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Oral Pathology > All Topics (with details-not just images,tx,etiologies, more!) > Flashcards

All Topics (with details-not just images,tx,etiologies, more!) Flashcards

Use this if you want to study more details like epidimology, location, clinical manifestations)

1
Q
A
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2
Q

What are the two types of Odontogenic Cysts?

A

Inflammatory
or
Developmental

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3
Q

List the type of Inflammatory cysts

(4)

A
  • Periapical (radicular)
  • Residual periapical
  • Buccal bifurcation
  • Paradental
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4
Q

List the types of Developmental Cysts?

(9)

A

‐ Dentigerous
‐ Eruption
‐ Gingival cyst of newborn
‐ Gingival cyst of adult
‐ Lateral periodontal
‐ Glandular odontogenic
‐ Odontogenic keratocyst
‐ Orthokeratinized odontogenic
‐ Calcifying Odontogenic

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5
Q

All of the following are histologically the same because they are all what?

-Periapical (radicular)
‐ Residual periapical
‐ Buccal bifurcation
‐ Paradental

‐ Dentigerous
‐ Eruption
‐ Gingival cyst of newborn
‐ Gingival cyst of adult

A

squamous epithelial lined cysts

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6
Q

What are the sources of epithelium
within the jaw bone ?

(6 sources)

A

▪ Epithelial rests of Malessez
▪ Reduced enamel epithelium
▪ Fissural cysts – when 2 pieces of bone come together
▪ Odontogenic cysts
▪ Epithelial component of odontogenic tumors
▪ Salivary gland inclusions – rare, incorporated in development

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7
Q

radicular cyst, inflammatory cyst are other names for

A

Periapical Cysts

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8
Q

▪ The most common cyst of the jaws

A

Periapical Cysts

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9
Q

Periapical Cysts

Demographic and location

A

▪ Any age (peak in 3rd ‐ 6th decades, rare in 1st decade)
▪ No sex predilection
▪ MX > MD (anterior MX most common)

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10
Q

Tooth vitality and Periapical Cysts

A
  • Involved tooth usually non‐vital/non‐responsive with thermal and electric pulp testing
  • Should test vitality of tooth if see radiolucency in apex\
  • If tooth vital, and still see radiolucency ► should do biopsy
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11
Q

Periapical Cyst

(Radiographic)

A
  • Usually appears as well‐circumscribed periapical radiolucency with widening of the PDL space and/or loss of lamina dura
  • Typically small (< 1 cm) but can grow to large dimensions if left untreated
  • Radiographic findings can NOT be used for definitive diagnosis
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12
Q

Why the Radiographic findings of Periapical Cyst can NOT be used for definitive diagnosis?

A

‐ similar appearance with:

  • periapical granuloma
  • odontogenic tumors
  • early COD {Cemento Osseous Dysplasia}
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13
Q

Lateral radicular cyst appears on the lateral surface of the root of a non‐vital/non‐responsive tooth
‐ A differential for which cyst?

A

lateral periodontal cyst

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14
Q

What is this radiographic finding?

A

Periapical Cysts

►Would need to test both teeth for vitality.

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15
Q

What is this radiographic finding?

A

Periapical Cyst

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16
Q

What is this radiographic & clinical findings?

A

Periapical cyst

shows inflammation at site
abscess developed fistula tract thru
soft tissue. Pt will have pain until
pressure is released

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17
Q

The wall of which cyst?

A

Periapical Cyst

Open clear areas = Cholesterol clefts where fat
used to be. Multinucleated cells (purple dots)
trying to break down cholesterol

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18
Q

What is this and what is it associated with?

A

keratin pearl – can be associated w/SCC

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19
Q

What are these radiographic findings?

A

Residual Cysts

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20
Q

What is the radiographic finding?

A

Residual Cyst

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21
Q

Periapical Cyst

treatment

A
  • endodontic therapy or extraction of involved teeth
  • larger lesions may require biopsy along with endodontic therapy
  • lesions which fail to resolve should be biopsied
  • follow-up at 1-2 years
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22
Q

Residual Cyst

Etiology

A
  • After tooth extracted, not properly cleaned ► the residual cells of the cyst lining and inflammatory cells continue to proliferate
  • Has to be at site where tooth was previously removed
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23
Q

Residual Cyst

Radigraphically

A
  • well defined round to oval radiolucency in the site of a previous extraction
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24
Q

Residual Cyst

Histologically is identical to which cyst?

A
  • identical to the radicular cyst (periapical cyst)
  • Should biopsy to rule out other causes
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25
Q

What is the radiographic finding?

A

Paradental Cyst

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26
Q

What is the radiographic finding?

A

Paradental Cyst

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27
Q

Residual Cyst

Treatment

A

-Removal

  • Enucleation if small
  • Marsupialization if large
  • Note:*
  • Enucleation* means: removal of an organ or other mass intact from its supporting tissues

Marsupialization means: surgical technique of cutting a slit into an abscess or cyst to empty its contents and suturing the edges of the slit to form a continuous surface from the exterior surface to the interior surface of the cyst or abscess.
Promotes Decompressing and shrinkage.

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28
Q

Paradental Cyst

Etiology

A

Some controversy over this designation
‐ some think they are inflammatory cyst
‐ some think they are developmental cysts
▪ Etiology: remains unclear

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29
Q

Paradental Cyst

Radiographically

A
  • Radiolucent area noted
  • most frequently, along the distal aspect of an impacted or partially erupted third molar
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30
Q

What is the radiographic finding?

A

Buccal Bifurcation Cyst

as seen in occlusal radiographs

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31
Q

What is the radiographic finding?

A

Buccal Bifurcation Cyst

as seen in occlusal radiographs

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32
Q

Which cyst has been associated w/ enamel extensions into furcation areas of the
involved teeth?

A

Paradental Cyst

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33
Q

Paradental Cyst

Treatment

A

Extraction of the tooth along with the lesion

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34
Q

Buccal Bifurcation Cyst

is similar to what Cyst ?

A

Similar to a paradental cyst

‐ EXCEPT: location is central on the buccal of mandibular first molars

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35
Q

Buccal Bifurcation Cyst

Etiology

A

unclear

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36
Q

Buccal Bifurcation Cyst is most commonly seen with eruption of what tooth?

A

The eruption of the permanent first molar

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37
Q

Buccal Bifurcation Cyst

Clinically

A

seen as

  • swelling
  • tenderness of soft tissue over involved area
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38
Q

dentigerous cyst or
follicle ?

A

_dentigerous cys_t
b/c *attachment at CEJ

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39
Q

What is the radiographic finding?

A

Dentigerous Cyst

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40
Q

What are these radiographic findings?

A

dentigerous cyst

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41
Q

What are these radiographic findings?

A

dentigerous cyst

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42
Q

What is the radiographic finding?

A

dentigerous cyst

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43
Q

What is this gross finding?

A

Grossly image of

Dentigerous Cyst

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44
Q

Dentigerous Cyst

Treatment

A
  • Decompression: Try to open window in the jawand put tube into cyst lumen and have pt irrigate a few times a day for a few weeks ► release pressure and allows bone to grow back ► cyst will shrink
  • If get rid of whole area surgically► c_an risk_ fracturing the jaw
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45
Q

Which

Radiograph type is best to see

Buccal Bifurcation Cyst?

A

▪ Radiolucency best seen with an occlusal radiograph

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46
Q

Buccal Bifurcation Cyst
Treatment

A

▪ Enucleation of cyst; tooth extraction unnecessary
▪ Some cases resolve w/o surgery
▪ Some resolve w/ daily irrigation of buccal pocket with saline/hydrogen peroxide

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47
Q

Dentigerous Cyst
also known as ?

A

Follicular Cyst

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48
Q

What is most common type of developmental odontogenic cysts?

20% of all epithelial lined cysts of the jaw

A

Dentigerous Cyst

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49
Q

What is the clinical finding?

A

Eruption Cyst

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50
Q

What is the clinical finding?

A

Eruption Cyst

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51
Q

Dentigerous Cyst

Origin & Etiology

A

Originates: by the separation of the follicle from the crown of an unerupted tooth

Pathogenesis: accumulation of fluid between the tooth and the reduced enamel epithelium

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52
Q

Dentigerous Cyst

Clinically

A

▪ Small cysts typically asymptomatic and picked up
on routine radiographic exam
▪ Large lesions may show expansion of bone
▪ Cysts may become infected, especially if partially erupted
tooth

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53
Q

Dentigerous Cyst

Demographics & Location

A
  • Mostly mandibular 3rd molars (rarely unerupted deciduous teeth)
  • Most commonly present in 2nd and 3rd decades
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54
Q

What is a key characteristic of Dentigerous Cyst location?

A
  • Attached to the tooth at the CEJ
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55
Q

Small Dentigerous Cyst
are hard to differentiate radiographically from —?

A

enlarged/hyperplastic follicle

Rule of thumb:

  • If 4‐5mm or more of radiolucency ► dentigerous cyst
  • If <4mm of radiolucency► can be hyperplastic follicle
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56
Q

What is the clinical finding?

A

Cysts of the Newborn:
Palatal cysts

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57
Q
A

Gingival cyst of the newborn/ Dental lamina cysts/Cysts of the Newborn-gingival

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58
Q

What is the Soft tissue counterpart of a dentigerous cyst?

A

Eruption Cyst

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59
Q

Eruption Cyst also known as

A

eruption hematoma

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60
Q

Eruption Cyst

Etiology

A
  • Results from accumulation of fluid in the follicular space when the tooth has erupted over the alveolar bone *NOT in bone*
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61
Q

What is the clinical finding?

A

Gingival Cyst of the
Adult

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62
Q

What is the clinical finding?

A

Gingival Cyst of the
Adult

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63
Q

What is the clinical finding?

A

Gingival Cyst of the
Adult

notice the bluish hue

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64
Q

Eruption Cyst

Demographic & Location

A

▪ Usually seen in 1st decade (children)

▪ Most often involves 1st permanent molar and maxillary incisors

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65
Q

Eruption Cyst

Clinically

A

Frequently normal mucosal color, BUT surface trauma (ex. chewing) may result in bleeding into the cystic space► may look purple or blue
▪ Usually soft or fluctuant(like a balloon) upon palpation

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66
Q

Eruption Cyst

Treatment

A
  • Unless symptomatic, no treatment required, cysts resolve upon eruption of teeth
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67
Q

Cysts of the Newborn

can either be — or —

A

Palatal cysts

or

Gingival cyst

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68
Q

Palatal cysts

Types

&

Location

A

‐ Bohn’s nodules: scattered over HP (hard palate), often junction of HP and SP (soft palate)

‐ Epstein’s pearls: along median palatal raphe

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69
Q

Which is here is

Lateral Periodontal Cyst

Lateral Radicular Cyst

Lateral Odontogenic Kertocyst

A
  • Could be differential for lateral Odontogenic keratocyst, except this does not grow in size
  • Lateral radicular cysts from an accessory canal if tooth is non vital
  • or it could be Lateral Periodontal Cyst if tooth is vital!
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70
Q

What is the radiographical finding?

A

Lateral Periodontal
Cyst

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71
Q

What is the radiographical finding?

A

Lateral Periodontal
Cyst

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72
Q

What is the histological finding?

A

Lateral Periodontal Cyst

see the alternating
thin to thick epithelium
a characteristic of these cysts

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73
Q

What is the histological finding?

A

Lateral Periodontal Cyst

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74
Q

Cysts of the Newborn:

Palatal cysts

Demographics

A
  • Seen in 60‐80% of neonates
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75
Q

Cysts of the Newborn:
Palatal cysts

Clinically

A
  • 1‐3 mm cream to white papules (keratin filled cysts)

*NOT in bone*

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76
Q

Cysts of the Newborn:
Palatal cysts

Treatment

A

No treatment is required
‐ Resolve (degenerate or rupture) on their own in a
few months
‐ Once baby eats solid foods, will go away

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77
Q

What is the radiographical finding?

A

Botryoid Odontogenic
Cyst

well circumscribed, between 2 teeth (similar to
lateral odontogenic cyst), multilocular

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78
Q

What is the radiographical finding?

A

Botryoid Odontogenic
Cyst

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79
Q

Cysts of the Newborn:
Gingival cyst of the Newborn

Also known as

A

Dental lamina cysts

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80
Q

Gingival cyst of the newborn

demographics & Location

A
  • Found superficially on the alveolar ridge mucosa
  • MX > MD
  • Rarely seen after 3 mos. of age
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81
Q

Gingival cyst of the newborn

Treatment

A

▪ No treatment is necessary

▪ Spontaneously resolve (degenerate or rupture)

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82
Q

Gingival cyst of the newborn

Clinically

A
  • 1‐3 mm creamy white papule (keratin filled cysts)
  • *NOT in bone*
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83
Q

What is the soft tissue counterpart of the lateral periodontal cyst ?

A

Gingival Cyst of the Adult

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84
Q

What is the radiographical finding?

A

“Primordial” Cyst

Assuming histologically it is different from OKC

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85
Q

Gingival Cyst of the Adult

Origin

A

Derived from dental lamina rests
‐ Rests of Serres

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86
Q

Gingival Cyst of the
Adult

Demogrophic & Location

A

▪Uncommon lesion
▪ 60‐75% mandibular canine/premolar area
‐ most common location on the facial or buccal aspect
▪ 5th and 6th decade most common

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87
Q

Gingival Cyst of the
Adult

Clinically

A
  • Painless, dome‐like swellings up to 5 mm in diamete
  • Often with a bluish or grayish hue
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88
Q

Gingival Cyst of the
Adult

has similar histology to which cyst?

A

lateral periodontal cyst

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89
Q

Gingival Cyst of the
Adult

Treatment

A
  • simple surgical excision
  • Unlikely to recur/come back
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90
Q

What are the site distribution of OKC?

A

Most of OKC in
posterior region

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91
Q

Lateral Periodontal Cyst represents the intrabony counterpart of which cyst?

A

gingival cyst of the adult?

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92
Q

Lateral Periodontal
Cyst

Origins

A
  • Developmental cyst believed to arise from dental lamina rests
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93
Q

Lateral Periodontal cyst is diagonsed when cysts occur in the lateral periodontal region and after what have been excluded?

A
  • an inflammatory origin cysts or the diagnosis of odontogenickeratocyst have been excluded
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94
Q

Lateral Periodontal Cyst

Charcterstics and tooth vitality

A

▪ Commonly asymptomatic and found on routine radiographic exam

▪ Associated teeth tests vital/responsive with electric pulp test

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95
Q

if you see a radilucency Lateral to a teeth

how would you know if it’s

Lateral Periodontal Cyst

or

Lateral Radicular Cyst

or

Lateral OKc

A

‐ If pulp alive► lateral periodontal cyst or Lateral Okc ( if huge lesion)

‐ If pulp dead► lateral radicular cyst

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96
Q

Lateral Periodontal Cyst

Demographic and Location

A

▪ Most likely found after age 30
▪ Males>Females
▪ ~65% mandibular canine/premolar area
‐ Can also be seen between canine and lateral incisor

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97
Q

What is the radiographical finding?

A

Odontogenic
Keratocyst
OKC

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98
Q

What is the radiographical finding?

A

Odontogenic
Keratocyst
OKC

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99
Q

What is the radiographical finding?

A

Odontogenic
Keratocyst
OKC

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100
Q

What is the radiographical finding?

A

Odontogenic
Keratocyst
OKC

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101
Q

What is the radiographical finding?

A

similar to
lateral
periodontal cyst
but is actually
OKC

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102
Q

What is the histological finding?

A

Odontogenic
Keratocyst

Histology

Notice the daughter cysts

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103
Q

Lateral Periodontal Cyst

Radiographically

A

Present as well circumscribed, unilocular radiolucencies between 2 teeth, located lateral to tooth root
▪ Most often 0.5‐1.0 cm in diameter
▪ Radiographic features are NOT diagnostic

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104
Q

What is this radiographic finding?

A

✎A patient who has Nevoid Basal Cell Carcinoma
Syndrome
✎We can see multiple cystics areas and lesions in
the jaws, maxillary and mandible
✎Both 3rd molar displaced in the maxilla because of
the cyst

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105
Q

What is this radiographic finding?

A

✎Multiple lesions, impacted 3rd molar in mandible
and displaced 3rd molar up into the sinus,
✎These too many lesions hard to manage the issue
with a surgery
✎This large area on the left mandible – good example of why we do
decompression because if you just remove this lesion
and the entire area is left open, this would be an area
risk for fracture

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106
Q

What is this called

which can be seen with

Nevoid Basal Cell Carcinoma
Syndrome

A

✎An example of the pitting that can be seen palmar
and plantar

~ This is a side of a hand
✎This is an early stage of basal carcinoma which
never goes on (like it is aborted)

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107
Q

What are these findings that is associated with

Nevoid Basal Cell Carcinoma
Syndrome?

A
  • thousands of basal cell carcinoma is developing on the skin

-very difficult to manage with surgery,
~ That’s why they remove
the larger ones, the deeper ones ~ They leave the one
that’s less as an issue until they get to a larger size to
be removed

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108
Q

Lateral Periodontal
Cyst

Treatment

A
  • consists of conservative enucleation
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109
Q

What cyst is a variant of lateral periodontal cyst?

A

Botryoid Odontogenic
Cyst

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110
Q

Botryoid Odontogenic
Cyst

Grossly and Microscopically

A

shows a grape‐like cluster of small
individual cysts

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111
Q

Botryoid Odontogenic
Cyst

Radiographically

A

▪ Either unilocular or multilocular on radiographs, depending on size of the lesion
▪ Cyst lining similar to lateral periodontal cyst

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112
Q

Glandular Odontogenic
Cyst

Charcterstics

A
  • A rare odontogenic cyst which exhibits features of glandular differentiation within the epithelium
  • Presumably represents the pluripotentiality of odontogenic epithelium
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113
Q

Glandular Odontogenic
Cyst

Demographics

A

▪ Wide age range from 2nd to 9th decades
‐ mean age 49
▪ ~ 80% of cases in mandible
▪ Anterior lesions
‐ More common
‐ May cross the midline

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114
Q

Glandular Odontogenic
Cyst

Radiographically

A

▪ Uni‐ or (more often) multilocular radiolucency

▪ Well‐defined with a sclerotic border

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115
Q

Glandular Odontogenic
Cyst

reccurance rate

A

(~ 25% recurrence rate)

Can be locally aggressive

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116
Q

Glandular Odontogenic
Cyst

Clinically

A

▪ Usually asymptomatic unless inflamed

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117
Q

What is this radiographic finding?

A 
**Calcifying
Odontogenic Cyst (COC)**
  • in the mandible and you can see it well circumscribed radiolucency
  • a little bit of blunt root resorption in this area
  • No calcifications in this one yet ►so this is still unilocular radiolucency
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118
Q

What are the clinical and radiographic findings here?

What is this lesion?

A
  • Clinical finding for this patient was Obliteration of the vestibule space, because the mandible is showing expansion
  • radiographically:we see radiolucency going as far as the first molar
  • This is a mixed radiolucent radiopaque lesion in developing calcifications.
  • This is an example of Calcifying Odontogenic Cyst (COC)
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119
Q

“Primordial” Cyst

why it is controversial!

A
  • Mixed up with OkC
  • Originally meant to describe cyst which develops in bone at a site where a tooth was meant to develop (usually a third molar)
  • If this lesion exists, it is truly rare and would have histology distinct from OKC
    • In the current literature, reference has been almost nonexistent
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120
Q

“Primordial” Cyst

is not a true ——-

A
  • lesion, was actually some other type of cyst
    • it is now thought that most of the reported Primordial cysts were actually OKCs
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121
Q

Odontogenic
Keratocyst

OKC

Also known as

A

keratocystic odontogenic tumor (KOT) -2005 WHO

but now it’s back to OKC

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122
Q

Odontogenic
Keratocyst (OKC)

Etiology

A
  • Growth and expansion of this lesion due not only to osmotic effects/pressure, but to unusual gene expressions
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123
Q

Which unusal gene expression causes growth and expansion of OKC ?

A
  • Expresses Ki‐67 (high rate of cell proliferation)
  • O_verexpression of Bcl‐2_ (antipoptotic protein)
  • Overexpression of MMP’s 2 and 9 (thought to allow growth into connective tissue)
  • Mutation of PTCH, a tumor suppressor gene
    • when PTCH is non‐functional → cell proliferation
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124
Q

Odontogenic
Keratocyst (OKC)

Demographic & Location

A
  • ~ 60% present in 2nd and 3rd decade, but can occur at any age
  • Mandible affected in 60‐80% of cases
    • tendency to occur in posterior mandible and ramus
  • 25‐40% of cases involve an unerupted tooth
  • ‐ 5% of patients have multiple cysts
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125
Q

Odontogenic
Keratocyst (OKC)

differes from

Meloblastoma

in its growth pattern

A

Odontogenic Keratocyst (OKC) :grows in anterior to posterior manner before causing cortical expansion

while

Meloblastoma: causes cortical expansion early

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126
Q

Which cyst make up ~10‐15% of all odontogenic cysts?

A

Odontogenic
Keratocyst (OKC)

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127
Q

5% of Odontogenic
Keratocyst (OKC) are associated with which syndrome?

A

nevoid basal cell carcinoma
syndrome(Gorlin syndrome)

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128
Q

Odontogenic
Keratocyst

Reccurance Rate

A
  • HIGH Recurrence Rate
  • Benign, but locally aggressive biologic behavior
  • Solitary OKCs have ~10% recurrence rate with appropriate treatment
  • _Multiple OKCs hav_e ~ 30% recurrence rate
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129
Q

Odontogenic
Keratocyst

(OKC)

Reccurance Rate Order

from highest to lowest reccurance rate

A

Syndrome OKC > Multiple OKC > Solitary OKC > Conventional odontogenic cysts

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130
Q

Odontogenic
Keratocyst

OKC

Radiographically

A
  • Usually a well‐circumscribed radiolucency with smooth, often corticated margins

▪ Cysts may be
‐ Unilocular (most common)
‐ Multilocular (larger lesions)

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131
Q

Odontogenic
Keratocyst

OKC

clinically

A

▪ Small cysts are typically asymptomatic and picked up on routine radiographic exam
▪ Larger cysts may or may not be asymptomatic
▪ *Cysts tend to grow in an antero‐posterior direction prior to lateral growth ►therefore cysts are usually quite large when they start to expand the cortical plate

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132
Q

Odontogenic
Keratocyst

OKC

Has similar Radiographic findings with ?

A
  • dentigerous cyst
  • ameloblastoma
  • and others
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133
Q

Odontogenic
Keratocyst
OKC

Treatment

A

▪ Marsupialization (decompression)
▪ Peripheral ostectomy
‐ Carnoy’s solution
▪ Resection
▪ Medications targeted to PTCH
▪ Long term follow‐up

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134
Q

Nevoid Basal Cell Carcinoma
Syndrome

is also known as —– ?

A

Basal Cell Nevus or Bifid Rib Syndrome

or

Gorlin syndrome

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135
Q

Which cyst is assoicated with

Nevoid Basal Cell Carcinoma
Syndrome

?

A

Odontogenic Keratocyst
“OKC”

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136
Q

Nevoid Basal Cell Carcinoma
Syndrome

(Gorlin syndrome)

_modes of inheritanc_e

A

Autosomal dominant inheritance

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137
Q

Which Gene mutation and pathway

associated with

Nevoid Basal Cell Carcinoma
Syndrome

(Gorlin syndrome)

A
  • Mutation of PTCH (tumor suppressor gene)
  • in the Sonic Hedge Hog pathway
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138
Q

Nevoid Basal Cell Carcinoma
Syndrome

Prognosis

A

■ Prognosis depends on progression of skin tumors

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139
Q

Nevoid Basal Cell Carcinoma
Syndrome

Treatment

A

✎Surgery (typically MOHS)
✎Sometimes curette them
✎ Radiation therapy (RT) is typically not the first line of therapy with small lesions RT
✎Cryotherapy which means they just use a little liquid nitrogen and freeze them
✎Photodynamic therapy with photosensitizer and topical medications
■ New medication: Vismodegib inhibits sonic hedgehog pathway by binding smoothened (SMO)

  • suppressive rather than curative cause it seems to work for short time and after ~7-8 months ..may also helps suppress growth of OKC
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140
Q

Why Basal Cell Carcinoma is very problematic ?

A

It’s not the lesion themselves causing metastasis
that’s the issue, it’s the lesion growing deeply and in affecting adjacent structures that really is the
issue with basal carcinoma

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141
Q

What is the Most common type of skin cancer?

A

Basal Cell Carcinoma
(BCC)

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142
Q

Basal Cell Carcinoma
(BCC)

Demographics

A
  • 2-3 million cases a year
  • About 3 out of 4 skin cancers are basal cell carcinomas
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143
Q

Basal Cell Carcinoma

Growth and location

(BCC)

A
  • Develop in the lowest layer of the epidermis, called the basal Layer
  • Develops on sun-exposed areas: cumulative DNA Damage
    - Slow-growing
    • If not treated, basal cell cancer can grow into nearby areas
    and invade the bone or other tissues beneath the skin
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144
Q

Basal Cell Carcinoma

Progrssion

(BCC)

A

within 5 years of being diagnosed with
BCC►35%-50% of people develop a new skin cancer

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145
Q

Calcifying Odontogenic Cyst

​COC

also known as

?

A
  • Calcifying Cystic Odontogenic Tumor
  • Gorlin Cyst ( don’t confuse it with Gorlin syndrome)
  • Ghost Cell Tumor

*

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146
Q

Calcifying Odontogenic Cyst
(COC)

can present in 3 types

A
  1. ■ Cystic Unilocular COC
    • COC with odontoma (~ 20%)
    • Extraosseous/peripheral – present in older patients
  2. ■ Solid COC (odontogenic ghost cell tumor)
    • Often demonstrate a more aggressive behavior
    • WHO once considered them all CCOT now back to COC
  3. ■ Odontogenic ghost cell carcinoma
    • very rare lesion
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147
Q

Collision Tumors is a term used to describe lesions involving Calcifying Odontogenic Cyst (COC), what does that mean?

A
  • where you see both features of ameloblastoma with COC or adenomatoid odontogenic tumor with COC
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148
Q

Calcifying Odontogenic Cyst
(COC)

may occur in association

with

which tumors or cysts?

A
  • Odontomas (a benign tumour linked to tooth development)
  • Ameloblastomas (rare, noncancerous (benign) tumor)
  • Adenomatoid odontogenic tumor (rare tumor of epithelial origin that is benign, painless, noninvasive, and slow-growing)
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149
Q

Calcifying Odontogenic Cyst
(COC)

Demographics & Location

A

■ Peak in second decade, most before age of 40
■ Frequently presents anterior to molars
■ ~ 20% extraosseous (peripheral), found in older age group (~ 50 years of age)

■ Female > Male

■ ~ 70% occur in MX
■ One third are associated with unerupted teeth, usually a canine

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150
Q

Calcifying Odontogenic Cyst

Radiographically

(COC)

A

■ Usually a well-circumscribed unilocular radiolucency, infrequent multilocular cases
■ One third to one half show radiopaque structures within the radiolucency
■ When you see calcifications within a lesion, you don’t use the term uni or multi locular anymore, but they are called mixed radiolucent/radiopaque lesions

■ May cause resorption or displacement of roots
■ One third are associated with unerupted Canine

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151
Q

The hallmark of Calcifying
Odontogenic Cyst COC Histology is

A

Ghost cells

They have that sort of polygonal shape or roundish shape with the pink that looks like the cytoplasm, but in
the location where the nucleus would have then, there’s an empty spot

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152
Q

Histologically speaking, Calcifying
Odontogenic Cyst COC, basically
looks similar to what epithelium?

A

ameloblastic epithelium

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153
Q

Calcifying Odontogenic Cyst COC

Treatment

A

■Enucleation with peripheral ostectomy ~ Very similar to odontogenic keratosis
■ Follow up is long term because s_ome of the solid tumors have a more aggressive behavior_

■ Peripheral lesions are treated with excision

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154
Q

When COC is associated with another tumor, ameloblastoma, how would you treat?

A

■ the treatment is based on the more aggressive tumor

~ So you would treat the ameloblastoma.

~You wouldn’t treat conservatively the COC though

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155
Q

Odontogenic ghost cell carcinoma

Prognosis

A

(5 year survival ~ 70%).

  • It is rare and shows cytologic atypia histologically
  • It has an unpredictable biologic behavior
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156
Q

Fissural Cysts

(6)

A

❑ Nasolabial cyst
❑ Globulomaxillary cyst (historic)
❑ Nasopalatine (incisive canal) cyst
❑ Incisive papilla cyst
❑ Median palatal cyst
❑ Median mandibular cyst (historic)

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157
Q

Nasolabial Cyst

also known as

A

aka Nasoalveolar cyst

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158
Q

where a number of the visual cysts would develop

A

(1) That’s the nasopalatine, which is sort of up in the labial nasal fold and it’s in the soft tissue.
(2) Sort of where the nasal alveolar cyst would occur.
(3) Where the globular maxillary cyst would occur between the canine and the lateral sometimes between the lateral and the first premolar
(4) The nasopalatine in the cyst of the nasopalatine papilla
(5) Is the median palatal

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159
Q

Nasolabial Cyst

Etiology

A

■ Thought to be caused by:

  • either epithelial remnants of the nasolacrimal duct
  • or cells left after fusion of the maxillary, medial and lateral nasal processes during development of the midface
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160
Q

Nasolabial Cyst

Location

A

Rare soft tissue cyst of the upper lip, lateral to the midline (right under the ala of the nose) *NOT in bone*

■ Clinically see a swelling which can cause elevation of the ala of the nose ■ Intraorally see a swelling in the maxillary vestibule lateral to the midline (usually sort of in the canine area or just a little bit distal to the canine area) ■ Pain is uncommon, unless cyst becomes infected

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161
Q

Nasolabial Cyst

Clinically & Intraoray

A

■Clinically we see a swelling which can cause elevation of the ala of the nose

■ Intraorally see a swelling in the maxillary vestibule lateral to the midline (usually sort of in the canine area or just a little bit distal to the canine area)

■ Pain is uncommon, unless cyst becomes infected

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162
Q

Nasolabial Cyst

Demographics

A

■ Peak in 4th and 5th decades

■ 3 to 4 times more common in females

■ ~ 10% of cases are bilateral

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163
Q

Nasolabial Cyst

Treatment

A
  • Surgical Excision via intraoral approach,
  • usually do not recur ~ very low risk of occurrence
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164
Q

What is this clinical finding?

A

Nasolabial Cyst

The lesion here just below the nose and you can tell that it’s sort of raising the edge of the nose slightly

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165
Q

What is this clinical finding?

A

Nasolabial Cyst

the lesion raising the edge of the nose slightly

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166
Q

_Nasolabial Cys_t has a a respiratory type epithelium and so it’s very similar to what you would see in ?

A

either in the sinus or in the nasopalatine ducts

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167
Q

Is this

Globulomaxillary Cyst

lateral granulomas

OKCs

COCs

A
  • we can see the displacement of the root
  • A teardrop or pear shaped radiolucency between the lateral and the canine
  • Well circumscribed maybe leaving a little sclerotic edge up here
  • ended up being in a odontogenic keratocyst (OKC)
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168
Q

Is this Globulomaxillary Cyst , lateral granuloma or OKC?

A

~ it is kind of a teardrop or pear shaped size

~Little less well differentiated in this particular instance but again unilocular radiolucency between the roots of two teeth

This one ended up being an OKC

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169
Q

“Globulomaxillary Cyst”

Origin controvesy

why the name in quotations?

A
  • it’s in quotations, because really there is no such thing as a globulomaxillary cyst
  • because it was thought that this was remnants after fusion of the globular portion of the nasal process with the maxillary process, and now we know that these two processes are always united from the start and that there is no fusion
  • When biopsied these cysts are odontogenic in origin
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170
Q

what does it mean for Globulomaxillary Cyst to be odontogenic in origin?

A

✎This is term used to describe a cyst in a particular anatomic location it is not a diagnosis

✎An odontogenic cyst (inflammatory cyst, lateral periodontal or even sometimes OKC) that forms in the area between the maxillary lateral incisor and the canine roots

~ It’s really associated with a_n anatomic location not with any particular cyst._

✎So it can be any of the odontogenic lesions such as lateral granulomas or cysts, OKCs, COCs, etc.

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171
Q

Globulomaxillary Cyst

Radiographically

A

✎Presents as a “inverted pear” shaped well-circumscribed radiolucency

✎Frequently causes displacement of the roots

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172
Q

What are two different ways nasopalatine duct cyst arise?

A
  • *A**. It can either be the cyst totally within bone
  • *B**. It can actually cause widening of the orifice and causing the soft tissue expansion in this way
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173
Q

Most common non-odontogenic cyst of the oral cavity

A

Nasopalatine Duct Cyst

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174
Q

Nasopalatine Duct Cyst

also known as

A

incisive canal cyst

nasopalatine canal cyst

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175
Q

Nasopalatine Duct Cyst

Origin

A
  • arise from epithelial remnants of the nasopalatine duct which, embryologically, connects the oral and the nasal cavities
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176
Q

What is this radiographic finding?

A

Nasopalatine Duct Cyst

✎This person is edentulous
✎ an inverted pear shape
✎The nasal spine is superimposed
on your radiolucency ► a heart shape

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177
Q

What is this radiographic finding?

A

Nasopalatine Duct Cyst

✎Between the roots of the two teeth, a well circumscribed
radiolucency, not showing any changes to the adjacent structures
✎could be an enlargement of the incisive canal due to variation in size ~ early lesions can be hard to diagnose
✎the treatment in such cases: a follow up with another radiograph in six months to see if there’s been any change in size
✎ No surgical intervention until you see the cyst expanding

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178
Q

What is this oral finding?

A

This is showing you the how the
papilla can be enlarged if it’s only
in soft tissue or if there’s a partial
soft tissue partial bone expansion

Nasopalatine Duct Cyst

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179
Q

Nasopalatine Duct Cyst

Demographic and Location

A
  • Peak presentation in the 4th to 6th decades, but can occur at any age ~ because it takes a little bit of time for the cyst to grow within the bone
  • commonly found on the anterior palate ~ typically in the nasal area of the papilla.
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180
Q

What is this radiographic finding?

A

Median Palatine Cyst

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181
Q

Nasopalatine Duct Cyst

Clinically

A

■ present with swelling o_f the anterior palate_ (in the nasal area of the papilla)

■ Most are asymptomatic, but they may have pain or drainage

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182
Q

Is this Median Mandibular Cyst

Or something else

A

Remember

Median Mandibular Cyst is a term used to describe a cyst in a anterior mandible not a definitive diagnosis

So, this turned out to be an early ameloblastoma. It wasn’t a cyst

The lesion radiolucency in the anterior mandible and again

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183
Q

Nasopalatine Duct Cyst

Radiographically

A

■ a well-circumscribed unilocular radiolucency on the midline of the anterior hard palate
between and apical to the central incisors
■ The radiolucency often have an oval or inverted pear shape with a sclerotic border
■ Superimposition with the nasal septum can create an appearance of the classic “heart” shape

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184
Q

Cysts of the incisive papilla

Incisive papilla cyst

A

Is a soft tissue cyst (no bone involvement) located in
the same area as the Nasopalatine Duct Cyst

on the midline of the anterior hard palate
between and apical to the central incisors

. They may be symptomatic or asymptomatic and usually are not seen radiographically.

some consider them to be uncommon variants of the nasopalatine duct cysts

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185
Q

Nasopalatine Duct Cyst

Treatment

A
  • surgical excision
  • recurrence is rare
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186
Q

What is this radiographic finding?

A

Surgical Ciliated
Cyst of the Maxilla

In this premolar shot (middle image) you can see a well-circumscribed lesion
✎Because the maxillary sinus is radiolucent, it almost looks like this is radiopaque but it’s not
✎ If you did a CBCT you would see that it’s an empty space within the bone of the maxilla. It’s not actually radiopaque

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187
Q

Median Palatine Cyst

is

a variant of which cyst?

A

nasopalatine duct cyst

  • it represents a more posteriorly placed nasopalatine duct cyst
  • ~ It’s probably due to some sort of anatomic variation in the patients; that their palatine duct is just placed more posteriorly
  • So instead of being between the roots of these two teeth, it’s placed more posteriorly
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188
Q

Median Mandibular Cyst

A
  • A controversial cysts whose existence is questioned ~ similar to the globulomaxillary cyst

■ Originally thought to arise from the fusion of the “halves” of the mandible, but current embryology finds that
the mandible forms from a single bilobed process, therefore, no epithelial remnants would be found
■ Now, it is thought that cysts in this area represent odontogenic cysts or tumors

  • Median Mandibular Cyst is a term used to describe a cyst in a particular anatomic location not a definitive diagnosis
    • ~ It is other lesions that occur in that particular location
    • The Anterior Mandible
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189
Q

Surgical Ciliated
Cyst of the Maxilla

Etiology

A

■ Occurs after trauma or sinus surgery (iatrogenic - reactive not neoplastic)

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190
Q

Surgical Ciliated
Cyst of the Maxilla

Formation

A

■a portion of the sinus lining is separated from the sinus and forms an epithelial lined cavity in bone
■ Cavity fills with mucin produced by the mucous cells of the cyst lining
■ These cysts enlarge as the intraluminal pressure increases, causing destruction of bone

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191
Q

Surgical Ciliated
Cyst of the Maxilla

occurs frequently

after

which procedures?

A
  • after a Caldwell-Luc procedure
  • sometimes with difficult maxillary extractions
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192
Q

In which country Surgical Ciliated
Cyst of the Maxilla

are reported with higher frequency ?

A

Japan

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193
Q

What are pesudocysts?

A
  • They have no epithelial lining.
  • They’re called cysts by convention just because that’s what everybody is used to
  • They’re not true cysts.
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194
Q

pesudocysts

List

(5)

A
  • Aneurysmal Bone Cyst
  • Antral Pseudocyst
  • Simple Bone Cyst
  • Osteoporotic Bone Marrow Defect
  • Stafne Bone Cyst
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195
Q

Aneurysmal Bone Cyst

Demographics

A

■ Most common site in the body is long bones or vertebrae
_■ In the jaw_s, most frequently seen in the 1st and 2nd decade
■ MD > MX

it’s a pesudocyst

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196
Q

Aneurysmal Bone Cyst

Clinically

A
  • swelling, frequently a rather rapid swelling
  • often with pain and/or paresthesia (signs which can be suggestive of the presence of a malignant or aggressive lesion)
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197
Q

Aneurysmal Bone Cyst

Etiology

A
  • Etiology is unclear, may result from trauma or a vascular malformation
  • most agree that it is a reactive and *not* a neoplastic lesion
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198
Q

Aneurysmal Bone Cyst

Radiographically

A

■ a radiolucency which can be either unilocular or multilocular in appearance

■ Borders are variable, often irregular in shape and may be ill-defined (again, giving the suggestion of malignancy)

■ Teeth may be displaced

■ we may see cortical expansion and thinning ~ the cortex itself can become quite thin

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199
Q

What does this person have?

A
  • you might think that he has an odontogenic infection but he didn’t. You can see that there’s
    a pretty significant swelling on the left side of his face

This is a Aneurysmal Bone Cysts

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200
Q

What is this radiographic finding?

A

Aneurysmal Bone Cyst

you can see that there is kind of a
multilocular radiolucency in this particular area

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201
Q

What is this radiographic finding?

A

Aneurysmal Bone Cyst

✎ There’s a radiolucency involving the second molar
that’s going as far anterior as the first molar and back
to the third molar
✎ There is a little bit of spiking root resorption and
that’s one of the signs that we associate with
malignancy
✎ It’s a little bit ill-defined ~ hard to say exactly
where it begins and ends

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202
Q

What is this gross finding?

A

Aneurysmal Bone Cyst

✎ It looks like a blood soaked sponge

✎ There’s these open sinusoidal spaces and then fibrous connective tissue surrounding them.

✎The sinusoidal spaces can vary in size; some of them are fairly small and others are large

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203
Q

Aneurysmal Bone Cyst

Treatment

A

■ Treatment is surgical enucleation and curettage

■ lesions can recur ~ Usually the recurrence is because
you didn’t get the entire thing out the first time around

■ Some surgeons follow enucleation with cryotherapy

■ Irradiation is contraindicated

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204
Q

Is bleeding a concern during surgical removal of Aneurysmal Bone Cyst?

A

■ No, vascularity is predominantly “low flow”, therefore not as much concern for bleeding upon surgical removal

■ As compared with central hemangioma where there is a concen for bleeding

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205
Q

Antral Pseudocyst

A

They are different than surgical ciliated cyst

in their lining, etiology, location and appearance!

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206
Q

What is this radiographic finding?

A

Antral Pseudocyst

  • a Dome-shape swelling on the floor of the sinus.
  • They can sometimes be fairly subtle

Antral Pseduocyst are NOT Mucoceles

Mucoceles would have more of meniscus-like
appearancewhere it would come up tothe edge of
the sinus

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207
Q

As opposed of surgical ciliated cysts, Antral psuedocysts are not —-

( in term of their lining)

A

Not epithelial lined spaces

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208
Q

What are these radiographic findings?

A

Aneurysmal Bone Cyst

✎ A dome shape swelling on the floor of the sinus that’s associated with some _sort of inflammation of tooth of t_he premolar caused inflammation underneath the apex of the bone (right) and then that leads to accumulation of fluid which causes the sinus lining to elevate off the bone and fill with fluid
✎ After root canal therapy and once the infection gets under control, these will typically resolve on their own

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209
Q

As opposed of surgical ciliated cysts, Antral psuedocysts are not —-

( in term of location)

A

Not within the bone but are in the sinus

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210
Q

As opposed of surgical ciliated cysts, Antral psuedocysts Develop as —-

( in term of etiology)

A

develop as an accumulation of an inflammatory exudate (often serum) between the sinus epithelial lining and the bone

-It develops because of an inflammatory event in the jaw, usually the maxilla, often from the roots of the maxillary teeth that cause inflammation

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211
Q

As opposed of surgical ciliated cysts, Antral psuedocysts appear as —-

( in term of Radiology)

A

Appears as a dome shaped elevation of the floor of the sinus

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212
Q

Simple Bone Cyst

also known as

A

aka traumatic bone cyst

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213
Q

What is this radiographic finding?

A

Simple Bone Cyst

✎A well-circumscribed with cortication in the body of the
mandible, affecting the posterior aspect (premolars and the molars )

✎Note the scalloping that happens up between the roots. It
doesn’t cause root resorption and actually the lesion will grow up between the roots of the teeth

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214
Q

What is this radiographic finding?

A

Simple Bone Cyst

  • A well-circumscribedshowing the scalloping up between the roots of the teeth radiolucency
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215
Q

What is this radiographic finding?

A

Simple Bone Cyst

✎Big lesion example: It’s going back to the molar area here.

✎You can see that the lesion extends over to the canine on the other side

✎Most lesions are usually in the anterior mandible

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216
Q

Simple Bone Cyst

Charcterstics

A
  • A benign, empty or fluid filled, cavity in bone which is devoid of an epithelial lining – a pseudocyst
  • Thought to be reactive, NOT neoplastic
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217
Q

Simple Bone Cyst

Etiology

A

Etiology ununcertain, theories include:

  • trauma
  • ischemic necrosis of medullary space
  • cystic degeneration of a primary bone lesion
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218
Q

Simple Bone Cyst

Demographics

A
  • In jaws, most likely in the 2nd decade
  • Almost exclusively the mandible
  • Twice as common in males
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219
Q

Simple Bone Cyst

Radiographically

A
  • a well-circumscribed radiolucency with an irregular outline
  • Tendency to “scallop” around and between roots (highly suggestive, but not diagnostic of this lesion)
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220
Q

Simple Bone Cyst

Treatment

A
  • exploration and curettage of space to create bleeding. Clot will organize and allow bone repair
  • Recurrence is rare
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221
Q

What is this radiographic finding?

A
  • You can see there’s a little bit of radiolucency.
  • There happened to actually still be teeth in the area, but
  • when it was biopsied it showed that it was a
  • hematopoietic or osteopoietic bone marrow defect
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222
Q

Stafne Bone Cyst

Charcterstics

A

■ An asymptomatic focal concavity of the cortical bone on the lingual aspect of the MD

■ A pseudocyst, not a true cyst

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223
Q

Osteoporotic Bone Marrow Defect

Demographic

A

■ Uncommon finding

■ > 75% of cases are in females

■ ~ 70% occur in the posterior MD, often in an edentulous area

it’s a pesydocyst

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224
Q

Osteoporotic Bone Marrow Defect

Etiology

A
  • Etiology unclear
  • may be hyperplasia of marrow due to need for RBCs or
  • abnormal regeneration of bone after an extraction or persistence of fetal marrow
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225
Q

Osteoporotic Bone Marrow Defect

Charcteristics

A
  • it’s a pesydocyst
  • a radiolucency in an area typically
    where tooth has been removed. Instead of filling in with bone, it fills in with marrow.
  • When we biopsy it, you’re seeing the hematopoietic elements. (fat, early stages of (the -blasts of) red cells,
    white cells.
  • We see basic bone forming marrow content
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226
Q

What is this radiographic finding?

A

Stafne Bone Cyst

This is the classic look.

  • a well-circumscribed corticated radiolucency
  • below the inferior alveolar nerve, away from the teeth.
  • They can be either oval, like this, or round in appearance
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227
Q

What is this radiographic finding?

A

Stafne Bone Cyst

Less common location

Check if the teeth were vital with vitality test

Get a CBCT in that area
to see what was going on first and then once you saw
the CBCT you’d be able to make the diagnosis.

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228
Q

Osteoporotic Bone Marrow Defect

A

Hematopoietic bone marrow defect

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229
Q

Osteoporotic Bone Marrow Defect

Clincalally

A

■ Typically asymptomatic and found on routine radiographic exam

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230
Q

Osteoporotic Bone Marrow Defect

Radiographically

A
  • Irregularly shaped radiolucency with either a well-defined or ill-defined border (It can be in the differential diagnosis with malignancy)
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231
Q

Osteoporotic Bone Marrow Defect

Treatment

A

■ Must biopsy to make a definitive diagnosis
■ No further treatment is then necessary

~ You don’t have to remove it; you can just leave it as it is

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232
Q

Stafne Bone Cyst

also known as

A

static bone cyst, Stafne defect

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233
Q

Stafne Bone Cyst

Demographics and Location

A
  • Most commonly found near the angle of the mandible below the inferior alveolar nerve (but also seen in the anterior MD)
  • > 80% in Males
  • usually noted only in adults
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234
Q

Stafne Bone Cyst

Radiographically

A

Oval round well-circumcribed radilucency

Below the Inferior Alveolar Nerve

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235
Q

Stafne Bone Cyst

Etiology

A
  • Believed to be developmental in origin, but usually noted only in _adults_
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236
Q

Stafne Bone Cyst

Treatment

A
  • lesions in the posterior MD are usually pathognomonic
  • no further treatment is necessary
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237
Q

Dermoid Cyst

Charcterstics

A
  • Benign developmental cystic lesion
  • Considered a form of teratoma

Remember: Teratomas have
all four embryologic layers and so you can see these cysts that have teeth, bone, hair, muscle, and nerves.

Dermoid cyst is sort of a lesser version of a teratoma in that it just has dermis, rather than all the other layers

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238
Q

Dermoid Cyst

Clinically

A
  • Depending on whether the cyst is above or below the mylohyoid muscle►the lesion will cause swelling into the oral cavity elevating the tongue or under the chin in the submandibular area, respectively
  • Usually found on the midline
  • Painless and slow growing, if not infected
  • Upon palpation, cyst feels doughy or rubbery
  • Usually roundish to oval-ish swelling
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239
Q

Dermoid Cyst

demographic and locations

A
  • Most common in the 1st and 2nd decade ( young pts)
  • Can be found anywhere, but in the oral cavity they are ususally located in the anterior floor of the mouth (FOM) - usually on the midline
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240
Q

Dermoid Cyst

Treatment

A
  • surgical excision
  • recurrence is rare
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241
Q
A

Dermoid Cyst

a dome shaped
swellingin the floor of the
mouth.

If these were left long
enough, they could cause issues
with swallowing

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242
Q

What is this clinical finding?

A

Dermoid Cyst

✎This is a larger lesion on the floor of the mouth, causing
elevation of the tongue
✎If you let this go/grow, it would be similar to Ludwig’s angina where you would basically eventually obstruct the airway
✎The difference is this is very slow growing while Ludwig’s happens rather quickly. with fever and other symptoms.

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243
Q

What is this clinical finding?

A

Dermoid Cyst

  • This is showing you when they occur below the mylohyoid muscle.
  • You get an elevation under the chin.
  • This is a fairly small one but they can get much larger
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244
Q

Epidermoid Cyst

also known as

A

infundibular cyst

epidermal inclusion cyst

“sebaceous” cyst (laymen’s term, not really sebaceous) ~

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245
Q

Epidermoid Cyst

Charcterstics

A
  • A very common skin cyst
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246
Q

The epidermoid cyst is similar to which cyst?

A

similar to the dermoid cyst, except we don’t see those adnexal structures

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247
Q

Epidermoid Cyst

Etiology

A
  • Often occur after _inflammation of a hair follicl_e
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248
Q

Epidermoid Cyst

Demographics and Location

A

■ Males > Females

■ Young adults more likely to have cysts of the face

■ Older adults have cysts of the back

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249
Q

Epidermoid Cyst

Associated with which

syndrome?

A

Associated with Gardner’s syndrome

Gardner syndrome is associated with polyps
in the intestine.

Gardner syndrome is associated with epidermoid cysts.

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250
Q

What is this clinical finding?

A

Epidermoid Cyst

A dome-shaped swelling.

There’s no change in the
overlying skin color, no redness, no pain

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251
Q

Epidermoid Cyst

Clinically

A

■ Subcutaneous nodular, firm to fluctuant, papule

~ It tends to be a subcutaneous, dome-shaped nodule that
can be either firm to fluctuant, depending on how much stuff is within the lumen

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252
Q

What is the key difference between a dermoid and epidermoid cyst?

A
  • The key difference between a dermoid and
  • epidermoid cyst, is that there’s no adnexal structures in an epidermoid cyst. There are adnexal structures in a dermoid cyst.
  • The adnexal structures are: sebaceous glands, sweat glands, hair follicles, etc.
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253
Q

Epidermoid Cyst

Treatment

A

■ Treatment is excision

■ Recurrence is rare

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254
Q

What is this clinical finding?

A

Thyroglossal Duct Cyst

This is NOT a goiter.

It looks like an enlargement of the thyroid, but this ended up being just
a cyst, so they had a thyroglossal duct cyst

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255
Q

Thyroglossal Duct Cyst

Etiology/Origin

A
  • A developmental cyst that develops from epithelial remnants of a tract which forms when the thyroid anlage descends into the neck from an area that later forms the foramen caecum
  • Follows a path that goes anterior to the hyoid bone and ends below the thyroid cartilage
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256
Q

Thyroglossal Duct Cyst

Clinically

A

■ Cysts are typically painless fluctuant swellings, unless infected
■ If the cyst remains attached to the hyoid bone or the tongue ► i_t will move up and down when swallowing or protruding the tongue_
■ ~ 1/3 will present with a fistulous tract ~ so they’ll be draining.

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257
Q

Thyroglossal Duct Cyst

Treatment

A

■ surgical excision

■ recurrence are not uncommon

■ Rare cases of thyroid carcinoma developing in these cysts have been reported

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258
Q

Thyroglossal Duct Cyst

Demographics and locations

A

■ 60-80% of cysts are below the hyoid bone

■ Most commonly present in the first 2 decades (~ 50% prior to 20 years of age)

■ Cyst classically forms at the midline

■ The most common developmental cyst of the neck

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259
Q

What is the most common

developmental cyst of the neck?

A

Thyroglossal Duct Cyst

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260
Q

Branchial Cleft Cyst

Also known as

A

cervical lymphoepithelial cysts

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261
Q

What is this clinical finding?

A

Branchial Cleft Cyst

a small one in a child.

You can see that
there’s a small cystic lesion here on the neck

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262
Q

What is this clinical finding?

A

Branchial Cleft Cyst

Then you can see it in an older person; this is getting
to be maybe 4-5 centimeters at least in size. He left
his for a little bit longer

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263
Q

Branchial Cleft Cyst

Demographic and location

A

■ Most commonly presents in the 3rd to 5th decades

■Located on the lateral aspect of the neck, usually anterior to the sternocleidomastoid muscle

■2/3 of the reported lesions have been on the left side

■Although cyst are uncommon in the parotid gland, can see multiple lymphoepithelial cysts bilaterally in HIV positive patients

■These cases present as painless uni- or bilateral swellings of the parotid glands

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264
Q

Branchial Cleft Cyst

Clinically

A
  • presents as a soft fluctuant swelling ranging from 1 to 10 cm in diameter
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265
Q

Branchial Cleft Cyst

Etiology

A

Etiology is disputed

  • Some think it is from remnants of the branchial cleft
  • Others think it is cystic change of parotid gland epithelium which became entrapped in a cervical lymph node during development
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266
Q

What is this clinical finding?

A

Oral Lymphoepithelial Cyst

A pale dome-shape swelling in the floor of the mouth. ​because the lesion is so close to the surface; you’re seeing little capillaries of the mucosa lining the lesion

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267
Q

Branchial Cleft Cyst

&

HPV patients

A

We can see multiple Branchial Ceft cysts bilaterally on the parotid gland

Painless swelling bilaterally or unilaterally on the parotid gland

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268
Q

Branchial Cleft Cyst

Treatment

A

surgical excision, recurrence is rare

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269
Q

Oral Lymphoepithelial Cyst

Demographics and Location

A

■ Uncommon lesion

■ The Most frequent location is the floor of the mouth (FOM) (> 50%)

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270
Q

Oral Lymphoepithelial Cyst

Clinically

A

■ Usually less than 1 cm in diameter
■ May feel firm or soft on palpation
■ Typically creamy to yellow in color
■ Painless unless infected

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271
Q

Oral Lymphoepithelial Cyst

Treatment

A
  • Surgical Excision
  • Reccurance is Rare
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272
Q

What is the relationship between lesion’s agrressivness, rate of reccurance and follow up duration ?

A

the more aggressive the biologic behavior, the higher risk of
recurrence, and the longer the follow up needed for the patient

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273
Q

What is the spectrum of benign and malignant lesions

A
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274
Q

Which lesions are considered benigns

A

Things that have a very low rate of recurrence when you do a conservative excision or a nucleation ►they’re going to be very benign and they’re not going to be likely to be recurrent:
▪ Odontoma and radicular cysts are way down here near the benign side
▪ AOT (Adenomatoid Odontogenic Tumor) is benign.
▪ COCs (Calcifying odontogenic cyst) are benign.
▪ OKCs (Odontogenic keratocyst) ‐ they’re benign.
▪ Even Ameloblastomas are benign

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275
Q

which lesions are on the malignant side?

A

But eventually you get over to the side over here where you can have something like an Ameloblastic carcinoma ‐ truly malignant –> We know that it can metastasize and it can lead to death
▪ Lesions like Ameloblastomas and CEOTs will need to be managed more aggressively. (Not just curettage, aka surgical scraping or cleaning)
o You have a resection ‐ either a portion of the mandible is
removed or a segment of the mandible is removed.

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276
Q

What are the 3 Classification of
benign tumors?

A
  1. Epithelial
  2. Mesenchymal
  3. Mixed
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277
Q

What are the list of Epithelial Benign Tumors?

(5)

A

▪ Ameloblastoma
▪ Adenomatoid odontogenic tumor
▪ Calcifying epithelial odontogenic tumor
▪ Squamous odontogenic tumor
▪ Odontogenic keratocyst (aka Keratocystic odontogenic tumor)

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278
Q

What are the list of Mesenchymal Benign Tumors?

(5)

A

▪ Odontogenic myxoma
▪ Central Odontogenic fibroma
▪ Cementifying fibroma
▪ Cementoblastoma
▪ Granular cell odontogenic tumor

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279
Q

What are the list of Mixed Benign tumors?

5

A

▪ Odontoma (complex and compound)
▪ Ameloblastic fibroma/odontoma
▪ Primordial odontogenic tumor
▪ Dentinogenic ghost cell tumor
▪ Calcifying cystic odontogenic tumor(aka COC, ghost cell tumor)

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280
Q

Ameloblastoma

Charcterstics

A
  • An epithelial odontogenic neoplasm (Tumor of Epithelial Origin)
  • with a close histologic resemblance to the enamel organ
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281
Q

Ameloblastoma

Origin

A

Potential sources of epithelium include:

o Enamel organ – look like they’re about to deposit a
substance but never do

o Odontogenic rests (Malassez, Serres)

o Reduced enamel epithelium

o Epithelial lining of odontogenic cysts ‐ can actually have an ameloblastoma arise within a dentigerous cyst

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282
Q

Ameloblastoma

Radiographically

A

-Osteolytic tumor (radiolucent – no hard tissue formed)

  • Well-circumscribed uni- or multilocular radiolucency
  • Often with sclerotic or corticated borders
  • May see blunt root resorption and displacement of teeth
  • Frequently seen in association with unerupted teeth
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283
Q

Ameloblastoma

Clinically

A
  • Rather slow growing tumor
  • Larger lesions present as painless expansion or swelling of bone
  • Smaller ones are asymptomatic, can be seen on routine imaging
  • Buccal and lingual cortical expansion is common
  • May perforate cortical plate and invade surrounding soft tissue
  • Can arise in a dentigerous cyst (see transition from stratified
  • squamous to ameloblastic epithelium)
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284
Q

Ameloblastoma

Types

A

Conventional/multicystic/solid/ (~ 80%)

  • Unicystic (~6-15%) need entire specimen (excision) to know
  • Desmoplastic
  • Peripheral
  • Malignant
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285
Q

Ameloblastoma

Demographics

A

▪ 11‐18% of non‐cystic lesions of the maxillofacial bones
▪ 4th and 5th decade most common, but occurs over a broad age range (rare in first decade)
o Usually starts 2nd decade, can go up to 80‐90s. Late 30s/early 40s are usually the peak
▪ > 80% occur in the mandible (most in molar/ramus area)

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286
Q

What is

the second most common

odontogenic neoplasm?

A

Ameloblastoma

(after odontoma)
o although odontomas are more like hamartomas

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287
Q

Which tumor can arise in a dentigerous cyst?

A

Ameloblastoma

(we see transition from stratified squamous to ameloblastic epithelium)

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288
Q

ameloblastoma

location

A

▪ Almost 80% or a little over 80% (of ameloblasts) are down in the mandible.
▪ And the vast majority are in the posterior mandible
▪ Do occur in maxilla but at lower rate

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289
Q

What is this radiographic finding?

A

Unilocular and unicystic ‐ An example of a unilocular ameloblastoma that is
not associated with an impacted tooth
▪ Is between roots of two teeth, may be confused with lateral
periodontal cyst. Well‐circumscribed radiolucency

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290
Q

What is this radiographic finding?

A

▪ Typical appearance for ameloblastoma

Multilocular, very well‐circumscribed, associated with impacted tooth.

Can see bowing of inferior aspect of mandible

lateral oblique radiograph.was used here

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291
Q

What is this radiographic & clinical finding?

A

Ameloblastoma

clinically: Have expansion of the buccal plate, obliterating the vestibule in this area.

Radiographically: Root resorption of molar, unilocular radiolucency in mandible

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292
Q

What is this radiographic finding?

A

Ameloblastoma

  • Small lesion distal to impacted tooth.
  • Unilocular radiolucency with elevation of alveolar ridge + some expansion of soft tissue
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293
Q

What is this radiographic finding?

A

Ameloblastoma

▪ Well‐circumscribed radiolucency with a sclerotic or
corticated margin.

▪ If you had a CBCT, it would probably show you that there
was a thin septa in this area of residual bone trabeculae.

▪ Fracture could be caused by very large cysts.

▪ Resolve by decompressing unless with odontogenic tumor – need to remove the mandible 1cm+ on either side of lesion

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294
Q

Ameloblastoma

Etiology

A

▪ Over expression of Bcl‐2 (anti‐apoptotic protein)
▪ Expression of fibroblast growth factor (FGF)
▪ Over expression of matrix metalloproteinases (MMPs 9 and 20) – like in OKC, allowing tumor to grow into surrounding area
▪ Surprisingly, no significant increase in Ki‐67 expression (cell
proliferation marker) – ameloblastomas do NOT turn over rapidly

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295
Q

Case

16yo female

Describe the lesion and what is the diagnosis?

A

▪Left mandible, multilocular radiolucency associated with impacted tooth
▪ It’s well circumscribed, edge may be a little bit sclerotic or corticated
▪ It has displaced an impacted tooth down towards the inferior
aspect of the mandible
▪ Appears to be expanding the cortex of the mandible in areas
▪ There’s blunt resorption of the teeth adjacent (PMs and molar)

Ameloblastoma

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296
Q

Case

▪ Well‐circumscribed radiolucency, no impacted tooth
▪ But notice that it’s coming up to posterior aspect of first molar
▪ Surgery done to remove lesion, left inferior aspect of mandible

Follow‐up image: conservative surgery but still removed bone up to mesial aspect. Less conservative would be removing entire mandible
▪ Concern with that is paresthesia (from removing the nerve as well)

A

Conventional/Solid Ameloblastoma

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297
Q

Unicystic
ameloblastoma

types

Subgroup of
ameloblastomas

A

▪ Unicystic (Simple or luminal)

  • lumina- confined to the surface lining of the cystic space

▪ Plexiform (intraluminal)

  • intralumina-one or more areas of the ameloblastic epithelial lining, proliferate into the lumen of the cystic space

▪ Mural – hard to distinguish from conventional,
so pathologists think they should NOT be treated the same as unicystic (which would be a more conservative treatment)
▪ Ameloblastoma arising in a cyst ‐ can usually be treated in a similar way as unicystic ameloblastoma.

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298
Q

What is this radiographic finding?

A

Unicystic Ameloblastoma

but could be

Dentigerous Cyst

based on clinical presentation!

So radiograph is not diagonstic

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299
Q

What is this radiographic finding?

A

Desmoplastic
Ameloblastoma

  • Spherical growth. Within it, has both radiodense and radiolucent areas (is
  • mixed radiolucent‐radiopaque)– similar appearance to benign fibro‐osseous lesions.
  • Well‐circumscribed, corticated.
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300
Q

Conventional/Solid Ameloblastoma

Treatment

A
  • Resection (treatment depends on extent of the lesion and anatomy of involved bone)
  • Segmental
  • Composite
  • Long term (decades) follow up is needed for these patients
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301
Q
A

Peripheral
Ameloblastoma

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302
Q

Unicystic Ameloblastoma

Demographcics and Locations

A

▪ Younger initial presentation (~ 50% in 2nd decade)
▪ 90% in MD (mandibular)
▪ Typically asymptomatic and found on routine radiographic exam

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303
Q

Unicystic Ameloblastoma

Radiographically

A
  • Commonly a well‐circumscribed radiolucency that surrounds the crown of an unerupted tooth
  • Commonly accompanied by root resoprtion
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304
Q

Unicystic Ameloblastoma

radiographically can be confused with which cyst?

A
  • Radiographically can be confused with dentigerous cyst
    • Presence of root resorption should increase your suspicion of ameloblastoma
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305
Q

Unicystic Ameloblastoma

Treatment

A
  • Treatment is typically enucleation and curettage
    • Reports of lower rate of recurrence (10‐20%) than conventional ameloblastoma (50‐90%) with similar treatment
    • Some recommend decompression prior to surgery
  • Use of Carnoy’s solution after enucleation- resulted in a recurrence rate lower
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306
Q

Desmoplastic
Ameloblastoma

Location

A
  • Anterior jaws (particularly maxilla)
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307
Q

case

A

Calcifying Epithelial Odontogenic Tumor

(CEOT)

Clinically: we see a little expansion on inferior aspect of mandible + lingual too

Radiographically: we see well‐circumscribed, a little corticated/sclerotic edge, impacted tooth
▪ we can see bowing of inferior aspect of mandible
▪ Within areas of radiolucency, see areas of opacity (calcified lesions = classic CEOT)
▪ When smaller► could have looked *unilocular*

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308
Q

Desmoplastic
Ameloblastoma

Radiographically

A
  • looks “fibro‐osseous” due to mixed radiolucentradiopaque appearance
    • Mineralization of dense collagen
  • Well‐circumscribed, corticated.
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309
Q

What is this radiographic finding?

A

Calcifying Epithelial Odontogenic Tumor(CEOT)

  • flecks of calcifications.
  • Calcifications all around crown is common
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310
Q

What is this radiographic finding?

A

Calcifying Epithelial Odontogenic Tumor(CEOT)

  • Multilocular radiolucency with calcifications.
  • an expansion up to PMs and back to 2nd molar
  • as well as bowing of mandible.
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311
Q

What is this radiographic finding?

A

Calcifying Epithelial Odontogenic Tumor(CEOT)

  • Fewer calcifications here, well‐circumscribed and corticated, impacted tooth.
  • periosteal reaction causing elevation at the bottom of image!
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312
Q
A

Calcifying Epithelial Odontogenic Tumor(CEOT)

  • well‐circumscribed radiolucency with calcifications in lower anteriors
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313
Q

Peripheral
Ameloblastoma

Origin and Charcterstics

A
  • Thought to arise from epithelial rests or basal cells in the gingiva
  • Uncommon
  • Does not invade underlying bone
  • Histology is the same as conventional type
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314
Q

Peripheral
Ameloblastoma

location

A
  • Found on gingiva or alveolar mucosa (*that’s why it’s named peripheral or extraosseous)
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315
Q

What are the two types of “Malignant”
Ameloblastomas ?

A
  1. Malignant ameloblastoma
  2. Ameloblastic carcinoma
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316
Q

Adenomatoid odontogenic tumor

(AOT)

Origin

A
  • thought to arise from remnants of the dental lamina in the gubernacular cord /canal
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317
Q

What is Ameloblastic carcinoma?

A
  • a primary lesion has atypical poorly‐differentiated
  • neoplastic(malignant) histology
  • may metastasize
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318
Q

What is the DD?

A

well‐circumscribed radiolucency at crown of an impacted canine
Hard to tell if attaches at CEJ.

If further down, less likely a dentigerous cyst and more likely AOT, ameloblastoma, or OKC

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319
Q

What is this radiographic finding?

A

we see calcifications forming, with both radiolucent and radiolucent areas.
▪ Dentingerous cyst, ameloblastoma, and OKC are NO LONGER in the differential diagnosis.

This is clearly AOT

_(_Adenomatoid odontogenic tumor)

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320
Q

What is this clinical finding?

A

Adenomatoid odontogenic tumor

(AOT)

Swelling in maxillary vestibule

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321
Q

What is this clinical finding?

A

Adenomatoid odontogenic tumor

(AOT)

fibrous capsule of AOT is at least partially encapsulated.

Easy to remove; “popped right out”.

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322
Q

What is this clinical finding?

A

Adenomatoid odontogenic tumor

(AOT)

An expansion into lingual area as well as into vestibule

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323
Q

What is this radiographic finding?

A

Adenomatoid odontogenic tumor

(AOT)

Snowflake‐like calcifications within mixed, well‐circumscribed radiolucency

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324
Q

What is this radiographic finding?

A

Adenomatoid odontogenic tumor

(AOT)

  • Teardrop shape / inverted pear between roots of teeth.
  • Well-circumscribed, corticated margin & snowflake‐like calcifications within
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325
Q

What is a malignant ameloblastoma?

A

▪ Malignant ameloblastoma
o Primary lesion and metastasis have normal welldifferentiated
ameloblastic (benign) histology
o Most commonly to lung

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326
Q

CALCIFYING EPITHELIAL ODONTOGENIC TUMOR

CEOT

also known as ?

A

Pindborg Tumor

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327
Q

Calcifying Epithelial Odontogenic Tumor

(CEOT)

A

▪ Uncommon (~1% of odontogenic tumors)
▪ Does not have inductive effect

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328
Q

Calcifying Epithelial Odontogenic Tumor

(CEOT)

Demographics and Location

A

o 2nd to 10th decades, peak ~ 4th decade
o MD (mandibular) 2 : 1 MX (maxillary)
o Usually posterior mandible

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329
Q

Calcifying Epithelial Odontogenic Tumor

(CEOT)

Clinically

A
  • Presents as painless slowly expanding swellings
  • sessile swellings of the gingiva or alveolus ( 2 times more on mandible than maxilla
  • Peripheral lesion may be seen, but are rare
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330
Q

Calcifying Epithelial Odontogenic Tumor

(CEOT)

Radiographically

A
  • May be unilocular, but most commonly as a multilocular lesion
  • May be entirely radiolucent or a mixed radiolucent-radiopaque lesion
  • Often associated with an unerupted tooth
    • MD third molar most common
  • Calcifications in the lesion, if present, are typically prominent around the crown of the impacted tooth.
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331
Q

What is this radiographic finding?

A

In addition to fracture, there is semilunar loss of bone around the molars ► (SOT)

Squamous Odontogenic Tumor

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332
Q

What is this radiographic finding?

A

SOT

Squamous Odontogenic Tumor

  • Semilunar loss of bone.
  • Alveolar bone is gone due to impacted canine that is visible
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333
Q

Calcifying Epithelial Odontogenic Tumor

(CEOT) have clinical presentation similar to what lesion?

A
  • CEOT clinically is similar to ameloblastoma
  • Also, CEOT has potential to be locally invasive, if in the right anatomic location, but has a less aggressive biologic behavior compared to ameloblastoma
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334
Q

Calcifying Epithelial Odontogenic Tumor

(CEOT)

Treatment

A

▪ Enucleation _with peripheral ostectom_y
▪ Resection with rim of normal bone
▪ Recurrence rate is ~12%
▪ ~ 2% demonstrate malignant transformation

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335
Q

What is this radiographic finding?

A

Central odontogenic fibroma (COF)

  • well‐circumscribed radiolucency posterior to molar
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336
Q

What is this radiographic finding?

A

Central odontogenic fibroma (COF)

round mass of opacity due to FCT. Ground glass‐like appearance

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337
Q

Adenomatoid odontogenic tumor

(AOT)

Demographics and Location

A

▪ 2/3 anterior jaws
▪ 2/3 females
▪ 2/3 associated with an impacted canine
▪ 2/3 MX
▪ 2/3 2nd decade – kids and teenagers\

That’s why it’s known as the tumor of two thirds

▪ ~ 3‐7% of all odontogenic tumors

New research showing more in _ant md_ though

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338
Q

Adenomatoid odontogenic tumor

(AOT)

Clinical charcterstics

A
  • Frequently asymptomatic, discovered upon routine radiographic exam or when lesion becomes large enough to expand bone
  • Tumor of Epithelial Origin
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339
Q

Adenomatoid odontogenic tumor

(AOT)

Radiographically

A

▪ ~ 75% are well‐circumscribed unilocular radiolucency involving the crown of an unerupted tooth
o less often, they are found between the roots of teeth
▪ Mixed radiolucent/radiopaque appearance is likened to “snowflake” calcifications
▪ May be totally radiopaque in some cases
▪ Divergence of roots is frequently seen

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340
Q

If an Adenomatoid odontogenic tumor (AOT) is not showing any calcifications yet, it’s in the differential
diagnosis with —— ?

A

a dentigerous cyst.

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341
Q

What is this radiographic finding?

A

Odontogenic Myxoma

  • Classic example of enlargement of the mandible caused by multilocular radiolucency.
  • Enlarged into oral cavity ‐ alveolar ridge elevated
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342
Q

What is this radiographic finding?

A

Odontogenic Myxoma

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343
Q

Case

A

Clinically: obliteration of vestibule on patient’s left mandible

Radiographically:lesion running from posterior by third molar all the way anterior to canine. Well‐circumscribed, multilocular radiolucency is scalloping up
between teeth, causing some root divergence

Grossly: gelatinous appearance of myxoma makes it hard to remove

After treatment: post‐surgery; had excised all the way to right 2nd PM

This is Odontogenic Myxoma

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344
Q

Adenomatoid odontogenic tumor

(AOT)

Treatment

A
  • Treatment is usually enucleation
  • recurrence is rare
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345
Q
A

CEMENTOBLASTOMA
(True Cementoma)

  • First molar has tumor attached to the root.
  • Mostly radiopaque but has some less radiodense areas within = classic for cementoblastoma.
  • Radiolucent halo around region.
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346
Q

What is this gross and histological finding?

A

Cementoblastoma

Grossly continuous growth from tumor to the root of the tooth. Brownish
areas were more vascular.
Histologically: tubular dentin in tooth, attached to mass of tissue with calcifications

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347
Q

Squamous Odontogenic Tumor

(SOT)

Demographics and Location

A

▪ Typically involves alveolar ridge
▪ Anterior > Posterior jaws
▪ Seen from 2nd to 7th decade (mean 40 years of age)

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348
Q

Squamous Odontogenic Tumor

(SOT)

Clinical charcterstics

A
  • Tumor of Epithelial Origin
  • Rare
  • Usually asymptomatic, but may present with tooth mobility and slight pain
  • Multiquadrant ~ 20-25%
    • A couple reported cases in families
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349
Q

Squamous Odontogenic Tumor

(SOT)

Radiographically

A
  • Well‐circumscribed radiolucency , often a semilunar radiolucency of alveolar ridge
    • Can mimic periodontal disease
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350
Q

Squamous Odontogenic Tumor

(SOT)

Origin

A
  • Thought to arise from epithelial rests (Malassez) in the periodontal ligament space
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351
Q

Squamous Odontogenic Tumor

(SOT)

Treatment

A
  • Treatment is conservative local excision
  • Recurrence is rare
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352
Q

Compound Odontoma

Vs

Complex Odontoma

A

Compound Odontoma

  • Mature normal appearing pulp, enamel and dentin
  • Organization like teeth, with enamel surrounding dentin which surrounds pulp ( Well developed rudimentary “tooth” forms)
  • appear as small tooth‐like structures in the Anterior jaws (esp. MX)

Complex Odontoma

  • Mature pulp, enamel and dentin
  • No organization, mass of dentin and enamel matrix and pulp tissue (**Poorly developed mass of calcified deposits)
  • appear as masses of radiopaque material with
  • variable densities in the Posterior jaws (esp. MD)
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353
Q

What is this radiographic finding?

A

Classic appearance of Odontoma

  • multiple tooth‐like shapes aggregated together
  • Typically with some sort of radiolucent halo around them
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354
Q

What is this radiographic finding?

A

Compound Odontoma

little teeth‐like structures blocking canine eruption

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355
Q

What is this radiographic finding?

A

Complex Odontoma

  • 2‐2.5cm mass overlaying the molar.
  • radiolucent rim/halo that is mixed, mostly radiopaque
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356
Q

Squamous Odontogenic Tumor SOT
Histologically may be mistaken for what other lesions?

A
  • Ameloblastoma
  • Squamous cell carcinoma (SCCa)
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357
Q

Central odontogenic fibroma (COF)

also known as ?

A
  • *Odontogenic Fibroma
    (central) **
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358
Q

Central odontogenic fibroma

(COF)

Origin

A
  • Tumors of Mesenchymal Origin
  • Some believe represents the counterpart to the peripheral ossifying (odontogenic) fibroma (in soft tissue)
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359
Q

Case

A

Primordial
Odontogenic Tumor
(POT)

unilocular radiolucency

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360
Q

Central odontogenic fibroma

(COF)

Location

A
  • MX ≈ MD
  • lesions in MX tend to be anterior to first molar
  • those in MD anterior ≈ posterior
  • 1/3 associated with an unerupted tooth
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361
Q

Central odontogenic fibroma (COF)

Clinically

A

-Small lesion tend to be asymptomatic

-Larger lesions can cause cortical expansion and tooth mobility

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362
Q

Central odontogenic fibroma

(COF)

Radiographically

A
  • Small lesions tend to be well-circumscribed unilocular radiolucencies
    • often periradicular
      • can mimic periapical granulomas and cysts
  • Larger lesions tend to be well-circumscribed multilocular radiolucencies
  • Borders are usually sclerotic
  • Root resorption or divergence may be seen
  • ~ 10- 15% will show radiopaque flecks within the radiolucency
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363
Q

What is this radiographic finding?

A

Ameloblastic Fibroma
(AF)

1‐3 potential locules, no impacted tooth associated

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364
Q

Central odontogenic fibroma

(COF)

Treatment

A
  • Enucleation with curettage or excision
  • usually don’t recur
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365
Q

What is this radiographic finding?

A

Ameloblastic Fibro-odontoma (AFO)

  • well‐circumscribed radiolucency
  • corticated edge + calcification
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366
Q

What is this radiographic finding?

A

Ameloblastic Fibro-odontoma (AFO)

has expansion into oral cavity. Flecks of calcification
in lesion with impacted tooth = odontoma

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367
Q

What is the Microscopic Differential Diagnosis of Central odontogenic fibroma (COF)?

A

o Desmoplastic fibroma ‐ a more aggressive lesion
o Fibromyxoma ‐ variant of odontogenic myxoma with
abundant collagen
o Hyperplastic tooth follicle ‐ typically loose immature stroma, but when hyperplastic can have abundant collagen

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368
Q

Odontogenic Myxoma

Origin

A
  • Tumors of Mesenchymal Origin
  • Thought to arise from the tooth follicle or dental papilla
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369
Q

Odontogenic Myxoma

Demographics and Location

A
  • ~3-5% of all odontogenic tumors
  • Wide age range, but 3rd decade most common
  • Found anywhere in the MD or MX
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370
Q

Odontogenic Myxoma

Radiographically

A
  • Small lesions present as asymptomatic radiolucencies found upon routine exam
  • Larger lesions can cause painless expansion of bone
  • All are radiolucent lesions, but the appearance can vary from well‐ circumscribed to irregular and diffuse
  • Unilocular to, more commonly, multilocular (“soap bubble” or “honeycomb”) radiolucency
  • Borders are often scalloped, can see sc_alloping around the roots of teeth_
    • But can cause displacement of teeth and resorption of the roots of teet
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371
Q

What is this radiographic finding?

A

Ameloblastic Fibrosarcoma

in the mandible developed after two years from AF

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372
Q

Odontogenic Myxoma

Grossly

A
  • the tumor is described as loose, soft and gelatinous
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373
Q

Odontogenic Myxoma

Treatment

A
  • Surgical excision or resection
  • Because the lesion is not encapsulated and has a gelatinous loose consistency► it is difficult to remove completely
    • this is thought to be why myxoma has a fairly high recurrence rate
  • Maxillary posterior lesions should be treated more aggressively
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374
Q

CEMENTOBLASTOMA

Origin

(True Cementoma)

A
  • Tumor of Mesenchymal origin
  • Benign tumor of cementoblasts
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375
Q

CEMENTOBLASTOMA

Demographics and Location

(True Cementoma)

A
  • Typically present in 2nd and 3rd decade (~75% prior to the age of 30)
  • 75% MD
    • ▪ ~ 90% in molar/premolar region
      *
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376
Q

CEMENTOBLASTOMA
(True Cementoma)

Clinically

A
  • 2/3 of cases have pain and swelling
  • Can cause cortical expansion if large enough
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377
Q

CEMENTOBLASTOMA
(True Cementoma)

Radiographically

A
  • Radiopaque mass fused to the root of the affected tooth
  • Usually has a thin radiolucent halo or rim surrounding the radiopacity
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378
Q

CEMENTOBLASTOMA

Treatment

(True Cementoma)

A
  • surgical extraction of the involved tooth with attached tumor
  • Root amputation (with attached tumor) and endo is an option for smaller lesions
  • Recurrence is unlikely
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379
Q

Cementoblastoma has similar histologic presentation to what?

A

osteoblastoma

Difference is Osteoblastoma is NOT a_ttached to the root of a tooth_ (whereas cementoblastoma must be)

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380
Q

What are Odontogenic Tumors
of
Mixed Origin
(Epithelial and
Mesenchymal)

A

They are tumors in which the _odontogenic epithelial componen_t causes induction of the mesenchymal component to produce a product

Examples:

  • Odontomas
  • Ameloblastic fibroma
    • (and Ameloblastic fibrosarcoma)
  • Ameloblastic fibro-odontoma
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381
Q

Odontoma

Origin

A
  • Odontogenic Tumors of Mixed Origin (Epithelial and Mesenchymal
  • They are hamartomas rather than true neoplasms
  • They are masses of enamel and dentin with variable amounts of pulp and cementum
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382
Q

What is the most common odontogenic “tumor”?

A

Odontoma

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383
Q

Odontoma

Demographics and Locations

A

▪ First 2 decade most common (mean age of 14)

Location is based on the type of Odontoma

  • Compound Odontoma
    • Anterior jaws (esp. MX)
    • **Well developed rudimentary “tooth” forms
  • Complex Odontoma
    • Posterior jaws (esp. MD)
    • **Poorly developed mass of calcified deposits
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384
Q

Odontoma

Charcterstics

A
  • Often associated with an unerupted tooth
  • Lesions may prevent eruption of teeth
  • Usually small in size, but rare cases of > 6cm reported
  • large lesions can cause bone expansion
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385
Q

Odontoma

Radiographically

A

▪ Radiographically see a radiopaque structure(s) surrounded by a radiolucent rim
▪ As with any calcified lesion, those found early in development may appear totally or predominantly radiolucent
▪ Compound odontomas appear as small tooth‐like structures
▪ Complex odontomas look like masses of radiopaque material with variable densities

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386
Q

Odontoma

Treatment

A

▪ Simple excision or enucleation
▪ Unlikely to recur

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387
Q

Primordial
odontogenic tumor
(POT)

Origin

A
  • Tumor of mixed origin
  • Very rare! first reported in 2014 -less than 30 cases so far
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388
Q

Primordial
odontogenic tumor
(POT)

Demographics and Location

A
  • Most common in 1st and 2nd decades
    • Mean age 12.5 years
  • MD:MX 6:1
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389
Q

Primordial
Odontogenic Tumor
(POT)

Clinical Charcterstics

A
  • Asymptomatic found on routine imaging
  • Can cause tooth displacement and cortical expansion
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390
Q

Primordial
Odontogenic Tumor
(POT)

Radiographically

A
  • Well-defined radiolucency associated with an impacted tooth
    • Most commonly a third molar
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391
Q

Primordial
Odontogenic Tumor
(POT)

Treatment

A
  • conservative excision/enucleation
  • So far no recurrence
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392
Q

Ameloblastic fibroma (AF) and ameloblastic fibro-odontoma (AFO)

Charcterstics

A
  • Uncommon benign mixed odontogenic neoplasms.
  • Considered together because it is thought they are variations of the same process
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393
Q

Ameloblastic fibroma (AF) and ameloblastic fibro-odontoma (AFO)

demographics and location

A
  • Typically presents in first 2 decades
    • mean is 12 years of age
  • ~ 70% occur in the posterior mandible
  • ~ 75% associated with unerupted teeth
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394
Q

Ameloblastic Fibroma (AF)

clinical and radiographic presentations

A
  • Small lesions are asymptomatic and found on routine exam
  • Large lesions can cause bone expansion
  • Smaller lesions are unilocular Radiolucencies
  • Large ones are multilocular radiolucencies
  • Border is well defined and often sclerotic
  • Untreated, can grow to very large size
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395
Q

Ameloblastic Fibro-odontoma (AFO)

Clinical and Radiographic features

A
  • Clinical features similar to Ameloblastic Fibroma AF (Small lesions are asymptomatic and found on routine exam
    & Large lesions can cause bone expansion)

Radiographically, we see a mixed radiolucent/radiopaque lesion because of the formation of odontomas

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396
Q

Ameloblastic fibroma (AF) and ameloblastic fibro-odontoma (AFO)

Treatment

A
  • Conservative surgical excision or curettage,
    easily removed from surrounding bone
  • Prognosis is excellent, recurrence is unusual
  • ▪ Rare cases reported of development of ameloblastic fibrosarcoma in area of AF or AFO
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397
Q

Ameloblastic
Fibrosarcoma

Charcterstics & Origin

A
  • _Malignant counterpar_t of ameloblastic fibroma
  • Rare lesion which may arise in the site of a previous AF/AFO or arise de novo
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398
Q

Ameloblastic
Fibrosarcoma

Demographics and location

A
  • 1.5 times more common in males
  • ~ 80% MD
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399
Q

Ameloblastic
Fibrosarcoma

Clinically

A
  • Pain, swelling and rapid growth are common presenting signs
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400
Q

Ameloblastic
Fibrosarcoma

Radiographically

A
  • presents as an ill-defined destructive radiolucency with irregular borders
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401
Q

Ameloblastic
Fibrosarcoma

Treatment

A
  • Radical surgical excision as the tumor is very aggressive and infiltrative
  • Prognosis is dependent on complete removal of tumor
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402
Q

Odontogenic carcinomas

List them (5)

A

-Ameloblastic carcinoma

-Primary intraosseous carcinoma, NOS

-Sclerosing odontogenic carcinoma

-Clear cell odontogenic carcinoma

-Ghost cell odontogenic carcinoma

All fairly rare lesions!

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403
Q

What is the Differential Diagnosis D/D of Multilocular Radiolucency

A

MOCHA

  • M odontogenic Myxoma
  • O Odontogenic keratocyst
  • C Central giant cell granuloma
  • H Central Hemangioma
  • A _A_meloblastoma

Others:

  • Aneurysmal bone cyst
  • early CEOT
  • ameloblastic fibroma AF
  • central MECa
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404
Q

Key Concepts of
Malignant Lesions on
Imaging

A

Rapidly growing and infiltrative

–finger-like extensions into surrounding anatomy

Remember: in some instances, a benign lesion can mimic a malignant
one.

Therefore we should be wary of all the information that is available.

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405
Q

Key Concept of
Malignant Lesions on
Imaging

A

ill-defined invasive borders followed by bone destruction

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406
Q

Key Concept of
Malignant Lesions on
Imaging

A

Destruction of the cortical boundary (floor of maxillary antrum) with an adjacent soft tissue mass (arrows)

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407
Q

Key Concept of
Malignant Lesions on
Imaging

A

Tumor invasion along the periodontal membrane space causing irregular thickening of this space

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408
Q

Key Concept of

Malignant Lesions on Imaging

A

Multifocal lesions located at root apices and in the papilla of a developing tooth destroying the crypt cortex and displacing the developing tooth in an occlusal direction (arrow)

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409
Q

Key Concept of

Malignant Lesions on Imaging

A

Four types of effects on cortical bone and periosteal reaction, from top to the bottom:
•cortical bone destruction without periosteal reaction
•laminated periosteal reaction with destruction of the cortical bone and the new periosteal bone
•destruction of cortical bone with periosteal reaction at the periphery forming Codman’s triangles
•a spiculatedor sunray type of periosteal reaction

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410
Q

Key Concept of Malignant Lesions on Imaging

A

Bone destruction around existing teeth, producing an appearance of teeth floating in space.

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411
Q

What is this radiographic finding?

A

Chondrosarcoma

  • its consistent widening as opposed to seen in periodontitis and inflammatory disease
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412
Q

Case

CC of loose teeth wanted extractions and a
denture

A

Chondrosarcoma

  • Ill defined lesion of anterior maxilla
  • Areas of radiolucency
  • Classic area of moth‐eaten look
  • Circular area of radiolucency with trabecular
  • pattern
  • Patient left without surgery, not heeding medical advice

Then patient came back
▪ Someone was willing to do the dentures for her
▪ CC‐ denture was not fitting
▪ Expansion of cortical plate
▪ Hyperkeratotic because of denture rubbing

▪ Still has malignancy
▪ Advise for surgery
▪ Refused again

Then the lesion kept on Lesion still growing
▪ Metastasize to lungs
▪ Admitted to breathing issues
▪ About 5 ½ years from initial dx to
pt passing away

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413
Q

What is this clinical finding?

A

Chondrosarcoma

  • Alveolar process and floor of mouth affected
  • Limitations of movement of the tongue
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414
Q

Case

  • 83 year old female with nodular areas under denture on anterior mandibular ridge
  • ▪ c/c of her denture rocking
A

Can see in the anterior region there’s an
elevation

histology shows it’s not chondrosarcoma

because it contained Cutright lesion

papule or nodule on alveolar ridge

  • Osseous and/or chondromatous metaplasia within the soft tissue of the gingiva

o Lesion is NOT central in bone or connected to bone
▪ NOT a malignant lesion
o Thought to be reactive metaplasia due to a poorly fitting denture

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415
Q

Chondroma & Chondrosarcoma

A
  • *Chondroma –** benign
  • *Chondrosarcoma**‐ malignant
  • Both are listed here because
    • a benign cartilaginous tumor central In the jaw is extremely rare (or may not exist)
    • Lesions tend to recur many times and eventually metastasize ( Basically chondromas are not really benign)
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416
Q

Chondrosarcoma

Charcterstics

A
  • Malignant tumor that forms cartilage
  • 10% of all primary bone tumors, but rare in the jaws
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417
Q

What is this clinical finding?

A

Osteosarcoma

▪ Swelling on left side of face
▪ Difficult opening

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418
Q

What is this clinical finding?

A

Osteosarcoma

  • See something in the operculum
  • Infection in third molar?
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419
Q

What is this radiographic finding?

A

Osteosarcoma

  • AP Plain Film
  • Most of jaw was missing
  • Radiolucency affecting entire ramus and condyle
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420
Q

What is this radiographic finding?

A

Osteosarcoma

  • Classic sunburst pattern
  • Fuzzy appearance on outer edges of cortex
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421
Q

What is this radiographic finding?

A

Osteosarcoma

  • cloudy bone formation on surface of cortex on facial and lingual aspect
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422
Q

What is this clinical finding?

A

Osteosarcoma

a patient with swelling with side of face

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423
Q

What is this radiographic finding?

A

Osteosarcoma

▪ Lytic lesion
▪ Slightly ill defined
▪ Loss of bone in the inferior aspect of mandible

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424
Q

Chondrosarcoma

Clinical presentations

A
  • Patient’s chief complaint is painless swelling, may be associated with tooth mobility
  • Symmetric widening of the PDL space
    • Can be initial presentation with chondrosarcoma and osteosarcoma
    • Along radicular surface of the tooth there is the same rate of widening all the way down the tooth
      • In contrast to periodontal disease, where there is a triangular shaped loss of space
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425
Q

Chondrosarcoma

Radiographically

A
  • Poorly defined radiolucency, often with scattered radiopaque foci
    • Radiopaque foci can be seen since the cartilage in the tumor can ossify
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426
Q

Chondrosarcoma

Treatment

A
  • Radical surgical excision on initial treatment
    • Maxillectomy/Mandibulectomy
      • If anterior region they remove the entire anterior portion of the jaw
  • These lesions don’t respond to radiation or chemotherapy
  • Although used as adjuncts for lesions that can’t be treated surgically
  • For example a posterior sinus lesion since that is the base of the skull
    • These patients have poorer prognosis than those with more accessible sites such as the mandible
  • Prognosis is poorer than for osteosarcoma (which contrasts with the prognosis in extragnathicsites)
  • Treatment failure (and mortality) is usually due to uncontrolled local disease not metastasis
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427
Q

Why any diagnosis of chondroma in the jaws should be viewed with suspicion?

A
  • Since 20% of chondrosarcomas of the jaw are initially misdiagnosed as chondromas ► any diagnosis of chondromain the jaws should be viewed with suspicion
  • All cartilaginous tumors arising in the jaws should be excised widely
    • (>60% of cartilaginous tumors of the jaw recur and ~7% metastasize to the lung and/or bone )
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428
Q

Osteosarcoma

_Demographics & Location_MD > MX, Male > Female

A
  • Most common malignant bone tumor in the jaws is metastatic disease
  • Most commonly primary (meaning started at this location) malignant bone tumor in patients under 40 years old
    • 2nd most common overall after multiple myeloma
  • Mean age at presentation for jaw lesions is 33 years old, 10‐15 years older than that for long bones
    *
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429
Q

Osteosarcoma

Clinically & Radiographically

A
  • Swelling and pain are the common presenting symptoms (25% have “toothache”)
  • Can also have loosening of teeth,** **paresthesia of lip** and **nasal obstruction
  • Symmetric widening of the PDL is often an early radiographic change
  • Lesions vary from dense sclerotic, mixed sclerotic and radiolucent to all radiolucent
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430
Q

Osteosarcoma

Treatment

A
  • Important to distinguish from chondrosarcoma as treatments are different
  • Osteosarcoma is currently treated with pre-op multi-agent chemotherapy followed by surgery
  • Radiation therapy alone is insufficient for cure
    • Favorable jaw site – MD symphysis
    • Worst site – MX sinus
  • 5 year survival is ~ 20% (up to 80% if caught early and treated with radical resection)
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431
Q

What is this clinical finding?

A

Langerhans Cell
Disease

Infant with Acute disseminated type
▪ See lesions on head/ear

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432
Q

What is this clinical finding?

A

Langerhans Cell
Disease

we see lesions on maxilla

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433
Q

What is this clinical finding?

A

Langerhans Cell Disease

▪ Older child
▪ Chronic disseminated form
▪ Alveolar ridge involvement
▪ Lot of bone loss and mobility
▪ Painful to brush

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434
Q

What are these clinical findings?

A

Langerhans Cell Disease

Torus and molar involvement

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435
Q

What is this clinical finding?

A

Eosinophilic
Granulations

Erythematous area

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436
Q

What is this radiographic finding?

A

▪ Child with disseminated form
▪ Punched out radiolucency in the skull

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437
Q

What is this clinical finding?

A

▪ Child with bone loss surround the teeth
▪ Floating teeth

disseminated form

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438
Q

What is this radiographic finding?

A

▪ Floating teeth
▪ Only attached by soft tissue due to extensive bone loss

disseminated form

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439
Q

What is this radiographic finding?

A

Eosinophilic granuloma

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440
Q

Peripheral (juxtacortical) Osteosarcoma

Location

A
  • Arise on the surface of the bone (vs. medullary site for usual forms of osteosarcoma)
  • Usually long bones
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441
Q

What are the two types of Peripheral (juxtacortical) Osteosarcoma ?

A

parosteal – well differentiated, but will recur with less than an en bloc or radical surgery

periosteal – higher grade with prominent cartilaginous component

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442
Q

Parosteal Peripheral Osteosarcoma

Charcterstics

A

o Mushroom like growth on bone surface
o No elevation of periosteum
o No new bone formation
o Low grade

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443
Q

Periosteal Peripheral Osteosarcoma

Charcterstics

A

o Usually sessile growth on bone surface
o Elevation of periosteum
o New bone fills in space under periosteum
o Prognosis is better than medullary osteosarcoma but worse
thanparosteal type

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444
Q

Langerhans Cell
Disease

also known as

?

A
  • Histiocytosis X (old name)
  • Langerhans cell granuloma
  • Eosinophilic granuloma
  • Langerhans cell histiocytosis
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445
Q

Langerhans cell histiocytosis

Etiology

A

Etiology unclear
o Demonstration that LCH cells are clonal, along with the recent discovery of activating BRAF mutations in LCH cells, ►strongly suggests that LCH is a neoplastic disease

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446
Q

Langerhans cell histiocytosis

Demographics & Location

A
  • Males>>> Females
  • More than half of cases seen under the age of 10
  • Jaw affected in 10 ‐20% of cases
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447
Q

What is this radiographical finding?

A
  • Punched out radiolucency
  • Lytic radiolucency without cortication

MM

Multiple Myeloma

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448
Q

What is this radiographical finding?

A
  • more punched out radiolucency in iliac crest in the image
  • Bone marrow biopsy usually done in this area since it’s frequently involved

multiple Myeloma

MM

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449
Q

What is this radiographical finding?

A

Multiple Myeloma

▪ Radiolucency without sclerotic border

▪ Multiple and separated

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450
Q

What is this clinical finding

A

Swelling of gingiva

▪ Plasmacytoma

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451
Q

Langerhans Cell
Histiocytosis

Clinically & Radiographically

A

Clinically:

Common sites: skull, rib, vertebrae, and mandible
▪ Often have associated pain or tenderness

Radiographically:

▪ In jaws we see loss of alveolar bone in molar area
o Mimics severe periodontitis

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452
Q

Types of Langerhans Cell
Disease

List 3

A

▪ Acute disseminated form (Letterer‐Siwe disease)
▪ Chronic disseminated form (Hand‐Schuller‐Christian Disease,
▪ Eosinophilic Granuloma (chronic localized)

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453
Q

Acute disseminated form (Letterer‐Siwe disease)

charcterstics

A
  • Multisystem (bone, skin, liver spleen and lymph nodes)
  • Infants
  • high mortality
  • rapidly progressive
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454
Q

Chronic disseminated form (Hand‐Schuller‐Christian Disease, Multifocal Eosinophilic Granuloma)
Charcterstics

A
  • Unisystem (frequently bone, but also skin and viscera)
  • Children
  • fairly high mortality
  • more chronic progression
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455
Q

What is this gross finding?

A

Ewing Sarcoma

▪ Long bone

▪ Large expansion

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456
Q

What is this radiographical finding?

A

Ewing Sarcoma

  • an _expansion of tissu_e
  • Dissolution of bone in that area
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457
Q

Eosinophilic Granuloma (chronic localized)

Charcterstics

A
  • Solitary or multiple bone lesions without visceral involvement
  • Adults
  • very low mortality
  • Some reports of association with smoking marijuana
    • In these cases the lungs are involved
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458
Q

The site of invovelement of Langerhans Cell
Disease depends on ?

A

Site of involvement depends on clinical form

  • Neoplastic proliferation of Langerhans cells
    • Langerhans cells
      • Dendritic mononuclear cells normally found in the epidermis and mucosa
      • Antigen presenting cells to T lymphocytes
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459
Q

What is this radiographical finding?

A

Metastatic Carcinoma to Jaw Bones

▪ A. Metastatic breast carcinoma surrounding the apical half of the second and third molar roots and extending inferiorly. It has destroyed the inferior border of the mandible.

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460
Q

What is this radiographical finding?

A

Metastatic Carcinoma to Jaw Bones

B. Bilateral metastatic lesions from the lung destroying the mandibular rami.

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461
Q

What is this radiographical finding?

A

Metastatic Carcinoma to Jaw Bones

D. Destruction of the left mandibular condyle (arrows) from a thyroid metastatic lesion

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462
Q

What is this radiographical finding?

A

Metastatic Carcinoma to Jaw Bones

A. Partial panoramic image of prostate metastatic lesions involving the body and ramus; note the sclerotic bone reaction (arrows).

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463
Q

What is this radiographical finding?

A

Metastatic Carcinoma to Jaw Bones

B. Occlusal image of prostate lesions causing sclerosis and spiculated periosteal reaction (arrows)

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464
Q

What is this radiographical finding?

A

Metastatic Carcinoma to Jaw Bones

C. Periapical image of a metastatic lesion of breast carcinoma; note the irregular widening of the periodontal membrane spaces and patchy sclerotic bone reaction, especially around the roots of the molars

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465
Q

Chronic disseminated form (Hand-Schuller-Christian Disease, Multifocal Eosinophilic Granuloma)

What is its classic Triad?

A
  • Exophthalmus
  • Diabetes insipidus
  • Lytic defects of bone
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466
Q

Chronic disseminated form of Langharan Disease

Clinically and radiographically

A

Clinically:

  • we see mobility of teeth

Radiographically:

  • picture of child with “teeth floating in air”
  • Sharply punched out radiolucent lesions, ill- defined radiolucency in some cases
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467
Q

Eosinophilic Granuloma

Charcterstics & Demographics

A
  • Elderly men often present with lung lesions (increased incidence with smoking)
  • Localized lesions, usually affecting one bone
  • If found to be an accessible solitary lesion, treatment is usually curettage and possibly low dose RT
  • in some instances it can be initial presentation of systemic disease – but that would typically be in children or young adults
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468
Q

Langerhans Cell
Histiocytosis
Histology

It contain rod shape called

A

Birbeck granules

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469
Q

What is the differential diagnosis for Alveolar Bone Loss in Children?

A

o Juvenile periodontitis

o Langerhans cell histiocytosis

o Papillon‐Lefevre syndrome

o Cyclic neutropenia/agranulocytosis

o Burkitt’s Lymphoma

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470
Q

Multiple Myeloma

charcterstics

A

Monoclonal Expansion of malignant plasma cells

  • Plasma cells make a lot of immunoglobulin ► So we will see a lot of immunoglobulin
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471
Q

Multiple Myeloma

Demographics and Location

A
  • Most common in 40‐70 year old
    • Means 63 years old
  • Bones most commonly involved include ribs, vertebrae and skull
    • 70‐90% will have jaw involvement at some point
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472
Q

Multiple Myeloma

Clinically

A
  • Present with bone pain (>70%) and pathologic fractures
  • Anemia, thrombocytopenia and neutropenia due to crowding out of normal cells within bone marrow by proliferating malignant cells
  • 50‐60% have Bence‐Jones proteins in urine (light chains, usually kappa)
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473
Q

▪ Solitary plasmacytoma Vs Extramedullary plasmacytoma Vs Multiple myeloma – multifocal disseminated disease

A

▪ Solitary plasmacytoma

  • Individual lesion in bone
    • When affecting oral cavity, ~95% of the cases are ramus and angle of the mandible
  • In many cases p_rogress to more systemic disease_

Extramedullary plasmacytoma

  • individual soft tissue lesion (not central In bone)

Multiple myeloma

  • multifocal disseminated disease
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474
Q

Multiple Myeloma

Radiographically

A
  • “punched out” radiolucencies (no sclerotic margin) often with an irregular outline
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475
Q

Multiple Myeloma

Lab findings

A
  • Elevated M spike in serum
  • Elevation of immunoglobulin in serum (hyperglobulinemia) most commonly IgG
  • Deposition of amyloid in tissues (macroglossia)
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476
Q

Multiple Myeloma

Treatmet

A

Treatment can include :

  • chemotherapy with or without Radtiaion Therapy
  • bone marrow transplant
  • interferon
  • antibodies made against tumor cells
  • thalidomide
  • Even with treatment, many patients do not survive more than 18‐24 months, however treatment modalities are improving
  • Older patients are treated less aggressively
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477
Q

Ewing Sarcoma, Ewing’s family of sarcomas

Charcterstics

A

▪ Highly malignant, undifferentiated, small round cell tumor/small blue cell tumor

o The cell of origin is in question, may be of neural crest origin

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478
Q

Ewing Sarcoma

Demographics and Location

A
  • ​Primarily a disease of children and adolescents (90% of patients are between 5 and 30 years old) ▪ >60% males ▪
  • Twice as common in mandible
  • Caucasians>>>>Blacks and Asians
  • Make up ~6% of primary malignant bone tumors
    • In the jaws, the ratio of primary tumor to metastasis is 14 to 1
  • 50% of cases in the femur and pelvic bones
  • ~1% occur in the jaw bones
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479
Q

Ewing Sarcoma

Clinically

A
  • Patients often present with pain, swelling, fever and elevated ESR (similar to signs of inflammation)
  • May be misdiagnosed as an infection or osteomyelitis
  • Paresthesia and loosening of teeth are common findings with jaw lesions
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480
Q

Ewing Sarcoma

Radographically

A
  • an irregular lytic lesion with ill‐defined margins
  • Root resorption may be seen
  • May see thickening of the periosteum with a characteristic “onion skinning” pattern (like with peripheral periostitis)
    • seen more in long bones
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481
Q

Ewing Sarcoma

Treatment

A
  • Combined therapy with multi‐agent chemotherapy, radiation therapy and surgery has led to 40% ‐ 80% survival rates
  • Gnathic Ewing sarcoma has a lower mortality rate than all other primary sites
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482
Q

What are the most common carcinomas that metastasize to the jaw

A

The most common carcinomas to jaw: Breast Lung Thyroid and Colon Kidney Prostate ▪

“B. L. T. and Cold Kosher Pickle”

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483
Q

Malignant tumors of jaw

Review

A

Metastatic tumors to the jaw are more common than primary lesions

● Think osteosarcoma, chondrosarcoma, or osteoblastic metastasis (breast or prostate) if lesion radiographically looks malignant and has radiopaque internal pattern

● Ewing’s sarcoma is clinically accompanied by signs of inflammation

●Multiple myeloma characteristically presents as multiple, well‐ defined, punched‐out radiolucencies

● Bone affected by Non‐Hodgkin’s lymphoma radiographically appears to be dissolving

● Langerhans cell histiocytosis characteristically presents as scooped‐ out radiolucencies at the mid‐root level

● Remember to include metastatic carcinoma to jaw as a radiographic differential diagnosis for malignant lesions

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484
Q
A
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485
Q

What are Gastrointestinal Diseases

what are example of them?

A

Inflammatory bowel diseases associated with oral findings

▪ Crohn disease
▪ Ulcerative colitis
▪ Pyostomatitis vegetans
▪ Celiac Disease

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486
Q

Crohn Disease
Regional Ileitis

What areas does affect?

What are the symptoms?

A

What areas does affect?

● Primarily affecting distal small intestine and proximal colon

What are the symptoms?

● Symptoms include abdominal cramping, pain, bloating, diarrhea, and nauseas (similar amongst the GI diseases)
● Patients often have weight loss and malnutrition
● 20% have abrupt onset of symptoms resembling acute appendicitis or bowel perforation

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487
Q

Crohn Disease
Regional Ileitis

When it is diagnosed?

Etiology?

Prevalence?

What are the oral implactions?

A

When it is diagnosed?

● Usually initially diagnosed in adolescents

Etiology?

● Etiology unknown‐ immunologically mediated?
o Theory of being too clean as a child and having a negative response as we grow older since we’re not used to normal bacteria

Prevalence?

● Prevalence increasing, reason unknown

What are the oral implactions?

●Oral lesions can be first sign of disease

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488
Q

Crohn Disease
Histopathology

A

● Superficial or deep ulceration with adjacent granulation tissue extending into deep submucosa or below
● A transmural granulomatous inflammation
o Sarcoid‐like, non‐caseating, poorly formed granulomas, in all tissue layers (50‐70% of cases) usually adjacent to blood
vessels or lymphatics
● Transmural inflammation with lymphoid aggregates throughout bowel wall

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489
Q

Crohn Disease
Oral Findings

A
  • Recurrent oral ulcerations can mimic those seen with recurrent aphthous lesions
  • Diffuse or nodular swelling of the oral and perioral tissues
    • Can look like epulis fissuratum
  • Deep linear granulomatous‐appearing ulcerations (often in the buccal vestibule area)
    • Cobblestone mucosal appearance
  • Polypoid tag‐like lesions on vestibular and retromolar mucosa
  • Enlargement of lips caused by granulomatous inflammation: orofacial granulomatosis
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490
Q

Crohn Disease
Treatment

A
  • Current strategies aim for deep and long‐lasting remission, with the goal of preventing complications, such as surgery, and blocking disease progression
  • Immunosuppressant such as cyclosporine
  • In more severe cases;
  • *high dose corticosteroids and**
  • chemotherapeutics to induce a remission
  • Nutritional supplements (iron, folate)
    • Because they are unable to absorb nutrients
  • If medical means do not keep patient under control► surgical removal of a portion or all of the intestine
  • When intestinal symptoms are under control►oral ulcerations resolve
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491
Q

Which systemic disease manifests like this?

A

Crohn Disease

  • Patients can also get angular cheilitis
  • Above the Linear ulceration, can see a flap like structure which is the hyperplastic margin
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492
Q

Which systemic disease has this oral manifestation?

A
  • we see the ulceration and hyperplastic tissue surrounding it.
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493
Q

Which systemic disease has this oral manifestation?

A

Crohn Disease

Nodular appearance of buccal mucosa

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494
Q

Which systemic disease has this oral manifestation?

A

Crohn Disease

we see more nodules

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495
Q

Which systemic disease has this oral manifestation?

A

Crohn Disease

Linear granulomatous ulcerations
But they are not the aphthous ulcerations but the more
linear type

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496
Q

How different is Ulcerative Collitis from Crohn Disease?

A

Unlike Crohn’s, lesions extend in a continuous fashion proximally from the rectum (no skip lesions) and histologically don’t have granulomas

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497
Q

Pseudomembranous
Ulcerative Colitis

Causes?

A

Bactrial Overgrowth in the pseduomemberane

(C.difficile Overgrowth)

Causes:

  • Clindamycin prolonged use ~2 weeks can cause the C. difficile overgrowth.
  • Always warn patients if you prescribe clindamycin about possible side effects and stop usage since do not want them to develop untreatable strains
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498
Q

Ulcerative Colitis

  1. What are the symptoms
  2. What type of Cancer risk it presents?
A

What are the symptoms

  • A chronic inflammatory disease of the colon (mucosa and submucosa) presenting with diarrhea, rectal bleeding, abdominal pain, weight loss and fever

What type of Cancer risk it presents?

  • Increased risk of colon cancer
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499
Q

Pyostomatitis
vegetans

Treatment

A

● Treatment is not well standardized, fairly rare disease and good double blind studies rare
● Can use topical corticosteroids
● Werchniak et al had good results with topical tacrolimus
● Sulfasalazine or Prednisone for GI lesions
● If GI symptoms are under control► oral lesions will resolve

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500
Q

Oral Manifestations of which systemic disease?

A

Pyostomatitis
Vegetans

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501
Q

Oral Manifestations of which systemic disease?

A

Pyostomatitis
vegetans

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502
Q

Oral Manifestations of which systemic disease?

A

Pyostomatitis
vegetans

Snail track
appearance

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503
Q

Ulcerative Colitis

Oral Lesions

A

● In some cases, patients get recurrent oral ulcerations (can have aphthous‐like lesions)
● Papillary mucosal projections with deep linear ulcers and fissures
● Intraepithelial pustules of the mucosa (pyostomatitis vegetans)

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504
Q

Ulcerative Colitis

Management

A

● Use of anti‐inflammatory medications
o Sulfasalazine or Prednisone
● If medical means do not succeed► then removal of part or all of colon

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505
Q

What is the difference between Inflammatory Bowel
Disease IBD & Irritable
Bowel Syndrome IBS

A

● IBD
o Classified as a disease
o Can cause destructive inflammation and permanent harm to the intestines
o The disease can be seen during diagnostic imaging
o Increased risk for colon cancer

● IBS
o Classified as a syndrome, a group of symptoms
o Dose not cause inflammation; rarely requires hospitalization or surgery
o There is no sign of abnormality during an exam of the colon
▪ Usually because it’s only periodic
o No increased risk form colon cancer or IBD

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506
Q

Pyostomatitis
Vegetans

what is it?

Demographics?

Symptoms onset?

A

What is it?

  • Thought to be an unusual presentation of inflammatory bowel disease, especially ulcerative colitis (sometimes with Crohn’s)\

Demographics

  • In only a rare subset of patients
  • Typically present before 30 years of age

Symptoms onset

  • ~25% of cases seen in absence of GI symptoms
  • May see oral symptoms before the GI symptoms
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507
Q

Pyostomatitis
Vegetans

Oral Symptoms

and

Most common sites in the mouth?

A

Oral Symptoms

● Recurrent oral ulcerations _concurrent with, or prior to GI symptoms_
● Oral mucosa is erythematous and thickened with multiple
cream/yellow‐colored pustulesandsuperficial erosions
● Linear “snail track” oral pustules

Most common sites in the mouth?

● Most common sites include buccal and labial mucosa, soft palate, and ventral tongue

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508
Q

Celiac (Sprue) Disease

What is it?

Which gene is involved?

Symptoms?

A

What is it?

● Chronic disease (diffuse enteritis) of the small intestine which improves upon withdrawal of gluten proteins

Which gene is involved?

● >90% express HLA‐B8 histocompatibility antigen

Symptoms?

● Patients present with diarrhea, gas, weight loss, fatigue, impaired nutrient absorption, etc

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509
Q

Oral manifestation of which Systemic Disease?

A

Amyloidosis

Nodular “waxy” depositions in skin

deposition on the eyelid

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510
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

orange, red, yellow tinge

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511
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

Macroglossis and crenation of tongue (indentation near the teeth area)

skin deposits on the comissure,

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512
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

macroglossia

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513
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

Amyloid deposition on the tongue is amyloid, you have papule and nodule like area, can see the crenation of the tooth

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514
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

Submucosal amyloid deposit

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515
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

Amyloid deposition with ulceration and petechiae

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516
Q

Which systemic disease has these oral manifestations?

A

Amyloidosis

▪ different color compared to normal tongue with amyloid

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517
Q

Patients with Celiac (Sprue) Disease have risk of developing which cancer?

A

● 10‐15% risk of GI lymphoma

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518
Q

Celiac (Sprue) Disease

Oral Symptoms

A

● 10‐15% risk of GI lymphoma

● Oral symptoms include aphthous‐like ulceration of mucosa
● Patients can have enamel defects and pitting

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519
Q

Amyloidosis

What is it?

From what does it form?

Seen with what disease?

A

What is it?

  • Protein deposits in tissue
    • Paucicellular eosinophilic deposits amorphous eosinophilic deposit

From what does it form?

  • Form fibrillar β‐pleated sheets within the tissue

Seen with what disease?

  • multiple myeloma
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520
Q

Amyloidosis

what are its Types and what they are associated with?

A
  1. ▪ Primary amyloidosis is associated with multiple myeloma
  2. Reactive systemic amyloidosis
  3. Hemodialysis associated amyloidosis kidney dysfunction
  4. Hereditary amyloidosis (Familial Mediterranean Fever), present with polyneuropathies, cardiac arrhythmias, renal failure, CHF
  5. Localized dermal amyloidosis
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521
Q

Primary amyloidosis is associated with which cancer?

A

multiple myeloma

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522
Q

Hemodialysis associated amyloidosis leads to ——

A

kidney dysfunction

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523
Q

Amyloidosis

Organ Limited

Clinically

A
  • Rare in oral cavity
  • Amyloid nodule, asymptomatic submucosal deposit
  • Not associated with systemic symptoms
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524
Q

Primary or Muliple Myeloma associated Amyloidosis

Systemic

Demographics & Clinical presentations

A
  • Older adults > 65yrs
  • Male predilection
  • Amyloid deposits lead to macroglossia, carpal tunnel syndrome, hepatomegaly, dry mouth
  • Skin lesions: Waxy papules and plaques, smooth surface (eyelid area, retroauricular, neck, lips), orangy, red appearance
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525
Q

Secondary Amyloidosis

systemic

Etiology & Effects

A
  • Due to chronic inflammatory process
  • *(osteomyelitis, TB,** sarcoidosis)
  • Affects liver, kidney, spleen, adrenals but not heart
  • can affect multiple organs, heart is usually spared
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526
Q

Hemodialysis associated Amyloidosis

Etiology & Effects

A

o Accumulation of normal protein (beta‐2 microglobulin) in plasma
_o Deposits in bones and joint_s
o Carpal tunnel syndrome, cervical spine pain
o Tongue deposits can have macroglossia

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527
Q

Amyloidosis

Clinical Presentations

A
  • Deposition of an extracellular proteinaceous material‐often immunoglobulins
    • all types have common feature of a β‐pleated sheet molecular configuration
  • Macroglossia
    • can be massive and exhibit dental indentations (crenation) with yellowish peripheral nodules
  • Gingiva: usually normal in color, but may be bluish, spongy and enlarged
  • Xerostomia if deposits in salivary glands
  • Mucosal petechiae can be seen
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528
Q

Amyloidosis

Mangement

A
  • Medical work‐up to determine type of amyloidosis
  • Treat underlying disease when possible
  • No treatment available for most types
  • Chemo drugs (Colchicine, Prednisone, Melphalan, Thalidomide, Cyclophosphamide) for multiple myeloma
  • Serum electrophoresis – monoclonal gammopathy very complicated and time consuming treatment
  • Renal transplant for dialysis‐associated type
  • Death due to cardiac failure, arrhythmias or renal failure is not uncommon within a few year of dx
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529
Q

Diabetes Mellitus

A

Endocrine Disease

  • a group of metabolic disorders with one common manifestation: hyperglycemia
    • Basic problem is either a decreased production of insulin or tissue resistance to insulin
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530
Q

Diabetes Mellitus
Pathophysiology

A

▪ Insulin is hormone produced by beta cells of the pancreatic islets of Langerhans
▪ It is required for the uptake of glucose by body cells
▪ Insulin binds specific receptors which trigger the intracellular events necessary for glucose uptake

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531
Q

Diabetes Mellitus
Types

A

Type 1

Type 2

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532
Q

Diabetes Mellitus

Type I

Definition

Demographics

Symptoms

Etiology

A

Definition

insulin‐dependent diabetes mellitus (IDDM)

Demographics

5‐10% of cases
Juvenile onset (avg age 14)

Symptoms

  • Severe absolute lack of insulin
  • Hyperglycemia and ketoacidosis
  • Blood glucose levels of 200‐400 mg/dl (70‐120 normal)
  • Ketoacidosis from using protein and fat for energy instead of glucose body can’t use glucose
  • Thin body habitus

Etiology

  • Autoimmune disease
  • Thought to be possible viral infection as trigger to Islet cell antibody destruction of beta cells
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533
Q

Diabetes Mellitus

Type II

Definition

Demographics

Symptoms

Etiology

A

Definition

  • non‐insulin‐dependent diabetes mellitus (NIDDM)

Demographics

  • About 90% of cases
  • Onset in older, obese adults (80‐90%); ketoacidosis is rare

Symptoms

  • _Patients produce some insuli_n, can typically be treated with oral medication
  • “insulin resistance”‐ insulin levels appear WNL or elevated

Etiology

  • Decreased number of insulin receptors or defective receptors
  • Genetic abnormalities, multifactorial
  • Growing percent of the US population as well as around the world
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534
Q

Diabetes Mellitus

Complications

A

▪ Decreased neutrophil chemotaxis ►do not fight off infections as well as
you should
▪ Peripheral vascular disease►microangiopathy
o Results in ischemia: kidney failure, gangrenous complications of lower limbs, retinal involvement leading to blindness
o Amputations, CVA or MI
o Ketoacidosis may lead to diabetic coma

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535
Q

Diabetes Mellitus
Oral Findings

Most often associated with Type I but may be seen with Type II

A
  • Periodontal disease‐ more frequent occurrence, more rapid progression
  • Poor healing post oral surgery/extractions
  • Enlargement and erythema of the attached gingiva
  • Increased risk of infections
    • Candidiasis
  • Xerostomia‐ 1/3 of pts complain of dryness
  • Diabetic Sialadenosis‐ both type I and type II
  • Mucormycosis‐ in uncontrolled disease and the tissue becomes necrotic because it is not getting any blood supply
  • Dental Carieso Benign migratory glossitis
    • Increased prevalence in type I
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536
Q

Diabetes Mellitus

TYPE I

Management

A
  • Insulin injections
  • Insulin shock‐ if blood glucose falls below 40 mg/dl
    • Treat with dextrose
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537
Q

Diabetes Mellitus

TYPE II

Management

A
  • Dietary modification and weight loss
  • Oral hypoglycemic agents
    • ex. tolbutamide, glyburide, metformin
  • Drugs may cause a lichenoid drug reaction
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538
Q

Oral Manifestation of which systemic disease

A

Diabetes Mellitus

Gingivitis = puffy red papillae here between the
central and lateral incisors

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539
Q

Oral Manifestation of which systemic disease ?

A

Diabetes mellitus

Anterior papillae are very puffy and red and fill of pus

Posterior gingiva are very
hyperplastic

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540
Q

Oral Manifestation of which systemic disease ?

A

Hyperplastic gingiva

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541
Q

Oral Manifestation of which systemic disease ?

A

Diabetes Mellitus

Sialadenosis

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542
Q

Oral Manifestation of which systemic disease ?

A

Diabetes Mellitus

diabetic patient who
developed Mucormycosis

Notice it is causing necrosis in the palate

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543
Q

Which systemic disease has this oral manifestation?

A

Lichenoid mucositis looks like lichen
planus
-same reticular white pattern, but there are
areas of erosion and some ulceration as
well
-some diabetic medications can lead to this

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544
Q

Hyperthyroidism
Treatment

A
  • Treatment includes:
    • Surgery – complete or partial removal of thyroid gland
    • Medications
      • Propylthiouracil and methimazole block normal use of iodine by thyroid gland
    • Radioactive iodine 131I
  • Treatment often results in hypothyroidism
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545
Q

Which systemic disease has this oral manifestation?

A

Hyperthyroidism

  • enlargement of the neck
  • characteristic stare
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546
Q

Hyperthyroidism

what is its most common form?

A

Graves’ Disease is the most common form

o An autoimmune disease attacks thyroid (TSH receptor)
o Leads to elevated release of thyroxine
o Most often a diffuse thyroid enlargement (goiter)

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547
Q

In Hyperthyroidism, what happens to

T4 (thyroxine) and TSH values

A
  • Serum T4 (thyroxine) is elevated

and

  • TSH is decreased
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548
Q

Hyperthyroidism
Demographics

A

▪ 5‐10X more common in females ‐ 2% of women

▪ 3rd ‐ 4th decade of life

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549
Q

Hypothyroidism

Treatment

A

▪ Treatment is thyroid hormone replacement
▪ Prognosis is generally good
▪ If children are not treated in a timely fashion ► permanent CNS damage can occur (mental retardation)

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550
Q

Which systemic disease has this oral manifestation?

A

hypothyroidism

woman who had
hypothyroidism, lips are thickened, thick creases in the face

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551
Q

Which systemic disease has this oral manifestation?

A

hypothyroidism,

in child, still has
deciduous teeth even though its an older child

Radiographically we see the teeth have not erupted in the oral cavity

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552
Q

Which systemic disease has this oral manifestation?

A

Hypothyroidism

Macroglossia and crenation (scalloping)

of the lateral tongue

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553
Q

Before and after tx of which systemic disease?

A

hypothyroidism

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554
Q

Hyperthyroidism

What patients might complain of?

What are the symptoms?

A

What patients might complain of?

  • nervousness
  • heart palpitations
  • heat intolerance
  • muscle weakness
  • emotionally labile

What are the symptoms?

  • weight loss, excessive perspiration, tachycardia,

tremors, eyelid retraction and exophthalmos

  • 20‐40% have ocular involvement

o Early in the disease‐ characteristic stare with eyelid retraction and lid lag
o Exophthalmos or proptosis
▪ Oral findings in children can include early eruption of teeth

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555
Q

Benign and malignant tumors of thyroid and pituitary gland can cause which systemic disease

A

hyperthyroidism

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556
Q

Hypothyroidism

What happens in Hypothyroidism?

What it is called in children & adults?

How it is diagnosed?

A

What happens in Hypothyroidism?

  • Decreased levels of thyroid hormone

What it is called in children & adults?

  • cretinism in children
  • myxedema in adults

How it is diagnosed?

  • Diagnosed by measuring T4 (free thyroxine) in serum
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557
Q

Hypothyroidism

Primary and secondary etiologies and T4,TSH profile?

A

▪ Primary Hypothyroidism

‐ due to abnormality in thyroid gland
o T4 low, TSH elevated

▪ Secondary Hypothyroidism (less common)

‐ pituitary gland doesn’t produce adequate
amounts of TSH
o T4 low, TSH low or borderline

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558
Q

Hashimoto’s thyroiditis or thyroid surgery are main causes in adults of which systemic disease?

A

Hypothyroidism

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559
Q

Hypothyroidism

Symptoms

Oral findings

A

Symptoms

  • Symptoms include lethargy, dry skin, thinning hair, swelling (edema) of face and extremities, huskiness of voice, weakness and fatigue
  • ▪ Infants have failure to thrive

Symptoms

o Thickened lips and macroglossia due to accumulation of glycosaminoglycans (GAGs)
o In children can see failure of tooth eruption even though teeth have normal development (enamel pitting can be seen)

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560
Q

An Oral Manifestaion of which systemic disease?

A

Hyperparathyroidism

in young children

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561
Q

Primary Hyperparathyroidism

Charcterstics

A

o Uncontrolled PTH production
o 80‐90% caused by parathyroid adenoma
o ~15% caused by hyperplasia
o ~ 2% caused by parathyroid carcinoma

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562
Q

Secondary Hyperthirydoism

Charcterstics

A

o PTH continuously produced in response to chronic low serum calcium (usually associated with chronic renal disease)

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563
Q

Hyperparathyroidism

Classic triad

of

A

bones, stones, and groans (& moans)

  • Bones – Changes in the bones:
    • Subperiosteal resorption of distal phalanges (early in disease)
    • Loss of lamina dura around roots (early in disease)
    • Loss/blurring of trabecular density in bone with resultant “ground glass” appearance in radiographs
    • Brown tumor
  • Stones – renal calculi (especially with primary disease) due to elevated serum calcium basically kidney stones
  • Groans – duodenal ulcers
  • Moans – changes in mental status mild dementia
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564
Q

Which systemic disease has this oral manifestation?

A

Pseudohypoparathyroidism

pulp chambers are very
elongated

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565
Q

Which systemic disease has this oral manifestation?

A

Pseudohypoparathyroidism

issues with eruption, no
pulp stones present

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566
Q

Hyperparathyroidism

A

Can be Primary or Secondary

  • Reduced amounts of PTH
  • Parathormone normally stimulates osteoclasts in bone and resorption in kidney, to bring serum levels of calcium back to normal with decreased parathyroid function, serum calcium levels drop → hypocalcemia
  • Lab findings ‐ PTH ↓, calcium ↓, phosphate↑, and normal renal function
  • Postive Chvostek’s sign ( sign of low Calcium)

Females 2 to 4 times more than males

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567
Q

Hyperparathyroidism

Bones Manfestiation

A
  • Subperiosteal resorption of distal phalanges (early in disease)
  • Loss of lamina dura around roots (early in disease)
  • Loss/blurring of trabecular density in bone with resultant
  • “ground glass” appearance in radiographs
  • Brown tumor
  • Steitis fibrosa cystica
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568
Q

What systemic disease causes this oral symptoms?

A

Hereditary
Hypophosphatemia/vitamin D‐resistant rickets

teeth look fairly
normal, have a draining abscess with ulcers and perilous

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569
Q

What systemic disease causes this oral symptoms?

A

Hereditary
Hypophosphatemia/vitamin D‐resistant rickets

teeth look fairly
normal, have a draining abscess with ulcers and perilous

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570
Q

Hereditary
Hypophosphatemia
Histology

A

 Enlarged pulp horns
o Can extend up to DEJ
 Abnormal globular dentin
o Dentin may exhibit clefting
 Enamel clefts
 Bacteria noted in enamel, dentin and pulp
o Pulpal involvement leads to necrosis and development of the periapical pathology

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571
Q

What is the most severe bone manifestation in people with hyperparathyroidism

A

Steitis fibrosa cystica

Where we see central degeneration and fibrosis of longstanding brown tumors

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572
Q

What are the manifestation of Brown tumor in Hyperparathyroidism

A
  • uni‐ or multilocular Radiolucency (pelvis, ribs, mandible)
  • seen with persistent disease
  • histology of giant cell lesion (like CGCG)
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573
Q

Hyperparathyroidism

Treatment

A

It is typically surgical removal of a portion or all of the
parathyroid glands

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574
Q

Hypoparathyroidism

Etiology

A

▪ Can be due to inadvertent surgical removal when thyroid gland is excised or to autoimmine destruction.

▪ DiGeorge syndrome (anomaly) and endocrine‐candidiasis syndrome can show this.

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575
Q

What is a Chvostek’s sign?

A
  • The Chvostek sign is a clinical finding associated with hypocalcemia, or low levels of calcium in the blood.
  • This clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual’s when the facial nerve below the zygomatic process
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576
Q

Hypoparathyroidism

in young children

A
  • If develops in young children tooth development can be affected ​
    • pitting enamel hypoplasia and failure of eruption
  • Persistent oral candidiasis in a young patient may be a sign of the onset of endocrine‐candidiasis syndrome (check for other endocrine abnormalities)
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577
Q

Hyperparathyroidism
Management

A
  • Oral vitamin D precursor
    • vitamin D2 (or ergocalciferol)
  • Dietary supplements of calcium
  • Teriparatide (a portion of PTH) injections twice daily
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578
Q

Pseudohypoparathyroidism

Also known as?

What is it?

How it appears clinically

What is its lab findings?

A

Also known as?

Albright hereditary osteodystrophy

What is it?

▪ Normal parathyroid and PTH, but activation of target cells is dysfunctional

How it appears clinically?

▪ Clinically, patient appears to have hypoparathyroidism
o Based on elevated serum levels of PTH seen with hypocalcemia,hyperphosphatemia and normal renal function

Lab findings

PTH ↑, calcium ↓, phosphate ↑

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579
Q

Pseudohypoparathyroidism

Types

What causes it

Type of inheritance & mutation

A

Types

Two broad disorders multiple subtypes

Type I and Type II

What causes it

Abnormal biochemical pathways that result in lack of target cell activation despite normal levels of PTH

Type of inheritance

Can be autosomal dominant inheritance –
defective PTH receptor on the target cells

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580
Q

Pseudohypoparathyroidism

Management

A
  • Vitamin D and calcium supplements
  • Serum and urinary calcium are monitored
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581
Q

Pseudohypoparathyroidism

Oral Findings

A
  • *- Generalized enamel hypoplasia**
  • Widened pulp chambers with pulpal calcifications (“dagger” shaped pulp stones)
  • Oligodontia
  • Delayed eruption
  • Blunting of root apices
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582
Q

Hereditary
Hypophosphatemia

Also known as?

What type of inheritance?

What mutation causes it?

A

Also known as?

vitamin D‐resistant rickets looks like they have rickets.

What type of inheritance?

▪ Most cases are X‐linked inheritance (males)

What mutation causes it?

o Mutation in PHEX ‐ zinc metalloproteinase gene
▪ phosphate regulating gene with endopeptidase activity on
the X chromosome
▪ Mutation affects metabolism of vitamin D precursors to the active metabolite
o Therefore low or no absorption of calcium
▪ Decreased capacity for reabsorption of phosphate from the renal tubules

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583
Q

Hereditary
Hypophosphatemia/vitamin D‐resistant rickets

Clincal Findings

Lab findings

A

Clinical Findings

▪ Clinical features similar to those of rickets, but resistant to treatment with vitamin D
o Short stature (upper body fairly normal, lower body shortened)
o Lower limbs short and bowed
▪ Similar to Vitamin D‐dependent rickets except no hypocalcification of teeth
▪ Teeth have enlarged pulp chambers and elongated pulp horns (extend to DEJ)
▪ With minor attrition of occlusal cusps, pulp is exposed to the oral cavity
▪ Exposures are often very small and when note periapical radiolucencies, it appears that otherwise normal teeth have periapical pathology

Lab findings:

↓ serum phosphate

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584
Q

Hypophosphatasia

What is it?

Type of inheritance?

Clincal findings?

Lab Findings?

A

What is it?

Rare metabolic bone disease

Type of inheritance:

Autosomal recessive inheritance, generally the younger the age of
onset the more severe the expression

Clincal findings:

 Bone abnormalities resemble rickets
 Often presents with premature loss of primary teeth
o not from periodontal disease, thought that marked reduction, or lack, of cementum allows exfoliation

Lab findings:

↓ alkaline phosphatase, ↑ blood and urinary
phosphoethanolamine

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585
Q

Hypophosphatasia

Types

4

A

 Perinatal

 Infantile

 Childhood

 Adult

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586
Q

Hypophosphatasia

Perinatal

A

o Most severe manifestations
o Death in a few hours secondary to respiratory failure
o Marked hypocalcification of skeleton

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587
Q

Hypophosphatasia

Infantile

A

o Diagnosed ~4‐6 months due to failure to grow
o Skeletal malformations
 shortened bowed limbs, rib and skull abnormalities
o Nephrocalcinosis, nephrolithiasis
 Can have premature exfoliation of teeth

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588
Q

Hypophosphatasia

Childhood

A

o Diagnosed at later age, variable clinical expression
o Early sign is premature loss of primary teeth, may be the only teeth affected
o Large pulp chambers and alveolar bone loss
o Premature fusion of cranial fontanels can lead to increase
intracranial pressure and brain damage

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589
Q

Hypophosphatasia

Adult

A

o Mild presentation
o Premature loss of primary or permanent dentition; patient may be edentulous
o Stress fractures in feet
o Increased number of fractures assoc. with minor trauma

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590
Q

Acromegaly

vs

Gigantism

A

Acromegaly – excess production of growth hormone after closure of the epiphyseal plates

Gigantism – excess production of growth hormone before
closure of the epiphyseal plates

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591
Q

Acromegaly

Etiology

Clinical signs

Oral Findings

A

Etiology

▪ Usually due to a pituitary adenoma

Clinical signs

▪ Renewed growth of small bones of the hands and feet as well as membranous bones of the skull and jaws
▪ Soft tissues are also affected

Oral Findings

▪ Mandibular prognathism, macroglossia, and diastema formation

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592
Q

Which systemic disease has these clinical manifestations?

A

Acromegaly

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593
Q

Addison’s Disease

also known as

etiology

when do clinical symptoms appear?

A

also known as

Hypoadrenocorticism

etiology

Insufficient production of corticosteroid hormones due to destruction of
adrenal cortex (autoimmune, infection, tumors, etc.)

when do clinical symptoms appear?

▪ Need ~90% destruction of gland before clinical symptoms

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594
Q

Which systemic disease manfiest like this?

A

Addison’s Disease

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595
Q

Which systemic disease manfiest like this?

A

Addison’s Disease

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596
Q

Addison’s Disease /Hypoadrenocorticism

Clincal symptoms

Lab findings

A

Clincal symptoms

  • diffuse hyperpigmentation of skin (bronzing), fatigue,
  • irritability, depression, weakness, etc.
  • Oral mucosa shows diffuse or patchy macular pigmentations flattened pigmentations

Lab findings

failure of cortisol to rise in response to a rapid ACTH stimulation

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597
Q

Which systemic disease is associated with this symptom?

A

Pellagra

Deficience in Vitamine B3 (Niacin)

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598
Q
A

Pellagra

Deficience in Vitamine B3 (Niacin)

Dermititis of the skin

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599
Q

Which systemic disease manifests like this?

A

Pellagra

Deficience in Vitamine B3 (Niacin)

erythema of the tongue

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600
Q

Vitamin B3 (Niacin)

Deficiency known as

Classid Triad

Oral symptoms

A

Deficiency

pellagra

Classic triad

Dermatitis, Dementia, Diarrhea

Oral symptoms

stomatitis and glossitis

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601
Q

Plummer‐Vinson
Syndrome

Why it is a concern?

A

Why it is a concern?

Premalignant process
o ↑ incidence of oral and esophageal SCCa

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602
Q

Which systemic diseaswe associated with these oral manifestations?

A

PLUMMER‐VINSON
SYNDROME

denuded tongue
and angular chelitis

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603
Q

Which systemic diseaswe associated with these oral manifestations?

A

PLUMMER‐VINSON
SYNDROME

Angular chelitis (top) hard to get rid of them

Atrophic Glossitis (bottom) red beefy tongue

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604
Q

How blood looks with

A

Top photo: in Iron Deficiency Anemia, Plummer‐Vinson Syndrome, small area that is pale in the center

Bottom photo : normal smear, center is not pale

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605
Q

Vitamin C

Deficiency

Known as

A

scurvy

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606
Q

Iron Deficiency
Anemia

Charcterstics of the Anemia

Symptoms

A

Charctersics of Anemia

a hypochromic, microcytic anemia

decrease in color, smaller
than normal

Symptoms

fatigue, light headedness, lack of energy

.

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607
Q

Iron Deficiency
Anemia

Oral Symptoms

A
  • Angular cheilitis (corner of the mouth ulceration)
  • Dysphagia (difficulty swallowing)
  • Atrophic glossitis (bald tongue, loss of papilla) beefy colored tongue
  • Glossodynia (burning tongue)
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608
Q

Smear blood of Pernicious Anemia vs normal blood smear

A

not biconcave

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609
Q

Iron Deficiency
Anemia

Treatment

A

Treated with iron supplements, extreme cases with blood infusions

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610
Q

Which systemic disease manifests like this?

A

Pernicious Anemia

glossitis, denuded papillae

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611
Q

This is a before and after of which systemic disease?

A

Pernicious Anemia

denuded tongue and then the papillae is back again after the treatment. You have to get injections for the rest of your life

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612
Q

Plummer‐Vinson
Syndrome

What is it ( assiosited with what difficiency)?

Demographics?

A

What is it ( assiosited with what difficiency)?

  • Iron deficiency anemia with glossitis and esophageal strictures
    • Similar signs and symptoms as iron deficiency

Demographics

  • Mostly women 30‐50 years old
    • Northern European heritage more common
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613
Q

Which systemic disease has this oral manifestation?

A

Uremic Stomatitis

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614
Q

Plummer‐Vinson
Syndrome

Iron Deficiency
Anemia

Treatment

A
  • Treated with iron supplements
  • Need long term follow up for eval of SCCa
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615
Q

Before and after treatment of which systemic disease?

A

Uremic Stomatitis

Before and
After Tx with Dialysis

changes on ventral and lateral side
of the tongue, better outcome after dialysis

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616
Q

Which systemic disease has these oral manifestations?

A

Reiter’s Syndrome (Reactive arthritis)

This not actually a geogrpahic tongue!

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617
Q

Which systemic disease has these oral manifestations?

A

Reiter’s Syndrome (Reactive arthritis)

Top: erythema on the palate and
areas of ulceration

Bottom: classic look of geographic
tongue, but it is not geo tongue. They are symptoms of Reiter’s

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618
Q

Infective endocarditis

A

▪ Janeway lesions
o Seen on palms of hands and soles of feet (tiny micro emboli that are causing lesions on the hands and feet)
▪ Erythematous macule or petechiae
▪ Painless
▪ Septic micro emboli

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619
Q

Which systemic disease has these clinical manifestations

A

Infective Endocardiatios

Janeway lesions

These are Septic Emboli

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620
Q

Which systemic disease is this?

A

Hyperparathyroidism

Here we see we see

  • a granular appearance of the max and mand bone everywhere, it is not localized.
  • There is a loss of bone density and the loss of definition of cortical bone.
  • Here we see a loss of definition of lamina dura as well because it is now granular, and is not as clear.
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621
Q

Which systemic disease shows radiographically like this ?

A

Hyperparathyroidism; this is the brown tumor which is sometimes well or ill defined, multi or unilocular radiolucency with granular septation.

If you have a patient that is younger than 15-20 years old that has a central giant cell granuloma ► you have to check that patient for hyperparathyroidism, because it could be a brown tumor.

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622
Q

Which systemic disease shows radiographically like this ?

A

This is another medical CT scan. You see the granular appearance of
the maxilla, skull, and well-defined multilocular radiolucency with
granulation. We call this a brown tumor because it is associated with
hyperparathyroidism.

( systemic endocrine diseases)

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623
Q

Which systemic disease shows radiographically like this ?

A

Hyperparathyroidism

On our intraoral radiographs, we see loss of definition of lamina dura because the bone now has a granular appearance which extends to the lamina dura.

The teeth are usually normal, but there is a loss of lamina
dura around the teeth. These teeth are not mobile.

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624
Q

Which systemic disease shows radiographically like this?

A

a medical CT scan of a patient with secondary hyperparathyroidism.

We see a lack of cortical bone – no normal cortical bone. Inside the skull

we have a granular appearance, with radiolucent and radiopaque dots, we call this a salt and pepper dots.

This is why we call this a salt and pepper appearance, there is no normal cortical bone.

( systemic endocrine diseases)

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625
Q

Pernicious Anemia

Type of Anemia?

What difficiency?

Causes?

A

Type of Anemia?

Megaloblastic Anemia

What difficiency?

Vitamin B12 difficiency

Causes?

  • Poor absorption of vitamin B12 (extrinsic factor, cobalamin)
  • These patients lack intrinsic factor, usually due to autoimmune destruction of parietal cells
    • Intrinsic factor produced by parietal cells in the stomach is needed for absorption of B12
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626
Q

Pernicious Anemia

Symptoms

A
  • Have burning sensation of tongue, lips and buccal mucosa
    • One of the things you need to rule out in patients with burning mouth syndrome
  • 50‐60% of patients have tongue symptoms, see atrophy (papilla denuded) and erythema
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627
Q

Which systemic disease shows radiographically like this?

A

we have 2 Pas of patients

with pseudohypoparathyroidism.

  • hypoplasia of enamel, tooth material
  • hypoplastic tooth bud ( hypoplastic means arrested development)
  • delayed eruption,
  • external root resorption.
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628
Q

Pernicious Anemia

Treatment

A
  • monthly IM injections of cyanocobalamin
  • cannot take ​B12 orally, you need injections
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629
Q

Pernicious Anemia

CLASSIC TRIAD

A

1 – Generalized weakness
2 – Painful tongue
3 – Numbness or tingling of the
extremities

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630
Q

UREMIC STOMATITIS

What is it?

What causes the oral lesions?

A

What is it?

  • Uncommon complication of renal failure
    • Patients have markedly elevated levels of urea in their blood stream

What causes the oral lesions?

  • Cause of oral lesions is unclear, may be urease produced by normal flora degrades urea in saliva liberating free ammonia which damages mucosa
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631
Q

UREMIC STOMATITIS

Clinical Presentation

A

Most cases in patients with acute renal failure
▪ Abrupt onset of white plaques or crusts
o Bad taste and burning also possible
o May be painful
▪ Usually on the buccal mucosa, tongue and floor of mouth
o If localized to the tongue can mimic oral hairy leukoplakia
▪ May detect an odor of ammonia or urine on the patients breath

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632
Q

Uremic Stomatitis
Treatment

A

▪ Usually clears within a few days after renal dialysis has begun
▪ Mildly acidic mouth rinses seem to clear oral lesions (ex. diluted hydrogen peroxide)
▪ Palliative treatment for pain includes ice chips or a topical anesthetic

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633
Q

Reiter’s Syndrome

also known as?

Corrlate with which antigen?

Associated with what?

A

also known as?

Reactive arthritis

Corrlate with which antigen?

Correlation with HLA B27 (> 70%)

Associated with what?

Typically seen after patient has either a bacterial dysentery or an STD sometimes chlamydia

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634
Q

Reiter’s Syndrome (Reactive Arthritis)

Etiology

Demographic

Clinical Presentation

A

Etiology

  • Thought to be due to an abnormal immune response to the infection

Demographic

  • Almost exclusively seen in males in their twenties

Clinical Presentation

  • Oral lesions (~ 20% of cases) include painless oral ulcerations, erosions/erythema of mucosa, as well as erosions of the tongue which can mimic geographic tongue (both clinically and histologically)
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635
Q

Reiter’s Syndrome

Classic Triad

A

Reiter’s Syndrome

Classic Triad

▪ 1 – Polyarthritis (lasting more than one month)
▪ 2 – Conjunctivitis or uveitis
▪ 3 – Urethritis

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636
Q

Hyperparathyroidism

Radiographic features

A

▪ Stones, bones, moans, and groans
▪ Radiolucent appearance (generalized osteopenia) What we see in the bones is one of the earliest radiographic features that we see = sudden erosions in the phalanges in the bones of the hands followed by mineralization of the skeleton including max and mand, skull base. As a
result, you have generalized osteopenia. 10% of these patients have brown tumors
▪ Brown tumors: Brown tumors are the same as central giant cell granulomas. When they are associated with hyperparathyroidism, we call them brown tumors.
▪ Punctate or nodular calcifications in the joints and kidneys =stones

▪ Entire calvaria has a granular appearance classically known as the “salt and pepper” skull as a result of the generalized osteopenia, we have this granular appearance in the skull

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637
Q

Hypoparathyroidism

Radiographic features

A

What is Hypoparathyroidism:

Insufficient secretion of PTH
o Damage or removal of the parathyroid glands during thyroid surgery

Principal radiographic change: calcification of the basal ganglia
Sometimes we have pseudohypoparathyroidism. This happens when we have a normal amount of PTH, but there is something wrong with the response of the target tissue. So, we have normal PTH but abnormal response to PTH.

dental enamel hypoplasia, external root
resorption, delayed eruption, or root dilaceration

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638
Q

Hyperpituitarism

What is it?

What is its types

A

What is it?

  • Hyperfunction of the anterior lobe of the pituitary gland caused by a benign functioning tumor of the anterior lobe
  • it’s a systemic endocrine disease

What is its types ?

▪ Types based on age of onset

  • Gigantism happens in children, generalized overgrowth of most long bones, hard and soft tissue. These patients are usually very tall. Proportion in these patients may be normal, but very large appearance.
  • Acromegaly Increased hyperfunction in adult patients. In these patients, the epiphysis of the long bones already closed, you can see in the mand or max. One of the observable features is enlargement of the whole mandible/skull/sinuses/soft tissue. Patients usually present with “My hat is not fitting anymore, my denture is not fitting anymore”
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639
Q

Hyperparathyroidism

What is it?

What are its types?

A

What is it?

  • Excess of circulating parathyroid hormone important in formation of osseous structures
  • Increase bone remodeling but tips the balance of osteoblastic and osteoclastic activity in favor or osteoclastic resorption
  • it’s a systemic endocrine disease

What are its types?

o Primary hyperparathyroidism Type 1
▪ Uncontrolled parathyroid hormone production by
parathyroid neoplasm (adenoma >> hyperplasia >
adenocarcinoma)
o Secondary hyperparathyroidism Type 2
▪ Continuous parathyroid hormone production in
response to chronic low serum calcium levels
▪ Renal osteodystrophy

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640
Q

Which systemic disease is this?

A

Hyperparathyroidism

Here we see we see

  • a granular appearance of the max and mand bone everywhere, it is not localized.
  • There is a loss of bone density and the loss of definition of cortical bone.
  • Here we see a loss of definition of lamina dura as well because it is now granular, and is not as clear.
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641
Q

Which systemic disease shows radiographically like this ?

A

Hyperparathyroidism; this is the brown tumor which is sometimes well or ill defined, multi or unilocular radiolucency with granular septation.

If you have a patient that is younger than 15-20 years old that has a central giant cell granuloma ► you have to check that patient for hyperparathyroidism, because it could be a brown tumor.

How well did you know this?
1
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2
3
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642
Q

Which systemic disease shows radiographically like this ?

A

This is another medical CT scan. You see the granular appearance of
the maxilla, skull, and well-defined multilocular radiolucency with
granulation. We call this a brown tumor because it is associated with
hyperparathyroidism.

( systemic endocrine diseases)

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643
Q

Which systemic disease shows radiographically like this ?

A

Hyperparathyroidism

On our intraoral radiographs, we see loss of definition of lamina dura because the bone now has a granular appearance which extends to the lamina dura.

The teeth are usually normal, but there is a loss of lamina
dura around the teeth. These teeth are not mobile.

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644
Q

Which systemic disease shows radiographically like this?

A

a medical CT scan of a patient with secondary hyperparathyroidism.

We see a lack of cortical bone – no normal cortical bone. Inside the skull

we have a granular appearance, with radiolucent and radiopaque dots, we call this a salt and pepper dots.

This is why we call this a salt and pepper appearance, there is no normal cortical bone.

( systemic endocrine diseases)

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645
Q

Which systemic disease shows radiographically like this?

A

we have 2 Pas of patients

with pseudohypoparathyroidism.

  • hypoplasia of enamel, tooth material
  • hypoplastic tooth bud ( hypoplastic means arrested development)
  • delayed eruption,
  • external root resorption.
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646
Q

Which systemic disease shows radiographically like this?

A

Acromegaly (Hyperpituitarism)

  • enlargement of the mandibular bone with a high degree of enlargement
  • a class III appearance
  • enlargement of sella tursica because of the pituitary gland enlargement
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647
Q

Ranula

Definition

Associated with

Clinical features

Treatment

A

• Definition: mucocele-like lesion that forms unilaterally on the floor of the mouth
• may break through the mylohyoid muscle & enter neck space = “plunging ranula”
• associated with: the ducts of the sublingual & submandibular glands
• clinical features:
- must be on floor of the mouth for it to be considered a ranula
- big & have deep blue color if exophytic
- sometimes can grow downward/deep & won’t see blue as much
• treatment: surgical excision

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648
Q

Hyperparathyroidism

Radiographic features

A

▪ Stones, bones, moans, and groans
▪ Radiolucent appearance (generalized osteopenia) What we see in the bones is one of the earliest radiographic features that we see = sudden erosions in the phalanges in the bones of the hands followed by mineralization of the skeleton including max and mand, skull base. As a
result, you have generalized osteopenia. 10% of these patients have brown tumors
▪ Brown tumors: Brown tumors are the same as central giant cell granulomas. When they are associated with hyperparathyroidism, we call them brown tumors.
▪ Punctate or nodular calcifications in the joints and kidneys =stones

▪ Entire calvaria has a granular appearance classically known as the “salt and pepper” skull as a result of the generalized osteopenia, we have this granular appearance in the skull

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649
Q

Which systemic disease shows radiographically like this?

A

Osteoporosis

  • reduction in bone density,
  • larger bone marrow spaces.

We need more tests to confirm osteoporosis besides dental radiographs.

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650
Q

Hypoparathyroidism

Radiographic features

A

What is Hypoparathyroidism:

Insufficient secretion of PTH
o Damage or removal of the parathyroid glands during thyroid surgery

Principal radiographic change: calcification of the basal ganglia
Sometimes we have pseudohypoparathyroidism. This happens when we have a normal amount of PTH, but there is something wrong with the response of the target tissue. So, we have normal PTH but abnormal response to PTH.

dental enamel hypoplasia, external root
resorption, delayed eruption, or root dilaceration

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651
Q

Which systemic disease shows radiographically like this?

A

medical CT scan with a patient with osteopetrosis- very dense. Not a
nice definition of the cortical bone. We see decreased in size of skull
foramina.

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652
Q

Which systemic disease shows radiographically like this?

A

pt with Osteopetrosis

we see

Hypovascular bones so they are more prone to osteomyelitis. This is a sign of sequestrum which is a sign of osteomyelitis.

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653
Q
A

pt with Osteopetrosis

  • Generalized increase in bone density, increased trabeculation, loss of large bone marrow spaces.
  • These patients are more prone to osteomyelitis because they are Hypovascular.
  • We have to be careful in extractions because they don’t have the same vascularity as other healthy patients have.
  • We see an onion skin appearance by the white arrow.
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654
Q

Hyperpituitarism

What is it?

What is its types

A

What is it?

  • Hyperfunction of the anterior lobe of the pituitary gland caused by a benign functioning tumor of the anterior lobe
  • it’s a systemic endocrine disease

What is its types ?

▪ Types based on age of onset

  • Gigantism happens in children, generalized overgrowth of most long bones, hard and soft tissue. These patients are usually very tall. Proportion in these patients may be normal, but very large appearance.
  • Acromegaly Increased hyperfunction in adult patients. In these patients, the epiphysis of the long bones already closed, you can see in the mand or max. One of the observable features is enlargement of the whole mandible/skull/sinuses/soft tissue. Patients usually present with “My hat is not fitting anymore, my denture is not fitting anymore”
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655
Q

Hyperpituitarism

Radiographic
Features

A

▪ General features

  • Enlargement (ballooning) of the sella turcica
  • Enlargement of the paranasal sinuses (especially the frontal sinus)
  • Thickening of the outer table of the skull

▪ Jaws

  • Enlargement of the jaws, most notably the mandible
  • Class III skeletal as a result of the mandible enlargement with growth centering in the condylar head

▪ Teeth and associated structures

  • Spacing of the teeth, enlargement of tongue, it could result in spacing of teeth in the anterior region

o Hypercementosis the forces are higher now

  • so you may see Hypercementosis
  • Hypercementosis is excessive deposition of non-neoplastic cementum over normal root cementum, which alters root morphology. This cementum may be either hypocellular or cellular in natur*
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656
Q

Which systemic disease has this radiographic manifestation?

A

Ricket / Osteomalacia

hyperplasia or thinning of mineralization of teeth. We
can see hyperplasia of enamel in patients.

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657
Q

Hypopituitarism

What is it?

What is it called?

How it appears radiographically?

A

What is it?

Reduced secretion of pituitary hormones

it’s a systemic endocrine disease

What is it called?

Dwarfism

How it appears radiographically?

▪ Finding of the jaws
o Normal eruption of primary dentition but delayed exfoliation
o Small jaws -> crowding and malocclusion because there is not enough space for the teeth to erupt

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658
Q

Which systemic disease manifest radiographically like this?

A

Renal
Osteodystrophy 1

Presentation is variable. Sometimes you see denser or granular
appearance of bone. You see increase here

but you sometimes will also see loss of definition of lamina dura, sometimes a sclerotic appearance
and trabeculation.

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659
Q

Which systemic disease manifest radiographically like this?

A

Renal
Osteodystrophy 2

sometimes you see:

  • increase in bone density
  • loss of definition of lamina
  • dura and cortical bone
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660
Q

Osteoporosis

What is it?

Why it happens?

What the bone are like?

A

What is it?

▪ Generalized decrease in bone mass in which the histologic appearance of bone is normal, it is a metabolic bone diseases (MBD)

Why it happens?

  • Aging process (postmenopausal women) bone mass usually increases until 30 years of age, and then there is a gradual decrease- about 8% loss in females and 3% loss in males
  • Nutritional deficiencies
  • Hormonal imbalance
  • Inactivity
  • Corticosteroid or heparin therapy

What the bone are like?

▪ More prone to fracture (distal radius, proximal femur, ribs, and vertebrae)

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661
Q

Which systemic disease manifests radiographically like this?

A

Hypophosphatasia

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662
Q

Which systemic disease manifests radiographically like this?

A

large root canal structures, large root chambers, premature loss of
teeth = hypophosphatasia.

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663
Q

Osteopetrosis

What is it?

How is the bone is like?

What are the effects on other structures?

What are the consquences?

A

What is it?

Defect in the differentiation and function of osteoclasts, (osteoclasts that are used to resorb bone in the bone modeling process. They are not functioning properly ►so we have an increase in bone density.) It is a metabolic bone diseases (MBD)

How is the bone like?

Bone is dense, fragile, and susceptible to fracture _and infection ►we now have a_n osseous structure but small bone marrow spaces

What are the effects on other structures?

It compromised vascular structures and cranial nerves

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664
Q

Osteopetrosis

What are the consquences?

A
  • Compression of the cranial nerves as they pass through the narrowed skull foramina -> blindness, deafness, vestibular nerve dysfunction, and facial nerve paralysis.
  • Compromises hematopoiesis Poor vascularity -> osteomyelitis
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665
Q

Which systemic disease manifests radiographically like this?

A

Hypophosphatemia

  • Periapical lesions with radiolucency but no caries on the crown.
  • There is loss of definition of cortical bone.
  • On the teeth, you have:
    • large pulp chambers
    • hypoplasia of enamel and dentin
    • periodontal and periapical lesions.
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666
Q

Which systemic disease manifests radiographically like this?

A

Progressive Systemic
Sclerosis
(scleroderma)

sharp areas of resorption in the bones near muscles attached to the
angle of the mandible= masseter and medial pterygoid. You see
resorption at the coronoid process at the attachment of the temporal
bone as well.

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667
Q

Which Systemic disease manifests radiographically like this?

A

Progressive Systemic
Sclerosis
(scleroderma)

  • presence of widening of the PDL space everywhere around the root of the tooth.
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668
Q

Rickets and
Osteomalacia

What are they

Differences

Effects on Bones

A

What happens?

They are metabolic bone diseases (MBD)

Inadequate serum and extracellular levels of calcium and phosphate, failure of normal activity of vitamin D.

There are different levels in the conversion from I,12- dihydroxy vitamin D that can have errors, not just
the consumption of vitamin D.

Differences

Rickets: disease affects the growing skeleton in infants and
children
Osteomalacia: disease affects the mature skeleton in adults

Effects on bones:

A softening and weakening of bones

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669
Q

Which systemic disease mainfest radiographically like this?

A

On a sickle cell anemia patient, you see:

  • loss of this cortical bone area
  • the hair-on-end appearance on the skull
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670
Q

Which systemic disease mainfest radiographically like this?

A

Sickel Cell Anemia

enlargement of bone marrow spaces, less trabeculation, more
osteoporotic bone. You see periapical pathology associated with teeth
with no obvious reason. You see the radioluscencies around the apex of
the mandibular teeth.

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671
Q

In Rickets and
Osteomalacia, there is Failure of normal activity of vitamin D, what causes it?

A

o Lack of vitamin D in the diet
o Gastrointestinal malabsorption problems
o Lack of exposure to UV light
o Liver disease
o Kidney disease
o Defect in the intestinal target cell response

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672
Q

Clinical presentation

Ricket

vs

Osteomalacia

A

Rickets

o Growth retardation
o Short stature
o Bowing of long bones of the legs, waddling gait
o Radiograph manifestations in the teeth (especially <3 years of age) and jaws

Osteomalacia

o Weak fragile bone structure

o Diffuse skeletal pain

o Susceptible to fracture with minor injury

o Radiographic manifestations in the jaws are uncommon

o you may see hyperplasia or thinning of mineralization of teeth. You can see hyperplasia of enamel in patients.

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673
Q

Which systemic disease mainfest radiographically like this?

A

Thalassemia

  • osteopenic bone (loss bone mass and bones get weaker)
  • radiolucent appearance of bone
  • thinning of cortical bone around the mandible and maxilla.
  • Usually there is hypoplasia of the paranasal sinuses.
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674
Q

Renal
Osteodystrophy

What is it?

what can it lead to?

A

What is it?

Chronic renal failure produces bone changes by interfering with the hydroxylation of vitamin D in the kidneys -> hypocalcemia -> inhibit the normal calcification of bone and teeth (it is a metabolic bone disease)

what can it lead to?

(secondary hyperparathyroidism)

level of calcium is low leads to having hyperparathyroidism secondary to osteodystrophy

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675
Q

Which systemic disease manifests radiographically like this?

A

Dwarfism

  • hypopituitarism*
  • We see* multiple dental anomalies: hypodontia, radicular fusion, fused roots of left lateral incisor and left canine and impacted permanent teeth.
  • (from google)*
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676
Q

Hypophosphatasia

What is it?

What are the types?

A

What is it?

  • Rare metabolic bone disease due to lack of tissue-nonspecific alkaline phosphatase

What are its types?

Four types: prenatal, infantile, childhood, adult

  • The younger the age of onset, the more severe the
  • manifestations
  • It may have premature loss of these patients because loss of function of the lungs in these patients
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677
Q

Hypophosphatasia

Common factors?

Dental manfestations?

A

Common factors?

  • Low levels of tissue-nonspecific alkaline phosphatase
  • High blood and urinary phosphoethanolamine
  • Rickets-like skeletal malformations

Dental manfestations?

  • Premature shedding of primary incisors
  • Enamel hypoplasia
  • Enlarged pulp chambers and root canals
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678
Q

Hypophosphatemia

What is it?

_Clinical Manifestations?

Dental Manifestations?_

A

What is it?

  • A rare, heterogeneous group of inherited metabolic disorders characterized by decreased phosphate reabsorption in the distal renal tubules
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679
Q

Hypophosphatemia

Clinical Manifestations?

Dental Manifestations?

A

Clinical Manifestations

  • Rickets-like skeletal malformations

Dental Manifestations

  • Enlarged pulp chambers and root canals
  • Periapical and periodontal abscesses of no obvious cause
  • Enamel hypoplasia
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680
Q

Progressive Systemic
Sclerosis
(scleroderma)

What is it?

Demographics?

A

What is it?

  • Excessive collagen deposition resulting in hardening (sclerosis) of the skin and other tissues can have involvement of GI tract, heart, kidney,etc

Demographics?

  • Middle aged female
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681
Q

Progressive Systemic
Sclerosis
(scleroderma)

Clinical symptoms

Oral Manifestations

A

Clinical Presentation

  • Thickened, leathery quality skin
  • joint pain
  • exaggerated response to cold (Raynaud’s disease)
  • heartburn.
  • more prone for heart problems and respiratory
    insufficiencies,

Oral Manifestations

  • microstomia (small mouth)
  • Xerostomia (dry mouth)
  • telangietasia (“spider veins”)
  • Increased decayed, missing and filled teeth.
  • higher Gingivitis scores (usually)
  • Deeper Periodontal Pockets
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682
Q

Progressive Systemic
Sclerosis
(scleroderma)

Treatment

A

Treatment for generalized symptoms may involve:

  • corticosteroids
  • immunosuppressants, such as methotrexate or Cytoxan
  • nonsteroidal anti-inflammatory drugs

Depending on your symptoms, treatment can also include:

  • blood pressure medication
  • medication to aid breathing
  • physical therapy
  • light therapy, such as ultraviolet A1 phototherapy
  • nitroglycerin ointment to treat localized areas of tightening of the skin

(from google)

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683
Q

Sickle Cell Anemia

What is it?

What causes it?

A

What is it?

Chronic hemolytic blood disorder

What causes it?

▪ Abnormal hemoglobin, resulting in anemia -> by increasing the production of red blood cells -> requires compensatory hyperplasia of the bone marrow

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684
Q

Sickel Cell Aniema

Radiographics findings

A
  • loss of this cortical bone area
  • See the hair-on-end appearance on the skull
  • enlargement of bone marrow spaces
  • less trabeculation, more osteoporotic bone
  • periapical pathology associated with teeth
    with no obvious reason
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685
Q

Thalassemia

What is it?

What causes it?

A

What is it?

  • Defect in hemoglobin synthesis

What causes it?

  • RBC with reduced hemoglobin content and short life span
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686
Q

Thalassemia

Clinical and Radiographic findings

A
  • Hyperplasia of the bone marrow component of the bone which results in fewer trabeculae per unit area and can change the overall shape of the bone
  • Protrusive premaxilla
  • Radiographic appearance very similar to Sickle Cell Anemia
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687
Q

Suspect systemic endocrine and metabolic disease if radiographs show what?

A

generalized decrease in bone density of jaws (thin cortices; granular cancellous bone; loss of lamina dura).

  • Refer to physician for lab tests to make the diagnosis
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688
Q

We can include certain systemic endocrine and metabolic diseases as radiographic differentials in the presence of:

o Localized focus of radiolucency- think what?
o Mandibular prognathism and incisor flaring- think what?
o Premature shedding of primary incisors-think what?
o Enamel hypoplasia, enlarged pulp chambers and periapical abscesses of no obvious cause- think what?

A

o Localized focus of radiolucency► think brown tumor and
hyperparathyroidism
o Mandibular prognathism and incisor flaring► think acromegaly
o Premature shedding of primary incisors► think
hypophosphatasia
o Enamel hypoplasia, enlarged pulp chambers and periapical
abscesses of no obvious cause► think hypophosphatemia

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689
Q

Palatine Torus/Torus Palatinus

A
  • Tori are incredibly common, a normal of variant
  • Part of physical exam is to visualize as well as running index finger over the hard palate every time
  • Sometimes, torus palatinus is quite small and unnoticeable until you touch it (feel a hard bump and it’s just a bony growth)
  • Sometimes, they are pedunculated; Sometimes, they get so large they become traumatized; vascular supply on surface can sometimes form ulcerations and even get a little bone exposure.
  • If patient with history of use of bisphosphonates (bone modifying agents given to women who have osteoporosis or osteopenia and to prevent metastesis for certain cancers), he will remove that dead bone, and it will slowly heal. That’s one of the perils of having an enlarged palatine torus
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690
Q

What is this clinical finding?

A

Palatine Torus/Torus Palatinus

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691
Q

What is this clinical finding?

A

Palatine Torus/Torus Palatinus

692
Q

What is this clinical finding?

A

Mandibular Torus:
Torus Mandibularis

693
Q

What is this clinical finding?

A

Mandibular Torus:
Torus Mandibularis

694
Q

What is this clinical finding?

A

Buccal Exostoses

695
Q

Mandibular Torus: Torus Mandibularis

A
  • Sometimes pt’s tori are so large that the sublingual frenum gets stuck underneath
  • repeated irritation/trauma can create a little white rim on the tori
  • these tori are rock hard and may grow overtime, but we don’t really understand why people get them
696
Q

What is this clinical finding?

A

Unencapsulated Lymphoid Aggregates

697
Q

What is this clinical finding?

A

Lymphoepithelial
cyst

we see a tiny yellowish cyst. we see the blood vessels on the surface; this is quite characteristic.

698
Q

What is this clinical finding?

A

Unencapsulated
Lymphoid
Aggregates

Post-tonsillectomy

Can even develop these on area of tonsils.
(left pic) Red/salmon is a lymphoid aggregate (unencapsulated lymphoid tissue). This is someone
who had a tonsillectomy , and you can see these
lymphoid aggregates on posterior pharyngeal wall (salmon color).They move around the area.
(right pic) It grew back even in post-tonsillectomy patients.

699
Q

What is this clinical finding?

A

Fordyce Granules

700
Q

What is this clinical finding?

A

Fordyce Granules

701
Q

Buccal Exostoses

A
  • Sometimes patient develops exostoses (another word for torus).
  • Can get buccal exostoses, all just bone. Can pick these up on radiograph, the bone is a lot denser.

Why does it happen?

  • Maybe it’s related to parafunctional habits – but don’t really understand the
  • basis for the exostosis.
  • They’re going to be bilateral. If it’s unilateral, we start thinking about other bony diseases

a variant of normal

702
Q

What is this clinical finding?

A

Fimbriated
fold/Plica
semiluminaris

703
Q

What is this clinical finding?

A

Frenal tag

704
Q

Unencapsulated Lymphoid Aggregates

A
  • the lymphoid aggregates are part of the foliate papillae (they contain some taste buds as well).
  • This is lymphoid tissue -- when you get a cold or upper respiratory tract infection, sometimes these areas can become hyperplastic in response to infection – can become a little enlarged.
  • These are usually bilateral.
  • a variant of normal
705
Q

What is this clinical finding?

A

Sublingual Varices

706
Q

What is this clinical finding?

A

Sublingual Varices

707
Q

What is this clinical finding?

A

Sublingual Varices

708
Q

What is this clinical finding?

A

Circumvallate papillae

709
Q

What is this clinical finding?

A

Parotid Papillia (Stenson duct)

710
Q

What is this clinical finding?

A

Parotid Papillia (Stenson duct)

711
Q

What is Lymphoepithelial
cyst?

A

a cystic structure.develops in that area where there are already unencapsulated lymphoid tissue.

This is not normal – Pathologic
Sometimes when you get a cyst in this area – because of lymphoid tissue, you can develop lymphoepithelial cyst – a tiny yellowish cyst. we see the blood vessels on the surface; this is quite characteristic.

712
Q

What is this clinical finding?

A

Linea Alba

713
Q

What is this clinical finding?

A

Leukoedema

714
Q

Fordyce Granules

A
  • Occurs on the buccal labial mucosa, retro molar pad and tonsillar area and lips
  • They are white or yellow ectopic sebaceous glands
  • They can be present in small or large quantity
  • Why do we have sebaceous glands in mouth? we dont know, evolutionary advantage? we don’t really understand.
  • a variant of normal
715
Q

What is this clinical finding?

A

Palatal Rugae

716
Q

Fimbriated
fold/Plica
semiluminaris

A
  • Some patients have more obvious fimbriated folds or plica semilunaris in their mouths than others
  • When you look at the ventral surface of the tongue, you’ll sometimes be able to pick these up.
  • These are duct opening from a series of salivary glands, minor glands, but they’re a little bit different than other minor glands in the mouth.
  • They produce more of a viscous type of saliva, and they are the glands of the Blandin and Nuhn
  • a variant of normal
717
Q

What is a Frenal tag?

A
  • Frenal attachments are thin folds of mucous membrane with enclosed muscle fibers that attach the lips to the alveolar mucosa and underlying periosteum.
  • Most often, during the oral examination of the patient the dentist gives very little importance to the frenum, for assessing its morpholology and attachment.
  • Sometimes occur; essentially normal of varient
718
Q

Sublingual Varices

A
  • Tortuous dilated vessels (enlarged engourged veins) on the ventral surface of the tongue, and sometimes stretch onto lateral border
  • Appears bluish purple in color
  • More prominent with increasing age; we don’t see it in younger pts.
  • Nothing to be concerned about, a variant of normal
719
Q

Circumvallate papillae

A
  • Located in the posterior region of the tongue; dividing the body from the base
  • They are mushroom shaped and arranged in V-shape formation
  • Although they are usually not apparent in most patients, you may be able to visualize them in some
  • a variant of normal
720
Q

Parotid Papillia (Stenson duct)

A
  • Located in right and left buccal mucosa at the level of the occlusal plane close to the maxillary first and second molar.
  • This structure may appear as a small dot or have a prominent pink to red papillae presence.
  • This is the parotid papilla, and It is the opening of the parotid duct which drains saliva from the parotid gland.

A normal of variant

721
Q

Linea Alba

A

•a white line or keratotic area that present along occlusal plane in some patients

  • due to some friction In that area. (the buccal mucosa)
  • It varies in thickness and opacity
  • Can be seen in some patients who have bruxism
  • a variant of normal
722
Q

Leukoedema

A
  • A bluish and white filmy opalescence of the mucosa is observed
  • In order to differentiate it from other white lesions à gently stretch the patient’s cheek forward and the leukoedema will disappear or partly fade and appears less apparent
  • It is commonly found in people of color and some smokers.
  • a variant of normal
723
Q

Palatal Rugae

A
  • Raised ridges or folds
  • Located in the anterior palate on either side of the mid-palatine raphe behind the incisive papilla
  • They vary in number and size
  • May increase with age
  • a variant of normal
724
Q

Irritation Fibromas

Composed of

Etiology

Clinical features ;Color

Location

Treatment

A
  • AKA – Fibroma, Traumatic Fibroma
  • Composed of dense, scar-like, fibrous connective tissue
  • Occurs as a result of chronic trauma
  • Clinical Features: Exophytic lesion
  • Usually less than a centimeter in diameter
  • Color: lighter pink than surrounding mucosa,the surface can be white sometimes bc it’s rubbing and bumping into other oral structures (like teeth), so they get surface keratinization
  • Locations: buccal mucosa, tongue, lips, gingiva
  • Very common; totally benign soft lesion
  • Treatment: You don’t have to remove them, but the surgical Tx = to excise them bc pts will stop biting them and they’ll heal and stop the irritation
725
Q

What is this clinical finding?

A

Irritation Fibromas

726
Q

What is this clinical finding?

A

Irritation Fibromas

727
Q

What is this clinical finding?

A

Chronic Hyperplastic Pulpitis (pulp polyp)

728
Q
A

Giant Cell Fibroma

729
Q

Chronic Hyperplastic Pulpitis

What is it?

Location?

Age?

Clinical Appearance?

Treatment?

A

• AKA: pulp polyp
• An e_xcessive proliferation of chronically inflamed dental pulp tissue_ – granulation tissue/ fibrous tissue with inflammatory cells (like a little fibroma that
occurs from pulp tissue​) ( benign soft tissue leasion)
• Location:
• Teeth with large, open carious lesions
• Primary or permanent molars
• Age: Children & young adults
• Clinical Appearance: A red or pink nodule of soft tissue protruding from the
pulp chamber and fills the entire cavity of the tooth
• Treatment: RCT or extraction of tooth

730
Q

Giant Cell Fibroma

A
  • Very small form of fibrous tumour that show giant cells
  • Age: relatively rare in paediatric patients.
  • Clinically it is presented as a painless, sessile, or pedunculated growth which is usually confused with other fibrous lesions like irritation fibromas or Retrocuspid papilla
  • Location: Largely occur on lower gingivae and on palate\
731
Q

What are these clinical findings (what is the name of the syndrome or complex?)

A

Tuberous sclerosis complex

we see A lot of gingival enlargement – is this overgrowth from disease or from seizure medication? Multi organ system involvement

732
Q

What is this clinical finding?

A

Epulis Fissuratum

733
Q

Cowden Syndrome

A
  • (multiple hamartoma and neoplasia syndrome)
  • • Autosomal dominant disorder affecting multiple organ systems
  • • Caused by mutations in the phosphatase and tensin homolog gene (PTEN, a tumor suppressor gene)
  • • Oral and perioral findings include
  • *multiple papules on the lips and gingivae,**
  • papillomatosis (benign fibromatosis) of the buccal, palatal, faucial, and oropharyngeal
  • mucosae often producing a “cobblestone” effect, and the tongue may also present as pebbly or fissured.
  • • Multiple papillomatous nodules (histologically inverted follicular keratoses or
  • trichilemmomas) are often present on the perioral, periorbital, and perinasal skin, the pinnae of the ears, and neck.
  • • These nodules are often accompanied by lipomas, hemangiomas, neuromas, vitiligo, café au lait spots, and acromelanosis .
  • • A variety of neoplastic changes occur in the organs exhibiting hamartomatous lesions,with an increased rate of breast and thyroid carcinoma and gastrointestinal malignancy.
  • Squamous cell carcinoma of the tongue and basal cell tumors of the perioral skin have also been reported.
  • Incredibly rare ( board loves it)
734
Q

What is this clinical finding?

A

Inflammatory Papillary Hyperplasia of the Palate

735
Q

What is these clinical findings? (what is the name of the syndrome or complex?)

A

Cowden Syndrome

Very rare!

736
Q

Tuberous sclerosis complex

A

• is an inherited disorder caused by mutations in the tuberous sclerosis complex (TSC1 or TSC2) genes
• Characterized by seizures and mental retardation associated with hamartomatous glial proliferations and neuronal deformity in the central nervous system.
• Fine wart-like lesions (adenoma sebaceum) occur in a butterfly distribution over the cheeks and forehead, and histologically similar lesions (vascular fibromas) have been described intraorally.
• Characteristic hypoplastic enamel defects (pitted enamel hypoplasia)
occur in 40 to 100% of those affected.
• Rhabdomyoma of the heart and other hamartomas of the kidney,

737
Q

Epulis Fissuratum

AKA

Cause

Location

Clinical presentation

Composed of

Treatment

A

• AKA: denture-induced fibrous hyperplasia, fibrous inflammatory hyperplasia
• Cause: ill-fitting denture
• Location: vestibule (maxilla or mandible), along the
denture border
•Clinical presentation: Arranged in elongated folds of tissue into which the
denture flange fits; • Surface ulceration within the folds is common
• Composed of dense fibrous connective tissue
• Treatment: surgical excision (scalpel vs CO2 laser -laser is better)
and reline then remake of denture

738
Q

What is the clinical finding?

A

Pyogenic Granuloma

We can see the corresponding radiograph;

-although the radiograph suggests generalized bone loss, there is a lot of calculus on
the distal of #16 > it makes sense that this is a pyogenic granuloma

739
Q

What is this clinical finding?

A

Pyogenic Granuloma:

740
Q

Pyogenic Granuloma

Histology

A

They are filled with blood vessels so they’re very very rich
in vascularization > they tend to bleed easily

741
Q

What is this clinical finding?

A

A parulis

It is not a pyogenic granuloma

A parulis is a proliferation of granulation tissue at the opening of a sinus tract
When the infection breaks through the alveolar bone and presents itself,
it will sometimes cause this proliferation of granulation tissue

742
Q

Inflammatory Papillary Hyperplasia of the Palate

Majority occur with what disease?

Associated with what?

Clinical appearance

Treatment

A
  • Majority occur with denture stomatitis
  • Associated with a removable full or partial denture or orthodontic
  • appliance (Something you see in patients who wear denture all the time, don’t take it out, chronic denture wear)
  • Clinical Appearance: Palatal vault is covered by multiple erythematous papillary projections (fibrous connective tissue surfaced by epithelium) –(papillary but no papilla, instead it’s bumpy and bosselated)
    • Granular or cobblestone appearance
    • Erythema is usually due to superinfection with candida
  • Treatment:Treat underlying candidiasis, fix denture. These bumps can be removed, take electrosurgery loop, and scrape off the bumps – heals well
743
Q

What is this clinical finding?

A

Peripheral Ossifying or Cementifying Fibroma

Lesion in the image is pedunculated – put a periodontal probe on normal gingiva and glide along underneath it, there’s a stalk

744
Q

Peripheral Ossifying Fibroma

Histology

A
  • When sessile, when removing it, take scalpel blade and just cut into it
  • If has a little bone or cementum formation inside it, you can feel the bone with the scalpel
745
Q

What is this clinical finding?

A

Peripheral Giant Cell Granuloma

746
Q

Peripheral Giant Cell Granuloma

Histology

A

Giant cells inside the lesion

747
Q

What are the 3P

or 4P?

A

• Pyogenic granuloma/pregnancy tumor
• Peripheral ossifying**_or_**cementifying fibroma
• Peripheral giant cell granuloma
• Peripheral fibroma (4P)

Memorize these well!

All benign soft tissue lesions

748
Q

Pyogenic Granuloma

What a differential diagonsis to consider if we see it

A
  • if it’s on the gingival tissues, take a radiograph
  • always consider SCC as a differential diagnosis
749
Q

What is this clinical finding?

A

Inflammatory Gingival Enlargement

Example of someone with true hyperplastic gingivitis
Maybe related to very poor plaque control
In this case, either porcelain or porcelain fused to metal full coverage restorations that have very
bulky margins, and that may play a role for food to pick up

750
Q

Pyogenic Granuloma

What is it?

Etiology

Assossiated with which demographics?

Location?

Treatment?

A
  • What is it? Reactive connective tissue hyperplasia - exuberant granulation tissue; Misnomer – not pyogenic and not a true granuloma
  • Etiology: Response to injury - calculus or overhang restoration
  • Assosiated with? Often occurs in pregnant women (“pregnancy tumor”), also associated with puberty
  • Treatment: Excision and removal of irritant (eg calculus, overhanging restorations)
751
Q

What is the Differential diagnosis of gingival enlargement

A

Acute Myelogenous Leukemia (AML)

Wegener’s Granulomatosis

Kaposi Sarcoma

Plasma Cell Gingivitis

Generalized gingival enlargement – all different cases and diseases

752
Q

How to differentiate Pyogenic Granuloma from the other 2Ps ?

(Peripheral ossifying or cementifying fibroma & Peripheral giant cell granuloma)

A
  • They often occur in the gingival, but can occur in multiple areas
    • that’s the one thing that distinguishes this from the other 2 P’s: pyogenic granuloma can occur on ANY oral site, most commonly on the gingival tissues
753
Q

What is this clinical finding?

A

Hereditary Gingivofibromatosis

754
Q
A

Infantile
Hemangioma

(“strawberry” hemangioma).

Infant with two red, nodular masses on
the posterior scalp and neck

Neville Cr

755
Q

Pyogenic Granuloma

Clinical appearance

Location

Size

Developing rate

Age:

A
  • Clinical appearance
  • Usually ulcerated
  • Soft exophytic lesion, either sessile or pedunculated
  • Deep red to purple in color, bleeds easily
  • Location:
    • Most common – gingiva
    • Also occurs in other areas of the oral mucosa ( can happen anywhere)
  • Size: small to large (millimeters to centimeters)
  • Develop rapidly and then remain static
  • Age: Any age
756
Q

How to recogonize a capillary Malformation?

A

When you apply pressure to it, it evacuates the lesion (disappears!), when you pull away, it refills and you see it again – that tells you it’s a vascular lesion

757
Q

What is this clinical finding?

A

Capillary
Malformation (Low
flow)

758
Q

How to differentiate between

Venous
malformation (low
flow)

from

Arteriovenous or
arteriolar malformations
(High flow)

A

Venous malformation
(Low flow)
No bruit, non-pulsatile
vs
Arteriovenous or
arteriolar malformations
(High flow)
Bruit and pulsatile

In other word, Venous lesion = Does not have pulse

Histopathologically they look different too

Treatment:

-Don’t biopsy this unless it’s rapidly growing, if it is rapidly growing then suspect ► angiosarcoma? ( unlikely)

-can be surgically treated by oral surgeons -clamping off the blood vessel and dissecting it out, or putting a sclerosis agent

759
Q

What is this clinical finding?

A

Venous
malformation (low
flow)

Many pts can live with this without treatment

760
Q

What are these clinical findings ( which syndrome or complex is this)?

A

Osler-Weber-Rendu
Syndrome

761
Q

What are these clinical findings? (What is the syndrome or complex)?

A

Sturge-Weber
Angiomatosis

Sturge-Weber syndrome

762
Q

What are these clinical findings (What is the syndrome or complex)?

A

Sturge-Weber
Angiomatosis

Sturge-Weber syndrome

Notice how the vascular malformation is only one side..

Remember: Vascular changes follow trigeminal nerve, so it doesn’t cross midline

763
Q

What is this clinical finding?

A

Lymphangioma

764
Q

What is this clinical finding?

A

Cystic Hygroma

a type of Lymphangioma

765
Q

Peripheral Ossifying or Cementifying Fibroma

What is it?

Clinical appearance

Derived from

Age

Sex

Reccurance rate

Treatment

A
  • a reactive benign soft tissue lesion
  • Clinical appearance: Well-demarcated, sessile or pedunculated lesion that appears to originate from the gingival interdental papilla
  • Derived from: cells of the periodontal ligament
  • Age: children and young adults
  • Sex: females more than males
  • Recurrence rate – about 16%
  • Treatment: Surgical excision
766
Q

What is this clinical finding?

A

Neuroma

(Traumatic Neuroma)

Not a benign true neoplasm, it’s reactive lesion
This is an edentulous patient, so resorbed bone, so flange of denture is impinging in the area of mental foramen – develop from repeated trauma
Sometimes have to cut into nerve, peel the neuroma from nerve, careful not to sever nerve

767
Q

What are these clinical findings (Which syndrome or complex)?

A

Multiple Endocrine
Neoplasia (MEN)
Syndrome

768
Q

What is this clinical finding?

A

neurofibroma

-it looks like lymphoepithelial cyst, but this is further anterior and not where you would get
lymphoid tissue – so it’s not lymphoepithelial cyst, it’s neurofibroma
Yellow – nerves typically yellow

769
Q

What is this clinical finding?

A

neurofibroma

770
Q

Peripheral Giant Cell Granuloma

​What is it?

Location?

Age?

Clinical appearance:

Radiographic finding?

A
  • What is it? Probably a reactive lesion due to local irritating factors (giant cells develop inside the lesion which is a benign soft tissue lesion)
  • Location: Gingiva, usually anterior to the molars
  • Age: Most frequently seen between 40-60 years old
  • Clinical appearance: dusky purple, sessile or pedunculated, smooth-surfaced, dome-shaped papule or nodule. Most lesions are less than 1.5 cm in diameter, though infrequently, may grow as large as 5 cm in greatest dimension
  • Radiographic Features: Usually none, but superficial destruction of the alveolar bone may occur
771
Q

What are these clinical findings (which syndrome or complex)?

A

Neurofibromatosis syndrome

von Recklinghausen’s Disease

  • Lisch nodules on iris, pigmented (eye picture)
  • Neurofibromatosis in mouth (bottom left picture)
  • Café au lait (bottom right picture)
772
Q

What is the clinical finding?

A

Schwannoma/ Neurilemoma

773
Q

What is this clinical finding?

A

Schwannoma/ Neurilemoma

774
Q

Schwannoma/ Neurilemoma

Histology

A

Antoni A and Antoni B.

Streaming fascicles of spindle-shaped Schwann cells characterize Antoni A tissue.

These cells
often form a palisaded arrangement around central acellular, eosinophilic areas known as Verocay bodies. Antoni B
tissue is less cellular and less organized; the spindle cells are randomly arranged within a loose, myxomatous stroma.

775
Q

What is this clinical finding?

A

Granular Cell Tumor

776
Q

What is this clinical finding?

A

Granular Cell Tumor

777
Q

Granular Cell Tumor

Histology

A

Has pseudoepitheliomatus hyperplasia of epithelium (seen on left picture)
Characteristic feature are the granular cells on the right picture
Infiltrate down into the muscle layers, that’s when pathologist confirms granular cell tumor

778
Q

Diagnosis and Treatment

of the 3Ps

A

•Diagnosis: All 3 “P” lesions usually occur on gingival interdental papillae ( however pyogenic granuloma can occur anywhere)
• Since they can look similar clinically, excisional biopsy necessary to
determine diagnosis
• Treatment: complete excision and removal of local irritant (scaling
and root planing)

779
Q

What is this clinical finding?

A

Congenital Epulis

780
Q

Gingival Enlargement

Etiology

A
  • Response to chronic inflammation
  • Hormonal changes (pregnancy/puberty)
  • Immune-mediated/plasma cell gingivitis
  • Drug induced
  • Genetic/ Inherited

NOTE: Gingival enlargement is not always hyperplastic tissue

781
Q

What is this clinical finding?

A

Neuroectodermal tumor of infancy

look how they removed it here surgically

is rare, rapidly growing, pigmented neoplasm of neural crest origin. It is generally accepted as a benign tumour despite of its rapid and locally destructive growth.

782
Q

Lipoma

What is it?

Location?

Cliniclly?

Histologically?

Treatment?

A
  • What is it: Benign tumor of mature fat cells; Relatively rare
  • Location:Won’t see on gingival tissue, will see on buccal mucosa, on the tongue, and floor of the mouth
  • Clinically appears as a yellowish mass surfaced by thin overlying epithelium, When you feel it, it’s soft
  • Histologically: a well-delineated tumor composed of mature fat cells with a thin capsule
  • Treatment: surgical excision,does not recur
783
Q

What is this clinical finding?

A

Lipoma

Usually very orange looking lesion in site where there’s adipose tissue

Very obvious, nothing as orange as lipoma

784
Q

Drug Induced Gingival
Enlargement

What are the famous drugs that are known to cause it?

A
  • Phenytoin: (or Dilantin) – the drug that used to be given to every single
  • person that had seizures
  • Calcium-channel blockers
    • Nifedipine not as prescribed anymore
    • Dilitiazem still prescribe
    • Amlodipine: is prescribed as one of the first line therapy for hypertension (very commonly prescribed); it doesn’t typically cause gingival overgrowth except in some selected patients, usually
      those with pretty poor oral hygiene
  • Cyclosporine A (used for for bone marrow transplant, graft vs
    host disease, solid organ transplant)
    • Cyclosporine is universally recognized as causing gingival hyperplasia
    • Cyclosporine is largely replaced with Tacrolimus, which typically doesn’t cause gingival overgrowth
  • Cyclosporine A is largely replaced with Tacrolimus, which typically doesn’t cause gingival overgrowth
    Some drugs have more connective tissue component, others have more epithelial component
    Not all identical under the microscope
  • Cyclosporine provides more epithelial change, Dilantin causes more of a connective tissue change
785
Q

What is this clinical finding?

A

Vascular leiomyoma

High-power view showing spindle-shaped cells with bluntended
nuclei. Immunohistochemical analysis shows
strong positivity for smooth muscle actin (inset).

786
Q

What is this clinical finding?

A

Rhabdomyoma

Will see the striated muscle
Differential diagnosis… looks like granular cell tumor – don’t know til you remove it
If patient presents with relatively slow growing tumor like this, will I get incisional biopsy or
excisional biopsy? Hard to say
If confident benign tumor and it’s this size and I don’t think it’s vascular (no pulse, can do
aspiration), feels firm – try to excise it
If it looks different, like you think it’s malignant minor salivary gland neoplasm (won’t find it in this
site, but if it’s on hard palate) – incision?

787
Q

What is this clinical finding?

A

Leiomyosarcoma

788
Q

Hereditary Gingivofibromatosis

What causes it?

How common?

what effects on oral cavity?

Treatment?

A

What causes it?

  • Various genes that are implicate (Putative inherited mutations are in the SOS1 or CAMK4 genes.) Linked to both autosomal dominant and recessive patterns of inheritance

​How common?

  • Very rare

what effects on oral cavity?

  • Sometimes gingival overgrowth will completely obliterate the teeth, grow around entire tooth
  • Enlargement may be present at birth or may become apparent only with
    the eruption of the deciduous or permanent dentitions.
  • Tooth migration, prolonged retention of the primary dentition, and
    diastemata are common, and enlargement may completely cover the
    crowns of the teeth, resulting in compromised oral function.

Treatment

  • Need surgical (usually laser) treatment – just grows back, so have to get it done periodically
789
Q

What are these clinical findings?

A

Rhabdomyosarcoma

In this case, hasn’t broken through epithelium
They don’t all break through

790
Q

Infantile
Hemangioma

When do they appear?

Rate of Development

Clinical presentation

Treatment

A
  • When do they appear? They are rarely present at birth, infants are Born with this in place.
  • Rate of development: the tumor will demonstrate rapid development that occurs at a faster pace than the infant’s overall growth in the first few weeks of life,
  • Clinical presentation: Either superficial or deeper tumors
    • Superficial tumors of the skin appear raised and bosselated with a bright-red color (“strawberry” hemangioma); They are firm and rubbery to palpation, and the blood, cannot be evacuated by applying pressure.
    • Deeper tumors may appear only slightly raised with a bluish hue.
    • May be left with a pink or magenta macule in site where hemangioma occurred after its involute
  • Treatment: Typically will involute with time, Some cases don’t involute, so need to be removed
  • It is a vascular Anomaly
791
Q

What is this clinical finding?

A

Fibrosarcoma

792
Q

Capillary
Malformation (Low
flow)

A
  • a type of vascular anomaly
  • CMs are commonly known as port wine stains.
  • They look like a pink, red or purple patch of skin
  • occur in 1 in 300 newborns.
793
Q

What is this clinical finding?

A

Kaposi Sarcoma

Solitary vascular lesion on hard palate – it was so small so he decided to just excise it in this case^

794
Q

What are these clinical findings?

A

Kaposi Sarcoma

  • Widespread Kaposi, can see cutaneous lesions
  • Oral images of this patient: on palate, starts with macule on patient’s left posterior palate –macular stage
  • Then in becomes proliferative – exophytic nodular stage (seen on patient’s right anterior palate,surrounding canine and some incisors)
  • Can see engorged blood vessels in area on histology slide
795
Q

What is this clinical finding?

A

Plasmacytoma in Multiple Myeloma

  • They already had multiple myeloma then developed plasmacytoma
  • When you biopsy this, it’s filled with plasma cells bc they’re producing the abnormal immunoglobulins, which are the cause of the devastating issues of multiple myeloma
796
Q
A

Acute myelogenous
leukemiawith
granulocytic
sarcoma

  • *Complaining of lump inside of her cheek**
  • *Notsomuch worried about her gingiva**, despite her overgrowth – leukemic infiltrates that got into gingival tissues
  • *Left buccal mucosa**, kept biting on it, feeling incredibly fatigued though she was always working out
  • *Oral surgeon biopsied** her buccal mucosa and read by pathologist as pyogenic granuloma
  • *Physician** sent her for bloodwork, dental school sent her for bloodwork too
797
Q

What is this clinical finding?

A

Lymphoma

  • Well circumscribed ulceration in area
  • Associated swelling in periphery
  • White change in the patient’s left area
  • Been there for 3 weeks
  • It’s lymphoma
798
Q

What is this clinical finding?

A

Looks like it could be a salivary gland neoplasm, but it’s not
It was another lymphoma
Manifest in a number of different ways

799
Q

Case

40 year old male
Completely healthy otherwise
Not taking any medications
Presents with bump on the tongue

First question: did you do anything that might have led to this? Bite your tongue?
“possible I bit my tongue, or it could be when I had a dental procedure, maybe they accidentally
cut into the side of my tongue” – then it developed
This tells us, is this a reactive lesion?
Is it pedunculated or sessile? It’s pedunculated, larger at the top than the base
Let’s look at the surface: it’s ulcerated
When palpating, it’s only on the surface - don’t feel any submucosal presentation
Tongue underneath feels relatively normal
This bump is kind of firm and it bleeds like crazy when you touch it
When you look at teeth, no area where they’re too sharp

A

Do you think it’s a fibroma? No. Why?
Fibroma is covered with normal coloring epithelium – sometimes see a little white change on surface or see tiny traumatic ulcer on surface This is not like that, this is completely ulcerated
Not fibroma; fibroma is a chronic bump that patient is aware of
Is it squamous cell carcinoma? Interesting, it is indeed very friable; but no
Sometimes SCC can develop and can be exophytic and don’t have deep invasion, But this is pedunculated, SCC would not be pedunculated
History says there could be some kind of trauma, biting, or nick with bur – not squamous cell
Mucocele? No
Would you typically develop mucocele on lateral border of tongue? No
Not going to be as many mucoceles in this area, but there are the glands of Blandin and Nuhn, so it’s possible to develop on ventral surface of tongue
This bump doesn’t look like a fluid filled bump though, it has surface ulceration, redness ;Mucoceles have intact surface, would not bleed, or be red
Granular cell tumor? No
Granular cell tumor would have normal overlying epithelium (it’s pushing up from underneath)
This does not have normal overlying epithelium
Hemangioma reserved for congenital; not a vascular malformation either
Neurofibroma? No, not the same surface
Salivary gland neoplasms? Possible, there are salivary glands in that area; keep this in differential
The one that this is is pyogenic granuloma: usually red, ulcerated, and bleeds easily

800
Q

Osler-Weber-Rendu
Syndrome

AKA

What is it and its clinical appearance

Type of Herditary and Etiology

What can it cause?

Location?

A

AKA

• Hereditary Hemorrhagic Telangiectasia

What is it and its clinical appearance

• disorder of development of the vasculature characterized by telangiectases and
arteriovenous malformations in specific locations. These are essentially endothelial cell issue – get tafted area of abnormal blood vessels multiple different organ systems – causes complications

Type of Herditary and Etiology

•Autosomal dominant with mutations i_n at least five gene_s but mutations in two genes (ENG and ACVRL1/ALK1) cause approximately 85% of cases.

What can it cause?

• Can cause hemorrhage

Location?

often on fingers, lips,tongue, but always look at the fingers!

801
Q

Sturge-Weber
Angiomatosis

Sturge-Weber syndrome

A
  • Rare, non-hereditary developmental condition
  • Vascular proliferation involving tissues of the brain and face
  • Face: Unilateral distribution along one or more segments of the trigeminal nerve ( unilateral means don’t cross the midline) known as port wine stain/ nevus flammeus – they are deep-purple color.
    • Intracranial calcifications; neurological disorders
  • Intraoral involvement is common
802
Q

Lymphangioma

What is it?

Types

Locations:

Treatment

A

What is it?

• Benign tumor of lymphatic vessels
Types

  • Microcystic
  • Mixed
  • Cystic hygroma (macrocystic)

Location

  • Most frequent extra-oral location: posterior triangle of the neck;
  • intraoral location: tongue

Treatment:

monitor, surgery if needed, recurrence common

803
Q

Neuroma

AKA

What is it?

Clinical presentation

Location

A

AKA

  • traumatic neuroma

What is it?

  • Reactive (ie not a true neoplasm) proliferation of nerve tissue after injury, usually extraction or other surgical procedure

Clinical presentation

  • They are smooth-surfaced, nonulcerated nodules.
  • May be painful (30% of cases) and sometimes associated with altered nerve sensations that can range from anesthesia to dysesthesia to overt pain

Location

  • mental foramen area, tongue, lower lip
804
Q

Multiple Endocrine Neoplasia (MEN) Syndrome

What is it?

Inhertiance type?

Which type is associated with multiple mucosal neruoma?

What other presentations?

Increase risk of which cancer?

A

What is it?

Group of rare conditions

Inhertiance type?

Autosomal dominant

Which type is associated with multiple mucosal neruoma?

Type 2B associated with multiple mucosal neuromas (one of the first
visual signs)

What other presentations?
• Marfanoid features
• Multiple tumors and hyperplasias of endocrine organs (ie
pheochromocytoma)

Increase risk of which cancer?

• Increased risk for medullary thyroid cancer (prophylactic thyroidectomy)

Common board questions

805
Q

Neurofibroma

What is it?

Clinical presentation?

Location?

Treatment?

Mailgnancy?

A

What is it?

  • A benign tumor arising from peripheral nerve tissue

Clinical presentation:

  • Slow growing, painless lesion
  • Smooth-surfaced, nodular mass that varies in size
  • Skin more commonly involved than oral mucosa

Location:

  • Common oral mucosal sites: tongue and buccal mucosa
  • May develop centrally in bone

Treatment: surgical excision

Malignant transformation reported, but rare

806
Q

Neurofibromatosis syndrome

Most common form?

intheritance type?

Clinical presntation?

Malignant transformation?

A

Most common form?

Several forms, type I is most common (von Recklinghausen’s Disease)

intheritance type?

• 85-97% of cases inherited as autosomal dominant trait, chromosome 17 (NF1 gene)

Clinical presentations:

  • Skin nodules (neurofibromas)
  • Café au lait pigmentation on skin
  • Lisch nodules very diagnostic (a pigmented hamartomatou in the iris of the eyes)

Malignant transformation

  • reported in 5% of cases (neurofibrosarcoma)
807
Q

Schwannoma/ Neurilemoma

What is it?

Age?

Location?

Clinical presentation?

Treatment?

malignant
transformation ?

A

What is it?

• Benign neoplasm of Schwann cell origin
• Uncommon lesion: 28-48% occur in the
head and neck

Age?

• Most common in young and middleaged
adults

Location?

• Most common intraoral location:
tongue

Clinical presentation?

• The solitary schwannoma is a slow-growing, encapsulated
tumor that typically arises in association with a nerve trunk.

• May present with pain

• Treatment

• surgical excision

malignant
transformation

reported, but rare

808
Q

Granular Cell Tumor

What is it?

Location?

Age?

Treatment?

A

What is it?

Benign tumor derived from
Schwann cells

Location?
• Oral cavity is the most common
location
• Vast majority of cases seen on
dorsal tongue

Clinical presentation?

  • Typically an asymptomatic sessile nodule that is usually 2 cm or less in size (firm)
  • The mass is typically pink, but some granular cell tumors appear yellow.
  • The granular cell tumor is usually solitary, although multiple, separate tumors sometimes occur, especially in black patients.
  • The lesion often has been noted for many months or years, although sometimes the patient is unaware of its presence.

Age:

40-60, rare in children

Treatment
• Treated by surgical excision (Be careful with excision! no need
to get all of it out, just most of it)
rarely recurs

809
Q

Congenital Epulis

AKA

Cell resemble?

Cell origin?

Clinical features & location

Treatment?

A

• AKA: Congenital epulis of the newborn
• Cells resemble cells of the granular cell tumor
• Cell of origin is unknown, not derived from nerve
• Clinical features:

  • Sessile or pedunculated mass, usually found on
  • *the anterior** gingiva/ alveolar mucosa
  • Almost always occurs in baby girls
  • Present at birth

• Treatment:Surgical excision, does not recur

810
Q

Neuroectodermal tumor of infancy

Location?

Rate of development?

Treatment?

Origin?

Clinical presentation?

A

Location?

Often occur as soft tissue mass largely in anterior maxilla

Rate of development?

So fast developing that it envelops and moves the teeth

Treatment?

Needs to be surgically excised

Origin?
Thought to be of neuroectodermal source

Clinical presentation?
Pigmented change in tissue

811
Q

Lipoma vs Lipofibroma

A
  • Sometimes lipomas can be mixed with fibrous tissue, can be lipofibromous
  • Two lesions that look almost identical but one is lipoma, one is lipofibroma
  • Only difference is that one has fibrous tissue in it, no other difference
812
Q

Benign Tumors of Muscle

A

• Leiomyoma
• Benign tumor of smooth muscle
• Vascular Leiomyoma
• Benign tumor of smooth muscle walls of
blood vessels
• Rhabdomyoma
• Benign tumor of skeletal muscle

They are SUPERRR rare
If become malignant, they become leiomyosarcoma or rhabdomyosarcoma – malignant even
more rare

813
Q

Leiomyosarcoma

A
  • a type of rare cancer that grows in the smooth muscles.
  • So, so rare
  • Diseases that move rapidly, because they’re malignancies
  • You might see surface ulcerations, they’re moving so fast, they break through the epithelium
814
Q

Rhabdomyosarcoma

A
  • is a type of sarcoma.
  • Rhabdomyosarcoma usually begins in muscles that are attached to bones and that help the body move, but it may begin in many places in the body
815
Q

What is Sarcoma ?

A

Sarcoma is cancer of soft tissue (such as muscle), connective tissue (such as tendon or cartilage), or bone.

816
Q

Fibrosarcoma

what is it?

Age?

Rate of growth?

Treatment?

Survival rates?

A

•What is it? Malignant tumor of fibroblasts
• Age? Most common in young adults and
children
• Rate of growth? Slow growing lesion that is usually not
painful (Can be slow growing, can be rapidly growing – different criteria determining high or low grade)
• Treatment: surgical excision, recurrence is common(Aren’t always easy to surgically remove, because already metastasized into other reservoirs, spread into contiguous areas) Aren’t always radiosensitive, don’t always respond to radiation treatment
• 5-year survival rates range from 40-70%

817
Q

Vascular Malignant Neoplasms

A

• Angiosarcoma

• Malignant tumor of blood vessels

• Lymphangiosarcoma

• Malignant tumor of lymphatic vessels

• Kaposi’s sarcoma

  • Malignant neoplasm associated with endothelial cells
  • Seen predominantly in poorly controlled HIV infected patient population (not exclusively)
  • Elderly people can develop Kaposi
818
Q

Kaposi Sarcoma

Etiology

Types

Treatment

A

Etiology:Caused by HHV-8 (human herpesvirus 8) /part of herpes family

Types:

  • Classic: late adult life, Italian and Jewish men, skin of lower extremities
  • Endemic: African form
  • Iatrogenic immunosuppression-associated: most often occurs in recipients of organ transplants
  • AIDS-related

Treatment

  • Surgical excision, radiation therapy or systemic chemotherapy for multiple nonoral lesions, if it gets large, dose-radiation therapy!
819
Q

Plasmacytoma in Multiple Myeloma

A

Presents as soft tissue lesion
It is possible that a patient can present with plasmacytoma that would be the first sign of multiple
myeloma (it would be a rare sign, but it can happen)

820
Q

Lymphoma

A
  • Lymphoma is a general term for a complex group of heterogeneous lymphoreticular malignancies.
  • Lymphoma is the sixth most common malignancy and the second most common neoplasm of the head and neck after squamous cell carcinoma and accounts for 50-59% of head and neck neoplasms in children.
  • They constitute approximately 3-5% of all known malignancies and are generally divided into two morphologically distinct types: Hodgkin’s lymphoma (HL) and non-Hodgkin’s lymphoma (NHL).
  • These malignancies typically arise within the lymphatic tissues and can progress to extranodal disease as in NHL.
  • Cervical lymph node involvement can be present in any type of lymphoma.
  • HL extends by means of contiguous nodal spread whereas NHL tends to disseminate hematogenously and is typically a systemic diagnosis.
  • Within the head and neck, Waldeyer’s ring is the most common site of involvement, accounting for more than half of all extranodal head and neck lymphomas.
  • Oral involvement by lymphoma may represent a localized disease process but is more often part of a systemic process that secondarily involves the cervical lymph nodes.
  • Lymphoma arising within the oral cavity accounts for less than 5% of all oral malignancies, and approximately 85% of these lesions involve the pharyngeal tonsil and the palate
  • Extralymphatic sites include the salivary glands, paranasal sinuses, oral cavity, and larynx.
821
Q

What is this clinical finding?

A

Lymphoma

  • Well circumscribed ulceration in area
  • Associated swelling in periphery
  • White change in the patient’s left area
  • Been there for 3 weeks
  • It’s lymphoma
822
Q

What is this clinical finding?

A

Looks like it could be a salivary gland neoplasm, but it’s not
It was another lymphoma
Manifest in a number of different ways

823
Q

Case

40 year old male
Completely healthy otherwise
Not taking any medications
Presents with bump on the tongue

First question: did you do anything that might have led to this? Bite your tongue?
“possible I bit my tongue, or it could be when I had a dental procedure, maybe they accidentally
cut into the side of my tongue” – then it developed
This tells us, is this a reactive lesion?
Is it pedunculated or sessile? It’s pedunculated, larger at the top than the base
Let’s look at the surface: it’s ulcerated
When palpating, it’s only on the surface - don’t feel any submucosal presentation
Tongue underneath feels relatively normal
This bump is kind of firm and it bleeds like crazy when you touch it
When you look at teeth, no area where they’re too sharp

A

Do you think it’s a fibroma? No. Why?
Fibroma is covered with normal coloring epithelium – sometimes see a little white change on surface or see tiny traumatic ulcer on surface This is not like that, this is completely ulcerated
Not fibroma; fibroma is a chronic bump that patient is aware of
Is it squamous cell carcinoma? Interesting, it is indeed very friable; but no
Sometimes SCC can develop and can be exophytic and don’t have deep invasion, But this is pedunculated, SCC would not be pedunculated
History says there could be some kind of trauma, biting, or nick with bur – not squamous cell
Mucocele? No
Would you typically develop mucocele on lateral border of tongue? No
Not going to be as many mucoceles in this area, but there are the glands of Blandin and Nuhn, so it’s possible to develop on ventral surface of tongue
This bump doesn’t look like a fluid filled bump though, it has surface ulceration, redness ;Mucoceles have intact surface, would not bleed, or be red
Granular cell tumor? No
Granular cell tumor would have normal overlying epithelium (it’s pushing up from underneath)
This does not have normal overlying epithelium
Hemangioma reserved for congenital; not a vascular malformation either
Neurofibroma? No, not the same surface
Salivary gland neoplasms? Possible, there are salivary glands in that area; keep this in differential
The one that this is is pyogenic granuloma: usually red, ulcerated, and bleeds easily

824
Q

ADENOMA

A

benign tumor
of glandular origin

825
Q

Characteristics of a Benign Tumor:

A

 Encapsulated ‐ distinguishable from surrounding tissues
 Freely movable ‐ not fixed
 Slow growing
 Non tender ‐ patients do not complain of pain

826
Q

BENIGN SALIVARY GLAND
TUMORS

(list 3)

A

Pleomorphic adenoma aka mixed tumor
Monomorphic adenomas
o Canalicular adenoma
o Basal cell adenoma
Warthin tumor (papillary cystadenoma lymphomatosum)

827
Q

PLEOMORPHIC ADENOMA

(MIXED TUMOR)

A
  • This tumor comes in many forms/shapes
  • Most common salivary gland tumor
  • Painless, slowly growing, firm mass
  • Adults (30‐50 years old) ; slight female predilection
  • Sites:
    • 50% to 77% of parotid tumors (most commonly found in parotid-2/3rd to 3/4th of parotid tumors)
    • Minor SG: palate>upper lip>buccal mucosa> other site (most common intraoral site is the palate)
  • Malignant transformation possible in long standing lesions (about 5% cases) ‐> called Ca ex PA
828
Q

What is this clinical finding?

A

PLEOMORPHIC ADENOMA

(MIXED TUMOR)

829
Q

What is this clinical finding?

A

PLEOMORPHIC ADENOMA

Classic presentation: includes swelling in the parotid region

(MIXED TUMOR)

830
Q

What is this clinical finding?

A

PLEOMORPHIC ADENOMA

Palatal presentation: since salivary glands are only in lateral sides of the palate, usually
swellings are in one side and not the midline. Lateral swelling is a clue that you are
looking at a salivary gland lesion (left pics)
On the right pic, it involved midline and crossed over to other side, so there are
exceptions. But more commonly found in lateral side of the palate.

(MIXED TUMOR)

831
Q

What is this clinical finding?

A

PLEOMORPHIC ADENOMA

  • Upper lip presentation: sometimes swelling can be seen extra orally and intraorally.
  • Remember the swelling will be movable, not tender, not fixed to underlying structures.

(MIXED TUMOR)

832
Q

What is this clinical finding?

A

Untreated pleomorphic adenoma

slow growing, but can grow to enormous sizes

833
Q

Pleomorphic adenoma
histology

A

This is a mixed tumor with myxoid component (right) and
fibrous/epithelial component(left)

This type of tumor can produce a lot of different tissues, since the origin is from myoepithelial cells aka plasmacytoid cells, which are pluripotent cells which means they can differentiate into many different lineages of cells such as

834
Q

What is this clinical finding?

A

Canalicular Adenoma

835
Q

What is this clinical finding?

A

Canalicular Adenoma

  • Mucocele might look this way, but what would make it lower on
  • differential diagnosis is the location of the swelling. Mucocele is mostly seen on lower lip and this pic shows upper lip. Salivary gland tumors and mucoceles
  • can have the same clinical presentation, so always do a biopsy for formal histopathology diagnosis.
836
Q

Basal Cell Adenoma

A
  • Basaloid appearance of the tumor cells
  • Primarily parotid lesion
  • predominantly in women over 50 years of age. It is uncommon in young adults.

 (Basal cells are located in epithelium that is adjacent to interface with the connective tissue and they are separated from the CT by a basement membrane, stem cells of epithelium are located in basal cell layer)
 Basal cells are typically Blue in appearance and cuboidal,

837
Q

What is this clinical finding?

A

Basal Cell Adenoma

838
Q

What is this clinical finding?

A

PAPILLARY
CYSTADENOMA
LYMPHOMATOSUM
(WARTHIN TUMOR)

839
Q

MUCOEPIDERMOID
CARCINOMA

Charcterstics?

Location

Clinical appearance in minor gland

Can be mistaken for

Histopahtology

A

 Most common malignancy of salivary glands
 Most common malignant SG tumor in children

Locations
Palate, most common intraoral site
 Rare primary intrabony (jaws) tumors
 Most common in parotid
Minor SG: palate 2nd
Clinical appearance in minor gland: asymptomatic fluctuant swelling; blue or red colored
 Can be mistaken for mucocele
Histopathology: note the cells growing into adjacent tissue, showing infiltration

840
Q

Monomorphic Adenomas

What is it?

Types?

Treatment?

A

What is it?

Proliferation of 1 type of cell makes up the tumor.

Types? Includes:
o Canalicular Adenoma
o Basal Cell Adenoma
Treatment for all monomorphic adenomas is surgical excision & diagnosis is done with biopsy

841
Q

What is this clinical finding?

A

MUCOEPIDERMOID
CARCINOMA

842
Q

What is this clinical finding?

A

MUCOEPIDERMOID
CARCINOMA

Request all for biopsies!

843
Q

What is this radiographical finding?

A

CENTRAL
MUCOEPIDERMOID
CARCINOMA

  • Intrabony presentations, may have extraoral swelling depending on the stage
  • Started as small swelling and progressed rapidly:, need to pick it up early!
  • Patient recovered, but might need radiation, lost salivary glands, needed reconstruction of palate
844
Q

Canalicular Adenoma

A
  • Almost exclusively in minor SG
  • Striking predilection for upper lip (>75%)
  • Nearly always occurs in older adults
  • Slowly growing, painless mass
  • One clue for visualization of soft tissue swellings is increased vascularity with blue‐ish tint in the area.
845
Q

What is the clinical finding?

A

ACINIC CELL
ADENOCARCINOMA

846
Q

What is the clinical finding?

A

ACINIC CELL
ADENOCARCINOMA

blue‐ish tint

847
Q

What is this clinical finding?

A

Untreated acinic cell adenocarcinoma

 Because it is slow growing, and a low grade tumor, the
patient is alive and not dead with a tumor this size.
 Similar presentation to pleomorphic adenomas, but there is a lot of ulceration on the surface and prominent vascularization in acinic cell
adenocarcinoma.

848
Q

Adenoid Cystic Carcinoma

A

High grade salivary gland malignancy ( very bad cancer to get)
 Adults
Palatal mass; ulcerations
 Spread through perineural invasion ‐ tumor wraps itself around nerves and spreads through perineural spaces
Grows slowly in the beginning and then picks up speed
Histology: Duct like proliferation with cystic spaces

849
Q

What is this clinical finding?

A

Adenoid Cystic Carcinoma

850
Q

What are these clinical findings?

A

Adenoid Cystic Carcinoma

851
Q

What are these clinical findings?

A

Adenoid Cystic Carcinoma

852
Q

Adenoid Cystic Carcinoma

A

Swiss cheese appearance, cribriform pattern (full of holes aka cystic spaces)

853
Q

Perineural invasion Histology

A

Perineural invasion: nerve nuble in the
center and is wrapped by tumor

854
Q

What is this clinical presentation?

A

Polymorphous
Adenocarcinoma

855
Q

What is this clinical presentation?

A

Polymorphous
Adenocarcinoma

856
Q

What is this clinical finding?

A

Carcinoma Ex Pleomorphic
Adenoma

857
Q

PAPILLARY
CYSTADENOMA
LYMPHOMATOSUM
(WARTHIN TUMOR)

A
  • finger‐like projections, benign, cystic spaces, aggregates oflymphocytes)
  • Vast majority occur within the parotid gland
  • Very rare intraorally
  • Predominantly in men
  • Typically between 5th and 8th decades
  • Strong correlation with cigarette smoking
  • Most common SG tumor to occur bilaterally (bilateral parotid swelling), but can be unilateral
  • Etiology: Thought to arise within lymph nodes as a result of entrapment of
  • salivary gland elements early in development
  • Clinical Features:
    • swelling that has more subtle presentation
    • Doughy to cystic mass
    • In the inferior pole of the gland, adjacent and posterior to the angle of the mandible
  • Treatment: surgical excision, responds very well to it
858
Q

Summary for benign
tumors

A

Encapsulated, freely movable, not fixed to underlying structure, not tender, patients do not complain of pain, slow growing
 There is one tumor of the ones discussed that does have a risk of malignant transformation (only 5% and will take many, many years) and that is Pleomorphic adenoma

859
Q

MALIGNANT SALIVARY
GLAND TUMORS

List 5

A

 Mucoepidermoid carcinoma
 Acinic cell carcinoma
 Adenoid cystic carcinoma
 Carcinoma ex‐mixed tumor/malignant mixed tumor
 Polymorphous adenocarcinoma

860
Q

CLINICAL FEATURES OF
ADENOCARCINOMAS
(malignant gland tumors)

A

 Infiltrative
 Fixed to underlying structures, not moveable
 Rapid or slow growth, depending on grade and type of malignant salivary
gland tumor
 Larger, rapidly growing lesions may cause pain and/or paresthesia
 Ulcerated overlying mucosa

861
Q

MUCOEPIDERMOID
CARCINOMA

What are its compoenents?

Within jaw prognosis

Treatment

Prognosis

Therapy by gene?

A

What are its compoenents? Mixture of mucus‐producing cells and epidermoid or squamous cells

May arise within jaws from odontogenic epithelium of dentigerous cysts
• More common in the mandible than maxilla
• Molar‐ramus area

Treatment: Usually treated by surgical excision

Prognosis:

• Overall prognosis is fairly good
• 10% of patients die, due to local recurrence or metastasis
 Low‐grade tumors have good prognosis (>90% are cured)
 High‐grade tumors the prognosis is guarded (Only 30% survive)
Therapy by gene?

CRTC1–MAML2, CRTC3‐MAML2 gene fusions (targeted therapy)

862
Q

ACINIC CELL
ADENOCARCINOMA

A
  •  Occurs predominantly in major SGs,
  •  Found in all age groups, peak incidence in 5th and 6th grade
  • No gender predilection
  • Malignancy with serous acinar differentiation
  • Most common in the parotid (since 90% serous acini)
  •  Variable microscopic appearance
  •  May even appear encapsulated, since it is SLOW growing
  • Better prognosis than salivary gland malignancies
863
Q

Adenoid Cystic Carcinoma

Location

Growth rate

Clinical presentation

Treatment

Prognosis

A

Location:

 Approx. 50% occur within the minor SG ‐ palate most common site

Growth rate
 Usually a slowly growing mass

Clinical presentation
 Pain is a common and important early finding, occasionally occurring before there is noticeable swelling (described at annoying pain)
 Tendency to show perineural invasion, corresponds to pain

Treatment
 Excision usually the treatment of choice ‐ but edges of tumor may have perineural invasion and remain undetected ‐ makes tumor dangerous

Prognosis
 5‐year survival rate as high as 70% (maybe 90%)
 By 20 years, only 20% ‐ poor long term prognosis

864
Q

Polymorphous
Adenocarcinoma

Location

Gender

Appearance

growth patterns

Treatment

A
  • Location:
  • Almost exclusively in the minor SG
  • 60% on the hard or soft palate
  • Gender”
  • 2/3rds in females
  • Appearance:
  • Tumor cells have deceptively uniform appearance
  • Growth patterns:
  • Different growth patterns – polymorphous
  • Perineural invasion ‐ common ‐ but considered low grade tumor
  • Treatment: Wide surgical excision; overall prognosis relatively good, with 80% cure rate
865
Q

Carcinoma Ex Pleomorphic
Adenoma

What is it?

Mean age?

Growth pattern

Treatment?

Prognosis

A

What is it? (benign tumors that have underwent malignant transformation‐ takes a lot time, 15 to 20 years)

Mean age about 15 years greater than benign counterpart

Growth patterns: Mass present for many years with recent rapid growth with associated pain or ulceration

Treatment: Best treated by wide excision, with local node dissection and radiation

Prognosis: guarded, with 50% local recurrence or metastases and dying Prognosis is case to case scenario, may transform to high grade tumor

866
Q

What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION

Lower lip

A

o Mucocele
o Mucoepidermoid Ca
o Pleomorphic Adenoma

867
Q

What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION

upper lip

A

o Canalicular Adenoma
o Salivary Duct Cyst*
o Pleomorphic Adenoma

868
Q

What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION

Parotid

A

o Pleomorphic adenoma
o Warthin’s tumor
o Basal cell adenoma
o Mucoepidermoid ca
o Acinic cell ca
o Adenoid cystic ca
o Ca ex mixed tumor

869
Q

What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION

Palate

A

o Pleomorphic adenoma
o Adenoid cystic ca
o Mucoepidermoid ca
o PLGA
o Monomorphic adenoma

870
Q

SG Tumors: Summary of
Key Points

A

 Involve both major and minor glands
 Benign and malignant tumors both have similar
clinical presentation
 Most malignant salivary gland tumors do not show histopathologic
characteristics associated with malignancy
 Most occur in adults
 Warthin Tumor seen in parotid, may be bilateral
 Mucoepidermoid carcinoma
o Can occur in children
o May occur centrally in bone

871
Q

Inflammatory/Reactive Lesions of the Salivary Glands

List 5

A
  • mucocele/mucous cyst
  • ranula
  • necrotizing sialometaplasia
  • sialolithiasis
  • sialadentitis
872
Q

Mucocele

Definition

Clinical features

Location

Histological features

Treatment

A

• definition: a lesion that forms when a salivary gland duct is severed & secretion spills into the adjacent CT
• a pseudocyst (not lined by epithelium) — mucous builds up in the CT & causes a bump
• clinical features:

  • swelling in the tissue that may increase & decrease in size
  • may have a bluish hue, fluctuant on palpation — fluid filled, soft, compressible

• location: lower lip most common site, but may form in any area where there are minor salivary glands

• histologic features:
- a cyst-like space in soft tissue
- lined by compressed granulation tissue
- lumen filled with mucin, foamy macrophages & inflammatory cells
• treatment: surgical excision, removal of associated minor salivary glands
• may recur if don’t remove all associated injured minor salivary glands

873
Q

What is this clinical finding?

A

Mucocele

874
Q

What is this clinical finding?

A

Mucous Cyst

875
Q

What is this clinical finding?

A

Ranula

Notice how it’s unilateral

on the floor of the mouth

876
Q

What is this clinical finding?

A

Ranula

  • Notice how it’s unilateral*
  • on the floor of the mouth*
877
Q

Necrotizing Sialometaplasia

Definition

Predisposing factors

Clinical features

Histologic features

Treatment

A

• Definition: locally destructive inflammatory condition — looks malignant but is benign
• salivary gland ischemia — “heart attack of the palate”; blood flow is interrupted
• predisposing factors:
- local trauma
- palatal injection of local anesthesia
- previous surgery
- many are idiopathic..
• usually a clinical diagnosis based on history & how fast — palate uncommon for SCC
• clinical features:
- initially appears as a non-ulcerated swelling of the palate
- often associated with pain or paresthesia
- within 2-3 weeks, necrotic tissue sloughs off & becomes a crater-like ulcer
- patient may say: “a chunk of the roof of my mouth fell out”
• histologic features:
- necrosis of the salivary glands — coagulative necrosis (green circles in histology —>)
- salivary gland duct epithelium is replaced by squamous epithelium — appear as islands of squamous epithelium deep in the CT & resembles SCC (arrows in histology —>)
• Treatment: no treatment, spontaneously resolves within 6 to 10 weeks
• irrigating & debriding the area can reintroduce vascularity & help healing

878
Q

What is this clinical finding?

A

Necrotizing Sialometaplasia

879
Q

Sialolithiasis

Definition

Location

Origin

Clinical features

Radiological features

Histological features

Treatment

A

Definition: lith = stone ;; sialolith: a salivary gland stone

Location: occur in both major & minor salivary glands

• floor of the mouth is most common location (Wharton’s duct is a common place)

• often causes obstruction of the duct

Origin: arise from desposition of calcium salts around nidus of debris within the duct lumen

  • *clinical features:**- minor glands: hard yellowish structure in soft tissue
  • may be visible on a radiograph
  • recurrent swelling (due to the obstruction)
  • episodic pain & swelling during times of increased salivation
  • can be palpated if the stone is located toward the terminal portion of the duct
  • *Radiological features** : may be viewed as a radiopacity on an occlusal x-ray–well defined radiopacity
  • *Histological features-** concentric rings of calcification, color of it in stain depends on level of calcificatio
  • *Treatment**: promote passage of stone (massage, sialogogues, increase fluid intake) or surgical removal
880
Q

What is this clinical finding?

A

Sialolithiasis

881
Q

What is this clinical finding?

A

Sialolithiasis

Notice how it can appear radiographically as a well defined radiolucency

882
Q

What is this Radiographical finding?

A

Sialolithiasis

883
Q

Mucous Cyst

Definition

Clinical features

Histological features

Treatment

A

•Definition: a pseudocyst
• microscopicallly appears as an epithelial lined cystic structure that is actually a dilated duct
• clinically you CANNOT tell the difference between a mucocele & mucous cyst
• clinical features:
- same as a mucocele
• histologic features:
- same as mucocele but will see an epithelial lining (but actually a dilated duct)
treatment: same as mucocele; surgical excision

884
Q

Sialadenitis

definition

causes:

clinical features:

histologic features:

Treatment:

A

• definition: acute or chronic inflammation in major or minor salivary glands
• causes:
• obstruction of a salivary gland duct (sialolith)
• infection (mumps [viral], staph aureus [bacterial, most common], candida [fungal])
• decreased salivary flow (Sjogren’s, sarcoidosis)
• parotid gland = parotitis
• clinical features:
- acute: most common in parotid, swollen & painful gland, erythematous & warm overlying mucosa/skin, purulent discharge, low-grade fever
- chronic: caused by recurrent or persistent ductal obstruction, periodic swelling & pain
• histologic features:
- acute or chronic inflammatory cell infiltrate in the salivary gland
- in chronic cases = salivary gland replaced by fibrous CT & fat
- cells: acute = neutrophils ;; chronic = lymphocytes, plasma cells, macrophages
• Treatment: antibiotics, rehydration, surgical drainage, or surgical removal of gland

885
Q

What is this clinical finding?

A

Sialadenitis

Acute: parotid papilla purulent discharge

886
Q

What is this clinical finding?

A

Sialadenitis

Chronic: caused fibrosis

887
Q

Summery

of inflmattory salivaory conditions

A

Mucocele

  • fluctuant swelling
  • bluish hue
  • lower lip most common

Ranula

  • fluctuant swelling
  • floor of mouth

Sialolithisis

• major glands: episodic pain &
swelling of affected gland
• minor glands: asymptomatic/
local swelling or tenderness
• if superficial - firm to palpation
& yellowish color

Necrotizing
Sialometaplasia

• initial painful swelling
• later necrotic ulcer
• posterior lateral hard
palate & soft palate

Sialadenitis

• painful swelling of
affected gland
• purulent discharge if
acute infection

888
Q

Rx Topical
Treatments:
Cautery

A

‐ Debacterol (sulfonated phenolics; sulfuric acid solution)
o Chemical cautery
o Label: one time application for 5‐10 seconds
‐ NOT recommended to patients with frequent outbreaks

889
Q

What are the Topical Therapy
Categories to treat ulcers?

A

Topical anesthetic agents
o To numb the pain
‐ Surface protective agents/bioadhesives
o Cover the ulcer if small enough
‐ Anti‐inflammatory/immunomodulatory agents
o Applied to ulcer surface (corticosteroids)
‐ Anti‐microbials
o Some evidence that topical tetracycline may help
‐ Chemical/physical cautery Lasers
‐ Over‐the‐counter (OTC) versus prescription (Rx

All essentially do the same thing:
o Numbing agent
o Mucosal covering agent
‐ Bottomline:
o ALL canker sores will heal on their on with time

890
Q

Frequent Minor
RAS or Major RAS

Treatment

A

‐ Treatment to reduce pain
‐ vs.
‐ Abortive treatment to reduce healing time
‐ vs.
‐ Suppressive treatment to suppress recurrences
‐ Combination of all

Also Consider

  • Using Sodium Lauryl Sulfate‐Free Toothpastes
  • Remove Obvious Possible Causes
891
Q

Infrequent Simple
Minor RAS

Treatment

A

‐ Treatment to reduce pain

Also Consider

  • using Sodium Lauryl Sulfate‐Free Toothpastes
  • Remove Obvious Possible Causes
    • ‐ Repair sharp teeth/restorations
    • ‐ Remove plaque
    • ‐ Optimize lubrication
892
Q

Steps in Managing RAS patient

A

‐ History of RAS
‐ Medical History
o Medications
o Review of Systems
‐ Social History
‐ Dental History
‐ Diet/Nutritional History
‐ Physical Examination
‐ LaboratoryTests

893
Q

How do we treat this?

A

‐ Repair sharp teeth/restorations
‐ Remove plaque
‐ Optimize lubrication

Ulcer

894
Q

What is this clinical finding?

A

Behcet’s Disease

‐ Recalcitrant oral ulcers associated with Behcet’s Disease
‐ Later developed genital ulcers and other complications
‐ Image:
o Sores in the labial mucosa have classic aphthae appearance
o Other ulcers are major aphthae:
▪ Larger
▪ Irregular borders
▪ Intense proliferative erythema

895
Q

What is this clinical finding?

A

Behcet’s Disease

‐ Recurrent inflammatory disorder of unknown cause:
o Bacterial?
‐ Affects:
o Middle Eastern Males
o Asian Females
‐ Onset 3rd – 4th decade
‐ HLA‐B51 association

Recurrent aphthous ulcers generally precede other signs:

o Genital/skin/eye lesions & others (arthritis, Gl lesions, CNS symptoms, vascular lesions)
‐ Diagnosis based upon criteria (point system): no laboratory tests

896
Q

What is this clinical finding?

A

Hematinic
Deficiencies

‐ Superficial ulcers
o Not classic aphthous ulcers
‐ Equivocal associations with iron, Vit B1, B2, B6, B12, and folate.
‐ Blood tests are not recommended routinely in all patients with RAS.
‐ Indications for blood work (CBC):
o Older patient with recent RAS history
o Suspicious medical history/review of systems
o Strict vegetarian patients

897
Q

What is this clinical finding?

A

HIV‐Associated
Aphthous

  • CD4 counts <100 cells/mm3 are predisposed to major RAS
  • ‐ Other sites may be affected:
    • o Esophagus
    • o Genitals
    • o Anus/rectum
  • ‐ We see this less frequently since ART
  • ‐ Diagnosis is important, particularly if no prior history
898
Q

What are these clinical findings?

A

Inflammatory
Bowel Diseases

  • Specific lesions:
    • o Diffuse labial and buccal swelling
    • o Cobblestones
    • o Other specific lesions
    • ▪ Mucosal tags
    • ▪ Deep linear ulcerations
    • o Mucogingivitis
    • o Granulomatous cheilitis
      • Non‐specific lesions:
    • o Aphthous ulcerations
    • o Pyostomatitis vegetans
    • o Dental caries
    • o Gingivitis and periodontitis
    • o Other non‐specific lesions
899
Q

What is this clinical finding?

A

Transient Lingual
Papillitis

  • ‐ Relatively rare
  • ‐ Canker sore meets fungiform papilla of tongue
    • Multiple papilla can become inflamed (above image)
    • Very painful
  • ‐ Ulcer Appearance:
    • Tiny
    • Transient
    • On fungiform papilla of tongue
  • ‐ Typically resolves in 7‐10 days
900
Q

What is this clinical finding?

A

Herpetiform aphthous stomatitis

  • Apppears like herpesvirus but unrelated to it
  • account for 5% of cases (the least common)

Appearance:

  • begin as multiple (up to 100) 1- to 3-mm crops of small, painful clusters of ulcers on an erythematous base.
  • They coalesce to form larger ulcers that last 2 weeks.
  • A bunch of smaller ulcers that coalesce
901
Q

What is this clinical finding?

A

‐ Minor Recurrent
Aphthous Ulcers
(RAS)‐ Rare Case

o Keratinized
Mucosal
Site

‐ 11‐year‐old boy
‐ Canine is in process of erupting
‐ Canker sore present on his keratinized mucosa (RARE)
o 99% of canker sores occur on NON-KERATINIZED MUCOSA

902
Q

What is this clinical finding?

A

Minor Recurrent
Aphthous Ulcers
(RAS)

  • aka‐ “Canker Sores”
  • ‐ High prevalence: 5‐25%
  • ‐ Comprises the overwhelming majority of cases
    • o 75‐85% of ALL RAS cases
  • ‐ <10 mm in diameter
  • ‐ Ulcer appearance:
    • o Shallow
    • o Round/Oval Shaped
    • o Yellow pseudomembrane
  • ▪ Slightly raised margin
  • ▪ Erythematous Halo
  • ‐ Typically resolves in 7‐10 days
    • o *May take longer if in a “high‐traffic” site
  • ‐ No scarring
  • ‐ Recurrence rates vary
903
Q

What are the Hallmarks of
Aphthous Ulcers

A

‐ Hallmarks:
o 1. Central ulceration
o 2. Ring of erythema (erythematous border)
▪ Accentuated in right image

904
Q

What is this clinical finding?

A

‐ Aphthous Ulcer of the tongue

‐ Aphthous ulcers can occur on specialized structures of the mouth

905
Q

What is this clinical finding?

A 
Aphthous ulcer (“The
canker sore”)

What would it be like to have a canker sore on your uvula?
o Painful to swallow
‐ The location of the canker sore will predict the symptoms

907
Q

Rx Topical
Treatments:
Corticosteroid
Rinse‐

A

‐ Dexamethasone elixir 0.5mg/5ml (ETOH base) or solution (H20 base)
‐ Indicated for difficult to reach lesions to obtain access to all of them
o Disp:600ml
o Label: swish with 5‐10 ml for 5 minutes up to 0.5mg/5mL 4x/day and
expectorate 00s preservalve.) May be used as suppressive therapy in
selected patients with close surveillance
o Prevent recurrences
‐ May buy an EXTRA DAY of healing time

dr. Kerr prefers the elixir

911
Q

What is this clinical finding?

A

Major Recurrent
Aphthous Ulcers
(RAS)

  • ‐ 10 – 15% of all RAS cases
  • ‐ >10 mm in diameter
  • ‐ Ulcer Appearance:
    • o Deeper
    • o Irregular borders (usually)
  • ‐ Typically resolves in WEEKS or MONTHS
  • ‐ May be associated with fever or malaise
    • o The associated cytokine release can induce a fever
  • ‐ Predilection for the throat
  • ‐ Often DOES leave scarring
  • ‐ Recurrence rates vary
921
Q

Rx Topical
Treatments:
Corticosteroids

for

Ulcers

A

‐ Triamcinolone acetonide in Orabase 0.1% (intermediate)
o Disp: 5g tube Dental Past
o Label: apply a thin film over ulcer after meals and bedtime APOTHECON
o Do not use for more than 2 weeks

‐ Fluocinonide gel or ointment 0.05% (Potent)
o Disp: 15g tube
o Label: apply a thin film over
o Do not use for more than 2 weeks
‐ Clobetasol ointment 0.05% (Ultra potent)
o Disp: 15gtube Label: apply a thin film over ulcer bid

923
Q

Problem with topical tx

A

Topical Treatments
‐ Drug is easily washed away or rubbed off
‐ Topical anesthetics have a short‐lived effect
‐ Often difficult to apply due to location
‐ Cost may be a disincentive to buy OTC
‐ Once ulcers are established, these treatments are not as effective, therefore
abortive treatment early on is preferred

924
Q

What about
systemic
treatments – taking
pills to treat ulcers?

A

‐ Prednisone or systemic steroids were the one systemic treatment that Dr. Kerr
has has success with in practice

o 0.5 mg/kg of Prednisone would be prescribed for about 1 week

o Very successful in patients with frequent outbreaks of multiple canker
sores
‐ In some limited cases Dr. Kerr has seen some success with:
o Colchicine
o Pentoxifylline

925
Q

What is Human herpes virus (HHV)

what is it’s 8 types?

A

Large family of double stranded DNA viruses

❏ HHV‐1: HSV‐1‐Herpes simplex virus type 1 (most common in oral cavity)
❏ HHV‐2: HSV‐2‐Herpes simplex virus type 2
❏ HHV‐3: VZV‐Varicella zoster virus
❏ HHV‐4: EBV‐Epstein Barr virus
❏ HHV‐5: CMV‐Cytomegalovirus
❏ HHV‐6: Sixth disease/Roseola (commonly seen in children, spreads through saliva and respiratory droplets)
❏ HHV‐7: Roseola
❏ HHV‐8: KSHV‐Kaposi sarcoma‐associated herpesvirus

926
Q

What is the Mode of infection of HHV?

A

Primary infection → Latency → Reactivationn → Recurrent infection

927
Q

After the primary infection the HHV‐1/HSV1 stays in ————

A

Sensory ganglia

928
Q

After the primary infection the HHV‐2/HSV2 stays in ————

A

Sensory ganglia

929
Q

After the primary infection the HHV‐3/VZV stays in ————

A

Sensory ganglia (dorsal root ganglia)

930
Q

After the primary infection the HHV‐4/EBV stays in ————

A

B‐Lymphocytes

931
Q

After the primary infection the HHV‐5/CMV stays in ————

A

Myeloid cells, salivary gland cells, endothelium

932
Q

After the primary infection the HHV‐6 stays in ————

A

CD4+ T‐Lymphocytes

933
Q

After the primary infection the HHV‐7 stays in ————

A

CD4+ T‐Lymphocytes

934
Q

After the primary infection the HHV‐8 stays in ————

A
  • *B‐lymphocytes (latency)**, **endothelial cells (Kaposi
    sarcoma) **
935
Q

Herpes Simplex Virus

types

&

locations

A

❏ Type 1‐ adapted to oral, facial, and ocular areas (more common in
oral cavity)
❏ Type 2‐ adapted to genital area
❏ Other sites may also be affected
○ Herpetic whitlow (finger)
○ Herpes gladiatorum (wrestlers)
○ Herpes barbae (beard area)

936
Q

Herpes Simplex Virus

primary infection

A

○ Acute/Primary Herpetic Gingivostomatitis
○ The easy way to remember where the ulcerations occur?
➢ gingiva and oral cavity

gingivo (=gingiva or fixed keratinized mucosa)

+
stoma (= the movable part of the oral cavity where the CT is
looser, including the labial and buccal mucosa, and the
tongue).

937
Q

Herpes Simplex Virus

Recurrent infection

A

two manifestations:

  1. Herpes labialis: occurs on the vermillion border
  2. Intra‐oral herpes: occurs ONLY on the fixed keratinized
    mucosa (mucosa that doesn’t move around) MEMORIZE
    THIS
938
Q

What does it mean if a person has a primary infection?

A

 They don’t have antibodies

939
Q

Who’s the typical group that will get primary herpetic gingivostomatitis?

A

 Children and young patients

940
Q

What is this infectious disease?

Describe it

A

HSV‐1: Primary
Infection

it is a raised blister/papule on the
vermilion
The bottom arrow pointing to a mucosal
ulcer w/ tan pseudomembrane.

941
Q

What is this infectious disease?

Describe it

A

HSV 1- Primary Herpetic
Gingivostomatitis

Ulcer with an erythematous halo (top two arrows). We
also have ulcerations that are irregular in shape on the gingiva
(bottom two arrows).

❏ Clinical Features:

  • Cervical lymphadenopathy
  • Chills
  • Fever
  • Nausea
  • Anorexia
  • Irritability
  • Sores in mouth
  • Ulcerations on fixed and movable mucosa
  • Variable number of lesions
  • Ulcers coalesce and form larger irregular ulcerations
  • Gingiva enlarged and painful
  • Resolution in 5‐7 days
942
Q

What is this infectious diseease?

What is its pathogensis ?

A

HSV‐1: Primary
Infection

pathogensis

❏ Usually young age
❏ Often asymptomatic
❏ Symptomatic = Primary herpetic gingivostomatitis
❏ In adults is usually pharyngotonsillitis (back of throat)
❏ Spread through infected saliva or active lesions
❏ Incubation period = 3‐9 days

These photos represent

gingivostomatitis

multiple irregularly shaped
ulcers present on the fixed and movable mucosa, bilaterally

943
Q

What is this infectious disease?

What probably this patient also have?

A

HSV1: primary herpetic gingivostomatitis

there are multiple irregularly shaped
ulcers present on the fixed and movable mucosa –> most likely
diagnosis is primary herpetic gingivostomatitis since the patient has
fever and malaise.

945
Q

HSV‐ Histopathology

A

❏ Molding
❏ Margination
❏ Multinucleation
❏ Also Tzanck cells

946
Q

What is a
definitive diagnosis for HSV1 Herpes simplex

A

HSV‐ Cytology‐
Papanicolaou Stain
(PAP)

947
Q

How to interpere HSV‐ Laboratory
Results based on IGg and IGm a

A

If you have positive IgM and negative IgG → that means it’s an acute
recent infection.
Then you have to wait 4‐6 weeks
If you do the serology then and get positive IgG and negative IgM → that means the person has the established infection.

951
Q

How is Primary HSV
(Herpes Simplex) diagnosed?

A

❏ Clinical diagnosis → based on putting all the features together
❏ Culture (may take 2 weeks) → not worth it
❏ Tissue biopsy → very invasive
❏ Cytologic smear (less invasive)
○ easiest bc you take a popsicle stick to scrape an ulceration
then you put those cells on a slide, you send it to a
pathologist after fixing the cells with some alcohol then you
can see the virally‐altered cells
❏ Serologic testing→ to look for antibodies 4‐8 days after they were
exposed.

955
Q

What is the treatment of Primary Herpetic
Gingivostomatitis ?

A
  • ❏ Supportive/Palliative Treatment
  • ❏ Fluids, nutrition, rest, avoid spreading to others
  • ❏ Avoid touching eyes, genitals
  • ❏ Possible referral to MD if infant is not drinking because of pain
  • ❏ Medications:
  1. Topical anesthetic (OTC vs Rx)
  2. Mucosal coating (OTC)
  3. Analgesic (OTC vs Rx)
  4. Antiviral (Rx)
956
Q

What are the medications used to treat Primary HSV?

A

❏ OTC Magic Mouthwash Formulation: helps the person to actually be able to eat bc they have so many ulcerations
○ 1 Part‐ Diphenhydramine/ Benadryl (anticholinergic)
12.5mg/5mL elixir
○ 1 Part‐ Lidocaine (topical anesthetic)
○ 1 Part‐ Magnesium hydroxide/ Maalox (mucosal coating
agent)
○ Disp: 4 oz bottle
○ Label: Rinse with 5mL every 2 hours for 30 sec. then spit
out
❏ Rx‐Topical Anesthetic
○ Lidocaine 2% viscous solution* (viscous lidocaine)
○ Disp: 100mL bottle
○ Label: Rinse with 10 mL for 2 minutes and spit out
*May diminish the gag reflex therefore better suited for older
patients‐ shouldn’t be prescribed to kids. Remember serious sideeffects of seizures and methemoglobinemia in pediatric population.
❏ OTC Analgesic
○ Acetaminophen (Tylenol) OR ibuprofen (NSAID)
suspension/ tablets as directed for body weight
❏ Rx Antivirals
○ Generally only indicated for immunocompromised or
dehydrated patients
○ Limited evidence for other cases‐ see Cochrane Oral Health
Group Review* (*Amended recently)
○ Oral acyclovir suspension (Zovirax) is typically used
○ 15 mg/kg up to adult dose of 200mg
○ Rinse and swallow, 5 times a day for 5‐7 days

957
Q

HSV-1 RECURRENT INFECTION

A
  • §Secondary herpes
  • §Mild, self-limiting
  • §Vermilion border
  • §Intraorally on fixed keratinized mucosa
  • §7-10 days
  • §Unilateral
  • § Prevalence‐15‐45%
  • 90% of adults have the antibodies, but 15‐45% of them can get recurrent herpes. Most of us have the antibodies, but we never exhibited the primary infection or a recurrent infection*.
  • § 1‐6 outbreaks a year
958
Q

Reccurent HSV-1 Latency place is ——–

A

trigeminal ganglion

959
Q

What are the Stages of recurrent Hsv-1?

A

Prodrome►papules►vesicles►ulcer►crust►heals►no scar

960
Q

What is this infectious disease?

describe it

A

recurrent Hsv-1/Recurrent herpes

It is raised
(papule), so it’s in the middle stage

962
Q

What are some of triggers of the Recurrent HSV?

A
  • Old age, Allergy
  • UV light ,Trauma
  • Physical / emotional stress, Dental treatment
  • Fatigue, Respiratory illnesses
  • Heat, Fever
  • Cold, Menstruation
  • Pregnancy, Systemic Diseases
  • Malignancy
963
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

Punctuate ulceration
erythematous border, irregular shape, fixed mucosa, unilateral

964
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

This is recurrent intraoral herpes. We have
punctate (point‐like) ulcerations which sometimes have clusters of
coalescing ulcers. That’s the words you wanna use
Other features of the ulcers:
○ Erythematous border
○ Irregular shape
○ Fixed mucosa
○ Unilateral

965
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

Bilateral > THIS IS KEY
-differential diagnosis with a Staph infection
that occurs periorally with kids -> impetigo

966
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

Vesicle stage (unilateral)

967
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

crust → later
crust comes off and then
you’ll have
epithelialization
underneath

968
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

papule bc its
raised

969
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

healing stage cause
you might see this one day

970
Q

What is HSV‐ Recurrent Infection‐
Shedding ?

A

Asymptomatic shedding can occur in seropositive patients
❏ More common after surgical procedures and in
immunocompromised patients
❏ We need to take Universal precautions

978
Q

How to diagnose Recurrent HSV?

A

❏ Clinical‐ if you see punctate ulcers unilaterally on the palate, it is
usually recurrent herpes simplex.
❏ Culture (may take 2 weeks) ‐ takes too long
❏ Tissue biopsy‐ if it wasn’t typical
❏ Cytologic smear‐ the ideal way if you want a definitive diagnosis

979
Q

What is this infectious disease?

A

Atypical recurrent HSV

❏ Immunocompromised host
Atypical recurrent HSV can have this
appearance on the movable mucosa too, not just fixed

980
Q

What is this infectious disease?

A

HSV Associated
Erythema
Multiforme

❏ Skin immune reaction in response to infection

❏HSV implicated in trigger for erythema
multiforme where you get target lesions
and crusted ulcerations on the
lip

❏ need to prescribe :antiviral prophylaxis

981
Q

What is the Treatment Recurrent HSV-1?

A

❏ Depends on severity/frequency
❏ Preventive/suppressive vs episodic/abortive strategies
Two types of treatment:
Preventive/Suppressive: taking antivirals everyday to prevent an outbreak
Episodic: taking antivirals here and there to abort the process; episodic: abortive.
❏ Drugs used:
❏ Antiviral agents
❏ Antiviral‐steroid combination agents
❏ Avoid precipitating factors, like use sunscreens – avoid any triggers

982
Q

e At which stage should the
abortive/ episodic treatment be done to avoid the outbreak?

A

❏ the prodrome, prodrome treatment is abortive
**remember this!**

983
Q

RECURRENT HERPES LABIALIS-RX TOPICAL/SYSTEMIC AGENTS

A

Topical like Acyclovir

or Acylovir + steroid combination

There are many OTC topical medications

984
Q

suppressive or preventative therapy of Recurrent HSV-1

A

: taking antivirals everyday to prevent those 6 outbreak/year.

There is modest evidence
that systemic acyclovir or
valacyclovir prevents
recurrent herpes labialis

these drugs tend to only affect virally‐altered cells. They don’t
affect the mammalian cells; they’re very safe.

985
Q

Episodic/ Abortive
therapy of reccurent HSV1

A

❏ Episodic‐Occurring, appearing, or changing at usually irregular
intervals
❏ Abortive‐Tending to cut short the course of a disease
○ Medication has to be taken during Prodrome
○ When the patient feels a burning, itching, and tingling

986
Q

What are Recurrent Herpes
Labialis‐ FDA Approved
Topical Treatments?

A

❏ Rx: Acyclovir cream 5% (Zovirax)
Disp: 5g tube
Label: dab on lesion every 2 hours for 4 days
❏ Rx: Penciclovir cream 1% (Denavir)
Disp: 5g tube
Label: dab on lesion every 2 hours for 4 days
❏ Rx: Docosanal cream (Abreva) OTC
Disp: 2g tube
Label: dab on lesion five times per day for 4 days

Acyclovir and Penciclovir
should be taken during
the prodrome stage

❏ Rx: Acyclovir 5%/ hydrocortisone 1% cream (Xerese)
Disp: 5g tube
Label: dab on lesion 5 times a day for 5 days
❏ Rx: Acyclovir buccal tablets (Sitavig) 50mg
Disp: 2 dose pack
Label: apply to canine fossa within 1 hour of symptoms
(single dose)

987
Q

What are Recurrent Herpes
Labialis‐ FDA Approved
Systemic Antivirals ?

A

❏ Rx: Valacyclovir 1g tablets
Disp: 4 tabs
Label: 2 tabs stat PO, then again in 12 hours (ie 2 doses)
Given during prodrome.

❏ Rx: Famciclovir 500mg tablets
Disp: 3 tabs
Label: 3 tabs stat PO

988
Q

What are other Topical
Agents for treating Recurrent Herpes
Labialis?

A

❏ Ice
❏ L‐lysine
❏ Bioflavonoids
❏ Evaporants ‐ Desiccants
❏ Emollients
❏ Bioadhesives (Zilactin‐benzyl alcohol, topical pain reliever)
❏ Wound‐healing modification/ occlusive agents

991
Q

HHV3

What is it’s primary infection and Secondary infection known as?

A

❏ Primary infection
○ Varicella/ Chicken pox
❏ Secondary infection
○ Zoster/ Shingles
○ May affect oral cavity/ face if reactivation
along distribution of V1/2/3

992
Q

What is this infectious disease?

describe it

A

HHV3

Varicella (chickenpox)

It is caused by

Varicella Zoster
Virus Infection

a typical macular, papular, vesicular rash –
it’s bilateral

993
Q

What is this infectious disease?

A

Herpes Zoster/
Shingles

  • It is affecting the intraoral region
  • and the maxillary branch.
  • Picture on the far right looks like recurrent HSV (cluster of coalescing ulcers)
  • Looking at the picture on the left you can determine it is NOT a recurrent intraoral herpes because we have vesicles that opened up and crusted over on the skin.

VZV histopathology is the same as HSV.

VZV remains latent in the
dorsal root ganglion
travels down the sensory nerves to skin upon reactivation.
❏ The reactivation presents as a painful rash in one or two adjacent
dermatomes that does not cross the midline.
❏ The rash is maculopapular and develops into vesicles.
❏ One complication of zoster is post‐herpetic neuralgia: pain that
persists in the area where the rash once was present.

995
Q

What is this infectious disease?

A

HHV 5

Cytomegalovirus
Infection

Histopathology look like an owl eyes

means the cells are affected- they are nuclear inclusions and cytoplasmic inclusions.

996
Q

What is this infectious disease?

Desercibe it

A

HHV 5

Cytomegalovirus
Infection

When a person is immunocompromised, particularly those who’ve had a transplant or HIV+ patients, only these people will present with ulcerations

It’s very hard to identify
based on photo alone

  • it’s very nonspecific
998
Q

What is this diseases?

Which virus is asscoaited with it?

A

Nasopharyngeal carcinoma
❏ Associated w/ HHV‐4 (EBV)
❏ You might be one of the first people to detect this
cancer – the first sign is the swelling of the lymph
nodes

In this case, these are late stages of the disease.

this photo from google

999
Q

What is this disease?

Which virus causes it

describe it

A

Oral hairy leukoplakia

Epstein‐Barr Virus induced disease
❏ Corrugated white
keratotic lesion
on the lateral
tongue in HIV+ people

1000
Q

What is this infectious disease?

A

Infectious mononucleosis

Epstein‐Barr Virus/EBV‐induced disease

The virus spreads through saliva, which is why it’s sometimes called “kissing disease.” Mono occurs most often in teens and young adults. However, you can get it at any age. Symptoms of mono include:

Fever

Sore throat

Swollen lymph glands

  • when you have salivary transfer, your lymph nodes get swollen
  • people feel fatigue and fever
  • they have tonsilitis
  • can lead to the secretion of white or gray‐ green tonsillar exudate
  • they can get petechiae on the palate too.
1001
Q

HHV5

is it symptomatics?

where does the diseases predominantly found?

Latency?

A

Cytomegalovirus
Infection

❏ Usually asymptomatic
❏ Symptomatic infections are nonspecific: chills, fever, sore throat
❏ What’s interesting here: ❏ When the cells are affected, they form these owl eyes – they are nuclear inclusions and cytoplasmic inclusions.

❏ Disease states found predominantly in:

  • ○ pregnancy/neonates (congenital infection)
  • immunocompromised patients, particularly transplant and HIV+ patients

​
❏ Latency in myeloid cells, salivary gland
cells and endothelium

1002
Q

What is this diasese?

which viruse causes it

A

Burkitt
Lymphoma

Epstein‐Barr Virus
Infection

  • Fast growing tumor discovered by Dr. Burkitt
  • High grade lymphoma B cells‐ Usually affects the jaws of children.
  • It is the fastest growing tumor/cancer.
  • There is translocation of c‐myc
1003
Q

What is this infectious diasese?

A

EBV mucocutaneous ulceration

Very rare

Photos from google

1004
Q

Which disease has Stary sky pattern histopathology?

A

Burkitt
Lymphoma

caused by EBV

1005
Q

What is this disease?

Describe it

A

Kaposi sarcoma

HHV 8

Kaposi sarcoma on
the skin:
>1cm
Different color, so
this is called a patch.
Erythematous
patches present on
multiple areas of the
face.

1006
Q

Kaposi sarcoma

Histopathology

A

Histopathology shows malignant endothelial cells proliferating.
There are tiny spaces. Extravasation of RBCs can be seen

1007
Q

What is this disease?

A

Kaposi Sarcoma
(HHV‐8)

Right photo: we see Patch, slightly raised plaque stage
○ This is different from hemangioma because if you press on it, it
doesn’t blanch (where all the blood goes away, and it looks
white)
Left photo: Nodular is when it becomes very exophytic
You need to do a biopsy for this because it looks irregular.

1010
Q

What are HPV types that cause

Genital Benign Lesions?

A

6, 11, 16, 18

(condyloma – can be malignant)

1011
Q

What are HPV types that cause

Non‐genital Benign Involving Mucosa?

A

6 & 11

1012
Q

What are HPV types that cause

Non‐genital Benign Involving the Skin?

A

2 & 4

1013
Q

What are HPV types that cause

Malignant & Potentially Malignant Disorders?

A

16, 18

1014
Q

HHV‐8

What is it?

Assoicated with what?

How it evolved?

How it is treated?

A

Kaposi sarcoma–associated herpesvirus (KSHV)

❏ Vascular neoplasm of endothelium
❏ Associated with immunosuppression
❏ Usually evolves through 3 stages:
○ Patch►plaque►nodular

  • More commonly seen in patients with HIV infection.
  • Treated with topical agents and chemotherapy.
1015
Q

What is HPV Pathogenesis and Incubation period?

A

Incubation period: 3 weeks – 2yrs
▪ Basic Explanation: Basal epithelial cell infection ► Genome
replicates ► DNA released into stratum corneum
▪ Detailed Explanation:

  1. HPV accesses and infects cells of the epithelial basal
    layer through breaks in the skin or mucosa
  2. The virus becomes incorporated in the genome of the
    infected cell
  3. The site of HPV integration into the cellular genome is
    in the general region of known oncogenes
  4. The virus replicates during keratinocyte
    differentiation in the spinous and granular cell layers
  5. A portion of the HPV genome encodes proteins that
    are capable of inducing cell proliferation and
    transformation (E6, E7)
1016
Q

HPV Pathogenesis – High Risk
▪ Break in the skin ► HPV (dark dots) invades and infects basal cells
▪ HPV incorporates into DNA ► moves up epithelium as it matures ► releases
Then 2 things happen

1.

or

2.

A
  1. Completely have infection go away

or

2 .Stays and forms wart or affects maturation (becomes cancer, depending on strain)

1017
Q

HPV Genome
Organization

A

▪ LCR: long control region
▪ P97: promoter protein
▪ E1‐E7: early region genes
▪ L1,L2: late region genes

1021
Q

HHV‐4

Latency?

and

What are the EBV inducded diseases?

A

Epstein‐Barr Virus
Infection

Latency in lymphocytes

§Infectious mononucleosis
§Oral hairy leukoplakia
§Nasopharyngeal carcinoma
§EBV mucocutaneous ulceration
§Burkitt lymphoma
§Other lymphomas (Hodgkin, post transplant)

1028
Q

what are the charcterstics of

HUMAN PAPILLOMA VIRUS (HPV)

?

A

§Small, non-enveloped icosahedral DNA virus that infects
skin or mucosal cells of humans.
§Circular DNA
§198 types established
§High and low risk types

‐ HIGH risk = CANCER
‐ LOW risk = WARTS

1029
Q

What can HPV Epithelial Lesions
cause?

(3)

A

▪ Benign: neoplasms of squamous epithelium
▪ Pre‐malignant: epithelial dysplasia – can lead to cancer
▪ Malignant: squamous cell carcinoma – infiltration of epithelial cells

1034
Q

What are Routes of Transmission for HPV?

A

▪ Sexual/non‐sexual direct contact
▪ Salivary transfer
▪ Contaminated objects (fomite) – not well established
▪ Autoinoculation – child puts finger into mouth
▪ Perinatal/pre‐natal transmission

1038
Q

What is the Molecular Mechanism

of HPV?

A 
**E6 = degrades p53
E7 = inactivates pRb**

  1. E2 = attachment location of Integrated HPV
  2. transcription of E6 + E7
  3. Binding of the viral E7 protein to pRb ► release of E2F and other proteins ► signals for the cell cycle to progress
    ▪ As long as the E7 protein stays attached to pRb, uncontrolled cell proliferation will continue

HPV E6 protein is:
‐ A ubiquitin ligase
‐ contributes to oncogenesis by attaching ubiquitin molecules to p53 ► making
p53 inactive and subject to proteasomal degradation
▪ Normal function of p53 = to stop cell division + repair damaged DNA so that damaged cells do not reproduce (apoptosis)
▪ When p53 is inactive, cells with changes in the DNA, such as integrated viral DNA, are not repaired ► destabilizes the cell ► increases the risk of malignant transformation

1039
Q

What is Persistence of HPV

A

▪ Low‐risk types: clear faster, less likely to become persistent
▪ High‐risk types: clear slowly, more likely to become persistent

1040
Q

What is the Prevalence of Oral (HPV)

A

Overall: 6.9% (CI 6.7‐8.3)
▪ Gender: Men (10.1%) > Women (3.6%) – women clear faster
▪ Age: bimodal distribution – 30‐34yo and 60‐64yo (she says 30‐34 but Dr. Kerr’s
graph shows mid‐20s
▪ High Risk HPV (3.7%) > Low risk HPV (3.1%)
▪ HPV‐16 infection most prevalent (1% or 2.13 million Americans)
▪ Based on NHANES study w/ oral rinse sampling and PCR

1041
Q

What are Risk Factors Associated
w/ Prevalence of HPV?

A

▪ Ever had sex (7.6%) vs never had sex (0.9%)
▪ Male
▪ Increased number of sexual partners (vaginal or oral sex)
▪ Tobacco smoking
▪ HIV infection

1042
Q

Most prevelant HPV TYPE?

A

HPV 16 = most prevalent

1043
Q

What is the Prevalence in
HIV + ?

A

Ppl w/ HIV+ and low CD4 T‐cells lvl = higher risk of
HPV
HPV 16+ higher if CD4 <200

1044
Q

Compare between SCC in Squamous Cell Carcinoma caused by HPV vs Tobacco and Alcohol

A

▪ HPV associated SCCa
‐ Wild type TP53
‐ Low pRb
‐ Increased p16

▪ Tobacco and Alcohol associated SCCa
‐ *Mutated TP53 – mutated by carcinogens in tobacco and alcohol► cancer
‐ pRB overexpression
‐ Decrease p16

1045
Q

BENIGN ORAL LOW RISK HPV LESIONS

(WARTS)

How do they appear?

Color?

Size?

Histologic?

A

§Appear as single or multiple exophytic papules, either sessile and flat
or pedunculated and papillary.
§Color depends upon degree of keratinization, ranging from white to
pink.
§Size of papules generally <10mm in diameter.
§Histologically, lesions may have koilocytes.

1046
Q

What are the types of Benign Oral Low Risk HPV
Lesion ?

(5)

A

▪ Squamous papilloma
▪ Verruca vulgaris
▪ Condyloma acuminatum
▪ Focal epithelial hyperplasia
▪ Oral florid papillomatosis

1047
Q

What is this infectious diease?

A

SQUAMOUS PAPILLOMA

Benign Oral Low Risk HPV
Lesion

HPV 6+11
“finger‐like projections

  • The projections are almost feathery
  • exophytic lesion
1049
Q

SQUAMOUS PAPILLOMA

What is it?

Gender?

Age?

Location?

Apperance ?

Treatment?

A

▪ Benign proliferation of stratified squamous
epithelium resulting ► papillary, verruciform, rugose (ridged or wrinkled) mass
▪ HPV types 6 + 11 – Low risk
▪ M = F
▪ Any age (more common in 30‐50s)
▪ Any oral mucosal surface (palate most common)
▪ Soft, painless, usually pedunculated, exophytic lesion w/ numerous finger‐like projections
▪ HPV DNA detected in only ~50%
▪ **should remove from mouth – but WOULD NOT submit for HPV typing

1050
Q

What is this infectious diease?

A

SQUAMOUS PAPILLOMA

Benign Oral Low Risk HPV
Lesion

HPV 6+11
“finger‐like projections

1051
Q

What is this infectious disease?

A

Oral Verruca Vulgaris
HPV 2,4,6
Also “finger‐like
projections”

remember it’s contagious

1052
Q

Oral Verruca Vulgaris

What is it?

Contagious?

Age?

Location?

Apperance ?

A

▪ HPV 2, and others (1,4,6,7,11,26,27,29,41,57,65,75‐77)
▪ Benign, HPV‐induced focal hyperplasia of stratified squamous epithelium
▪ Contagious – transmitted by direct contact
▪ Any age – frequently seen in children
▪ More common Anterior > Posterior part of mouth
▪ Soft, painless, usually pedunculated, exophytic lesions w/ numerous fingerlike projections (similar to squamous papilloma)
‐ How to tell the difference? Under microscope

1053
Q

What is this infectious disease?

A

Condyloma Acuminatum
(Venereal Wart)
HPV 6,11 – can be
cancerous
Genital warts
“short, blunt, clusters”

Characteristic clustering of multiple lesions

1056
Q

What is this infectious disease?

A

(Multifocal) Epithelial
Hyperplasia/Heck’s
Disease

HPV 13,32
“Flat‐top papules”

1057
Q

What is this infectious disease?

A

(Multifocal) Epithelial
Hyperplasia/Heck’s
Disease

HPV 13,32
“Flat‐top papules”

1058
Q

Condyloma Acuminatum
(Venereal Wart)

What is it?

Contagious?

Transmission?

Age?

Location?

Apperance ?

A

HPV Types 6, 11 – condyloma can turn cancerous
▪ Virually induced proliferation of stratified squamous epithelium – usually genital or anal mucosa
▪ Contagious – transmitted by direct contact
▪ Incubation period: 1‐3mo
▪ Considered sexually transmitted disease (if corroborated by history)
▪ Oral lesions – usually anterior part of mouth
▪ Sessile, pink, well‐demarcated, non‐tender exophytic mass
▪ Short, blunted surface projections
▪ Larger than papilloma or verruca vulgar

▪ Characteristic clustering of multiple lesions

1059
Q

What is this infectious disease?

A

Oral Florid Papillomatosis

Very characteristic appearance

  • diffused, in multiple locations
  • papillary

“Multifocal, papillary lesions”

-if we biopsied these or had these removed for aesthetic regions, we’d
see that the epithelium have become white, long, taller, and bumpy

1061
Q

If you see Condyloma Acuminatum in a child, what is the next step?

A

-Since this is a sexually transmitted disease, we need to suspect sexcual child abuse and investigate further!

1062
Q

(Multifocal) Epithelial
Hyperplasia/Heck’s
Disease

What is it?

Appearance?

Which communities or environment?

Demographics age and gender?

Histology?

A

▪ HPV Types 13, 32 and others (1,6,11,16,18,55)
▪ HPV‐induced localized proliferation of oral squamous epithelium
▪ “Flat‐top papules”
▪ Endemic in some Inuit/Alaskan native + Native American communities, Puerto Rican communities
▪ Crowded situations, malnutrition
▪ Usually seen in children
▪ May be seen in HIV + individuals
▪ M = F
▪ Histology: focal epithelial acanthos

1065
Q

Oral Florid Papillomatosis

What is it?

What are its types?

What is clinical appearance?

A

IIt’s benign HPV disease

▪ HIV infection
‐ Increased prevalence since advent of HAART therapy
‐ Multiple HPV types
▪ Down syndrome
Oral Florid

Characteristics:
‐ Diffuse, multiple locations
‐ Papillary
‐ Bumpy and tall

1067
Q

Benign
Oral HPV Lesions

HISTOPATHOLOGY

A

§Acanthosis
§Koilocytosis
§Binucleatedandmultinucleated keratinocytes
§Dyskeratosis
§Mitosoid figures
§Basilar hyperplasia

1068
Q

HPV is thought to cause –% of
oropharyngeal cancers in the US

A

HPV is thought to cause 70% of
oropharyngeal cancers in the US

That’s why we want to know if high risk
HPV– better prognosis

1069
Q

HPV Testing

A

▪ Pathologists order it
▪ Only do testing if pathologist sees cancer
No HPV testing on low‐risk HPV lesions (warts)
▪ No medical indication for low‐risk HPV testing b/c
‐ infection NOT associated w/ disease progression
‐ no treatment or therapy change indicated when low‐risk HPV is ID’ed
▪ HPV testing using p16 surrogate on oropharyngeal squamous cell carcinoma (SCC)

1070
Q

Management of Oral HPV
Lesions

Solitary Lesions

A

‐ Usually appear exophytic and papillary
‐ Excision is warranted
‐ Consider possible recurrence

1071
Q

Oral Molluscum
Contagiosum

Which viruse causes it?

Clinical Appaerance?

Who get affected?

Histopathology?

Treatment?

A

▪ Poxvirus
▪ Presents as:
‐ pink, dome‐shaped, smooth‐surfaced or umbilicated (like belly‐button) papules ‐ with caseous plug involving skin, lips, buccal mucosa, and palate
▪ Florid cases seen in immunocompromised persons
▪ Children, young adults
▪ Histopathology characterized by:
‐ Large intracytoplasmic inclusion bodies – “Henderson‐Paterson bodies”
‐ Kids can have 6‐9mo and will go away

1072
Q

What is this infectious disease?

A

Oral Molluscum
Contagiosum

multiple pink, dome‐shaped, smooth‐surfaced or umbilicated (like belly‐button) papules ‐ with caseous plug

1073
Q

Management of Oral HPV
Lesions

Multiple Lesions

A

‐ Use high power evacuation to prevent transmission
‐ Treatment = controversial
‐ Excision/ablation vs Topical vs Intralesional therapy (or combo)

‐ Consider higher rate of recurrence

1074
Q

What is this infectious disease?

A

Measles

*Characterized by Koplik’s spots

salts/grains

1075
Q

HPV multiple lesions

Excision/Ablation

A

Excision/Ablation

▪ Scalpel
▪ Carbon dioxide laser – be cautious, don’t know what is burned away
▪ Electrosurgery

1076
Q

What is this infectious disease?

A

Hand, foot, and mouth disease

caused by

Coxsackie
Virus

affect children

contagious

The condition is spread by direct contact with saliva or mucus.

1077
Q

What is this infectious disease?

A

Herpangina

casued by

Coxsackie
Virus

red macules and vesciles on the soft palate

a sudden viral illness in children.

It causes small blisterlike bumps or sores (ulcers) in the mouth

1078
Q

What is this infectious disease

A

Acute lymphonodular pharyngitis

Caused by

Coxsackie
Virus

Affects children

Nodules on the soft palate.

-distinctive, raised, micronodular lesions occur primarily in the pharynx and related structures and regressed without ulceration.

1079
Q

HPV multiple lesions

Topical Therapy

A

▪ Podophyllin resin
▪ Imiquimod (extra‐oral use only)
▪ Cidofovir
▪ Interferon

1080
Q

What is this infectious disease?

A

Rubella

caused by

Family: Togavirus; Genus: Rubivirus

Forchheimer sign (left)
Palatal petechiae (right)

(German Measles)

1081
Q

Topical Podophyllin

for what is it used

Is it FDA approved

Safe or not Durging pregnancy?

A

▪ Topical cytotoxic agent which arrests mitosis
▪ Genital warts and other papillomas
▪ Not FDA approved for oral warts
▪ Serious adverse reaction if absorbed systemically
▪ Pregnancy category X

1082
Q

Topical Imiquimod

A

▪ Induces cytokines + chemokines w/ resutlant anti‐virl (HPV) effects

Not FDA approved for oral warts

1083
Q

HPV vaccine

A

Newest is Gardsail 9

against many types

for both men and women

▪ 2 doses recommended for boys/girls age 11‐12 and 6mo later
▪ Recommended for everyone <26yo (MAX)
▪ NOT recommended for 26+yo unless risk for new infections (less benefit since most already exposed)
▪ Virus like particles (VLP) of L1 capsid protein present in vaccine
Results of Vaccination ▪ Drops in infections w/ HPV types that cause most HPV cancers + genital warts in
teen girls, young adult women
▪ Among vaccinated women – cervical precancers dropped by 40%

1084
Q

What precentge of people will be infected with HPV in their lifetime?

A

▪ 80% ppl will be infected in lifetime

so better take the vaccine early!

1087
Q

Measles

Which viruse causes it?

How does it spread?

Symptoms?

Clinical charcterstics?

location?

A

▪ Paramyxovirus
▪ Spread through respiratory droplets

▪ Symptoms: runny nose, red/watery eyes, cough, fever, rash, desquamation of skin

▪ *Characterized by Koplik’s spots
‐ Pathognomonic for measles
‐ Discrete, bluish white punctate mucosal
macules
‐ Surrounded by rim of erythema
‐ Represent foci of epithelial necrosis
‐ Often precedes skin manifestations

▪ Most common location for Koplok’s spots:
Buccal mucosa
‐ Lesions may resemble “grains of salt sprinkled
on erythematous background”

1089
Q

Enterovirus‐Coxsackie
Virus

What diseases can it cause ?

(3)

Who do they effect?

How they are treated?

A

-Herpangina‐soft palate, red macules ► fragile vesicles (back of throat)
‐ Hand, foot, and mouth disease – oral lesions more in anterior regions (aphthous‐like), hand/foot (vesicles)
‐ Acute lymphonodular pharyngitis – nodules on the soft palate

▪ Usually seen in children

▪ Self‐limiting

1093
Q

Rubella
(German Measles)

Which viruse causes it?

How does it spread?

Symptoms?

Clinical signs?

Assosited with what syndrome?

Is there a vaccine?

How it is diagnosed?

A

▪ Family: Togavirus; Genus: Rubivirus

▪ Respiratory droplets

Symptoms:
‐ Fever, headache, malaise, coryza (runny nose), anorexia, pharyngitis,
lymphadenopathy
▪ Rash – maculopapular w/ desquamation

  • *▪ Forchheimer sign**
  • *▪ Palatal petechiae**

▪ Congenital rubella syndrome – pandemics in past

▪ Vaccine: MMR – so we barely see this anymore

▪ Diagnosis: by serology

1095
Q

What is the Most common opportunistic fungal pathogen/ infection?

A

Candida Species

● Over 200 species exist

● At least 15 distinct Candida species cause human disease

1096
Q

Mucosal/Oral infections, which are generally non‐invasive are
caused primarily by ——–

A

Candida albicans

1097
Q

>90% of invasive disease is caused by 5 most common species, which are?

A

‐ C. albicans
‐ C. glabrata
‐ C. tropicalis
‐ C. parapsilosis
‐ C. krusei

1098
Q

Candida Species
have what kind of symbiosis with humans?

A

● Commensalism:
‐ “long‐term biological interaction (symbiosis) in which members of
one species gain benefits while those of the other species neither
benefit nor are harmed”
● >50% of humans carry candida without harmful effects

1099
Q

What is Candida Species‐
Disease State

A
  • Becomes an “infection” called candidiasis when environment changes and encourages growth
  • ● Defect in cell‐mediated immune response
  • ‐ Ranges from mild superficial mucosal infection ►(can be) fatal disseminated disease (usually with people with HIV and transplants)
1100
Q

What causes Candida
Infection?

A

● A disrupted balance of the normal mucosal flora
● Impaired barrier functions
● Immunosuppression

such as:

‐ Use of broad‐spectrum antibiotic
‐ Leukemia
‐ HIV
‐ Cancer chemotherapy
‐ Diabetes
‐ Xerostomia (what we deal with, candidiasis can persist here)

1101
Q

Normally Candida is in the commensal state and once you reach a certain level where the fungal burden has increased, you increase the c‐FOS pathway
‐ This is when the organism forms —–; once these are formed,
you see invasion into the——- cells.

A

Normally it is in the commensal state and once you reach a certain
level where the fungal burden has increased, you increase the c‐FOS
pathway
‐ This is when the organism forms hyphae; once these are formed,
you see invasion into the epithelial cells.

1102
Q

Pathogenesis‐ Key
Features

A

● Commensalism

  • Fungus is tolerated (threshold not reached)
  • Immune cells are not activated

● Pathogenicity

  • Fungal burden is increased and hyphae form
  • Immune cells are recruited by cytokines, chemokines
  • Neutrophils are recruited and kill fungus
  • Dendritic cells present antigen to T‐cells
  • T‐cells also decrease fungal burden (IL‐22, IL‐17)
  • Innate and acquired clear fungus to levels below threshold
1103
Q

How does Candida
overcome host
defenses?

6

A
  1. Dimorphism (can be spore and a hyphae‐ 2 forms)
  2. Phenotypic switching (change shape)
  3. Adhesins/Invasins (aid in attachment)
  4. Molecular mimicry of mammalian integrins (helps to be avoided by the immune system)
  5. Secretion of hydrolytic enzymes (aids in invasion)
  6. Phospholipase B contributes to degradation of host tissue (aids in degradation to gain entry)
1104
Q

Dimorphism

of

Candida

Two forms?

A

SPORES‐ when they are in this form, they do NOT invade
HYPHAE‐ when they begin their invasion

1105
Q

Crosstalk: Candida ——- play an important role in the continuous
interchange that regulates the balance between saprophytism and
parasitism

A

Crosstalk: Candida glycans play an important role in the continuous
interchange that regulates the balance between saprophytism and
parasitism

1106
Q

TYPES OF
CANDIDIASIS
INFECTION

A

● Superficial and localized‐more common (mild disease)

‐ Intertrigo §Paronychia/Onychomycosis
‐ “Diaper Rash”
‐ Vulvovaginitis
‐ Esophageal Candidiasis §Oral Candidiasis (Candidosis)

● Invasive, disseminated and deep infection‐rare (moderate‐severe)

‐ Affects blood (candidemia‐hospitalized), heart, brain, eyes, bones)

1107
Q

What is this infectious disease?

A

Onychomycosis

a type of candidiasis

1108
Q

What is this infectious disease?

A

Oral candidiasis

a type of candidiasis

1109
Q

What is this infectious disease?

A

Esophageal Candidiasis

a type of candidiasis

1110
Q

What is this infectious disease?

A

Vulvovaginitis

a type of candidiasis

1111
Q

What is this infectious disease?

A

“Diaper Rash”

a type of candidiasis

1112
Q

What is this infectious disease?

A

Intertrigo

a type of candidiasis

1117
Q

What is this infectious disease?

A

PSEUDOMEMBRANOUS CANDIDIASIS

UNCONTROLLED
DIABETIC

When you wipe away these plaques, you might
see some Erythematous areas that causes
some of the symptoms that the patient feels

-This is MILD DISEASE

1118
Q

What is this infectious disease?

A
  • *Pseudomembranous Candidiasis‐**
  • Uncontrolled HIV*

● This can be mistaken with materia alba (this is just food)
‐ Should ask patient if they just ate

● This is MODERATE DISEASE

1119
Q

What is this infectious disease?

A

Pseudomembranous Candidiasis

Topical
Corticosteroid Use

Can be brought about from steroid use (steroid inhaler example)
‐ If you don’t rinse your mouth after using steroids, this can happen
■ A proliferation of hyphae

1120
Q

What is this infectious disease?

A

PSEUDOMEMBRANOUS CANDIDIASIS

Severe dry mouth

This is severe disease

we would want to use systemic treatments/
intervention

1122
Q

What is this infectious disease

A

Angular Cheilitis

● Erythema, fissuring and scaling at angles of mouth
and commissures of mouth
● Loss of vertical dimension
● Pooling of saliva
● May be mixed bacterial/fungal infection
● Differential diagnosis can be Vit B Deficiency

a subtype of Erythematous
Candidiasis

1124
Q

What is this infectious disease

A

Denture Stomatitis

● Chronic atrophic candidiasis
● Erythema in denture bearing areas of maxilla
● Petechiae may be noted
● Usually, asymptomatic
● Consider denture care/fit/allergy/inadequate curing of acrylic

● This can occur if the patient NEVER takes off their denture

● Inflammatory papillary hyperplasia is associated with condition

● Treatment‐Nystatin applied to intaglio surface of denture and wear denture and patient to remove denture at night

a subtype of Erythematous
Candidiasis

1125
Q

What is this infectious disease?

A

Median Rhomboid Glossitis

a subtype of Erythematous
Candidiasis

● “Central Papillary Atrophy”
● Well‐demarcated erythematous zone
● Loss of papillae on midline posterior dorsal tongue
● Usually, asymptomatic
● “Kissing” palatal lesion
‐ Because the tongue and the palate are in contact
with each other
● Can have a diamond shape

1126
Q

What is this infectious disease?

A

ATROPHIC CANDIDIASIS

● Erythematous on any mucosal
surface
● “Bald Tongue”
● Typically, painful
● (Chronic multifocal, looks
familiar)

a subtype of Erythematous
Candidiasis

1127
Q

Which Candida is the most common species with what kind of Candidal Sepsis and
Disseminated Candidiasis ?

A

C. albicans

  • Candidal sepsis means that you have the fungal moving around in your body
  • Life‐threatening event in individual with severely deficient cell
  • mediated immunity
  • Most commonly involves urinary tract infection (women/men 4:1)
  • Very rare
1128
Q

What is this infectious disease?

A

HYPERPLASTIC CANDIDIASIS

1129
Q

Oral Candidiasis

facts

A

● 30‐50% of people carry organism without infection (called candida
carriage)
● Rate of carriage increases with age and risk factors
● 70‐80% of oral isolates are Candida albicans

1130
Q

What are the Predisposing
Factors for Oral Candidiasis ?

Local and general

A

Local

  • denture wearing
  • smoking
  • atopic consitituion
  • steroid inhalation
  • hyperkeratosis
  • imblance of the oral microflora
  • quality and qunatity of saliva\

General

  • immunosupressive disease
  • impaired health status
  • immunosupressive drugs
  • endocrine disorders
  • hematinic deficiencies
1131
Q

Pseudomembranous Candidiasis

Also known as?

Key feature?

Symptoms?

In which patients it is seen?

A

● “Thrush”
● KEY FEATURE: Wipeable white plaques that resemble curdled milk
● Underlying mucosa is erythematous
● Asymptomatic usually
● Mild symptoms: burning, dysgeusia
● Seen in patients with: HIV, broad‐spectrum antibiotics, leukemia,
infants

1132
Q

What is this infectious disease?

A

Chronic
Mucocutaneous
Candidiasis

Severe infection of mucosal surfaces, nails, and skin

1133
Q

What is this infectious disease?

A

Mucocutaneous
Candidiasis

APECED

Autoimmune
Polyendocrinopathy
Candidiasis
Ectodermal
Dystrophy
Syndrome

Biopsy of the tonuge revealed SCC

1136
Q

What is treatment of
moderate to severe
Candiadisis Disease?

A
  • Oral fluconazole, 100–200mg daily for 7–14 days

● For fluconazole‐refractory disease:
‐ Itraconazole suspension 200 mg once daily OR posaconazole
suspension 400 mg twice daily for 3 days then 400 mg once daily,
for up to 28 days, are recommended

Alternatives for fluconazole‐refractory disease include:
‐ Voriconazole, 200 mg twice daily, OR AmB deoxycholate oral
suspension, 100 mg/mL 4 times daily(strong recommendation;
moderate‐quality evidence).

‐ Intravenous echinocandin (caspofungin: 70‐mg loading dose, then 50 mg daily; micafungin: 100 mg daily; or anidulafungin: 200‐mg loading dose, then 100 mg daily) (weak recommendation;
moderate‐quality evidence). §

Intravenous Amphotericin B deoxycholate, 0.3 mg/kg daily, are
other alternatives for refractory disease (weak recommendation;
moderate‐quality evidence).

1137
Q

What is the treatment of
mild
Candiadisis Disease?

A
  • Clotrimazole troches, 10 mg 5 times daily

or

  • miconazole mucoadhesive buccal 50 mg tablet applied to the mucosal surface over the canine fossa once daily for 7–14 days
  • Alternatives for mild disease include nystatin suspension (100 000 u/mL) 4–6 mL swished for >1min then swallow 4 times daily.
1140
Q

What are other ways to manage denture stomoatitis ?

A

● Bleach‐1 part bleach to 10 parts water (not for dentures with metallic
clasps)
● Polident (NYU Carries Polident)
● Microwave? ( could be risky, careful not to ruin the denture)

CLEANSERS FOR REMOVABLE PROSTHESIS- you have to use this everynight to avoid denture stomoatits

NYU Carries Polident

Formulation: sodium bicarbonate, citric acid, potassium
monopersulfate, sodium carbonate, sodium carbonate peroxide,
TAED, sodium benzoate, PEG‐180, sodium lauryl sulfate, VP/VA
copolymer, flavor, cellulose gum, FD&C blue 2, blue 1 lake, yellow 5, yellow 5

1141
Q

Erythematous
Candidiasis

what are its

Clinical finding?

Subtypes?

A

● Clinical Findings:

  • Red macules or patches
  • Can be due to multiple things

● Subtypes:

‐ Atrophic Candidiasis (acute‐feels like mouth has been scalded)
‐ Median Rhomboid Glossitis (asymptomatic)
‐ Denture Stomatitis (asymptomatic)
■ HAS THE SHAPE OF THE DENTURE
‐ Chronic multifocal (asymptomatic)
■ THIS HAS BEEN THERE FOR A LONG TIME

1143
Q

What is this infectious disease?

A

a subtype of Erythematous
Candidiasis

1144
Q

How is Histoplasmosis Diagnosed?

How about its histology?

A

● Histopathology (H&E and special stain‐GMS)
● Culture
● Serology

as for histology

● Epithelioid macrophages containing histoplasma capsulatum (white arrows)
● Lymphocytes
● Plasma cells

1145
Q

What is the infectious disease?

A

Histoplasmosis

● This can be squamous cell carcinoma, shanker, ulcers
‐ Differentials for non healing ulcerations on the lateral tongue
● The white area is called the pseudomembrane

1149
Q

Which regions can Blastomycosis happen?

A

● Eastern half of US which extends farther north

● Seen in the wild

1150
Q

What is Hyperplastic
Candidiasis?

A

● a Rare and controversial form of candidiasis

● Candidiasis superimposed on pre‐existing
leukoplakic lesion

● White plaque which cannot be removed by
scraping (NOT WIPEABLE)

● Increased frequency of epithelial dysplasia

● MUST BIOPSY then diagnose as hyperplastic
candidiasis if you see fungi post biopsy

1152
Q

What is Chronic
Mucocutaneous
Candidiasis?

A

● Group of rare disorders with immunologic pathogenesis
● Clinical: Severe infection of mucosal surfaces, nails and skin
● Oral‐ lesions‐thick white plaques that do not rub off but may see other
forms

1153
Q

Chronic Mucocutaneous Candidiasis May be associated with endocrine abnormalities (APECED);

what does APECED stands with?

A

‐ A: autoimmune
‐ PE: polyendocrinopathy
‐ C: candidiasis
‐ E: ectodermal
‐ D: dystrophy

Chronic Mucocutaneous Candidiasis is also genetic

associted with AIRE gene

1154
Q

What is this infectious disease?

A

Blastomycosis

1155
Q

How to diagonse Blastomycosis?

A

● Histopathology (Granulomatous inflammation , Broad based budding , Double refractile cell wall)

● Cytology

● KOH

● Culture from sputum (3‐4 weeks)

● DNA probe (where you actively look for the DNA of the blastomycosis)

1156
Q

Chronic
Mucocutaneous
Candidiasis

is

at

increased

risk of what?

A

● Increased risk of squamous cell carcinoma

1159
Q

How is Oral
Candidiasis Diagnosed?

A

● Clinical signs
● Therapeutic diagnosis
● Cytologic smear: scrape cells and look at them under the microscope
and stained with PAS stain
● Periodic Acid Schiff Stain (PAS stain)
● KOH float §Biopsy (esp. hyperplastic candidiasis)
● Culture

1160
Q

What are Antifungal Drug
Classes?

3

A

● Polyene‐Nystatin, Amphotericin B (not absorbed; used for deep fungal infections)
● Imidazole‐Clotrimazole, Ketoconazole (GI absorption)
● Triazole‐Fluconazole, Itraconazole, Posaconazole, Echinocandins

1163
Q

What is Chronic Suppressive
Therapy?

A

this is when you keep the fungal infection under control for a
long time

Usually unnecessary in immunocompetent patients
● For patients who have recurrent infections:

‐ For HIV‐infected patients, antiretroviral therapy is strongly
recommended to reduce the incidence of recurrent infections
(strong recommendation; high‐quality evidence).

‐ Fluconazole, 100 mg 3 times weekly, is recommended (strong
recommendation; high‐quality evidence).

● Clotrimazole 10mg troches 1 week out of every month? (no evidence

1164
Q

What is Denture Stomatitis
Treatment?

A

YOU APPLY THE MEDICATION TO THE INTAGLIO PORTION

antifungal medication

(1) Topical Antifungal Agents
‐ Rx. Clotrimazole cream 1% vs OR
‐ Rx. Nystatin‐Triamcinolone Acetonide ointment or cream (why?
To keep the inflammation down)
■ Disp: 15g tube
■ Label: apply to angles of mouth after meals and before
bedtime
(2) Denture adjustment, reline, remake

YOU APPLY THE MEDICATION TO THE INTAGLIO PORTION

1166
Q

What is the Most common systemic fungal infection in US?

A

Histoplasmosis

1167
Q

What causes Histoplasmosis?

what is its mode of pathogensis ?

A

● Histoplasma capsulatum

● Dimorphic (yeast at body temperature and mold in soil)

1168
Q

Histoplasmosis

is endemic where

who can get infected by it?

How does is spread?

A

● Endemic in fertile river valleys
‐ Seen in people who spend a lot of time outside; near Ohio and Mississippi rivers

● Bird and bat excrement
● Airborne spores enter lungs through inhalation
● Macrophage ingests fungusàT‐lymphocyte immunity
● Antibodies develop several weeks later
● Macrophages may confine fungus (express disease later)

1171
Q

what is the treatment for Histoplasmosis?

acute

chronic

Disseminated

A

● Acute‐Supportive (analgesics and antipyretics)

● Chronic‐IV lipid preparation of amphotericin B or itraconazole

● Disseminated‐Lipid preparation of amphotericin B (2 weeks or more) followed by daily itraconazole for 6‐18 months

1172
Q

Blastomycosis

What is it?

What causes it?

What is its mode of pathogenesis?

A

● Uncommon fungal infection

● Blastomyces dermatitidis

● Dimorphic

1173
Q

Histoplasmosis‐ Clinical
Features

A

● Most cases produce no symptoms or only mild symptoms

● Acute‐Self‐limited lung infection (similar to influenza; the flu)
● Chronic‐Lung infection similar to tuberculosis
● Disseminated‐Extrapulmonary spread in immunocompromised (spreads from the lungs)
● Tongue, palate, buccal mucosa
● Solitary ulcer with firm rolled borders
● Clinically appear indistinguishable from malignancy (squamous cell carcinoma)

1175
Q

How does Blastomycosis spread?

Is there any gender prediclation?

A

● Airborne spores enter lungs through inhalation

● M>F

1176
Q

Acute Blastomycosis resembles ———-

A

● Acute‐ Resembles pneumonia

1177
Q

ChronicBlastomycosis resembles ———-

A

Chronic Resembles tuberculosis

1178
Q

What are the clinical features of Blastomycosis?

A

● Skin lesions‐extrapulmonary dissemination from lungs

● Oral lesions‐extrapulmonary dissemination or local inoculation

● Skin lesions

● Granular(rough looking) erythematous plaques which may become verrucous(wart‐like) or ulcerated

● Oral lesions

‐ Erythematous or white ‐ Intact surface or ulceration with rolled borders

‐ Painful ‐ Ddx‐Squamous cell carcinoma

1181
Q

How to treat Blastomycosis?

A

● Most cases asymptomatic

● Itraconazole (mild to moderate disease)

● Systemic amphotericin B (severe cases)

● There is a connection with people taking TNF‐alpha inhibitors

1182
Q

Paracoccidio Mycosis

What is it?

What causes it?

A

A deep fungal infecion

causes by:

Paracoccidioidomycosis brasiliensis

1183
Q

Which regions Paracoccidio Mycosis happen?

A

● South American blastomycosis

1184
Q

Paracoccidio Mycosis is seen in the soil around ——- (name of an animal)

A

nine‐ringed armadillos

1185
Q

Paracoccidio Mycosis

what gender is more common ?

which workers are more affected?

A

● More common in males

● Agriculture workers

1186
Q

Paracoccidio Mycosis presents intially as which infection?

A

Pulmonary infection

1187
Q

What is infectious disease?

A

Paracoccidio Mycosis

looks like the three tail in Naruto lol

1189
Q

what is this infection disease ?

A

Paracoccidioidomycosis

looks like strawberry gingiva but it is not

1190
Q

How is Paracoccidioidomycosis diagnosed?

A

● Histopathology (- Granulomatous inflammation, Epithelioid macrophages and multinucleated giant cells,GMS or PAS, Multiple daughter buds)

● Culture

● KOH

1191
Q

what are the clinical presentation of Paracoccidioidomycosis?

A

●affects the Alveolar mucosa, gingiva and palate lesions with “Mulberry‐like” ulceration (little bumps around it)

● Looks like strawberry gingivitis (differential diagnosis)

1194
Q

How is Paracoccidioidomycosis treated?

A

● Trimethoprim/ sulfamethoxazole (mild‐moderate)

● IV Amphotericin B (severe disease)

1195
Q

What is Coccidiomycosis?

A

deep fungal infection that present as Pulmonary infection

1196
Q

Coccidiomycosis is known as ——-

A

Valley Fever

1197
Q

What are the two types of Coccidiomycosis ?

A
  • Coccidioides immitis
  • Coccidioides posadasii
1198
Q

What is this infectious disease?

A

Coccidioidomycosis

1199
Q

How is Coccidioidomycosis diagnosed?

A

● Histopathology ( Round spherules with numerous endospores , Granulomatous inflammation, Suppurative neutrophils infiltrate, Special Stains used: GMS, PAS)

● Culture

● In situ hybridization (ISH)

● Cytology‐ scraping ulcers then stained with GMS

● Serology‐ check for antibodies

● Skin testing (limited value)

1200
Q

What is the mode of pathogenesis of Coccidiomycosis?

A

Dimorphic organism (spores and hyphae)

1201
Q

Coccidioidomycosis

What is the Clinical Features?

how does the oral and skin lesions appear?

A

● Oral lesions

ulcerated granulomatous nodules

● Skin lesions: papules(slightly raised), abscesses, verrucous(patchy), plaques, granulomatous nodules

1202
Q

Coccidioidomycosis

symptoms?

What is the Clinical Features?

how does the oral and skin lesions appear?

A

● Most cases are asymptomatic ~60%

● Flulike

● Fatigue, cough, chest pain, myalgia, headache

● May see a hypersensitivity reaction (valley fever) ‐ When you are over responding; immune system is over reacting

● Chronic‐mimics tuberculosis

● Disseminated‐ <1% of cases

1205
Q

How is Cryptococcus diagnosed?

A

● Biopsy ● Culture ● Serology

Note: Histopathologically they appear as Granulomatous inflammation (epithelioid histiocytes trying to confide the infection)

● Yeast are surrounded by a clear halo (capsule)

1206
Q

How is Coccidioidomycosis treated?

A

● Mild symptoms‐ no treatment usually

● Amphotericin B (‐ Immunosuppressed ‐ Severe pulmonary infection ‐ Disseminated disease ‐ Pregnant patients ‐ Life‐threatening situation )

● Itraconazole or fluconazole (fewer side effects and complications)

1207
Q

Cryptococcus

How common is it?

What causes it?

A

●Uncommon

● Cryptococcus neoformans

● Incidence increased due to AIDS epidemic in 1990s

● Pulmonary infection

● Meningitis

1208
Q

Cryptococcus is seen in ————–

A

pigeon excrement (poo)

1209
Q

Cryptococcus can cause what kind of infections?

A

● Pulmonary infection

● Meningitis ( after it spreads from the lungs to the brain. )

1210
Q

What is this infectious disease?

A

Mucormycosis‐

arrow refers to ESCHAR‐ always look for this and extreme-Black and necrotic ulcer (

we can see massive tissues destruction

1211
Q

What is this infectious disease?

A

Mucormycosis‐ CT

Sinus opacificatio

● First thing to do is to find out more about this lesion, how did this patient get this lesion?

1212
Q

Mucormycosis‐ Histopathology has a sepcial shape?

A

● Non‐septate hyphae with 90degrees branching

● You see necrosis of tissue in the area because this attacks the blood vessels

1213
Q

What are the Clinical Features of Cryptococcus?

A

Lung infection often asymptomatic

● Flulike illness

● Dissemination

‐ Meninges ‐ Skin ‐ Bone ‐ Prostate ‐ Oral‐papillary/granular erythematous plaques

1215
Q

How is Cryptococcus treated?

A

● Mild case: Fluconazole or Itraconazole

● Cryptococcal meningitis: amphotericin B + other antifungals

1216
Q

Mucormycosis is caused by what?

A
  • Infections caused by molds belonging to the order Mucorales
  • Grow in natural state on decaying organic materials (saprobic‐ recycling)
  • Spores may be liberated into air and inhaled by humans
1217
Q

Mucormycosis can affect people with what underlying conditions?

A

‐ Insulin dependent diabetics

‐ Bone marrow transplant recipients

‐ AIDS

‐ Patients receiving systemic corticosteroids

‐ Neutropenic patients (no white blood cells)

1218
Q

Which infectious disease has fruting body in its histopathology?

A

Aspergillosis

Histopathology includes:

●Branching septate hyphae

● Acute angle branching

● “Fruiting body

1219
Q

What are the Clinical Features of Mucormycosis?

A

● Rhinocerebral form

● Nasal obstruction

● Bloody nasal discharge

● Facial pain

● Facial paralysis

● Facial swelling/cellulitis

● Visual disturbances

● Into cranial vault‐blindness, lethargy, seizures

● Oral swelling/ulceration of the maxillary alveolar process/palate as a result of sinus involvement

● Black and necrotic ulcer (eschar)

● Massive tissue destruction

1220
Q

what is this infectious disease?

A

Aspergillosis

arrow points toward a violaceous‐ purple colour

1224
Q

How is Mucormycosis diagnosed?

A

● Histopathology

● Culture

1225
Q

How is Mucormycosis treated?

A

● Surgical debridement (massive tissue destruction)

● High doses of lipid formation of amphotericin B

● Control underlying disease (main one)

● Prosthetic obturation of palatal defects

1226
Q

What is Aspergillosis and what causes it?

A
  • Saprobic (in an environment rich of oxygen)
  • it caused by Aspergillus flavus and Aspergillus fumigatus
1227
Q

Where is Aspergillosis typically seen?

how it is spread?

A

● Seen in hospitals and construction sights

●caused by Aspergillus flavus and Aspergillus fumigatus

● Spores are inhaled

1228
Q

What is this infectious disease?

A

Necrotizing Gingivitis (NG)

o No periodontitis features

o SIMILAR APPEARANCE to gonorrhea

▪ Distinguishing characteristic of NG – Fetid Odor

1229
Q

What is this infectious disease?

A

Necrotizing Periodontitis (NP)

o Bone loss of the periodontium seen

1230
Q

Aspergillosis‐ Clinical Features

Two types

noninvasive

and invasive

A

● Noninvasive

‐ Allergic fungal sinusitis

‐ Aspergilloma (fungus ball, mycetoma [‐oma: like a tumour made of aspergillus])

● Invasive

‐ Localized (possibly after tissue damage in oral cavity)

‐ Disseminated ‐immunocompromised

1232
Q

How is Aspergillosis diagnosed?

A

● Histopathology

● Culture

1234
Q

How is Aspergillosis treated?

A

● Aspergilloma‐debridement

● Allergic fungal sinusitis‐debridement and corticosteroid drugs

● Localized invasive‐debridement & voriconazole and amphotericin B

● Disseminated invasive‐consider poor prognosis even with treatment

1235
Q

What are Oral Manifestations of Bacterial Infections?

A

Caries (streptococcus mutans)

‐ Gingivitis/Periodontitis

‐ Necrotizing Periodontal Diseases

‐ Noma (Cancrum Oris)

Impetigo

‐ Erysipelas ‐

Streptococcal Tonsillitis and Pharyngitis

Scarlet Fever

‐ Diphtheria

‐ Syphilis

‐ Gonorrhea

‐ Tuberculosis

Leprosy Actinomycosis

‐ Cat Scratch Disease

‐ Bacillary Angioma

1236
Q

What is Necrotizing Periodontal Diseases?

A

Bacterial infection which presents with a spectrum of lesions

‐ Vary depending upon the localization of lesion and predisposing factors

1237
Q

Necrotizing Periodontal Diseases

include 4 types,what are they? What do they mean?

A

‐ Includes:

o Necrotizing gingivitis (NG):rapidly destructive, non-communicable microbial disease of the gingiva

o Necrotizing periodontitis (NP):apidly progressing disease process that results in the destruction of the periodontium

o Necrotizing stomatitis (NS):When the bacterial infection extends further to OTHER parts of the mouth

o NOMA (extension to skin of face) ▪ Extreme disfigurement due to bacterial infection extending onto the skin of the face

1238
Q

Necrotizing Periodontal Diseases

name has changed

how?

A

‐ The term “acute” has not been included since 1999 (ANUG=old name) o As the infections are ALWAYS acute

‐ The term “ulcerative” removed in 2017 World Workshop proposed classification “Necrotizing Periodontal Disease (NPD)” is term proposed in 2017 World Workshop for NG, NP and NS o There is ALWAYS ulceration as a result of necrosis

1239
Q

what are the Clinical Features of Necrotizing Periodontal Diseases?

A

‐ Ulceration with necrosis of interdental papillae

o Results in a “punched out” crater‐like appearance of the papilla

‐ Gray pseudomembrane

o Dead tissue ‐ EXTREMELY Painful

‐ Fetid odor

‐ Spontaneous hemorrhage Fever, lymphadenopathy, malaise

1240
Q

Which population affected by Necrotizing Periodontal Diseases?

A

Young and middle‐aged adults

Prevalence <0.1%

1243
Q

What are the risk factors of Necrotizing Periodontal Diseases?

A

Many related factors (Multifactorial etiology):

o Psychological stress

o Immunosuppression

o Smoking

o Local trauma

o Poor nutritional status

o Poor oral hygiene

o Inadequate sleep

1244
Q

Which infectious diseases was known by Trench mouth?

A

Necrotizing Periodontal Diseases

o During WW1, soldiers that were fighting in the trenches were under extreme stress

o they commonly developed necrotizing periodontal diseases

1245
Q

What are the Constant bacterial species found in Necrotizing Periodontal Diseases?

Will we be able to use microbiological testing to form a diagnosis?

A

o Treponema spp.

o Selenomonas spp.

o Fusobacterium spp.

o Prevotella intermedia

o *Also always present in healthy gingiva ▪ so, No, Microbiological testing is NOT used to form a diagnosis

1246
Q

What is the Treatment of Necrotizing Periodontal Diseases?

A

o Removal of bacteria (scaling)

o Chlorhexidine rinse

o Antibiotics (fever or signs of systemic illness)

▪ Metronidazole ▪ Penicillin

o Oral hygiene instruction

o Supportive therapy

▪ Rest ▪ Fluids ▪ Soft nutritious diet

o Predisposing (Immunosuppressive)factors

▪ Smoking

▪ HIV?

1247
Q

NOMA is also called as ————

A

cancrum oris

1248
Q

What is NOMA?

Where it is seen?

A

‐ Rapidly progressive opportunistic infection caused by many bacteria

o More commonly seen in other parts of the world

o Seen in the US in immunocompromised patients ▪ HIV

‐ WHO estimates the global yearly incidence = 140,000

1249
Q

Which bacteria involved in NOMA?

A

‐ Polymicrobial etiology

‐ Normal flora become pathogenic during immunocompromised states

‐ Key bacteria:

o Fusobacterium necrophorum

o Prevotella intermedium ‐ Other common bacteria:

o Actinomyces pyogenes

o Bacillus cereus

o Bacteroides fragilis

o Fusobacterium nucleatum

o Prevotella melaninogenica

1250
Q

What are the Predisposing Factors of NOMA?

A

‐ Previous necrotizing periodontal disease Poverty

‐ Malnutrition or dehydration

‐ Poor oral hygiene

‐ Poor sanitation

‐ Unsafe drinking water

‐ Proximity to unkempt livestock

‐ Recent illness Malignancy

‐ Immunodeficiency disorder, including AIDS

1251
Q

What is this infectious disease?

A

NOMA

This is an aid patient

Figure 2: Extension of infection onto the face

‐ Figure 3: Lost bone and gingiva

‐ Figure 4 & 5 Bone destruction

1252
Q

What is this infectious disease?

A

NOMA

This is an aid patient

Figure 2: Extension of infection onto the face

‐ Figure 3: Lost bone and gingiva

‐ Figure 4 & 5 Bone destruction

1253
Q

Which bacteria involved in NOMA?

A

‐ Polymicrobial etiology

‐ Normal flora become pathogenic during immunocompromised states

‐ Key bacteria:

o Fusobacterium necrophorum

o Prevotella intermedium ‐ Other common bacteria:

o Actinomyces pyogenes

o Bacillus cereus

o Bacteroides fragilis

o Fusobacterium nucleatum

o Prevotella melaninogenica

1254
Q

What is this infectious disease?

A

NOMA

Development of NOMA from day 1 to day 15

1255
Q

NOMA can affect who?

A

Children

Adults with debilitating disease

1256
Q

What is this infectious disease?

A

Impetigo

‐ “Cornflakes glued to Surface” Appearance

o Little papules that can form little vesicles around the mouth

o Vesicles burst open and dry up around the skin of the mouth

‐ Bilateral

1257
Q

What is this infectious disease?

A

NOMA

Development of NOMA from day 1 to day 15

1258
Q

What are the clinical features of NOMA?

A

Gingiva (NG) ► Adjacent tissue (necrotizing stomatitis)

+ Non‐ contiguous tissue (trauma)

► Blue black discoloration of skin

‐ Spreads through muscle, bone (osteomyelitis)

‐ Other features:

o Fetid odor

▪ Due to tissue necrosis

o Pain o Fever o Malaise

o Tachycardia o Increased respiratory rate

o Anemia o Leukocytosis o Regional lymphadenopat

1259
Q

What is this infectious disease?

A

Impetigo

‐ “Cornflakes glued to Surface” Appearance

o Little papules that can form little vesicles around the mouth

o Vesicles burst open and dry up around the skin of the mouth

‐ Bilateral

1260
Q

What is this infectious disease?

A

Erysipelas

Superficial skin infection in immunosuppressed adults

‐ Group A beta‐hemolytic streptococci

‐ Painful ‐ Bright‐red, well‐circumscribed, swollen, indurated (firm) ‐ Warm to touch

‐ Systemic manifestations: o High fever o Swollen lymph nodes

Diagnosis:

Cultures not useful ‐

Treatment: o Penicillin ‐ Complications without treatment

1261
Q

What are the Predisposing Factors of NOMA?

A

‐ Previous necrotizing periodontal disease Poverty

‐ Malnutrition or dehydration

‐ Poor oral hygiene

‐ Poor sanitation

‐ Unsafe drinking water

‐ Proximity to unkempt livestock

‐ Recent illness Malignancy

‐ Immunodeficiency disorder, including AIDS

1262
Q

What is the treatment of Noma?

A

o Antibiotics

▪ Penicillin ▪ Metronidazole

o Local wound care

▪ Conservative debridement to avoid iatrogenic tissue damage

o Consider nutrition, hydration and electrolyte imbalances

o May cause significant morbidity

1263
Q

What is this infectious disease?

A

Erysipelas

Superficial skin infection in immunosuppressed adults

‐ Group A beta‐hemolytic streptococci

‐ Painful ‐ Bright‐red, well‐circumscribed, swollen, indurated (firm) ‐ Warm to touch

‐ Systemic manifestations: o High fever o Swollen lymph nodes

Diagnosis:

Cultures not useful ‐

Treatment: o Penicillin ‐ Complications without treatment

1264
Q

What is this infectious disease?

A

Primary Syphilis

Chancre

at site of inoculation (3 – 90 days later)

‐ Papule ► Ulceration

‐ Most chancres occur in genital area (4% oral

1265
Q

What is this infectious disease?

A

Primary Syphilis

Chancre

at site of inoculation (3 – 90 days later)

‐ Papule ► Ulceration

‐ Most chancres occur in genital area (4% oral

1266
Q

What are the clinical features of NOMA?

A

Gingiva (NG) ► Adjacent tissue (necrotizing stomatitis)

+ Non‐ contiguous tissue (trauma)

► Blue black discoloration of skin

‐ Spreads through muscle, bone (osteomyelitis)

‐ Other features:

o Fetid odor

▪ Due to tissue necrosis

o Pain o Fever o Malaise

o Tachycardia o Increased respiratory rate

o Anemia o Leukocytosis o Regional lymphadenopat

1267
Q

What is this infectious disease?

A

Secondary Syphilis

‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection

‐ Resolve in 3‐12 weeks

‐ Diffuse maculopapular (flat, raised) rash

o May involve oral cavity ‐ Mucous patches

o Most common on tongue and lip

‐ Condylomata lata

o Resembles viral papillomas

‐ Systemic symptoms

1268
Q

What is this infectious disease?

A

Secondary Syphilis ( Rash)

here we see muscus patches (right) and Condylomata lata (left)

‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection

‐ Resolve in 3‐12 weeks

‐ Diffuse maculopapular (flat, raised) rash

o May involve oral cavity ‐ Mucous patches

o Most common on tongue and lip

‐ Condylomata lata

o Resembles viral papillomas

‐ Systemic symptoms

1269
Q

What is this infectious disease?

A

Tertiary Syphilis

Gumma

‐ Latent period for 1 ‐ 30 years

‐ 30% of patients develop tertiary syphilis

‐ Serious complications develop:

  • Vascular system
  • Central nervous system
  • Ocular lesions

What is “Gumma”?

  • o Granulomatous inflammation with tissue destruction
  • o Common on palate and tongue
  • o Causes a hole in the palate
1270
Q

What causes Impetigo?

A

‐ Caused by:

o Staphylococcus aureus

o Streptococcal pyogenes

Damaged skin allows infection to enter

Usually affects kids

1271
Q

What is this infectious disease?

A

Primary Syphilis

Chancre

at site of inoculation (3 – 90 days later)

‐ Papule ► Ulceration

‐ Most chancres occur in genital area (4% oral

1272
Q

What is this infectious disease?

A

Congenital Syphilis

‐ Hutchinson Incisors (left image)

‐ Mulberry molars (right image) - not part of the triad

1273
Q

Syphilis

Histopathology

stage 1 and 2

A

Not specific ‐ Stage 1 and 2 similar

o Ulceration

o Hyperplasia (Stage 2)

o Exocytosis of neutrophils into epithelium

Intense Iymphoplasmacytic inflammatory infiltrate in superficial stroma and around deeper vascular channels (blood vessels)

1274
Q

Syphilis

Histopathology

Stage 3

A

Stage 3 o Granulomatous inflammation o Ulceration may be present ‐ Special stain “Warthin Starry”, highlights corkscrew spirochetes ‐ Immunohistochemical stain

1275
Q

How is Syphilis diagnosed?

A

o Biopsy with histopathology

o Dark field examination of a smear of active lesion

o Serologic screening lab tests

  • ▪ Venereal Disease Research Lab (VDRL), RPR (non‐ specific and not highly sensitive)
  • ▪ Fluorescent Treponemal Antibody Absorption (FTA‐ ABS), TPHA, TPPA, MHA‐TP (specific and sensitive)
1276
Q

What is this infectious disease?

A

Tertiary Syphilis

Gumma

‐ Latent period for 1 ‐ 30 years

‐ 30% of patients develop tertiary syphilis

‐ Serious complications develop:

  • Vascular system
  • Central nervous system
  • Ocular lesions

What is “Gumma”?

  • o Granulomatous inflammation with tissue destruction
  • o Common on palate and tongue
  • o Causes a hole in the palate
1277
Q

What is this infectious disease?

A

Secondary Syphilis

Mucous Patch

1278
Q

What is this infectious disease?

A

Secondary Syphilis ( Rash)

here we see muscus patches (right) and Condylomata lata (left)

‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection

‐ Resolve in 3‐12 weeks

‐ Diffuse maculopapular (flat, raised) rash

o May involve oral cavity ‐ Mucous patches

o Most common on tongue and lip

‐ Condylomata lata

o Resembles viral papillomas

‐ Systemic symptoms

1279
Q

Syphilis

Histopathology

Stage 3

A

Stage 3 o Granulomatous inflammation o Ulceration may be present ‐ Special stain “Warthin Starry”, highlights corkscrew spirochetes ‐ Immunohistochemical stain

1280
Q

How is Syphilis diagnosed?

A

o Biopsy with histopathology

o Dark field examination of a smear of active lesion

o Serologic screening lab tests

  • ▪ Venereal Disease Research Lab (VDRL), RPR (non‐ specific and not highly sensitive)
  • ▪ Fluorescent Treponemal Antibody Absorption (FTA‐ ABS), TPHA, TPPA, MHA‐TP (specific and sensitive)
1281
Q

What is this infectious disease?

A

Gonorrhea

looks like necrotizing gingivitis (NG) but fetor oris not present

1282
Q

Syphilis

Histopathology

stage 1 and 2

A

Not specific ‐ Stage 1 and 2 similar

o Ulceration

o Hyperplasia (Stage 2)

o Exocytosis of neutrophils into epithelium

Intense Iymphoplasmacytic inflammatory infiltrate in superficial stroma and around deeper vascular channels (blood vessels)

1283
Q

What is this infectious disease?

A

Secondary Syphilis

Mucous Patch

1284
Q

What is this infectious disease?

A

Congenital Syphilis

‐ Hutchinson Incisors (left image)

‐ Mulberry molars (right image) - not part of the triad

1285
Q

What is this infectious disease?

A

Secondary Syphilis

‐ Disseminated lesions are discovered 4 ‐ 10 weeks after initial infection

‐ Resolve in 3‐12 weeks

‐ Diffuse maculopapular (flat, raised) rash

o May involve oral cavity ‐ Mucous patches

o Most common on tongue and lip

‐ Condylomata lata

o Resembles viral papillomas

‐ Systemic symptoms

1286
Q

What is this infectious disease?

A

Gonorrhea

looks like necrotizing gingivitis (NG) but fetor oris not present

1287
Q

What is this infectious disease?

A

Primary Syphilis

Chancre

at site of inoculation (3 – 90 days later)

‐ Papule ► Ulceration

‐ Most chancres occur in genital area (4% oral

1288
Q

What is Impetigo Differential Diagnosis

A

o Recurrent Herpes Labialis

▪ Resemblance to initial impetigo stages when still unilateral

o Perioral Dermatitis

▪ Triggered by cosmetics and other substances on the skin

o Exfoliative Cheilitis (chapped lips)

1289
Q

How is Impetigo diagnosed and treated?

A

Diagnosis:

o Presumptive from clinical features

‐ Treatment:

o Topical mupirocin

o Systemic antibiotics

1290
Q

What is this infectious disease?

A

‐ Tuberculosis

1291
Q

What is this infectious disease?

A

‐ Tuberculosis

1292
Q

What is the treatment of Noma?

A

o Antibiotics

▪ Penicillin ▪ Metronidazole

o Local wound care

▪ Conservative debridement to avoid iatrogenic tissue damage

o Consider nutrition, hydration and electrolyte imbalances

o May cause significant morbidity

1293
Q

What is differential diagnosis for Erysipelas?

A

o Systemic Lupus Erythematosus (SLE)

▪ Due to sparing of nasolabial folds

▪ Butterfly rash in SLE resembles erysipelas

o Cellulitis (dental infection induced):

▪ Tooth infection burrowing through the tissues rather than forming an abscess

o Actinomycosis

1294
Q

What is Syphilis?

What causes it/

A
  • Chronic infection
  • caused by spirochete Treponema pallidum
1295
Q

What are the three stages of Syphillis?

A

Three stages

  1. o Primary (chancre)
  2. o Secondary (rash)
  3. o Tertiary (gumma)
1296
Q

What is this infectious disease?

A

TB

Ulceration (tongue ulceration most common)

1297
Q

What is this infectious disease?

A

Miliary TB

compared to miliary seeds

1298
Q

What is this infectious disease?

A

‐ Tuberculosis

1299
Q

What is this infectious disease?

A

‐ Tuberculosis

1300
Q

How is Impetigo diagnosed and treated?

A

Diagnosis:

o Presumptive from clinical features

‐ Treatment:

o Topical mupirocin

o Systemic antibiotics

1301
Q

What are the three stages of Syphillis?

A

Three stages

  1. o Primary (chancre)
  2. o Secondary (rash)
  3. o Tertiary (gumma)
1302
Q

What is this infectious disease?

A

Miliary TB

compared to miliary seeds

1303
Q

What is this infectious disease?

A

TB

Ulceration (tongue ulceration most common)

1304
Q

What is Differential Diagnosis for Primary Syphilis (Chancre)?

3

A
  1. SCC
  2. Fungal Ulcer
  3. Trumatic Ulcer
1305
Q

What is Syphilis?

What causes it/

A
  • Chronic infection
  • caused by spirochete Treponema pallidum
1306
Q

What is Differential Diagnosis for Primary Syphilis (Chancre)?

3

A
  1. SCC
  2. Fungal Ulcer
  3. Trumatic Ulcer
1307
Q

What is differential diagnosis for Erysipelas?

A

o Systemic Lupus Erythematosus (SLE)

▪ Due to sparing of nasolabial folds

▪ Butterfly rash in SLE resembles erysipelas

o Cellulitis (dental infection induced):

▪ Tooth infection burrowing through the tissues rather than forming an abscess

o Actinomycosis

1308
Q

Differential Diagnosis for teritiary syphillis “Gumma”

A

Differential Diagnosis:

  1. ▪ T‐cell Lymphoma
  2. ▪ Cocaine abuse
  3. ▪ Granulomatosis
  4. ▪ Polyangiitis
  5. ▪ Mucor
1309
Q

Congenital Syphilis is associated with what Triad?

A

‐ Pathognomonic features in Hutchinson triad:

o 1. Hutchinson teeth

o 2. Ocular interstitial keratitis

o 3. Eighth nerve deafness

‐ Other Features:

o High arched palate

o Saddle nose

o Frontal bossing

Clinical changes secondary to fetal infection

1310
Q

What is Impetigo Differential Diagnosis

A

o Recurrent Herpes Labialis

▪ Resemblance to initial impetigo stages when still unilateral

o Perioral Dermatitis

▪ Triggered by cosmetics and other substances on the skin

o Exfoliative Cheilitis (chapped lips)

1311
Q

Congenital Syphilis is associated with what Triad?

A

‐ Pathognomonic features in Hutchinson triad:

o 1. Hutchinson teeth

o 2. Ocular interstitial keratitis

o 3. Eighth nerve deafness

‐ Other Features:

o High arched palate

o Saddle nose

o Frontal bossing

Clinical changes secondary to fetal infection

1312
Q

Differential Diagnosis for teritiary syphillis “Gumma”

A

Differential Diagnosis:

  1. ▪ T‐cell Lymphoma
  2. ▪ Cocaine abuse
  3. ▪ Granulomatosis
  4. ▪ Polyangiitis
  5. ▪ Mucor
1313
Q

What causes Impetigo?

A

‐ Caused by:

o Staphylococcus aureus

o Streptococcal pyogenes

Damaged skin allows infection to enter

Usually affects kids

1314
Q

How is Syphilis Treated?

A

o Single dose of parenteral long‐ acting benzathine penicillin G (primary, secondary, early latent)

o Intramuscular penicillin weekly for three weeks (late latent and tertiary

1315
Q

NOMA can affect who?

A

Children

Adults with debilitating disease

1316
Q

What is Gonorrhea?

What causes it?

A

‐ a Sexually transmitted (F>M)

caused by

‐ Neisseria gonorrhoeae

1317
Q

How Gonorrhea affects the body?

what complications can arrise?

A

‐ Genital area usually‐purulent discharge

‐ Systemic bacteremia (myalgia, arthralgia, polyarthritis, dermatitis)
‐ Pelvic inflammatory disease in women (affects pregnancies)
‐ Gonococcal ophthalmia neonatorum (infection of infant’s eyes)

1318
Q

What are the Clinical
Features of Gonorrhea?

A

‐ Oral lesions ‐ similar to aphthous

o Very rare

‐ Tonsils edematous and erythematous

‐ May simulate necrotizing gingivitis (NG) but fetor oris not present

1320
Q

How is Gonorrhea
diagnosed?

A

‐ Gram stain
‐ Culture of endocervical swab
‐ Nucleic acid amplification tests (NAATs)‐detect DNA, RNA

1321
Q

How is Gonorrhea
treated?

A

Many cases of resistance with antibiotics
§Cephalosporins

Adults with gonorrhea are treated with antibiotics. Due to emerging strains of drug-resistant Neisseria gonorrhoeae, the Centers for Disease Control and Prevention recommends that uncomplicated gonorrhea be treated with the antibiotic ceftriaxone — given as an injection — with oral azithromycin (Zithromax)

1322
Q

Gonorrhea can have coinfection

with what other infectious bacteria?

A

Chlamydia trachomatis

1323
Q

Chlamydia trachomatis can trigger which autoimmune disease

A

Reactive arthritis (reiter)
o Can’t see, Can’t Pee, Can’t Climb a Tree

▪ Causes:
● Conjunctivitis
● Urethritis
● Arthritis

Remember: Chlamydia trachomatis coininfect with Neisseria gonorrhoeae

1324
Q

What is Tuberculosis?

What causes it?

How does it spread?

A
  • Chronic granulomatous infectious disease
  • Caused by Mycobacterium tuberculosis

§Direct person-to-person spread through airborne droplets

1325
Q

Primary TB

A

affects previously unexposed, lungs - They breathe in the organisms that someone is coughing out

1st: C_hronic inflammatory reaction_ ► Next, a fibrocalcific nodule (Ghon focus) forms at initial site of infection

1326
Q

What are the chance
active disease if you get infected with Primary TB

A

Only 5%-10% infections lead to active disease i

1327
Q

“Secondary TB” reactivation

A
  • Leads to disseminated TB (miliary TB)
  • True, active TB
1328
Q

How is Syphilis Treated?

A

o Single dose of parenteral long‐ acting benzathine penicillin G (primary, secondary, early latent)

o Intramuscular penicillin weekly for three weeks (late latent and tertiary

1329
Q

What are the Clinical
Features of Gonorrhea?

A

‐ Oral lesions ‐ similar to aphthous

o Very rare

‐ Tonsils edematous and erythematous

‐ May simulate necrotizing gingivitis (NG) but fetor oris not present

1330
Q

What are the causes of secondary Tuberculosis?

A
  • Immunosuppressive medications
  • Diabetes
  • Old age
  • Crowded living conditions
  • AIDS
1331
Q

Tuberculosis
Clinical
Features

Extrapulmonary TB

A
  • Lymphatics
  • Skin
  • Skeletal system
  • CNS
  • Kidney
  • GI tract
  • Oral cavity (uncommon)
1332
Q

Tuberculosis
Clinical
Features

Primary TB

A

Usually asymptomatic

1333
Q

Tuberculosis
Clinical
Features

SecondaryTB

A

o Typically see lung lesions (productive cough)
o Fever, malaise, anorexia, night sweats

1334
Q

Tuberculosis

CLINICAL FEATURES OF ORAL LESIONS

A

§Ulceration (tongue ulceration most common)
§Mucosal granularity
§Diffuse inflammation
§Non-healing extraction socket

1335
Q

“Secondary TB” reactivation

A
  • Leads to disseminated TB (miliary TB)
  • True, active TB
1336
Q

What are the chance
active disease if you get infected with Primary TB

A

Only 5%-10% infections lead to active disease i

1337
Q

Tuberculosis
Clinical
Features

Primary TB

A

Usually asymptomatic

1338
Q

Tuberculosis
Clinical
Features

SecondaryTB

A

o Typically see lung lesions (productive cough)
o Fever, malaise, anorexia, night sweats

1339
Q

Tuberculosis

CLINICAL FEATURES OF ORAL LESIONS

A

§Ulceration (tongue ulceration most common)
§Mucosal granularity
§Diffuse inflammation
§Non-healing extraction socket

1340
Q

Tuberculosis
Clinical
Features

Extrapulmonary TB

A
  • Lymphatics
  • Skin
  • Skeletal system
  • CNS
  • Kidney
  • GI tract
  • Oral cavity (uncommon)
1341
Q

What are the causes of secondary Tuberculosis?

A
  • Immunosuppressive medications
  • Diabetes
  • Old age
  • Crowded living conditions
  • AIDS
1342
Q

Primary TB

A

affects previously unexposed, lungs - They breathe in the organisms that someone is coughing out

1st: C_hronic inflammatory reaction_ ► Next, a fibrocalcific nodule (Ghon focus) forms at initial site of infection

1343
Q

What is Tuberculosis?

What causes it?

How does it spread?

A
  • Chronic granulomatous infectious disease
  • Caused by Mycobacterium tuberculosis

§Direct person-to-person spread through airborne droplets

1344
Q

Gonorrhea can trigger which autoimmune disease

A

Reactive arthritis (reiter)
o Can’t see, Can’t Pee, Can’t Climb a Tree

▪ Causes:
● Conjunctivitis
● Urethritis
● Arthritis

1345
Q

Gonorrhea can have coinfection

with what other infectious bacteria?

A

Chlamydia trachomatis

1346
Q

How is Gonorrhea
treated?

A

Many cases of resistance with antibiotics
§Cephalosporins

Adults with gonorrhea are treated with antibiotics. Due to emerging strains of drug-resistant Neisseria gonorrhoeae, the Centers for Disease Control and Prevention recommends that uncomplicated gonorrhea be treated with the antibiotic ceftriaxone — given as an injection — with oral azithromycin (Zithromax)

1347
Q

How is Gonorrhea
diagnosed?

A

‐ Gram stain
‐ Culture of endocervical swab
‐ Nucleic acid amplification tests (NAATs)‐detect DNA, RNA

1348
Q

How Gonorrhea affects the body?

what complications can arrise?

A

‐ Genital area usually‐purulent discharge

‐ Systemic bacteremia (myalgia, arthralgia, polyarthritis, dermatitis)
‐ Pelvic inflammatory disease in women (affects pregnancies)
‐ Gonococcal ophthalmia neonatorum (infection of infant’s eyes)

1349
Q

What is Gonorrhea?

What causes it?

A

‐ a Sexually transmitted (F>M)

caused by

‐ Neisseria gonorrhoeae

1350
Q

What is the histological features of Tuberculosis

A

Granulomas

  • o Epithelioid histiocytes
  • o Multinucleated giant cells
    • ▪ * Langhans giant cells
      • ● Nuclei along the periphery
  • o Central caseous necrosis
1352
Q

What is this infectious disease?

A

Primary Oral TB

Oral Primary TB clinical manifestation is very rare

TB is directly in the epithelial cells.

Person coughs ⇒ organism enters broken skin somewhere in the
oral mucosa ⇒directly causing TB in the mouth
-this person would NOT have any issues in their lungs
-primary TB = infection went directly into their mucosa from another person

1353
Q

What is this infectious disease?

A

Primary Oral TB

tongue ulceration

1354
Q

TB staining

A

Special stain Epithelioid

o Ziehl‐Neelson or AFB

o Consider scarcity of organisms

o MAY NOT VISUALIZE ORGANISMS WITH STAIN

▪ NEGATIVE RESULT DOES NOT RULE OUT TB INFECTION

1355
Q

What is the Differential Diagnosis of non‐healing ulcer?

A

o TB
o Deep fungal infections
o Traumatic ulcer
o SCC
o Major Aphthous ulcer

1356
Q

How is Tuberculosis
diagnosed ?

A

o TB‐Test

§Delayed type hypersensitivity (Type 4)
§Checks if developed an immune response to TB
§PPD (purified protein derivative) (what they inject under the skin)
§T cells are attracted by immune system to the skin site
§Lymphokines induce hard raised area with clear margins
§Need to check 48-72 hours later (measure area)

1360
Q

What is this infectious disease?

A

Scrofula

1361
Q

How is Tuberculosis treated?

A

§Multiagent therapy for active infection to prevent mutation and resistance
§8 week course
§Pyrazinamide
§Isoniazid
§Rifampin
§Ethambutol
§Followed by 16 week course
§Isoniazid
§Rifampin

‐ Chemoprophylaxis
‐ For positive PPD but no active infection

‐ BCG vaccine
o Not used in US due to controversy regarding effectiveness

1363
Q

What is Non‐Tuberculosis
Mycobacterial
Infection

A

Scrofula

1364
Q

What causes scrofula?

A

Mycobacterium bovis

Infected milk leads to scrofula

RARE today as milk is pasteurized

1365
Q

What are the clinical features of scrofula?

A

o Enlargement of oropharyngeal lymphoid tissues and cervical
nodes
o Significant caseous necrosis may occur and cause sinus tracts
to skin

1366
Q

What is this infectious disease?

A

Leprosy

1367
Q

What is this infectious disease?

A

LEPROSY

Clinical features

  • *§Bone destruction** ( hole in the palate)
  • *§Nodular** will become nectortic and then destruction will follow
1368
Q

LEPROSY How is it diagnosed?

A

Diagnosis:
o Clinical presentation
o Acid fast stain

Histopahology

No well‐formed granulomas
o Lepromatous leprosy

diffuse presentation

1370
Q

Leprosy is also known as ———

A

Hansen disease

1371
Q

What causes Leprosy?

A

Mycobacterium leprae

1372
Q

What are the two types of Leprosy?

A

1. Tuberculoid leprosy

▪ High immune reaction
▪ Oral manifestations are RARE

2. Lepromatous leprosy

▪ Reduced cell‐mediated response

1373
Q

Leporsy prevelance & in which regions it is usually found?

A

EXTREMELY RARE

o 80% of cases occur in:
▪ Brazil
▪ India
▪ Indonesia
▪ Madagascar
▪ Myanmar
▪ Nepal
▪ Nigeria

1374
Q

What is this infectious disease?

A

Actinomycoses

it’s an external Sinus

1375
Q

What are the clinical features of Leporsy ?

A

Clinical features:
o Leonine facies
▪ Appearance of a lion
● Loss of eyebrows
● Scarring (fibrosis) from infection prevents hair
growth
o * Oral Manifestations seen in areas of mouth with lower
temperatures:
▪ Hard/soft palate
▪ Maxillary gingiva
▪ Tongue

Oral‐enlarging papules ► ulcer ► necrosis

1379
Q

what is the histology of Actinomycoses and stain used?

A

‐ Colony of actinomycotic organisms surrounded by neutrophils
‐ Grocott‐Gomori methenamine silver stain (GMS)

In this histo slide, we see:

* Sulfur Granule
o 1. Collection of actinomycoses israelii organisms
o 2. MANY neutrophils surround the periphery
o BOTH are requirements for a TRUE diagnosis of actinomycoses

1380
Q

‐ Actinomycoses
o Diagnosis

A
  • Culture
    • o < 50% of cases are positive
      • ▪ Due to various types of bacteria in the culture
  • Presumptive diagnosis from biopsy

in this histology: GMS stain was used
o Correlates with top H&E histopathology
o Filamentous branches are the actinomycotic organisms

1381
Q

How is Leprosy treated?

A

§Rifampicin, clofazimine, dapsone

1382
Q

What is Actinomycoses?

A

‐ Infection caused by filamentous branching gram positive anaerobic
bacteria
‐ Normal component of oral flora

1383
Q

What causes Actinomycoses?

A

‐ Associated Bacteria:

o Actinomyces israelii
o Actinomyces viscosus

‐ Normal component of oral flora -gram positive anaerobic
bacteria

1384
Q

What are the clinical features of Actinomycoses?

A

can be Acute or chronic

‐ Hard indurated swelling
o Result of injury / trauma
▪ Tooth extraction
o Erythematous

o Formation of external sinus
▪ Drains into the skin

‐ “Sulfur granules”
o May be present in suppuration

o Indurated area of fibrosis

1385
Q

Which locations Actinomycoses affect?

A

‐ 55% in cervicofacial area
‐ Hard indurated swelling
o Result of injury / trauma/tooth extraction
o Erythematous
‐ Area overlying angle of mandible
o Formation of external sinus
▪ Drains into the skin
‐ Other locations include:
o Abdomen
o Pelvis
o Lungs

1387
Q

How does Actinomycoses infection spread?

A

‐ Enters tissue through an area of prior trauma
o Soft tissue injury
o Periodontal pocket
o Non‐vital tooth
o Extraction socket
o Infected tonsil
‐ Direct extension through soft tissue to the surface

1388
Q

How is Cat‐Scratch Disease
diagnosed ?

A

‐ Clinical features:
o Presence of a cat
▪ Presumptive diagnosis can be made

‐ Serology (antibody detection)

‐ Histopathology (biopsy) (Stellate suppurative necrosis surrounded by a band of histiocytes and neutrophils) and the use of Immunohistochemistry and Warthin‐Starry silver stain to identify the organism

Left
o Histiocytes on the periphery
o Stellate necrosis in the center
‐ Middle Immunohistochemistry

o Antibodies allow for visualization of Bartonella henselae (red
little dots)
‐ Right : Warthin‐Starry silver stain
o Silver stain allows for visualization of Bartonella henselae
(black areas)

1389
Q

What is “Sulfur granules”

Where it is found?

In which infection?

color?

A

colonies of bacteria (o Actinomyces israelii
o Actinomyces viscosus)

found in suppuration (pus) which means Suppuration (pus) is dead tissue, bacteria, dead white blood cells, and other products of tissue breakdown..

Sulfur granules found in Actinomycoses

yellow in color

1390
Q

What is this infectious disease?

A

Cat‐Scratch
Disease

1391
Q

Differential Diagnosis to Actinomycoses

A

o Erysipelas

1392
Q

What are other presentations of Actinomycoses?

A

‐ Tongue
‐ Tonsillar crypts
‐ Salivary gland involvement
‐ Osteomyelitis
‐ Periapical inflammatory lesions

1395
Q

How is Actinomycoses treated?

A
  • * Prolonged high dose antibiotics for cervicofacial actinomycosis
    • Due to the fibrosis that occurs
    • Early cases 5‐6 weeks
    • Deep‐seated infections up to 12 months
  • Abscess drainage
  • Sinus tract excision
  • Penicillin
1396
Q

What is Cat‐Scratch
Disease?

A

‐ Infectious disease which is seen in lymph nodes

1397
Q

What causes Cat‐Scratch
Disease ?

A

‐ Causative organism:
o Bartonella henselae
‐ Previous contact with a cat (scratch or saliva)

1398
Q

What are the age of the patients that usually get Cat‐Scratch
Disease ?

A

‐ 80% in patients younger than 21

1399
Q

—– is the most COMMON cause of regional lymphadenopathy in children

(22,000 cases annually)

A

Cat Scratch Disease

1400
Q

What are the Differential Diagnoses: of Cat Scratch Disease ?

A

‐
o Swellings in the lymph node

o Unilateral swellings of the neck

1401
Q

What are the clinical features of Cat Scratch Disease ?

A

‐ Initial scratch
‐ Papule at inoculation site (3‐14 days later)
‐ Papule ► erythematous ► vesicular ►crusted
‐ Healing (1‐3 weeks)
‐ Lymph node enlargement with fever and malaise

1403
Q

How is Cat‐Scratch Disease
treated?

A

o Self‐limiting (resolves within 4 months)
o Local heat
o Analgesics
o Mechanical removal of suppuration (aspiration)
o May use antibiotics for severe cases
▪ Azithromycin

1404
Q

What are the 3 types of Benign Fibro‐Osseous
Lesions?

A
  1. Fibrous Dysplasia
  2. Cemento-osseous Oysplasia
  3. Ossifying Fibroma
1405
Q

Fibrous Dysplasia
Cemento‐osseous Dysplasia

are both type of

A

Type of Bone Dysplasia

1406
Q

Ossifying Fibroma is a ———

A

Benign neoplasm

1407
Q

What are the types of Fibrous Dysplasia?

A

 Monostotic
 Polystotic
 McCune‐Albright Syndrome
 Craniofacial
 Mazabraud Syndrome

1408
Q

What is the most common type of Fibrous dysplasia?

A

Monostotic

1409
Q

What is Monostotic Fibrous dysplasia?

A

a Fibrous dysplasia involving one bone

o Ex: when only the mandible involved or only the maxillae

(Most common type (70%)

1410
Q

What is Polystotic Fibrous dysplasia?

A

a Fibrous dysplasia involving more than one bone

1411
Q

What is the Second most common type of Fibrous dysplasia?

A

Polystotic Fibrous dysplasia

1412
Q

What are the two types of Polystotic Fibrous dysplasia?

A

 Jaffe Type
 McCune‐Albright Syndrome (involving multiple bones with
endocrine abnormalities)

1413
Q

What is Craniofacial Fibrous dysplasia?

A

-a Fibrous dysplasia limited to Skull and Facial Bones...

1414
Q

What is Mazabraud Syndrome

A

-Fibrous dysplasia with intramuscular myxomas

1415
Q

What happens in Fibrous Dysplasia?

A

an aberrations in osteoblastic/osteoclastic function ► normal bone turn over affected ► normal bone structure will be affected!

1416
Q

What is
fibrous dysplasia ?

A

Developmental lesion characterized by substitution of normal bone by poorly organized woven bone and fibrous tissue.

1417
Q

What is the etiology of fibrous dysplasia?

A

GNAS1 gene mutation in fibrous dysplasia is a potential diagnostic adjuvant, as it is not
found in normal bone tissue (etiolog

1418
Q

What gender and age affected by Fibrous Dysplasia?

A
  • No gender predilection
  • commonly seen in pediatric patients and young adults
1419
Q

What are the clinical charcterstics of fibrous dysplasia?

A
  • Clinically, it causes bone expansion and asymmetry
  • most typical presentation of monostotic fibrous dysplasia is a slow growing painless enlargement in the affected area.
    • so the patient may notice a slight asymmetry that won’t bother them intially, but over time~months to years ►they’ll notice that this area is slowly and steadily growing more and more ( slow and painless)
1420
Q

What are the most common sites of Fibrous Dysplasia?

A

• Most common sites of FD include the ribs, femur, tibia, maxillae and mandible

 the Maxillae is affected more than the mandible

1421
Q

What is this disease?

Patient CC: painless mass that is growing on one side

A

FD

Radiographically: you have altered trabecular pattern
Clinically: Painless mass slowly growing over time

is is typical
presntation of Fibrous Dysplasia

1422
Q

What is this disease?

A

Fibrous Dysplasia

  • ill‐defined radiolucent/radiopaque/mixed radiolucent‐radiopaque entities that blend with normal bone.
  • The left side is affected. Left body of the mandible and the ramus.
  • The cortical outlines have been expanded near the inferior border of the mandible.
1423
Q

What is the radiographic features of Fibrous dysplasia (FD)

A

• Maxillae affected more than mandible
• Ill‐defined borders, blends in with the surrounding bone (not necessary to be corticated)
• Variable density and orientation of the trabecular pattern (radiolucent, radiopaque or a combination)

  • *• Ground‐glass appearance** (common)
  • *• Peau d’orange (surface of an orange)** (common)
  • *• Cotton wool appearance** (common)
  • *• Fingerprint pattern** ( uncommon pattern)

• Typically the lesionss in the maxillae are more homogenous and radiopaque, whereas they may appear more heterogenous and mixed in the mandible.

*typically you’ll see the ground glass appearnce and Peau d’orange on the maxilla as they are homogenous the cotton wool appearance more commonly found in the mandible since it is heterogenous.

1425
Q

What is this trabecular pattern of the FD?

A

Fingerprint pattern

The arrow indicating the inter‐radicular area of this molar. You can see the trabecular
bone has been altered into a fingerprint pattern.
This is a case of localized fibrous dysplasia.

Very uncommon.

1426
Q

What is this trabecular pattern of the FD?

A

Cotton wool
appearance

Irregullary shaped and outlined radiopacities blending in with adjacent bone

1427
Q

What is this trabecular pattern of the FD?

A

Peau d’orange

surface of an orange – the bone shows a “pitting” appearance.

1428
Q

What is this trabecular pattern of the FD?

A

Ground Glass Pattern

it appears granular in nature. (Grainy)

1429
Q

What is this Radigraphical finding?

A

Fibrous dysplasia on
the right mandible.

Note the superior displacement of the IAN Canal
This is not odontogenic ( as they are usually above the canal)
Anything below th canal ►think of it as originiating from the bone itself

1430
Q

What is this Radigraphical finding?

A

Fibrous Dysplasia in
the left of the
maxillae.

Always compare both side left and right

  • We see granular/glass appearance of the bone ( blue arrow) and compare it to the contralateral maxillae. The trabucular pattern has changed signficantly.
  • Also compare the maxillary sinus space. The left maxillary sinus appears radiopaque.
  • That is because the maxillae has been enlarged to the point where it is pushing the floor of the maxillary sinus superiorly and reducing the total volume of the sinus.
  • The purple arrows indcate the displaced floor of the maxillary sinus.
1431
Q

what is this radiographic finding?

A

FD

Note the normal left maxillary sinus and the obliterated space of the right maxillary sinus ( blue arrows).
A ground glass appearing entity (humogenous radiopaque lesion) has obliterated the space secondary to expansion of the right maxilla.
These findings are consistent and quiet common in advanced cases Firbous dysplasia

1434
Q

How does Fibrous dysplasia affects the
Surrounding structures?

A
  • May have no effect ( especially if it hasn’t reached the cortical outlines)
  • Expansion and thinning of cortical walls
  • Displacement of teeth ( espically in advanced cases)
  • One of the few entities that cause SUPERIOR displacement of the mandibular canal
1440
Q

What is this radiologic finding

A

Periapical COD

green arrow

Simple bone cysts may develop in regions of COD ( periapical or florid type)
So look for areas void of trabucular bone and has scalopping of the lesion.

Red arrow

1441
Q

What is this radiologic finding

A

mature Periapical COD

Coronal cross section of the posterior mandible in the region of the premolar

~ mixed radiolucent/radiopaque entity, the center is radiopaque and the periphery is
radiolucent.

1442
Q

What is this radiologic finding

A

mature Periapical COD

You can have these lesions in endentulous areas as well.

So this is is an endeulous area, but if there was a tooth here, this would be in the
periapicel region or near it with mixed radiolucent/radiopaque entity  the differential
diagonsis of this area could include Periapical COD.

1443
Q

What is this radiologic finding?

A

mature Periapical COD

You see a nice radiolucent rim and radiopaque center

 so mixed radiolucent/radiopaque
entity in the periapical region of tooth #31

 most likely diagonsis would be Periapical
COD.

1444
Q

What is this radiologic finding

A

A very mature Periapical COD

( purple arrow)
Well‐defined radiopacity in the periapical region.
Sometimes you may or may not be able to differentiate a very thin radiolucent line as in
this case.

you might include ddx of other lesions which might present with
radiopacity in the preapical region
There are certain tests you can do clinically to differentiate too.

or do clinical tests

1445
Q

What is this radiologic finding

A

Periapical COD

Sagital cross section of the anterior Mandible.
Mixed radiolucent/radiopaque area (green circle)

1446
Q

What is this radiologic finding

A

Early & mature Periapical COD

Preapical radiographs of the anterior mandible of the same patient at different times.

Note the differnece in density between the two radiolecency:
Note the internal structure of the radiopacity is quite radiolucent ( purple arrow)
The Preapical radiographs of the same region taken at a later time shows a more
radiopaque internal structure (pink arrow). This reflect the maturing of the COD lesion.
The lesion with Pink arrow can be described as well‐defined mixed
radiolucent/radiopaque entity. ( because you have radioleucent part and radipaque part)

1447
Q

What is this radiologic finding

A

Early Periapical COD

well defined radiolucency surrounding the apeces of these two central

When looking at such cases, it is also imporant to:
1. look at the crowns to look for carious lesions. If there is no restorations or no
evidence of caries, it is likely that these lesions are arising from the bone and not
secondary to pulpal involvement.
2. It also important to look at the PDL and Lamina dura, typically in COD lesions they
should be visisulized and intact ( but because this is a 2D image and this area may
superimpose on this region and obsecure the visulizing of the lamina dura and the
PDL)

what’s the difference between COD and Inflammatory lesion?
COD won’t have effect on the PDL space itself, because it orginates from the bone!
Vitality testing can help us differntiate between inflmmatory lesion and something that happeing inside of the bone.

1450
Q

What is this radiologic finding

A

Florid COD

Axial section of the mandible.

  • Notice mixed radiolucent/radiopaque entity on the patient right side. And on the left the area is more radiopaque centrally and has a thin radioluceny around it.
  • The arrows indicate well‐defined radiopacities immedietly surrounded by radiolucent rims.
  • Note that the radiolucent rim on the left side is thin when compared to the lesion on the right. This likely means that the lesion on the left is more mature ( more time has passed for the entity to produce more woven bone).
1451
Q

What is this radiologic finding

A

Florid COD

Two periapical radiographs of the left and right posterior mandible of the same patient.

 In this case, note the areas of radiolucency and radiopacity are rather ill defined but widepsread to affect most of the teeth.

Most of the teeth noted here are restored.

 So even if the radiographs suggest a cemento‐osseous process, it is important to keep an eye for these teeth in term of vitality and prevent a periapical infections which would otherwise secondarily infect the altered bone of COD.

1452
Q

What is this radiologic finding

A

Florid COD

Multiple regions of COD.
Notice the wide areas of scelortic/radiopaque areas on mandible and also on maxillae

1453
Q

What is Differential Diagonsis
for Firbous Dysplasia
(FB)

?

A

Generalized FD

  • Metabolic bone diseases (hyperparathyroidism) (any disease that incrase trabacular bone density)
  • Paget’s disease

Localized FD

  • Osteomyelitis
  • Osteosarcoma
1454
Q

What is the management of Fibrous Displysia?

A
  • Consultation with an OMFR is advisable. Monitoring of the area is also advised.
  • Typically treatment is not needed unless there are clinical symptoms or patients present with cosmetic concerns if clinical symptoms are severe
  • Implants and surgical intervention should be avoided when possible as these areas are void of blood supply
1455
Q

Cemento‐ossifying
Fibroma

Types

and

Location

A

There are two types: classic and juvenile form

-juvenile seen in younger patients and
tend to be more aggressive in nature ( both radiographically and clinically aggressive features)
• Young adults and females affected mostly
• Bony expansion and displacement of teeth can be seen in many cases ( not suprising
since it acts like a neoplasm)

• More commonly seen in the mandible and in posterior regions

1456
Q

what is this radiographic finding?

A

Cemento‐ossifying
Fibroma

Note the internal granular appearance of the trabucular bone ( black arrows)
The purple arrows shows the wall of the expanded buccal/facial and lingual cortical plates caused by the neoplastic entity.
This was a confirmed cased of ossifying fibroma* mainly because of two things:
1. siginficant cortical expansion on buccal and lignual side
2. altered trabacular pattern.

ddx of fibrous dysplasia but you should look for a radiolucent rim
if you can and if not, they maybe considered under the same differential diagosnsis.
Note that may help you in differentiating :
The maxilla is affected more in Fibrous dysplasia
The mandible is affected more in Ossifying fibroma

1457
Q

What is this radiographic finding?

A

Cemento‐ossifying
Fibroma

Axial section of the
mandible

  • The granular radiopacity immediately surrounded by a radiolucent rim ( purple arrow)
  • Also note the extent of the expansion of the buccal and lingual cortical plates, a feature which is common of ossifying fibroma.
  • This is more clear radiographically where we see a radiolucent rim surrouding a mixed radiolucent/radiopaque center and there is a siginficant expansion of the buccal and lingual plates. ► very common in ossifying fibroma
1458
Q

Cemento‐ossifying
Fibroma

is classifed as ———–

and why?

A

Classified as a benign neoplasm

Because it acts like a benign neoplasm.

Once you examine it under microscope, you’ll see features resmeble benign fibrous osseous lesions. You’ll see:

 Fibrous connective tissues
 cementum like material
 even altered bone material (woven bone)

1459
Q

Cemento‐ossifying
Fibroma

Radiographic features

A
  • Well‐defined, round or oval lesion
  • Periphery of the lesion is corticated and may exhibit a radiolucent periphery (sometimes referred to as a soft tissue capsule)
  • Internally, the lesion is typically granular or radiopaque but may show variations (mixed radiolucent/radiopaque)
  • Strong tendency to displace teeth and cortical outlines
1460
Q

what is this radiographic finding?

A

Cropped Panaromic showing

a case of

Cemento‐ossifying
Fibroma

  • Appreciate the radiolucent rim indicated by the black arrows.
  • Also note the internal structure of the trabucular bone and compare it to adjacent unaffected areas. It is more granular and radopaque compared to adjacent areas.
  • Another important feature to appreciate is the displacement of the anterior teeth (diverging roots)
  • These features are usually seen in lesions with benign neoplastic characterstics.
1461
Q

What is CEMENTO‐OSSEOUS
DYSPLASlA (COD)?

A

Dysplastic lesions that are confined to the jaws.

1462
Q

What is this disease?

A

Cleido-Cranial
Dysplasia

Treatment: For children, facial reconstructive surgery on the bones of the face to reshape the forehead or cheekbones. Spinal fusion procedures to support the spinal column. Lower leg surgery to correct knock knees (knees that bend inward toward the center of the body)

1463
Q

What is this disease?

A

Gardner’s Syndrome

Synonym: Familial Multiple Polyposis.

Remember this:

 GarDENse Bone Island.
 GARDEN-FOREST:
 F- Familial adenomatous polyposis.
 O- Osteomas.
 RE- Retinal epithelial hypertropy.
 ST- Supernumerary teeth.

Treatment:

Because people with Gardner’s syndrome have a higher risk of developing colon cancer, treatment is usually aimed at preventing this.

Medications such as an NSAID (sulindac) or a COX2 inhibitor (celecoxib) may be used to help limit the growth of colon polyps.

Treatment also involves close monitoring of the polyps with lower GI tract endoscopy to make sure they do not become malignant (cancerous). Once 20 or more polyps and/or multiple higher risk polyps are found, removal of the colon is recommended in order to prevent colon cancer.

If dental abnormalities are present, treatment may be recommended to correct problems.

1464
Q

What is this disease?

A

Osteopetrosis

Osteomyelitis is a complication in patients with osteopetrosis as can be seen in pan image!

Treatment: Bone marrow transplant (to stimulate osteoclast formation).

1465
Q

What is this disease?

A

Paget’s disease stages

Early Linear lines: The bone is being resorbed in a very distinct
pattern > linear patterns of trabeculation

Middle -MAY see the “cotton wool” appearance (but this is more
pronounced in the third stage)
-the trabecular pattern may or may not be slightly affected

Late - There is MORE bone deposition -the “cotton wool” appearance
is very very clear in this stage! Also-hypercementosis and spacing of teeth.

1466
Q

What is this disease?

A

Paget’s Disease

Also Known As: Osteitis Deformans.

Skeletal disorder involving osteoclasts

Treatment: Osteoporosis drugs (bisphosphonates) are the most common treatment for Paget’s disease of bone

1467
Q

What is this disease?

A

Cherubism

Treatment: Usually not needed as the cyst-like lesions fill in with granular bone during adolescence- conservative surgical procedures may follow for cosmetic reasons.

1468
Q

What is this radiographic finding??

A

Idiopathic
Osteosclerosis

AKA: Dense Bone Island

 Not associated with any dysplastic, neoplastic, inflammatory or systemic disorder.
Common incidental finding.
 Slow growing, typically stops growing by the time of skeletal maturity.
 Peak prevalence in the third decade of life.
 No treatment required; monitoring is suggested.

1469
Q

Idiopathic
Osteosclerosis

vs

A

PCOD

Differentiating factor: Radiolucent zone surrounding the radiopacities of COD lesions. No such radiolucent areas for idiopathic osteosclerosis.
 Important: The root of the tooth #28 appears to be resorbed but is likely not.
Look at the root of #29. These teeth are still undergoing development in a young patient.
 Left is showing dense bone island.
 Right is showing Periapical COD- this is intermediate stage, not fully mature. You should see a radiolucent rim.
 Another more obvious radiographic feature: you see radiolucent areas surrounding in both images, the common feature is: because PCOD and dense bone island do not affect the PDL spaces – you should be able to see the PDL spaces.
 Sometimes it’s not the case. Look for the PDL, look for radiolucent area surrounding possible central radiopacity, idiopathic osteosclerosis can cause resorption; PCOD hasn’t been associated with root resorption.

1470
Q

Idiopathic
Osteosclerosis

vs

A

Hypercementosis

Differentiating Factor: A well-defined radiolucent border that is continuous with the PDL of the tooth, in the case of hypercementosis. This means that whatever is happening is within the confines of the tooth-bearing region. In this case, the
cementum.
 Hypercementosis- Cementum is overraeacting, so there’s enlargement of cementum.
 If cementum is larger, it should be pushing the PDL out (black arrow). So the PDL is enlarged meaning you should be able to see a radiolucent rim around the area. And the radiolucent rim should be continuous with the PDL of the
remaining root structure.

1471
Q

Idiopathic
Osteosclerosis

vs

A

Cementoblastoma

 Differentiating Factor: A well-defined radiolucent border that is continuous with the PDL of the tooth, similarly seen in the previous case of hypercementosis.
(sometimes it is difficult to differentiate hypercementosis and cementoblastoma, in this case, the beige arrow indicates the resorbed root surface, which normally occurs in benign neoplastic cases, such as cementoblastoma.
 Cementoblastoma is more of a heterogenous radiopacity- meaning you may see
gaps, like radiolucent voids, in between the areas.
 See radiolucent rim.
 But more common feature include root resorption because it’s a neoplastic condition. It should act like a neoplasms in which it’s destroying some of the root structure.

1472
Q

Idiopathic
Osteosclerosis

vs

A

 For condensing osteitis, look for heavily restored or carious teeth. Condensing osteitis typically surrounds the initial rarefying osteitis lesion. The teeth in these cases are non-vital as they represent a condition that is secondary to pulpal necrosis.
 Open necrosis, eventual PDL space widening and then once the infection reaches the bone, you have bone loss.
 Now you have an overreaction or inflammatory reaction surrounding the initial inflammation.

1473
Q

What is this disease?

A

Focal Osteoporotic
Marrow Defect

A large marrow defect that may mimic a
cystic/neoplastic radiolucency in the jaw.

common incidental finding

a variation of normal anatomy within trabecular bone.

1474
Q

What is this disease?

A

Simple Bone Cyst

Also known as

 1.) Solitary Bone Cyst.
 2.) Traumatic Bone Cyst.
 3.) Idiopathic Bone Cyst.
 4.) Hemorhhagic Bone Cyst.

Remember radiographic feature

tend to Scalop between teeth

 Treatment includes surgical curettage- spontaneous healing has been reported.

1475
Q

What are these two disease?

A

Sometimes, simple bone cysts should be differentiated from odontogenic keratocysts (OKCs)

1476
Q

 CGCG should be differentiated from ————-

A

brown tumor.

1477
Q

What is this disease?

A

central giant cell granuloma

CGCG

1478
Q

What is this disease?

A

Aneurysmal Bone Cyst

1479
Q

COD can be divided in to:

A

1) Periapical COD
2) Focal COD ( not covered)
3) Florid COD

Two types of COD
instead of three
Perapical COD
&
Florid COD

1480
Q

Cemento‐Osseous Dysplasia is Similar to Fibrous dysplasia where

A

cancellous bone is
replaced with fibrous tissues & cementum‐like material.

1481
Q

CEMENTO‐OSSEOUS
DYSPLASlA

COD

is it symptomatic?

is there bony expansion?

A
  • Typically asymptomatic, almost always captured as incidental finding
  • Generally, no bony expansion but is not uncommon in the florid type
1482
Q

Cemento‐osseous dysplasia COD

Gender?

Age?

Ethincity?

A

• Commonly seen in middle‐aged patients

female predilection

  • more commonly seen in the Black population
  • also frequently seen in Asian population
1483
Q

What are the Radiographic
features of Cemento‐osseous dysplasia COD?

A
  • Usually well‐defined borders in perapical type (may be ill‐defined in florid type).
  • Early lesions show radiolucent features in the periapical area of the teeth

_As times progresses, the lesion matures =_the entity may become radiopaque.
‐ as a result there is also an intermideate mixed phase

• The lesions mature from the center outwards
‐ as a result, a radiolucent rim surrounding the lesion is commonly noted.

• Typically the periodontal ligament space of affected areas are intact but my not be visualized because they are superimposed over the region.

1492
Q

What is Florid COD?

A

Widespread form of periapical COD

There is some discreppency on how to consider a lesion a florid COD
Some people say the radiopacity entities have to be on at least 2 qudarants And other says if you have the radiopacity entities crossing the midline of the bone.
If it is in 3 quadrant ► then you can defentitly say it’s the Florid type, but even if you see itone bone and it has crossed the midline ► you may consider it Florid COD

1493
Q

What is differential diagnosis for Periapical COD?

PCOD

A

Florid COD

Rarefying osteitis (radiolucent lesions) ( it would differentiate in the more early stages of the COD ( the radiolucent stage)
Condensing osteitis (considered in the differential when the lesion is more mature and more radiopaque lesions)
Cementoblastoma ( benign neoplasm of the cementum so we
should be able to see certain features that reflect benign neoplastic lesions )
Dense bone islands ( a common differential when considering COD)

1497
Q

What is differential diagnosis for florid COD?

FCOD

A
  • Paget’s disease ( t generalized areas)
  • Osteomyelitis ( localized area because we have mixed radioluecent/radiopaque areas)
1498
Q

What is the Management of COD?

A
  • Typically, no treatment is required unless these regions show clinical/radiographic
  • Ex if patient complain of some pain of that area –> we
    want to follow up that region
1505
Q

Treatment of
Cemento‐ossifying
Fibroma

A
  • Surgical excision ( need to send to biopsy in order to confirm the diagosnsis of that)
  • Wider resection with bone maybe necessary in soma larger or more clincally aggressive cases.
1506
Q

What is this clinical presentation?

A

Leukemia

o Dilantin hyperplasia (drug induced gingival hyperplasia) –
fibrotic looking

o Has to an addition of thromocytopenia

1507
Q

What is this clinical presentation?

A

Leukomia

o Leukemic infiltrate – have areas of erthema
o Looks like gingival hyperplasia, but in gingivail hyperplasia
you don’t have the same amount of redness. Leukemia has significant hyprotophy of gingivial papilla and areas that look like they have ptechia in them. With gingival
hyperplasia drug induced they are very fibrotic

1508
Q

What is this clinical presentation?

A

Leukemia

▪ Oral findings include gingival hyperplasia, spontaneous bleeding of gingiva, mucosal ulcerations, candidiasis, recurrent herpetic lesions, etc.
▪ Leukemic infiltrate in soft tissues (ex. gingiva) produces a diffuse,
boggy, nontender swelling that may or may not ulcerate
o most common with myelo‐monocytic types
▪ May create a tumor‐like mass in soft tissue
o granulocytic sarcoma/chloroma (clinically looks green)
▪ mass infiltrate into soft tissue

If you see children and notice they have prominent areas
of redness or red/purple and know the child has decent
oral hygiene, leukemia should be in your differential. Need
to be aware of that cause patients need to be treated in a
fairly quick fashion.

1509
Q

What is this clinical presentation?

A
1510
Q

What is this clinical presentation?

A

Leukemia

Acute and chronic myelo‐monocytic leukemia are the most likely
types of leukemia to exhibit oral manifestations
o Generalized gingival hypertrophy

May create a tumor‐like mass in soft tissue
o granulocytic sarcoma/chloroma (clinically looks green)
▪ mass infiltrate into soft tissue

1512
Q

What is this clinical presentation?

A

Agranulocytosis

Oral findings:

  • include multiple ragged ulcerations of the oral mucosa
  • can mimic recurrent aphthous (but often no erythematous halo)
  • Gingiva is a common site due -can resemble NUG)
1513
Q

What is this clinical presentation?

A

Agranulocytosis

Oral findings:

  • include multiple ragged ulcerations of the oral mucosa
  • o can mimic recurrent aphthous depending on sites involved
  • (but often no erythematous halo) – more like neutropenic ulcer
  • Gingiva is a common site due to the minor trauma caused bymastication (can resemble NUG)
1515
Q

What is this clinical presentation?

A

Cyclic Neutropenia

o Teeth floating in air

1516
Q

What is this clinical presentation?

A

Cyclic Neutropenia
▪ Gingiva is most severely affected with periodontal bone loss and
tooth mobility

1517
Q

What is this clinical presentation?

A

Cyclic Neutropenia

▪ Depending on surface involved, can mimic recurrent aphthous
ulcerations
o Usually do not see erythematous halo that is so typical of
aphthous

1518
Q

What is this clinical presentation?

A

Cyclic Neutropenia

▪ Oral ulcerations on any mucosal surface exposed to minor trauma (L,T, BM and oropharynx) last 5‐7 days
▪ Depending on surface involved, can mimic recurrent aphthous
ulcerations
o Usually do not see erythematous halo that is so typical of
aphthous
▪ Gingiva is most severely affected with periodontal bone loss and tooth mobility

1519
Q

What is this clinical presentation?

A

Cyclic Neutropenia

Oral ulcerations on any mucosal surface exposed to minor trauma & can mimic recurrent aphthous ulcerations without the
erythematous halo that is so typical of aphthous
▪ Gingiva is most severely affected with periodontal bone loss and tooth mobility

1520
Q

What is this clinical presentation?

A

Hematoma

because of THROMBOCYTOPENIA or Trauma

1521
Q

What is this clinical presentation?

A

Hematoma

because of THROMBOCYTOPENIA orTrauma

1522
Q

What is this clinical presentation?

A

o hematoma

because of THROMBOCYTOPENIA orTrauma

THROMBOCYTOPENIA:▪ Markedly decreased numbers of circulating blood platelets (severe
cases < 10,000/mm³)

Etiology: Can be from:
o Decreased production (malignancy, drugs)
o Increased destruction (immunologic, drugs)
o Sequestration in the spleen (splenomegaly)

▪ Clinically see spontaneous gingival bleeding, petechiae,
ecchymosis and hematomas
o Clinically see some type of bleeding
▪ Treatment is usually platelet transfusion

1523
Q

What is this clinical presentation?

A

o hematoma

because of THROMBOCYTOPENIA or Trauma

1525
Q

What is this clinical presentation?

A

Aplastic Anemia

▪ Failure of the hematopoietic precursor cells to produce adequate
numbers of all types of blood components
▪ Rare, but life threatening
▪ Associated with environmental toxins (benzene), certain drugs
(antibiotic chloramphenicol), or infection with certain viruses
(non‐A, non‐B, non‐C, non‐G hepatitis)
▪ Fanconi’s anemia and dyskeratosis congenita patients have an
increased risk of developing this

Oral signs: are associated with the thrombocytopenia and include
spontaneous gingival hemorrhage, mucosal petechiae, purpura,
and ecchymoses
▪ Nonspecific oral ulcerations (neutropenic ulceration) may also be seen on any mucosal surface, but especially in areas of trauma
(even minor trauma, ex. gingiva)
o Neutropenic = low neutrophils

1526
Q

What is this clinical presentation?

A

Sickle Cell Anemia

Can see prominent trabeculae left, looks like steps on a ladder

1527
Q

What is this radiographic presentation?

A

Sickle Cell Anemia

Radiographic findings include:

o decreased trabecular pattern in the mandible (due to
increased extramedullary hematopoiesis)

o laddering of inter‐radicular trabeculae
o “hair‐on‐end” appearance of skull films (less prominent
than with thalassemia)

Can see spontaneous pulpal necrosis in the absence of trauma or
caries

1529
Q

What is this clinical presentation?

A

Beta‐thalassemia

▪ Two defective genes – thalassemia major (Cooley’s anemia,
Mediterranean fever)
o Disease detected when fetal hemoglobin ceases to be
made (~3‐4 months old)
o Extramedullary hematopoiesis cause hepatosplenomegaly,
bone marrow hyperplasia, and lymphadenopathy
o In jaws, painless enlargement of maxilla and mandible
(“chipmunk” facies)
o Skull films show “hair‐on‐end” appearance
o Untreated, patient dies by about one year of age
o Treatment is repeated blood transfusions or bone marrow
transplant

this pt was treated with

1530
Q

What is this clinical presentation?

A

Macrocytic
(megaloblastic)
Anemias:

▪ Folic acid and B12 deficiencies

  • Glossitis
  • Denuded dorsal surface
  • Burning, stinging pain

Seen in older patients and seen in patients with poor nutrition

Etiology: alcoholism, malabsorption, medications
(trimethoprim, oral contraceptives, anticonvulsants

1531
Q

What is this clinical presentation?

A

Iron deficiency anemias
Microcytic hypochromic

▪ Atrophic glossitis – tongue has been a little denuded of papilla
▪ Angular cheilitis – white and redness at angle of mouth/
commissure
▪ Plummer‐Vinson Syndrome: type of iron deficiency anemia
o Chronic iron def, dysphagia (esophageal webs), atrophic glossitis.

  • Significantly increased risk of esophageal cancer (SCC)
  • More commonly seen in European women
  • Have difficulty swallowing
1532
Q

What is this clinical presentation?

A

microcytic,
hypochromic anemias
(iron deficiency):

Pallor

▪ Anemia: reduction in O2 carrying capacity
▪ Diagnosis: RBC counts, Hg, HCT, red cell indices for dx of type of
anemia
▪ Normal upper labial mucosa

▪ Pale lower labial mucosa

1533
Q

What is this clinical presentation?

A

Aplastic Anemia

  • One of the main differences between and neutropenic ulcer and an empthis ulcer? Is the red halo, the mucosa surroundingneutropenic ulcer Is pale and not red.
  • The center of a neutropenic ulcer has granulation tissue with a little bit of white
1534
Q

Aplastic Anemia

treatment

A 
supportive care initially, attempts to stimulate
bone marrow (androgenic steroids), and bone marrow transplants
for severe cases (prognosis is guarded at best)
1536
Q

What is this clinical presentation?

A

Multiple Myeloma

Elevated M spike in serum ‐ abnormal increase in
immunoglobulin (hyperglobulinemia), most commonly IgG
▪ Reversal of normal albumin/globulin ratio

1537
Q

Agranulocytosis

Symptoms

Treatment

A

Symptoms

  • ▪ Initial symptoms include non‐specific symptoms of infection malaise, sore throat, swelling, fever, chills, etc.
  • Oral findings include multiple ragged ulcerations of the oral mucosa, o can mimic recurrent aphthous but no erythematous halo, Gingiva is a common site & can resemble NUG

Treatment

  • Remove offending drug, numbers should replenish in 10‐14 days
  • Agranulocytosis secondary to cancer therapy ‐ meticulous oral hygiene, chlorhexidine rinse (non alcohol type) , etc.
1538
Q

What is this clinical presentation?

A

Non‐Hodgkins Lymphoma (NHL)

o Typically presents with painless lymphadenopathy
(often unilateral)
▪ up to 40% are extranodal
▪ 5‐10% arise in Waldeyer’s ring

▪ Inflamatory or reactive enlarged lymph nodes tend to be

  • *soft, tender, and movable**
  • *▪** Lymph nodes associated with malignancy tend to be
  • *hard/firm, fixed, and non‐tender**
1539
Q

What is this clinical presentation?

A

Non‐Hodgkins Lymphoma (NHL)

o The most common of the lymphoproliferative diseases
o Uncontrolled proliferation of B or T cell origin derived
from a single cell (or clone)
o Typically presents with painless lymphadenopathy
(often unilateral)
▪ up to 40% are extranodal
▪ 5‐10% arise in Waldeyer’s ring

1540
Q

What is this clinical presentation?

A

Non‐Hodgkins Lymphoma (NHL)

o The most common of the lymphoproliferative diseases
o Uncontrolled proliferation of B or T cell origin derived
from a single cell (or clone)
o Typically presents with painless lymphadenopathy
(often unilateral)
▪ up to 40% are extranodal
▪ 5‐10% arise in Waldeyer’s ring

1541
Q

What is this clinical presentation?

A

Adult acute myeloid leukemia (AML)

is a type of cancer in which the bone marrow makes a large number of abnormal blood cells.

We see in these images:
o Hemorrhagic ulcer right vestibule

o Ulcers are deep and can go down to bone

o Ulcers resolved after treatment

1542
Q

What is this clinical presentation?

A

leukomia

o Multifocal bony destruction
o Widened PDL with leukemic infiltrate

▪ Symmetric widening of PDL space in a patient that doesn’t have that normal vertical bone loss that you associate with periodontal
disease.
▪ If see symmetrical bone loss in PDL space think malignancy, neoplastic
● Lymphomas, leukemias, osteocarcoma, chondro scaroma can
do this

1543
Q

What is this clinical presentation?

A

leukomia

Cause of infiltrate they has bone loss

1544
Q

What is this clinical presentation?

A

Leukemia

This is Chloroma, inflitrate gets so dense they look green. On
buccal or lingual mucosa chloroma are more of a
solitary mass, gingival it more diffuses

1546
Q

What is this clinical presentation?

A

Hodgkins lymphoma

1547
Q

What is this clinical presentation?

A

Hodgkin Lymphoma

o Begins in lymph nodes
o 70‐75% cervical/supraclavicular
o Painless but unresolving,

o Night fevers/sweats

1548
Q

What is this clinical presentation?

A

Hodgkin Lymphoma

▪ Cell of origin is unknown
▪ Often begins as a unifocal disease above diaphragm and then
spreads to other sites
▪ Present with painless cervical lymphadenopathy in 60‐80% of
cases

▪ Bimodal ‐ late twenties and after 50 years old

▪ In North America and Europe, EBV positivity has been noted
in over 50 percent of mixed cellularity cases and 10 to 50
percent of nodular sclerosis cases

1549
Q

What is this clinical presentation?

A

T cell Lymphoma

Less common than B cell lymphomas
▪ One variant associated with palatal perforation
o Old name midline lethal granuloma

1550
Q

What is this clinical presentation?

A

Burkitt’s Lymphoma

Scattered throughout the lymphocytes are
macrophages containing nuclear debris (tingible body
macrophages)
o Creates a “starry sky” appearance

1551
Q

What is this clinical/radiographic presentation?

A

Burkitt’s Lymphoma

  • North American type (sporadic)
    • Typically older children (mean of 11 years)
    • Involves abdomen as a mass
    • uncommon in the jaws
    • No association with EBV
    • More localized disease
  • HIV type
    • Adults
    • 25% associated with EBV
    • GI, marrow and CNS

Teeth floating as shown in the image

1552
Q

What are the Lymphoma
Classifications?\

A
  • Low grade B cell (disseminated but slow growing)
    • Small lymphocytic, Mantle cell, Marginal zone
    • Follicular center (35‐40 % of all B cell lymphomas)
  • Moderate (aggressive)
    • Diffuse B‐cell, Peripheral T‐cell
  • High Grade B cell (disseminated and rapidly progressive)
    • Anaplastic large cell, lymphoblastic
    • Large cell (25‐30 % of all B cell lymphomas)
    • Burkitt’s
    • Immunoblastic (increasingly seen in AIDS)
      • As AIDS patients live longer we see this more
  • T cell lymphoma (less common than B cell, associated with palatal perforation [midline lethal granuloma]) (in differntial with deep fungal infections/candidiasis, TB, use of cocaine
    • Precursor T‐lymphoblastic, T cell chronic lymphocytic,
  • Hodgkin’s (bimodal ‐ late twenties and after 50 years old)
1553
Q

What is this clinical presentation?

A

Burkitt’s Lymphoma

African type (endemic)

  • More common
  • Peak incidence 3‐8 years of age
  • Twice as common in males
  • ~95% associated with the Epstein‐Barr virus
  • North american or non edemic type is not associated
  • with EBV
  • ~88% under 3 yrs of age have jaw lesions
    • Only 25% of those older than 15 do
  • Typically involves:
    • MD, MX, (often affects all 4 quadrants)
    • Mandible or maxilla
    • Abdomen
  • grow quickly
1555
Q

What is this clinical presentation?

A

Multiple Myeloma

Pathological fracture

1556
Q

What is this clinical presentation?

A

Multiple myeloma

1557
Q

What is this clinical presentation?

A

Multiple Myloma

Punched out translucency in crest

1558
Q

What is this clinical presentation?

A

Multiple Myeloma

Monoclonal expansion of malignant plasma cell
▪ Most common in 40‐70 year old (mean 63 yo.)
▪ Present with bone pain (> 70%) and pathologic fractures

Punched out radilucency

1559
Q

What is this histological presentation?

A

Plasma Cell Disorders

Clock face nucleaus

1560
Q

What is this clinical presentation?

A

Plasma cell gingivitis

▪ Allergen causes mass infiltrate into gingival
▪ Benign
▪ Diet log to identify allergen, allergy testing

1561
Q

Plasma cell gingivitis Treatment

A

▪ Diet log to identify allergen, allergy testing
▪ Ideally eliminate offending substance
▪ Can manage with topical steroids

1562
Q

What is this clinical presentation?

A

Plasma cell gingivitis

▪ Allergen causes mass infiltrate into gingival
▪ Benign

1563
Q

What is this clinical finding?

A

Multiple Myeloma

Deposition of amyloid in soft tissues
o Can cause macroglossia if tongue is involved

1564
Q

What is this radiographical presentation?

A

Plasmacytoma

▪ Unifocal, monoclonal neoplastic
▪ proliferation of plasma cells

▪ 30% develop into MM over 10 yrs
▪ 50% disseminate w/in 2‐3 yrs
▪ Central Bone lesion
o Unilocular radiolucency
o Swelling or bone pain
o Non‐tender soft tissue mass

▪ 90% occur in Head and neck

1565
Q

What is this clinical presentation?

A

Multiple Myeloma

1566
Q

o Differential diagnosis when you see this
“floating in air teeth” in children

A
  • Cyclic neutropenia
  • aggressive periodontitist
  • pamiona fav
  • burkitts lymphoma
  • langerhan cell histocytosis

o All these things can occur in children and lead bone
destructions and look like teeth are floating

1568
Q

How is Multiple Myeloma treated?

Prognosis?

A
  • Chemotherapy with or without RT
  • Bone marrow transplant, interferon, antibodies made
  • against tumor cells, thalidomide, bisphosphonates,
  • corticosteroids, melphalan, etc.
  • Even with treatment, most patients do not survive more than
  • 18‐24 months
    • older patients – better prognosis
    • younger patients – more aggressive and worse prognosis
  • IV bisphosphonate therapy puts patients at increase risk for MRONJ
1569
Q

What is this clinical presentation?

A

microcytic,
hypochromic anemias
(iron deficiency):

Pallor

▪ Anemia: reduction in O2 carrying capacity
▪ Diagnosis: RBC counts, Hg, HCT, red cell indices for dx of type of
anemia
▪ Normal upper labial mucosa

▪ Pale lower labial mucosa

1577
Q

If a patient has a Burning Tongue

What steps must we take

A

fungal (candidiasis) –> mucosal smear/ Empirically can give antifungals (to figure out if it is candidiasis can do a smear or give antifungal)
If not candidiasis order cbc
▪ Order CBC with diff
▪ Order blood levels on Fe, Folate, B12, zinc
▪ Rule out : diabetic neuropathy
If not candidiasis and blood work didn’t show anything abnormal patient has burning mouth syndrome
▪ TIBC tests to see if theres too much or too little FE in the blood,
measures the bloods capacity to bind fe with transferrin

▪ B12 def can be from pernicious anemia ( Schilling test for
Pernicious Anemia) lack intrinsic factor to allow proper absorption, malnutrition or malabsorption from GI conditions can lead to this as well.

1578
Q

What is Pernicious anemia?

What causes it?

Which age and race does it most affect?

A

Pernicious – “highly injurious or deadly”
▪ Lack of intrinsic factor protein in stomach decreases absorption of
vitamin B12

Etiology is usually the body making antibodies against parietal cells which make intrinsic factor
o Autoimmune disease effecting parietal cells leads to
decreased intrinsic factor

▪ More common in elderly
▪ More common in patients of Northern European and African
decent

This anemia can lead to death

1580
Q

Hemophilia A & dental treatment

A

▪ Partial thromboplastin time (PTT), prothrombin time (PT), bleeding time (BT) and platelet counts, as well as consultation with physician, should be done prior to any dental treatment
▪ (PT is like INR, Normal INR between 0.8 and 1.2)
▪ Clotting factor replacement therapy (synthetic) given as indicated
▪ Avoid aspirin

1583
Q

What is this clinical presentation?

A

Beta‐thalassemia

▪ Two defective genes – thalassemia major (Cooley’s anemia,
Mediterranean fever)

Hyperplasia of maxilla, body is trying to make more rbc so bone
marrow enlarges to support space of those red blood cells but rbc
are abnormal so spleen keeps destroying them

1585
Q

Sickle Cell Anemia Types and which is resistant to malaria?

A
  • Sickle cell trait ‐ one allele is affected, only 40‐50% of hemoglobin will be abnormal, no significant clinical manifestations
  • Sickle cell disease ‐ both alleles affected, close to 100% of hemoglobin is abnormal, significant clinical problems

▪ Abnormal gene confers resistance to malaria, therefore, sickle cell trait is seen most frequently in populations from areas endemic for malaria (Africa, the Mediterranean, and Asia)

1586
Q

What is Polycythemia

A

▪ Increase in the number of circulating red blood cells

1587
Q

People with chronic Polycythemia are at
increased risk of —— or ——-

A
  • *of MI or CVA (cerebral vascular accident or
    stroke) **
1588
Q

What are the types Polycythemia ?

A

▪ Types

  • Primary polycythemia: polycythemia vera
  • Secondary polycythemia: response to low O2 environment such as sleep apnea, living in high elevations, smoking
  • Relative polycythemia
    • Dehydration, diuretics, vomiting
1589
Q

What is this clinical presentation?

A

Secondary
Polycythemia

Oral manifestation

▪ Oral mucosa appears deep red
▪ Glossitis
▪ Gingiva appears edematous and bleeds easily
▪ Consequent “crowding out” of WBCs and platelets may result in
other manifestations

1593
Q

What is Aplastic Anemia?

What it is associated with?

Who are at increased risk of developing this anemia?

A

▪ Failure of the hematopoietic precursor cells to produce adequate numbers of all types of blood components

▪ Rare, but life threatening

▪ Associated with environmental toxins (benzene), certain drugs
(antibiotic chloramphenicol), or infection with certain viruses
(non‐A, non‐B, non‐C, non‐G hepatitis)

▪ Fanconi’s anemia and dyskeratosis congenita patients have an
increased risk of developing this

1595
Q

What is this clinical presentation?

A

o Hemophilia A

▪ A patient with only 25% of normal clotting factor VIII levels may function normally, but less than 5% will likely manifest as bruising and bleeding problems

▪ Deep hemorrhage in joints is a major complication resulting in
arthritis, ankylosis and deformity

▪ Oral findings include bleeding (often uncontrolled) upon scaling and root planing, tooth extractions and any oral lacerations
▪ Pesudotumor of hemophilia
o Tissue hemorrhage can result in a submucosal tumor‐like
mass
o Bone hemorrhage can result in intraosseous radiolucency

1596
Q

What is THROMBOCYTOPENIA?

What causes it?

A

Markedly decreased numbers of circulating blood platelets (severe
cases < 10,000/mm³)

Etiology: Can be from:
o Decreased production (malignancy, drugs)
o Increased destruction (immunologic, drugs)
o Sequestration in the spleen (splenomegaly)

1597
Q

What is the treatment of

THROMBOCYTOPENIA?

A

▪ Treatment is usually platelet transfusion

1598
Q

What is THROMBOCYTOPENIA?

How it presents clinically?

A

▪ Clinically see spontaneous gingival bleeding, petechiae,
ecchymosis and hematomas
o Clinically see some type of bleeding

1600
Q

What is Agranulocytosis?

Etiology?

pts at increase risk of what?

A

Agranulocytosis

Decrease in the number of cells from the granular cell lineage
(neutrophils, eosinophils, basophils, etc.)
o Decreased production or increased destruction

▪ Some cases are idiopathic, most are drug induced
▪ Anticancer chemotherapeutics ‐ inhibit mitotic division and
maturation of hematopoietic stem cells.
▪ In rare cases, agranulocytosis is a congenital syndrome.

▪ Increase risk of infections

1601
Q

etiology of leukemia

A
  • Probably caused by a combination of environmental and genetic factors
  • Some leukemias have specific genetic alterations (ex. CML –
  • Philadelphia chromosome)
    • t(9;22)(q34;q11) fusion gene BCR‐ABL1)
      • Translocation of 9 and 22 and fusion gene BCRABL1
  • Environmental factors include:
    • ionizing radiation
    • pesticides
    • benzene
    • viruses (ex. HTLV‐1)
1602
Q

What is Leukemia?

A

▪ Represents several types of malignancies derived from
hematopoietic stem cells

▪ ~ 2.5% of all cancers in USe

1603
Q

Types of leukemia

A

Divided into acute and chronic, myeloid and lymphoid
o Acute myeloid, chronic myeloid, acute lymphoid, and
chronic lymphoid
▪ Acute leukemia
o Typical course under 6 mos
o Untreated, runs an aggressive course often causing death
▪ Chronic leukemia
o 2‐6 or more years
o More indolent course, although, they too often result in
death
▪ Leukemia, like lymphoma, can cause bone destruction and the
radiographic appearance of “teeth floating in air” in children

1604
Q

AML in which age group is found and

which leukemia has peak in 3rd to 5th decade?

A 
**▪ Acute myeloid leukemia**
o Adult (and children)

▪ Chronic myeloid leukemia
o Peak 3rd ‐ 5th decade

1605
Q

which leukemia always in children?

A

Acute lymphoblastic leukemia (ALL)

Success in treatment of a previously fatal disease

Children age 1‐10 years have higher success with
treatments than teenager do (10‐20yrs)
o And infants (under 1yr) do the worst

Chemotherapy that are given for curing ALL actaully
causes problems when they are older.

1606
Q

What are the Clinical signs and symptoms of Leukemia

A

▪ related to crowding out of normal hematopoietic stem cells in the bone marrow
o ↓ in normal WBC, RBC, and platelets
▪ See fatigue, bleeding, bruising, fevers and infections, etc.

1607
Q

which leukemia in eldery and most common?

A

Chronic lymphocytic leukemia

o Elderly
o Most common type
o Considered incurable at this time
o unchecked proliferation of B‐cells
o no good treatment

1608
Q

What is the treatment of Leukemia?

A
  • Treatment depends on specific type of leukemia, but includes multi‐agent chemotherapy (often an initial high dose induction and then a lower maintenance dose)
    • And for lymphoma
  • Bone marrow transplant has been used with limited success
1610
Q

Cyclic Neutropenia

​length of the cycle

Symptoms

Diganosis

Treatment

A

▪ Usually a 21 day cycle

o Dx – when count falls below 500/ul for 4‐5 days every 21
days

▪ Patients experience recurrent fever, mallaise, anorexia, cervical
lymphadenopathy, oral ulcerations, etc.

▪ Treatment can be just supportive in mild cases, granulocyte
colony‐stimulating factor for more severe cases

1612
Q

What are the Clinical and radiological features

of

Multple Myeloma MM

A

▪ Bones most commonly involved include ribs, vertebrae and
skull
o 70‐90% will have jaw involvement at some point
▪ Anemia, thrombocytopenia and neutropenia due to
crowding out of normal cells within bone marrow by
proliferating malignant cells
▪ 50‐60% have Bence‐Jones proteins in urine (light chains,
usually kappa)
o Due increased plasma cells ⇒ plasma cells make
antibodies ⇒ antibodies/proteins gets excreted

Solitary plasmacytoma can be the first sign of multiple
myeloma
▪ Radiographically, see punched out radiolucencies (no
sclerotic margin) often with an irregular outline

1620
Q

What are the Stages of o Hodgkins lymphoma

A

▪ Stage I and II – localized disease curable with RT
▪ Stage III and IV – more widespread and treated with chemo
and RT, worse prognosis
▪ Stage determined by sites involved
o Above diaphragm – stage 1 and 2
o Above and Below diaphragm – stage 3 and 4

having it above diaphragm is bette than having it below so stage 1 and 2 are better than stage 3 and 4

1629
Q

o Palatal perforations differerntial diagnosis

A
  • Midline lethal granuloma (T cell Lymphoma)
  • deep fungal
  • malignancy
  • TB
  • tertiary syphilis gumma,
  • cocaine abuse (necrotizing sialometaplasia‐ soft
  • tissue)
1641
Q

What is the prognosis of Plasmacytoma

and how it is treated?

A

▪ Tx: radiation, better prognosis than MM

▪ Solitary better prognosis than disseminated MM

1642
Q

What is Neoplasias?

A
  • Immune cell tumors primarily involving bone marrow and peripheral blood are classified as leukemias
  • while those of lymph nodes are classified as lymphomas,
  • however there is often overlap of these entities
1645
Q

What causes Myelodysplastic Syndrome?

A

– environmental

1646
Q

What causes Megaloblastic Anemias
?

A

o Folic Acid def
o Vit B12 def (pernicious anemia)

1647
Q

What causes Iron Deficiency anemia?

A
  • *menstruation, pregnancy, malabsorption diseases
    (eg. Celiac)**
1648
Q

What causes Aplastic Anemia ?

A

– environmental, things like bensin

1649
Q

What causes Thalassemia & Sickle Cell anemia ?

A

Genetic

1650
Q

What causes Anemias of Chronic Disease?

A

inflammatory conditions, malignancy
– organ disease

1651
Q

What causes Anemias of Chronic Renal Insufficiency?

A

low levels of
erythropoietin – organ disease

1654
Q

What is the treatment for
Deficiency Anemias

B12 def?

A
  • 1mg IM injections weekly for 1‐2 months
  • Monitored for lifetime
1655
Q

What is the treatment for
Deficiency Anemias

Folic Acid def?

A

o 1mg PO, 5mg in malabsorptive disease
o Pregnant women given folic acid to decrease spina bifida
o Can be given IM injections if have malabsorption

1656
Q

What is the treatment for
Deficiency Anemias

Iron def?

A

▪ Ferrous sulfate 325 mg TID between meals
o can cause Constipation
▪ add on fiber to diet, green leafy vegetables
o IV doses for absorptive problems
▪ 125mg in 100ml saline infused over 1 hour

1657
Q

What is Thalassemia?

A

▪ A group of disorders of hemoglobin synthesis characterized by
decreased synthesis of either the alpha‐globin or beta‐globin
chains of the hemoglobin molecule

Patients get a microcytic, hypochromic anemia
▪ People with the abnormal gene have a resistance to malaria
▪ People who have the trait rather than the disease are more likely
to live and not die from malaria and spread that gene to their
children
▪ Severity depends on the specific genetic alteration and whether it
is homozygous (severe) or heterozygous (no clinical sign to mild
manifestations)

1659
Q

What type of Alpha‐thalassemia is not compatible with life

A

When there are Four defective genes – Hb Bart’s hydrops fetalis
o Lethal in utero or within a few hours of birth
o Not compatible with life

▪ Estimated that 5% of world population carries a variant of Alpha‐thalassemia (over 100 genetic forms)

▪ One defective gene –
o no disease detected
▪ Two defective genes – alpha‐thalassemia trait
o Mild degree of anemia (usually not clinically significant)
▪ Three defective genes – Hb (hemoglobin) H disease
o Hemolytic anemia and splenomegaly

1660
Q

Which ares alpha thalassemia is common?

A

Areas with a lot of malaria

1665
Q

What is Sickle Cell Anemia?

Type of inheritance

What causes it?

A

▪ Genetic disorder of hemoglobin synthesis (one of the
hemoglobinopathies)

▪ Autosomal recessive pattern

▪ Mutation in DNA of thymine for adenine causes alteration of
codon resulting in the substitution of the amino acid valine for
glutamic acid in the beta‐globin chain of hemoglobin

▪ This transformed hemoglobin is prone to molecular aggregation
and polymerization to form a rigid and curved shape (sickle shape)

1666
Q

What is Sickle cell crisis

treatment and how it diagnosed?

A
  • ▪ Transcranial Doppler scan used to evaluate blood flow in brain
    ▪ Hydroxyurea may be used as a therapy
    o Induces Hb F formation (doesn’t sickle)
    o But can be carcinogenic and teratogenic
1667
Q

What is Sickle cell crisis

What trigger it?

What are the symptoms?

effect on dental tx?

consequences?

A
  • sickling of the RBCs becomes severe
  • precipitated by such things as hypoxia, infection,
    hypothermia, or dehydration
  • Symptoms include pain (which may be severe) due to ischemia
    and infarction of affected tissues
    ▪ Long bones, lungs and abdomen are common sites of occurrence for “crises”
    ▪ Episodes last from 3‐10 days, some patients have monthly crises, some may go a year or more between
    ▪ May need pre‐medication prior to dental treatment
  • infections are the most common cause of death in sickle cell
    patients (in the US)
    ▪ Patients also have impaired kidney function and CNS involvement (strokes in 5‐8%, often prior to age of 10)
1669
Q

What is this

Hemophilia ?

What are its types

A

Bleeding disorders associated with a genetic deficiency of any
one of the clotting factors

o Hemophilia A (classic type, most common type )
▪ Factor VIII deficiency
▪ X‐linked recessive
▪ Abnormal PTT
o Hemophilia B (Christmas disease)
▪ Factor IX deficiency,
▪ X‐linked recessive, Abnormal PTT
o Von Willebrand’s disease
▪ Abnormal von Willebrand’s factor, abnormal
platelets
▪ Autosomal dominant
▪ Abnormal BT, abnormal PTT

1674
Q

What is Cyclic Neutropenia?

What causes it

When do symptoms begin?

What problems patients deal with?

A

Cyclic Neutropenia

▪ A rare idiopathic disorder characterized by regular periodic
reductions in the neutrophil population

Etiology: Underlying cause is a defect in hematopoietic stem cells in the marrow

▪ Symptoms usually begin in childhood
▪ Most symptoms when neutrophil count is at its lowest point
(nadir), usually lasts 3‐6 days (even when neutrophil counts are at their highest, it’s often lower than normal)
▪ Patients have repeated problems with infections

Oral ulcerations on any mucosal surface exposed to minor trauma & can mimic recurrent aphthous ulcerations without the
erythematous halo that is so typical of aphthous
▪ Gingiva is most severely affected with periodontal bone loss and tooth mobility

1675
Q

What is this radiographical presentation?

A

Mucositis

Thickening of the mucous of the sinus

  • normally we don’t see mucosa
    because it is very thin membrane

10 to 15 times thicker.

Most common
incidental findings
that we can see on
radiographs

1676
Q

What is this radiographical presentation?

A

Sinusitis

Sinus mucosa becomes inflamed and thickened from infection or
allergen, which may lead to ciliary dysfunction, retention of sinus
secretions and blockage of sinus drainage
● 10% of maxillary sinusitis are related to dental infections

1677
Q

What is this radiographical presentation?

A

Sinusitis

In this cone beam CT scan, we can see opacification of the sinus +
sometimes we see gaseous bubbles. It is fluid that is forming inside the
sinus.

1678
Q

What is this radiographical presentation?

A

Sinusitis

Sinusitis can be secondary to oral antral communication (communication
between maxillary sinus and oral cavity)

this can happen due to
extraction

1679
Q

What is this radiographical presentation?

A 
Antral Pseudocyst
(Retention
Pseudocyst)

Localized, submucosal accumulation of fluid forming a sessile, domeshaped
swelling along a sinus border
● Common incidental radiographic finding on panoramic
● Well-defined, non-corticated and dome shape radiopacity mostly along
the floor of maxillary sinus

1680
Q

What is this radiographical presentation?

A 
Antral Pseudocyst
(Retention
Pseudocyst)
1681
Q

What is this radiographical presentation?

A 
Antral Pseudocyst
(Retention
Pseudocyst)
1682
Q

What is this radiographical presentation?

A

Antrolith

Deposition of mineral salts (calcium phosphate/carbonate/magnesium) around an exogenous or endogenous (due to blood, pus or mucous) nidus
● Pediatric and adult population
‐ Small antroliths – incidental radiographic finding
‐ Large antroliths – sinus obstruction, sinusitis, nasal discharge,
pain
● Mostly adjacent to the floor of the maxillary sinus

● We see combination of radiopacity and radiolucency due to layers
of calcification.

1683
Q

Radicular Cyst VS
Antral Pseudocyst

A

One of the ways to differentiate antral pseudocyst from radicular cyst is by the presence of cortication.
‐ Reticulosis is a cystic lesion that happens around the apex of the nonvital
tooth.
‐ They have a round and domed shaped appearance too, but they are from
a different origin 􀀀 happening inside the alveolar processes

1684
Q

What is this radiographical presentation?

A

Antrolith

Deposition of mineral salts (calcium phosphate/carbonate/magnesium) around an exogenous or endogenous (due to blood, pus or mucous) nidus

We see a presence of radiopacity which is antrolith inside the
maxillary sinus

1685
Q

What is this radiographical finding?

A

Foreign Body in
Maxillary Sinus

1686
Q

What is this radiographical finding?

A

Foreign Body in
Maxillary Sinus

1687
Q

What is this radiographical finding?

A

Periostitis

•Lamellar, periosteal reaction from periapical inflammatory disease
•Exudate from infected tooth diffuses through the cortical bone,
(elevation of periosteum) lifts and stimulates the periosteal lining to
produce layer(s) of new bone
•Floor of maxillary sinus
•Inferior, buccal, lingual mandibular cortices

1688
Q

What is this clinical presentation?

A

Homogeneous leukoplakia

○ Thickened leathery, White plaque
○ Well-demarcated, Deepened fissures
○ Non-wipeable white patch

1689
Q

What is this clinical presentation?

A

Homogeneous leukoplakia.

○ Non-wipeable white patch

1690
Q

What is this clinical presentation?

A

homogenous leukoplakia

Just
white color

1691
Q

What is this clinical presentation?

A

Non-homogenous leukoplakia

Nodular leukoplakia ~ Largely white
Verrucous leukoplakia ~ Largely white
Erythroleukoplakia ~ Red and white

Speckled and verrucous leukoplakia have a greater risk for malignant
transformation than the homogeneous form

1692
Q

What is this clinical presentation?

A

Speckled leukoplakia.

Non-homogenous leukoplakia

1695
Q

What is this clinical presentation?

A

Hairy Leukoplakia

corrugated white lesion on the lateral tongue.
• It only occurs on the lateral tongue

1696
Q

What is this clinical presentation?

A

Hairy Leukoplakia

1699
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Patient with proliferative verrucous leukoplakia but manifesting more as
an erythroplakia in multiple sites than a leukoplakia

Proliferative verrucous leukoplakia has very high risk (49.5% in malignant transformation)
almost 10% risk for malignant transformation every year

1700
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Location
○ Gingiva (Frequent)
○ Buccal Mucosa
○ Palatal Mucosa

1701
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Multifocal

1703
Q

What is this clinical presentation?

A

Oral lichen planus

White lacy appearance, with
a network reticular appearance (Wickham’s striae)
sometimes punctate or plaque‐like lesions predominate

o Wickham’s striae→ very characteris► white wispy changes

1704
Q

What is this clinical presentation?

A

Oral lichen planus

on the buccal mucosa (most common site

reticular form.

1705
Q

What is this clinical presentation?

A

Oral lichen planus

slightly more red as you move to the left of the picture
● The white lines have small sunburst effect at the periphery
○ Very very characteristic of lichen planus
○ Will never see this in a leukoplakia

1706
Q

What is this clinical presentation?

A

Oral lichen planus

Lichen planus of the dorsum of the tongue

this is a hypertrophic form.

1707
Q

Leukoplakia

Etiology

A

Etiology

The exact etiology remains unknown. Tobacco, alcohol,
chronic local friction, and Candida albicans are important predisposing
factors. Human papilloma virus (HPV) may also be involved in the
pathogenesis of oral leukoplakia.

1708
Q

Leukoplakia

Treatment

A
  • Biopsy to rule out malignancy
  • Elimination or discontinuation of predisposing factors,
  • systemic retinoid compounds.
  • Smoking cessation (leukoplakias often disappear or become smaller within first year of smoking cessation)
  • Complete removal with surgical excision, electrocautery, cryosurgery, or laser ablation
1709
Q

What is this clinical presentation?

A

Lichenoid Reactions

Contact Lesions

a sensitivity in contact with a dental amalgam
▪ When you replace these amalgams, the lichenoid reaction will typically
disappear

1710
Q

What is this clinical presentation?

A

Oral Lichenoid

Contact lesion

chenoid reaction to dental amalgam and cold: white and erythematous
lesions on the buccal mucosa.

1711
Q

What is this clinical presentation?

pts takes Thiazide Diuretic

A

Oral Lichenoid Drug
Reaction

1712
Q

What is this clinical presentation?

pts takes allopurinol

A

Oral Lichenoid Drug
Reaction

1714
Q

Oral Lichenoid Drug
Reaction

Etiology

A
  • Lichenoid reactions may develop after exposure to a medication for periods of > 1 year
  • May develop very slowly after the problem is initiated so it can be very challenging to connect the dots

Many different medications that can lead to lichenoid reactions

  • Beta blockers, ACE inhibitors, Rituxumab etc…
  • A number of new targeted agents “mabs” and “nibs” can cause lichenoid reactions
  • In cancer centers, this has become quite a problem because they are taking disease‐modifying drugs
1716
Q

What is this clinical presentation?

A

Nicotinic Stomatitis

also known as

Smoker’s keratosis

smoker’s palate

  • the palatal mucosa becomes diffusely gray or white; numerous slightly elevated papules are noted, usually with punctate red centers
1717
Q

What is this clinical presentation?

A

Nicotinic Stomatitis

These papules represent inflamed minor salivary glands and their ductal orifices.

1718
Q

What is this clinical presentation

A

Nicotine Stomatitis.

1719
Q

Hairy Leukoplakia

Etiology

A

Epstein–Barr virus seems to play an important role in the
pathogenesis.

1720
Q

Hairy Leukoplakia

Treatment

A
  • Not required
  • however, in some cases aciclovir or valaciclovir
  • can be used with success.
  • Topical retinoids or podophyllum resin for temporary remission
1721
Q

What is this clinical presentation?

A

Pseudomembranous candidiasis

on the palate.

usually caused by Candida albicans

Predisposing factors are local

(poor oral hygiene, xerostomia, mucosal
damage, dentures, antibiotic mouthwashes)

1722
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

Multiple, well-demarcated zones of erythema (due to filiform atrophy) surrounded by slightly elevated, yellow-white, serpentine/ scalloped border

annular

  • serpiginous
  • atrophic
  • Fissured
1723
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

1724
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

1725
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

1726
Q

What is this clinical presentation?

A

Geographic tongue, localized lesion.

1729
Q

What is this clinical presentation?

A

Fordyce’s granules

on the buccal mucosa.

a normal anatomical variation.

ectopic sebaceous glands of the oral
mucosa.

1730
Q

What is this clinical presentation?

A

Leukoedema of the buccal mucosa.
Laskaris,

1732
Q

What is this clinical presentation?

A

White Sponge Nevus

Diffuse, thickened white plaques
of the buccal mucosa

1733
Q

What is this clinical presentation?

A

White Sponge Nevus

(Canon disease)

1734
Q

Proliferative Verrucous Leukoplakia

Treatment

A

complete removal: excision, electrocautery, cryosurgery, or laber ablation

Lesions rarely regress despite therapy

1735
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Early verrucous carcinoma of the buccal mucosa.

1736
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Large, exophytic, papillary
mass of the maxillary alveolar ridge.

1737
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Large, exophytic, papillary
mass of the maxillary alveolar ridge.

1738
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Extensive papillary, white
lesion of the maxillary vestibule

1741
Q
A

Traumatic Erythema /Traumatic Hematoma

on the lower lip.

1742
Q

What is this clinical presentation?

A

Geographic tongue: well-demarcated red patch on the tongue.

1743
Q

What is this clinical presentation?

A

Median rhomboid glossitis.

a Chronic hyperplastic, erythematous candidiasis

1746
Q

what is this clinical presentation?

A

Denture stomatitis.

1747
Q

Oral lichen planus

Etiology

A

Although the cause is not well known, T cell-mediated autoimmune
phenomena are involved in the pathogenesis of lichen planus.

1748
Q

What is this clinical presentation?

A

Erythroplakia

of the buccal mucosa

Well-demarcated erythematous patch or plaque with soft velvety texture

1749
Q

What is this clinical presentation?

A

Erythroplakia of the buccal mucosa.

1750
Q

What is this clinical presentation?

A

Erythroplakia

of the lateral margin of the tongue.

Well-demarcated erythematous patch or plaque with soft velvety texture

1751
Q

What is this clinical presentation?

A

Erythroplakia

Firey red Well-demarcated patch or plaque with soft velvety texture

transformed into SCC

1752
Q

Oral lichen planus

Treatment:

A
  • Incisional biopsy on non-keratinized, non-ulcerated mucosa

○ Asymptomatic → no tx
○ Symptomatic → 0.5mg/ml Dexamethasone Elixir.

1753
Q

What is this clinical presentation?

A

Erythroplakia.

Well-circumscribed red patch on the
posterior lateral hard and soft palate

1754
Q

What is this clinical presentation?

A

Erythroplakia.

Erythematous macule on the right
floor of the mouth.

Biopsy–

Turned out to be early invasive squamous cell
carcinoma.

1755
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Smokeless Tobacco–related Gingival Recession.
Extensive recession of the anterior mandibular facial gingiv

1756
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Severe

1757
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Mild. A soft, fissured,
gray-white lesion of the lower labial mucosa located in the area of
chronic snuff placement.

1759
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

. Multiple erosions affecting the
marginal gingiva.

1760
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Multiple erosions of the left
buccal mucosa and soft palate.

1761
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Large, irregularly shaped ulcerations
involving the floor of the mouth and ventral tongue.

1762
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

1763
Q

What is this clinical presentation?

A

Pemphigus vulgaris

● Multiple, chronic, mucocutaneous ulcers
● Many patients also have

● Relatively non‐specific
● Very superficial, only in epithelium
● Occur on any mucosal surface: oral, ocular, nasal, GI, esophageal,
genital

1764
Q

What is this clinical presentation?

A

Pemphigus vulgaris

PV Lesions can affect
virtually any mucosal
surface (oral, nasal,
ocular, pharyngeal,
esophageal, genital)

1765
Q

What is this clinical presentation?

A

Pemphigus vulgaris

usually suffer from Desquamative
gingivitis (DG)

More superficial erosion of the marginal gingiva, typically with an
intense erythema and inflammation, and very often in the absence of
local factors that would typically cause a gingivitis

o Hurts to brush their teeth

Immediately look for areas where there are no local factors and look for
inflammation there
o To check the possibility of systemic factors causing local
gingivitis

1766
Q

What is this clinical presentation?

A

Pemphigus vulgaris

Combination of PV
inflammation and
gingival inflammation
accumulating local
factors can result in
advanced loss of
attachment and tooth
loss

1769
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

1770
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal

can
result in functional
blindness

1771
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

Oral Hygiene: Plaque
related gingival
inflammation
contributing to
continued VB
desquamative
gingivitis

1772
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

REMEMBER:

▪ Plaque and calculus can be the consequence of painful MMP lesions
▪ When assessing MMP lesions/desquamative gingivitis, look for areas of intense inflammation WITHOUT local factors as evidence of VB disease

1774
Q

Oral Lichenoid
Contact Lesions

Etiology

A

Hypersensitivity

to

  • dental restorative materials, amalgam or other metal, composite resins
  • Foods, oral products
  • Especially cinnamon
  • dental plaque accumulation are the most common
1775
Q

MMP & PV BIOPSY

A

take two different sites
○ For H&E, still must be perilesional
○ If you get only ulcer just because the clinician thinks
○ that is the pathology → there is no epithelium!
○ The sample is useless and no diagnosis can be made

1776
Q

What is this clinical presentation?

A

Actinic cheilitis

(Solar cheilosis)

Early presetation:

Smooth, blotchy, pale, dry areas

Diffuse, irregular white plaque around line of the lip

Crusted, Scaly

​

1777
Q

What is this clinical presentation?

A

Actinic cheilitis

(Solar cheilosis)

Typical presentation of angular cheilitis with erythema, crusting and mild fissuring of the angles of the mouth bilaterally.

1779
Q

Oral lichenoid reaction

Treatment

A

Insicional biopsy Mandated to distinguish from OLP
○ Biopsy white areas on non-keratinized mucosa NOT ulcerated OR red areas

Treatment Replacement of the restorative material, polishing and
smoothing, and good oral hygiene are recommended.

Topical steroid
treatment for a short time is also helpful.

1781
Q

What is this clinical presentation?

A

SCC

arising from Actinic Cheilitis

1782
Q

What is this clinical presentation?

A

Oral Melanoma

Large, blue-black, irregularly bordered lesion on the upper lip of a male Japanese patient. The diagnosis is oral melanoma.

1783
Q

What is this clinical presentation?

A

Amalgam tattoo

This image depicts two diffusely bordered, dark gray macules in the left posterior buccal mucosa adjacent to molar teeth that have been restored. .

1784
Q

What is this clinical presentation?

A

Oral Melanoma

a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.

1785
Q

What is this clinical presentation?

A

Oral Melanoma

an ulcerated, blue-black, slightly elevated lesion in the edentulous, posterior right maxilla. The lesion extends across the residual alveolar ridge onto the palate and onto the facial aspect of the ridge.

1786
Q

What is this clinical presentation?

A

Oral Melanoma

patient with extensive, black-pigmented and irregularly bordered macule in the maxillary labial mucosa and midline facial gingiva, (teeth 8 and 9). (The patient’s fingers are depicted.)

1787
Q

What is this clinica presentation?

A

Oral melanoacanthoma.

the buccal mucosa of a middle-aged, black woman with a brown-black, irregularly bordered macule that arose suddenly. The patient was unaware of its presence.

1788
Q

What is this clinical presentation?

A

Oral melanotic macule

an irregularly shaped, tan-brown macule on the left hard palate in an edentulous patient.

1791
Q

Nicotine Stomatitis

Treatment

A

Smoking Cessation.

  • Nicotine stomatitis is completely reversible, even when it has been present for many decades.
  • The palate usually returns to normal within 1 to 2 weeks of smoking cessation.
1792
Q

What is this clinical presentation

A

Oral Melanoma

1793
Q

What is this clinical presentation

A

Oral Melanoma

1794
Q

What is this clinical presentation?

A

Traumatic

Granuloma

(traumatic ulcertaive granuloma)

1795
Q

What is this clinical presentation

A

Oral Melanoma

1796
Q

Nicotine Stomatitis.

Etiology

A

The elevated temperature, rather than the tobacco chemicals,
is responsible for this lesion.

1797
Q

What is this clinical presentation?

A

Traumatic ulcer

Most often on tongue, lips, buccal mucosa

Any sites that may be injured by dentition

1799
Q

What is this clinical presentation?

A

Traumatic ulcer

a chronic ulcer on the left posterior lateral border of the tongue caused by lingually tilted mandibular 3rd molar. Note central ulceration with peripheral keratosis

1800
Q

What is this clinical presentation?

A

Traumatic ulcer

caused by sharp or puncturing food stuff

1801
Q

What is this clinical presentation?

A

Traumatic

Granuloma

1802
Q

What is this clinical presentation?

A

Traumatic Granuloma

( Traumatic Ulcerative Granuloma)

1804
Q

What is this clinical presentation?

A

Squamous cell carcinoma

on the buccal mucosa)

1805
Q

What is this clinical presentation?

A

Erythroplakia and Squamous Cell Carcinoma

Erythroplakia is a general term for red, flat, or eroded velvety lesions that develop in the mouth. In this image, an exophytic squamous cell carcinoma on the tongue is surrounded by a margin of erythroplakia

1806
Q

What is this clinical presentation?

A

Leukoplakia and Squamous Cell Carcinoma

Leukoplakia is a general term for white hyperkeratotic plaques that develop in the mouth. About 80% are benign. However, in this image, squamous cell carcinoma is present in one of the leukoplakic lesions on the ventral surface of the tongue (arrow).

1809
Q

What is this clinical presentation?

A

Graphite tattoo

Gray, black, or blue-ish macule

1810
Q

What is this clinical presentation?

A

Graphite tattoo

Most common location on the palate and gingiva

Gray, black, or blue-ish macule

1813
Q

Geographic tongue/
areata migrans

Treatment

A
  • Generally no treatment is indicated
  • Reassuring the patient that the condition is completely benign is often all that is necessary.
  • In case of tenderness or a burning sensation that is so severe –topical corticosteroids, such as fluocinonide or betamethasone gel, may provide relief
1814
Q

Geographic tongue/
areata migrans

Etiology

A

The exact etiology remains unknown. It may be genetic.

1817
Q

Leukoedema

Etiology

Treatment

A

Etiology

It is due to increased thickness of the epitheliumand intracellular
edema of the prickle-cell layer.

Treatment

No treatment required

1820
Q

White Sponge Nevus

Etiology

A

Autosomal dominant skin disorder

Etiology:
● This condition is due to a defect in the normal keratinization of the oral mucosa in the 30-member family of keratin filaments, the pair of keratins known as keratin 4 and keratin 13 is specifically expressed in the spinous cell layer of mucosal epithelium.

1825
Q

Verrucous Carcinoma

Etiology

A

a low-grade variant of squamouscell
carcinoma.

Etiology

Leading theories include

  • human papillomavirus (HPV) infection
  • chemical carcinogenesis induced by smoking and chewing tobacco
  • alcohol consumption
  • betel nut chewing (oral lesions),
  • chronic inflammation
1826
Q

Verrucous Carcinoma

Treatment

A

○ Surgical Excision

○ Radiotherapy

1830
Q

Median Rhomboid Glossitis

Treatment

A

No treatment is required.

1831
Q

Median Rhomboid Glossitis

Etiology

A

Atrophy of central filiform papillae

Presumably developmental. Candida albicans may also be
involved.

but smokers, people with xerostomia , who use inhalation steroids
and denture wearers are at increased risk

1833
Q

Erythroplakia

Malignant transformation

A

Erythroplakia is a high risk for malignant transformation. So, if you
encounter an erythroplakia, it’s probably already a cancer or it’s fast‐tracking
towards a cancer

1838
Q

Erythroplakia

Treatment

A

○ Biopsy required for diagnosis

○ If a source of irritation can be identified and removed, biopsy may be delayed for 2 weeks to allow lesion to heal

○ Complete excision

1844
Q

Smokeless tobacco keratosis

Treatment:

A

typically resolves weeks after cessation

○ if persists 6+weeks -> biopsy to rule out dysplasia + SCC

1853
Q

Pemphigus vulgaris

Etiology

A

Pemphigus vulgaris is not fully understood.

Experts believe that it’s triggered when a person who has a genetic tendency to get this condition comes into contact with an environmental trigger, such as a chemical or a drug.

In some cases, pemphigus vulgaris will go away once the trigger is removed.

1854
Q

Pemphigus vulgaris

A

Treatment has 3 stages:
● Stage 1: Control
○ Suppress inflammation / lesion activity with Systemic Corticosteroid: Remains initial / 1st‐line treatment…
○ Then quickly add steroid‐sparing agents (mycophenolate mofetil) to minimize dose and duration of corticosteroid treatment as well as improve disease control
● Stage 2: Consolidation
○ Reducing auto‐antibody production with the addition of Immunosuppressants
○ Assessed by the lack of development of NEW lesions
● Stage 3. Remission / Maintenance:
○ achieving complete remission of lesion activity OFF medication is the GOAL
○ When lesion activity OFF medications cannot be achieved, principle of MINIMALLY effective therapy is the goal, typically with combination of immunosuppressant medications
○ RITUXIMAB has become the FIRST CHOICE treatment after
○ the consolidation phase to achieve DISEASE REMISSION

● TOPICAL / INJECTABLE CORTICOSTEROID MEDICATIONS
○ o Can be used to help control limited number of lesions resistant to systemic therapy: it treats ONLY the disease
○ outcome (lesions) and not the systemic illness / pathologic antibody production
○ ex:clobetesol 0. 05% , halbetesol 0.05% (most potent)

1859
Q

Mucous membrane pemphigoid

Etiology

A

Mucocutaneous autoimmune disease characterized by sub‐epithelial
blisters (bullae) which ruptures to form large, non‐healing ulcerations

1860
Q

Mucous membrane pemphigoid

Treatment

A

o Approach is similar to PV – but generally not as aggressive unless
hi‐risk areas ( ocular, esophageal ) where more intense immunosuppression indicated
▪ NON‐immunosuppressive treatments uniquely effective:

  • *o** Dapsone
  • *o Tetracycline + nicotinamide**
1864
Q

Actinic cheilitis

malignant transformation

A

Actinic cheilitis has 2 times of risk for developing SCC of the lip.

SCC on the lips is 11 times as likely to metastasize compared to SCC found on other parts of the body

1865
Q

Actinic cheilitis

Etiology

A

due to chronic ultraviolet light exposure.

1866
Q

Actinic cheilitis

Treatment

A
  • avoid sun exposure
  • Laser ablation is preferred for severe actinic cheilitis
  • surgical excision is recommended for severe actinic cheilitis with evidence of high-grade dysplasia
    • Lip Shaving” (Vermilionectomy)
  • can also use cryotherapy, electrodesiccation

It requires long term follow up and prognosis is good if caught early

1875
Q

Oral Melanoma

Etiology

A

Unknown. Ultraviolet radiation is an important causative factor for skin melanoma

Acute sun damage can cause it more than chronic exposure

1876
Q

Oral Melanoma

Risk Factors

A

Fair skin

A history of sunburn

Excessive ultraviolet (UV) light exposure.

Living closer to the equator or at a higher elevation

Having many moles or unusual moles

A family history of melanoma

Weakened immune system.

1877
Q

Oral Melanoma

Treatment

A
  • Surgical excision
  • Radiotherapy
  • Chemotherapy
1882
Q

Traumatic ulcer/Traumatic ulcerative granluoma

Etiology

A

Etiology

  • typically caused by trauma. In more than half the cases, the patient does not recall traumatizing the area although this may have occurred during sleep.
  • Chronic mucosal trauma from adjacent teeth
  • Some adjacent source of irritation
1884
Q

What is this clinical presentation?

A

Traumatic ulcer

Post-anaesthesia traumatic ulcer on lower lip.

1889
Q

Traumatic ulcer/Traumatic ulcerative granluoma

Treatment

A

Remove cause of irritation

Topical anesthetic or film for pain relief

If there is no obvious cause then ► biopsy

1893
Q

squamous cell carcinoma

Risk factors

A

HPV + SCC

Area affected: ( Oropharynx cancers largely involved tonsils, . Posterior 3rd of the Tongue)

Younger pts, 3:1 Males to females ratio, high socio-eco status

Incidence is decreasing

less aggressive → higher survival rates ( Better than HPV negative SCC)

HPV - SCC

The chief risk factors for oral squamous cell carcinoma are

Smoking (especially > 2 packs/day)

Alcohol use

Risk increases dramatically when alcohol use exceeds 6 oz of distilled liquor, 15 oz of wine, or 36 oz of beer/day. The combination of heavy smoking and alcohol abuse is estimated to raise the risk 100-fold in women and 38-fold in men.

( this affects these ares : the tongue, floor of mouth, buccal mucosa, or gingiva)

mostly men, low socio-economic factors

Incidence is decreasing

Very aggressive → lower survival rates

1894
Q

SCC treatment

A

Early stage: Radiation and/or Surgical removal

Late stage : combination of surgery, radiation therapy, or chemotherapy

1897
Q

Graphite tattoo

Etiology

A

result from pencil lead that is traumatically implanted, usually during the elementary school years

1898
Q

Graphite tattoo

Treatment

A

If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft

1899
Q

What is this clinical presentation?

A

Hemangioma of Infancy

a relatively common benign proliferation of
blood vessels that primarily develops during childhood.

display a rapid growth phase with endothelial
cell proliferation, followed by gradual involution.

1900
Q

What is this clinical finding?

A

Hemangioma of Infancy

1902
Q

What is this clinical presentation?

A

Traumatic ulcer of the tongue.

1904
Q

Hemangioma of Infancy

Treatment

A

○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”

1906
Q

What is this clinical finding?

A

Necrotizing Sialadenometaplasia

we see two ulcers on the palate

Mostly
● Palatal salivary glands
○ Possible for parotid
● 75% of case on posterior palate
● Hard>Soft palate
● 2/3rd are unilateral

1907
Q

What is this clinical finding?

A

Necrotizing Sialadenometaplasia

an uncommon, usually self-limiting, benign inflammatory disorder of the salivary glands.

Here it is on the palate

1908
Q

What is this clinical finding?

A

Xerostomia-related Caries

Or

Dry Mouth

. Extensive cervical caries of
mandibular dentition secondary to radiation-related xerostomia.

1909
Q

Necrotizing Sialadenometaplasia

Etiology

A

The cause is uncertain, although the hypothesis of ischemic
necrosis after vascular infarction seems acceptable.

1911
Q

Necrotizing Sialadenometaplasia

Treatment

A

No Treatment Needed

but we need to biopsy to rule out other diseases

1912
Q

Dry mouth

Subjective vs Objective

A

Xerostomia

The subjective experience of a dry mouth (ie a symptom)

Salivary Hypofunction

The objective measurement of a reduction in salivary flow (a sign)

1913
Q

What is the normal rate for Unstimulated Saliva
Production

A

300 ml/day
▪ Flow rate: mean 0.3 ml/min

1914
Q

What is the normal rate for Stimulated Saliva
Production

A

Stimulated Saliva
Production

▪ 200+ ml/day
▪ Flow rate: mean 1-2 ml/min, maximum 7 ml/min
o “Normal” range is very wide

1915
Q

What are Factors affecting unstimulated flow include?

A
  • Dehydration
  • Medical conditions
  • Body posture
  • Lighting conditions
  • Circadian/circannual rhythm (lowest during)
  • Medications

Age is an independent factor for whole saliva andsubmandibular/sublingual gland secretion (but notparotid).

1916
Q

What is this clinical presentation?

A

dry‐mouth

from radiation

Note the Ropy, frothiness on the palate.

  • The tissues are red and irritated due to candida infection as well.
1917
Q

What is this clinical presentation?

A

dry‐mouth

patient

a classic example

• Classic fissuring
• depapillation of the tongue papilla
• some white changes on the tongue.

1918
Q

What is this clinical presentation?

A

dry Mouth

Cervical caries related
to radiation.

The patient is a smoker and coffee drinker –> explains the staining

1919
Q

What is this clinical presentation?

A

dry Mouth

Incisal caries in a
radiation patient:

Incisal caries is a sure sign of severe dry mouth/ significant salivary gland hypofunction

1920
Q

What are Factors affecting stimulated flow include:

A
  • Mechanical stimuli
  • Vomiting
  • Gustatory/olfactory stimuli (acid/smell)
  • Gland size

Age is an independent factor for whole saliva (but not
for parotid and minor gland secretions)

1921
Q

Severity of patients
with xerostomia using
objective measures

A
1922
Q

What causes
dry mouth?

A

Central inhibition as a result of connections between the primary salivary centers and the
higher centers of the brain.

1923
Q

● What causes xerostomia in absence of measurable salivary hypofunction?

A
  • May be a reduction in baseline sialometry which is still above “normal.”
    • If they get a decrease in the salivary flow, they still may be in the normal range, but for them the experience is that they have got dry mouth.
  • Saliva film thickness
    • Palatal mucous gland secretions?
    • Anterior dorsum of tongue?
  • Relative contributions by glands
    • Mucins, proteins?
  • Alterations in sensory perception?
  • Mental status/central inhibition?
1924
Q

What cause
Salivary
Hypofunction?

A

● Dehydration
● Medications (Rx & OTC)

  • Direct damage to glands
  • Head and neck radiotherapy
  • As a result of radiation it’s irreversible damage to the glands
  • Chemotherapy (reversible)
  • Autoimmune diseases
  • Primary vs Secondary Sjögren’s Syndrome, GVHD
  • HIV disease

● Decreased mastication (tooth loss, soft diet)
● Conditions affecting the CNS:

  • Psychologic disorders (depression/anxiety?), Alzheimer’s, Parkinson’s, Cerebral palsy
1926
Q

What is this clinical presentation?

A

SJÖGREN’S SYNDROME

Dry Mouth

very severe
cervical disease & very dry lips

1928
Q

What is this clinical presentation?

A

a patient
with a
bacterial sialadenitis

who has

SJÖGREN’S SYNDROME

When we examine such patients and ”milk” the gland ► you actually see a purulent drainage from the gland itself.

1929
Q

What is this clinical presentation?

A

Depapillated &
Fissured Tongue

SJÖGREN’S SYNDROME

1930
Q

What is this clinical presentation?

A

Sjögren Syndrome

  • bilateral enlargement of the submandibular glands
  • angular cheilitis, dry and cracked lips and fissured and despapilated tongue
  • severe ocular lesions.
1931
Q

SJÖGREN’S SYNDROME

Management

A

These patients LOW USFR, no response to stimulation (aka abnormal USFR/SFR)

  • Rehydrate if dehydrated
  • Treat underlying conditions (i.e. DM)
  • Salivary substitutes (glycerin)
  • Minimize damage to glands from radiation
  • Prevention of complications & palliative treatment
    • Optimal hygiene
    • Restore caries
    • Smooth sharp edges in oral cavity
    • Fluoride therapy
    • Antifungals
    • Chlorhexidine rinses w/o alcohol
    • Sialendoscopy
    • Salitron - salivary pacemaker
  • ALTENS (acupuncture like transcutaneous electrical nerve stimulation)
1934
Q

To have dry mouth

xerostomia

what is the rate of Unstimulated and Stimulated Salivary flow

USFR

and

SFR

A

Abnormal unstimulated USFR= <0.1–0.2ml/min

Abnormal stiumated SFR = <0.5ml/min

1936
Q

How to manage with normal USFR and SFR?

A
  • Salivary stimulation (OTC) to stimulate their glands
  • Salivary lubrication ( to improve it)
  • Humidification ( like a humidifier in the room at night)
  • Hydration/prevent dehydration (ie avoid alcohol, caffeine both will act as a
  • diuretic and lead to dehydration).
  • Monitor closely to rule out emerging disease ( to see whether they are developing Sjogren’s or something else 􀀀 we want to follow them over time)
1937
Q

How to manage with abnormal USFR and abnormal SFR?

Abnormal unstimulated USFR= <0.1–0.2ml/min

Abnormal stiumated SFR = <0.5ml/min

A
  • If dehydrated ► rehydrate or treat underlying condition
    • People with uncontrolled diabetes, once you control the diabetes‐ their flow comes back.
  • All we can do is offering Salivary substitutes (sprays, gels, rinses )
  • For patients with high dose radiation treatment ► makes sure they get the INRT
  • Minimizing damage to salivary glands ( there are other strategies for that)
  • Prevention and treatment of oral complications
1938
Q

How to manage with abnormal USFR and normal SFR?

(respond to stimulated)

Abnormal unstimulated USFR= <0.1–0.2ml/min

A
  • Look for possible causes (major cause will be medications & can dehydration or others)
  • Restore chewing function (Masticatory issues)
  • Reduce medication‐induced salivary hypofunction
  • Prescribe Salivary stimulation OTC, Rx medications, others
  • Prescribe Salivary lubrication
  • Humidification ‐use humidifiers
  • Hydration/prevent dehydration (ie avoid alcohol, caffeine)
  • Treat oral consequences (such as candidiasis treated with an antifungal or caries with management of caries).
1939
Q

What are the

Prescription
Medications
for people with

low USFR and
some oral signs, but
responds to stimulation ?

(abnormal USFR, Normal/improved SFR)

(include dosage and usage)

A

– Muscarinic agonists:
– Pilocarpine 5‐7.5mg tid & qhs (can go as
high as 10mg qid)
– Cevimeline 30mg tid (can go as high as
60mg tid)

Contradicated for : CV disease, hepatic, renal or respiratory diseases or narrow angle glaucoma

Pilocarpine affects M1 & M3

side effects (sweating, flushing,
rhinitis, increased urination, weakness and
some experience the shakes. )

Cevimeline affects M3 only

fewer side effects

1941
Q

What is this clinical finding?

A

Frictional keratosis

on the tongue

1942
Q

What is this clinical finding?

A

Frictional Keratosis

the white surrounding a a traumatic ulcer

Symptomatic traumatic ulceration of the left mid-ventral tongue associated with a sharp left lower molar. The ulcer has flat edges and is surrounded by an area of frictional keratosis.

1943
Q

Frictional Keratosis.

Differential Diagnosis

A

Leukoplakia

Linea alba

Chronic cheek chewing (bite injury)

Candidiasis

Oral Lichen planus

Squamous cell carcinoma

1944
Q

What is this clinical finding?

A

Frictional Keratosis.

There is a rough, hyperkeratotic change to the posterior mandibular alveolar ridge (“alveolar ridge keratosis”),
because this area is now edentulous and becomes traumatized
from mastication.

Such frictional keratoses should resolve when the
source of irritation is eliminated and should not be mistaken for true
leukoplakia.

1945
Q

Frictional Keratosis

Etiology

A
  • Trauma from Sharp cusp & ortho appliance
  • Chronic mechanical irritation (chronic biting)
  • Masticatory function
  • Normal hyperplastic response
  • Dentures/missing teeth
1946
Q

Frictional Keratosis

Treatment

A
  • Remove the cauative factor that caused the trauma
  • observe large lesion regularly

excellent prognosis

1947
Q

What is this clinical presentation?

A

SJÖGREN’S SYNDROME

Autoimmune exocrinopathy

Dry mouth and eyes resulting from a chronic progressive loss of secretory function (Slowly but surely, the salivary glands and/or lacrimal glands (some cases are more lacrimal & less salivary or vice versa); slow & progressive

Patients with Sjogren’s can have bilateral salivary gland enlargement (parotid) (Sometimes we may see a unilateral enlargement of the salivary
glands due to retrograde infections.)

increased risk of lymphoma (MALT type)

1952
Q

For Smoking Cessations

Prescribe Nicotinic Drugs

(memorize any of them + dosage)

A

Nicotine Patch Generic Name-Nicodern CQ/Habitrol

  • 21 mg/24 hr> 10 dgs/d
  • 14 mg/24 hr or 7 mg/24 hr

<10 mg cig/d or <100 lbs

Nicotine Gum Generic Name -Nicorette

2 mg < 25 cig/d

4 mg > 25 cig/d

Nicotine lozenge - Commit

2 mg if smoke 1st cig more than 30 minutes after waking

4 mg 4 mg if smoke 1st cig within 30 minutes after waking

( no more than 20 a day)

Nicotine Inhaler -Nicotrol lnholer

6-16 cartridges/ d
Use 1 cartridge/hour

Nicotine Nasal Spray- Nicotrol NS

Mox 40 doses/d
(1 dose = 1 spray per nostril}

1953
Q

For Smoking Cessations

Prescribe Non-Nicotinic Drugs

(memorize any of them + dosage)

A

Sustained release buprorpion
Zyban or Wellbutrin
Can be used
w/NRT

Start 1-2 weeks
before quit date.

Option 1 : 150 mg/ day for
3 days then 150 mg BID
(doses at least 8 hrs apart)
Option 2: 150 mg q
AM is recommende~ Fewer
adverse eff eds better
tolerated iin older adult)

Varenidine tartrate

Chontix

Start 1 week
before quit date
0. 5 mg/ d for 3 days then
0.5 mg BID for next 4 days
(one in AM, and one in PM).
After firs1 7 days 1 mg/810

1954
Q

What are the adverse effects of Nicotine Inhaler
Nicotrol lnholer

A
  • Mouth and throat irritation
  • Cough

• Side effem generally caused by
inappropriate use

1955
Q

What are the adverse effects of Nicotine Nasal
Spray- Nicotrol NS

A
  • Nasal irrttation
  • Sneezing
  • Cough
  • Teary eyes
1956
Q

What are the adverse effects of Nicotine Patch ?

A
  • local skin irritation
  • insomonia
1957
Q

What are the adverse effects of Nicotine Gum?

A
  • hiccups
  • Dyspepsia
  • mouth sorness
1958
Q

What are the adverse effects of Nicotine lozenge?

A
  • Dyspepsia
  • local irrttation mouth & throat
  • Rarely causes coughing & hiccups
1959
Q

What are the adverse effects of Sustained release
bupropion (Zyban or Wellbutrin)?

A
  • Insomnia
  • Dry mouth
  • Anxiety
1960
Q

What are the adverse effects of Varenidine
tartrate Chontix ?

A
  • Nausea
  • Insomnia
  • Abnormal dreams
1961
Q

What is this clinical finding?

A

Urticaria

Well defined erythematous papules/plaques which are pruritic (itchy)

We’ll see them on the skin ‐ Not found intraorally

1962
Q

What is this clinical finding?

A

Urticaria

(HIVES)

this person was exposed to extreme temperature developed hives (
not really
red but very itchy)
no skin scarring is noted
it goes in about a day

1965
Q

What is this clinical finding?

A

Angioedema

❖ Diffuse edematous swelling of the soft tissues that most commonly
involves the subcutaneous and submucosal connective tissues
❖ Results from local vasodilatation and increased vascular
permeability of DEEPER blood vessels

1966
Q

What is this clinical finding?

A

Angioedema

1967
Q

Urticaria

Etiology

A

❖ Medications ► causing rash
❖ Foods ► like peanuts
❖ Airborne allergens ► pollen
❖ Physical stimuli ► ex cold weather

1968
Q

Urticaria

Treatment

A

❖Avoid known triggers avoid
the penicillin, any of
the triggers
❖ Antihistamines ( to prevent it
from happening in the first
place)
Corticosteroids (prevents the
inflammatory effect)

1969
Q

What is this clinical finding?

A

Cinnamon Contact
Stomatitis

  • It can present similar to leukoplakia
  • So you’d think it is pre‐malignant lesion
  • But after asking the patients ► you’ll realize they are chewing like 10 cinnamon gums every day.
1970
Q

What is this clinical finding?

A

Allergic Contact
Stomatitis

❖ Mild‐severe redness, edema, vesicles, erosions, ulcerations

❖ Burning, itching, stinging, tingling

●We can’t know what is this right away.

Patients may say it burns, tingles, there could be peeling
(desquamation). We might think it’s a vesiculobullous diseases.
● So these cases require more consulative‐investigative work.

1971
Q

What is this clinical finding?

A

Allergic Contact
Stomatitis‐Clinical

  • slight vesicales and diffused erythemya
  • we wouldn’t always know this is Allergic contact stomatitis
  • This occured due to allumnium chloride on gingival retraction cord.
1973
Q

What is this clinical finding?

A

Exfoliative cheilitis

Allergic Contact
Reactions‐ Non‐
Mucosal

dry, scaly, fissured, cracking lips

This is a mild case that affect the non‐mucosal around the the
skin

1974
Q

What is this clinical finding?

A

Exfoliative Cheilitis

caused by titanium implants and
some mercury in amalgam.

1975
Q

What is this clinical finding?

A

Perioral Dermatitis

Allergic Contact
Reactions‐ Non‐
Mucosal

erythematous
papules/vesicles
– papules ( raised) & vesicles
(actual blisters)

1976
Q

What is this clinical finding?

A

Erythema
Multiforme

Rapidly rupturing vesicles/bullae forming erosions/ulcerations and
hemorrhagic encrusted lip lesions, with greyish pseudomembrane
Fast expansion, ► the skin is just peeling off.

Type 4 hypersensitivity.

Has prodrome phasesudden

Rapid onset, crusted
hemorrhagic swollen
lips, and
desquamative
gingivitis.

1977
Q

What is this histological finding?

A

Granuloma

This is a granuloma. It’s composed of histeocytes that looks
epithelioid. This is a collection of epithelioid histeocytes

Found in:

  • TB (They’ll be holding TB inside. But in TB you have caseous necrosis of granuloma.
  • Deep fungal infections (they holding? fungal organisms)
  • GRANULOMATOUS DISEASES ( if with Asteroid bodies & Schaumann Bodies)

In these granulomas we don’t know why they are forming.

1978
Q

What is this clinical finding?

A

Orofacial
Granulomatosis

Cheilitis granulomatosa=Involvement of lips alone

Non‐tender, persistent swelling

NEED To BIOPSY to RULE OUT

angioedema

1979
Q

What is this clinical finding?

A

Orofacial
Granulomatosis

Papules, slightly raised areas, fissures, cobblestone appearance

DDx

We could suspect

a traumatic injury

early signs of Crohn’s

1980
Q

What is this clinical finding?

A

Orofacial
Granulomatosis

1981
Q

Orofacial
Granulomatosis

Treatment

A

❖ Discover cause ( we need to find out the cause.)
❖ Topical or intralesional corticosteroids (maybe try steroids)
❖ Other (topical tacrolimus, sulfazalazine, methotrexate, etc)
❖ Some cases resolve spontaneously

(This photo shows a person has puffiness because of granulomas.
Sometimes it goes away on its own. We can use injection steroids on
the lips too.)

1983
Q

What is this clinical finding?

A

Sarcoidosis‐Organ
Systems

❖ Lungs
❖ Lymph Nodes (bilateral hilar
lymphadenopathy)
❖ Skin (25% of time)
❖ Eyes
❖ Salivary Glands
❖ Other (endocrine,
gastrointestinal, heart, kidney, liver, nervous system, spleen, skeletal

1984
Q

What is this radiological finding?

A

Sarcoidosis‐Hilar
Lymph Node
Enlargement

popcorn‐like calcifications in the hilar lymph nodes.

granulomas from
sarcoidosis being inside
.

1985
Q

What is this clinical finding?

A

Sarcoidosis‐Skin
Lesions

Lupus pernio (nose, ears, lips and
face)
‐ when we have these erythematous
indurated, hard on face.

1986
Q

What is this clinical finding?

A

Sarcoidosis

DDX

in the oral cavity. It could be one of the three P’s:
❖ pyogenic granuloma
❖ peripheral ossifying fibroma
❖ peripheral giant cell granuloma.

1987
Q

What is this clinical finding?

A

❖ This is Strawberry gingivitis

Granulomatosis with
Polyangiitis “Wegener’s”

Orally

❖ Ulceration,
❖ Mucosal nodules
❖ Facial paralysis
❖ Enlarged major gland
from granulomas

  • we need to biopsy, as this also looks like a deep fungal
    infection. *
1988
Q

What is this clinical finding?

A

Granulomatosis with
Polyangiitis

Orally

We want to
biopsy to confirm because it Could be contact mucositis.

1989
Q

What is this clinical finding?

A

‐ Cinnamon contact mucositis

This could be oral hairy leukoplakia.
It could be hyperplastic candidiasis
it could be tongue chewing
it could be a leukoplakia.
We’ll know what it is by biopsy and investigate

1990
Q

What is this clinical finding?

A

Urticaria.

1991
Q

What is this clinical finding?

A

Erythema multiforme

1992
Q

What is this clinical finding?

A

* Erythema multiforme

1993
Q

What is this clinical finding?

A

‐ Orofacial granulomatosis.

We make sure there’s no tb, no fungal, no foreign material in the
granulomas

1994
Q

What is this clinical finding?

A

Sarcoidosis

*Erythemous papules (grey circle)
Asteroid bodies ( blue arrow)
Hilar lymph nodes (green circle)

1995
Q

What is this clinical finding?

A
1996
Q

What is this clinical finding?

A

orofacial granulomatosis.

What is
the common way to
describe this?

Cobblestone. This is the classic cobblestone.
Cobblestone and fissuring

DDx: people with Crohn’s with oral manifestations it looks like this
too.

1997
Q

What is this clinical finding?

A

Sarcoidosis

1998
Q

What is this clinical finding?

A

angioedema

1999
Q

What is this clinical finding?

A

Fixed Drug Eruption

–This case has both the skin and oral appearance.

This happened every time this person took NSAIDs that’s not used in
the USA.

A person gets a reaction to a medication they take. It occurs at the
same place each time because there’s some memory T cell at these
sites.

2000
Q

Angioedema

Etiology

A

Causes include:
❖ IgE mediated ( most common types are allergy related)

  • Hypersensitivity reaction
    • drugs, foods, plants, dust
  • Contact allergic reactions
    • foods, cosmetics, topical medications, rubber dam
  • Physical stimuli
    • heat, cold, exercise, emotional stress, solar exposure, vibration

❖ Drug reaction to ACE inhibitors

  • Does not respond well to antihistamines

❖ Hereditary or acquired activation of the complement
pathway
❖ Other (high levels of antigen‐antibody complexes and in
elevated blood eosinophil counts)

  • Complexes in lupus, viral and bacterial infections
  • Patients with grossly elevated blood eosinophilia
2001
Q

Angioedema

Treatment

A

❖ Antihistamine/IM epinephrine/IV corticosteroids ( typical treatment for allergy)

❖ Intubation and tracheostomy ( if the patient can’t breathe, so we can get air in)

❖ Avoid medications in ACE Inhibitor class of drugs ( for people who has Ace inhibitor induced angieodema)

❖ C1 esterase inhibitor concentrate and esterase inhibiting drugs

2002
Q

What is this clinical finding?

A

Granulomatosis with
Polyangiitis

extra-oral

Joint pain, weakness, tiredness
❖ Known as Saddle nose deformity

❖ First signs may be recurrent
respiratory infection, cough or
runny nose

❖ Oral lesions initial presentation in 2% of patients

2003
Q

Granulomatosis with
Polyangiitis

Treatment

A

First line: oral prednisone
❖ After remission immunosuppressive drugs:
❖ Methotrexate
❖ Cyclosporine
❖ Rituximab
❖ Treatment induces prolonged remission
❖ May have relapses

2007
Q

White wipeable plaque in the mouth

DDx

A

● pseudomembranous candidiasis
● Mucosal sloughing‐ Allergic Contact Stomatitis
● Food particles

2008
Q

What is this clinical finding?

A

Mucosal sloughing

Allergic Contact Stomatitis

caused by tooth paste (Colagate Total)

white area‐like a film peeling out slowly

Wipeable

could be confused with candidasis

2010
Q

Exfoliative cheilitis

causes

A

Medications, lipsticks,
sunscreens, toothpaste
floss, cosmetics

2011
Q

What is this clinical finding?

A

Erythema
Multiforme

Acute, vesiculobullous, ulcerative
mucocutaneous disorder

Immunologically mediated

Target lesions on skin (typical board question)

Healthy young adults in 20‐40’s

2013
Q

Erythema
Multiforme

Triggers

A

❖ 50% of cases precipitating cause is identified

  • Infectious Agents: Herpes simplex virus, Mycoplasma pneumonia, Adenovirus, Enterovirus, Coccidiomycosis
    • Most of the time, erythema multiforme is related to a previous infection with herpes simplex virus.
  • Drugs: Penicillin, Cephalosporins, Sulphonamides, NSAID’s, Phenytoin
  • Other: Foods (Benzoates, Nitrobenzene), Chemicals (Perfumes)

❖ it’s not an infection, it’s our body reacting to the infectious
organism or pieces of it in a wrong way

2014
Q

What is this histological finding?

A

Sarcoidosis

discrete clear
granulomas.

2nd

schaumann body in a giant cell (3rd to the right)

Asteroid bodies ( right)

2015
Q

What is this clinical finding?

A

Erythema Multiforme

Focal hemorrhagic crusting of
the lips is seen in conjunction with diffuse shallow ulcerations and
erosions involving this patient’s mandibular labial mucosa

2016
Q

What is this clinical finding?

A

Erythema multiforme

The concentric erythematous
pattern of the cutaneous lesions on the fingers resembles a target or
bull’s-eye.

2017
Q

What is this clinical finding?

A

Sarcoidosis

large red nodule on the lower lip.

2018
Q

What is this clinical finding?

A

Urticaria

developed after bites from an imported fire ant.

2019
Q

What is this clinical finding?

A

Erythema multiforme

multiple erosions on the lips and tongue.

2020
Q

What is this clinical finding?

A

(Granulomatosis with polyangiitis)

formerly Wegener Granulomatosis.

Hyperplastic and hemorrhagic
mucosa of the facial mandibular gingiva on the left side. ((strawberry gingivitis).

2028
Q

Orofacial
Granulomatosis

Etiology

A

❖ Idiopathic

❖ Abnormal immune reaction

❖ in orofacial granulomatosis, people form granulomas and it’s
idiopathic

❖ we don’t know why they’re forming them so that’s an abnormal
immune reaction.

2046
Q

Sarcoidosis
Treatment

A

Depends on the case!

❖ 60% of cases resolve within 2 years
❖ Initial diagnosis 3‐12 mo. observationàactive intervention as needed
❖ First line tx: corticosteroids
❖ Refractory dx:

  • Cytotoxic drugs (methotrexate, azithioprne)
  • TNF blockers
  • Hydroxychloroquine

❖ 4‐10% die of pulmonary, cardiac or CNS complications

2047
Q

Sarcoidosis
Etiology

A

❖ Granulomatous disorder
❖ Multisystem
❖ Unknown cause

2050
Q

Granulomatosis with
Polyangiitis

Etiology

A

First line: oral prednisone
❖ After remission immunosuppressive drugs:
❖ Methotrexate
❖ Cyclosporine
❖ Rituximab
❖ Treatment induces prolonged remission
❖ May have relapses

2051
Q

Urticaria

DDX

A
  • erythema multiforme
  • morbilliform drug eruption
2052
Q

Cinnamon Contact
Stomatitis

DDx

A
  • Oral hairy leukoplakia
  • hyperplastic candidiasis
2053
Q

What are List of
Agents that causes Allergic Contact
Stomatitis

A

❖ Foods
❖ Food additives
❖ Chewing gums
❖ Candies
❖ Dentifrices
❖ Mouthwashes
❖ Gloves
❖ Rubber dam material
❖ Topical anaesthetics
❖ Restorative metals
❖ Acrylic denture materials
❖ Dental impression materials
❖ Denture adhesive
preparations
❖ Cinnamon (mainly artificial flavoring)

2055
Q

Allergic Contact
Stomatitis

Treatment

A
  • *❖ Remove the suspected antigen**
  • *❖** Severe cases‐Antihistamine (combined with a topical anaesthetic) ( because it’s an allergy)
  • *❖** Chronic cases‐Apply topical corticosteroid

❖ Recommendations to AVOID:

  • ❖ Mouthwash
  • ❖ Gum/mints
  • ❖ Cinnamon
  • ❖ Excessive salty, spicy, acidic

❖ Patch testing (we send them to allergist )

2058
Q

Erythema
Multiforme

Treatment

A

❖Self‐limiting, resolves in a few weeks (It will go away on its own, you just have to manage symptomatically.)

❖Symptomatic management, IV rehydration, corticosteroids (topical and oral), antivirals in recurrent cases (We may use antivirals if they tell us they get cold sores every now and then this means they do have a history of herpes simplex.)

❖ Avoid causative drug (If drug‐related)

❖ Other second‐line systemic therapies (like cyclosporin,
azathioprine and other serious drugs)

❖ Usually not life threatening unless in major form.

2059
Q

Nicotine inhaler

Precautions/Contraindications

A

Reactive Airway Disease

2060
Q

Nictotine Nasal Spray

Precautions

A

Reactive Ariway diseases

Not recomended for pts with Chronic Nasal diseases ( nasal polyps & sinusitis)

2061
Q

Sustrained Release Buprooion

Contraindications

A
  • Seizure disorders
  • Current use of bullrin or MAO inhibitor
  • Eating disorder (bulimia, anorexia)
  • Alcohol
  • Head trauma

Moniter Blood presssure

2062
Q

Varenicline Tartlrate

Precaustions

A
  • women breasfeeding should avoid
  • pt with kidney problems -adjust dose
2063
Q

Nictoine Patch

Precutions

A
  • Caution with 6 months of MI
2064
Q

Nictotine Gum

Precuations

A
  • poor dentition
  • maybe inappropriate for use for pts with compelete or partial denture (hard for them to chew)
2065
Q

Nictotine Lozenge

Precautions

A
  • Xerostomia
2066
Q

Is Treating Tobacco is within the
Scope of Practice of dentists?

A

Yes

•New York State Education Department has deemed that treating tobacco use is part of the scope of practice for dentistry, this includes prescribing smoking cessation products.

2067
Q

First Line Pharmacotherapy

in combatting smoking?

A
  • Combination long- and-short acting Nicotine Replacement Therapy (NRT) (e.g., patch and gum, patch and inhaler)
  • Varenicline alone
  • Bupropion SR with NRT (long- or short-acting)
2068
Q
  • What is NRT at the POC?
  • Rationale for NRT at the POC
  • Who will hand the patient NRT?
  • What kind of NRT will be on stock?
  • How to distribute NRT at POC?
A

•What is NRT at the POC?

–Distribution of a free starter pack of NRT to all smokers by clinic staff during the clinic visit

•Rationale for NRT at the POC

–NRT doubles the success rate of patients’ quit attempts

–Inconvenience of purchasing RNT or filling a prescription creates barriers

–The clinic is an opportune time to intervene

•Who will hand the patient NRT?

–Dental Students

•What kind of NRT will be on stock?

•Nicotine Patch, Gum, and Lozenge

•How to distribute NRT at POC?

–Take faculty-approved NRT request form to dispensary, where NRT is stored.

2069
Q

What is the The most effective treatment for
smoking cessation

A

a combination
of pharmacotherapy and counseling

2070
Q

TREATING TOBACCO DEPENDENCE:
A 2-PART PROBLEM

A
2071
Q

Why is it so hard to quit: Nicotine addiction?

A
2072
Q

What are the symptoms of Nicotine Withdrawal?

A

■Irritability/frustration/anger

■Anxiety

■Difficulty concentrating

■Restlessness/impatience

■Depressed mood/depression

■Insomnia

■Impaired performance

■Increased appetite/weight gain

■Cravings

2073
Q

WHAT WORKS (5A’s)

A
  • Ask about tobacco use and secondhand smoke exposure
  • Advise to quit
  • Assess interest in quitting
  • Assist in quit attempt (referral and or pharmacotherapy)
  • Arrange for a follow-up
2074
Q

Assist-Prescribe FDA-Approved Medications

A

Oral Pathology (23 decks)

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