Images, etiologies, and treatments of most diseases Flashcards

1
Q

What is this radiographic finding?

A

Periapical Cysts

►Would need to test both teeth for vitality.

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2
Q

What is the most common cyst of the jaw?

A

Periapical Cysts

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3
Q

radicular cyst, inflammatory cyst are other names for

A

Periapical Cysts

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4
Q

What is this radiographic finding?

A

Periapical Cyst

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5
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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6
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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7
Q

What is this and what is it associated with?

A

keratin pearl – can be associated w/SCC

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8
Q

What are these radiographic findings?

A

Residual Cysts

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9
Q

What is the radiographic finding?

A

Residual Cyst

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10
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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11
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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12
Q

What is the radiographic finding?

A

Paradental Cyst

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13
Q

What is the radiographic finding?

A

Paradental Cyst

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14
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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15
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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16
Q

What is the radiographic finding?

A

Buccal Bifurcation Cyst

as seen in occlusal radiographs

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17
Q

What is the radiographic finding?

A

Buccal Bifurcation Cyst

as seen in occlusal radiographs

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18
Q

Paradental Cyst

Treatment

A

Extraction of the tooth along with the lesion

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19
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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20
Q

Buccal Bifurcation Cyst

Etiology

A

unclear

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21
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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22
Q

dentigerous cyst or
follicle ?

A

_dentigerous cys_t
b/c *attachment at CEJ

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23
Q

What is the radiographic finding?

A

Dentigerous Cyst

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24
Q

What are these radiographic findings?

A

dentigerous cyst

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25
Q

What are these radiographic findings?

A

dentigerous cyst

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26
Q

What is the radiographic finding?

A

dentigerous cyst

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27
Q

What is this gross finding?

A

Grossly image of

Dentigerous Cyst

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28
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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29
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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30
Q

Dentigerous Cyst
also known as ?

A

Follicular Cyst

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31
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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32
Q

What is the clinical finding?

A

Eruption Cyst

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33
Q

What is the clinical finding?

A

Eruption Cyst

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34
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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35
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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36
Q

What is the clinical finding?

A

Cysts of the Newborn:
Palatal cysts

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37
Q
A

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

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38
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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39
Q

What is the clinical finding?

A

Gingival Cyst of the
Adult

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40
Q

What is the clinical finding?

A

Gingival Cyst of the
Adult

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41
Q

What is the clinical finding?

A

Gingival Cyst of the
Adult

notice the bluish hue

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42
Q

Eruption Cyst

Treatment

A
  • Unless symptomatic, no treatment required, cysts resolve upon eruption of teeth
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43
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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44
Q

What is the radiographical finding?

A

Lateral Periodontal
Cyst

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45
Q

What is the radiographical finding?

A

Lateral Periodontal
Cyst

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46
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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47
Q

What is the histological finding?

A

Lateral Periodontal Cyst

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48
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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49
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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50
Q

What is the radiographical finding?

A

Botryoid Odontogenic
Cyst

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51
Q

Gingival cyst of the newborn

Treatment

A

▪ No treatment is necessary

▪ Spontaneously resolve (degenerate or rupture)

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52
Q

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

A

Gingival Cyst of the Adult

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53
Q

What is the radiographical finding?

A

“Primordial” Cyst

Assuming histologically it is different from OKC

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54
Q

Gingival Cyst of the
Adult

has similar histology to which cyst?

A

lateral periodontal cyst

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55
Q

Gingival Cyst of the
Adult

Treatment

A
  • simple surgical excision
  • Unlikely to recur/come back
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56
Q

Lateral Periodontal Cyst represents the intrabony counterpart of which cyst?

A

gingival cyst of the adult?

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57
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 alivelateral periodontal cyst or Lateral Okc ( if huge lesion)

‐ If pulp dead► lateral radicular cyst

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58
Q

What is the radiographical finding?

A

Odontogenic
Keratocyst
OKC

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59
Q

What is the radiographical finding?

A

Odontogenic
Keratocyst
OKC

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60
Q

What is the radiographical finding?

A

Odontogenic
Keratocyst
OKC

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61
Q

What is the radiographical finding?

A

Odontogenic
Keratocyst
OKC

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62
Q

What is the radiographical finding?

A

similar to
lateral
periodontal cyst

but is actually
OKC

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63
Q

What is the histological finding?

A

Odontogenic
Keratocyst

Histology

Notice the daughter cysts

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64
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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65
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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66
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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67
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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68
Q

Lateral Periodontal
Cyst

Treatment

A
  • consists of conservative enucleation
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69
Q

What cyst is a variant of lateral periodontal cyst?

A

Botryoid Odontogenic
Cyst

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70
Q

Botryoid Odontogenic
Cyst

Grossly and Microscopically

A

shows a grape‐like cluster of small
individual cysts

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71
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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72
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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73
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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74
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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75
Q

What is this histological finding?

A

Odontogenic
Keratocyst
OKC

Diagnosis of OKC is based on the characteristic histologic (not
radiographic) findings

Fibrous connective tissue (FCT) containing a pathologic space
lined by stratified squamous epithelium which is 6 to 8 cells in
thickness

Epithelium lining is thin, friable and easily detached from the
FCT, often see lining separated from FCT on histologic section
(thought to be a reason OKCs have a higher risk of recurrence
versus other odontogenic cysts,

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76
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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77
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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78
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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79
Q

What is this histological finding?

A

Odontogenic
Keratocyst
OKC

10-25% of cases show satellite or “daughter” cysts in
the connective tissue wall (thought to be another reason
the recurrence rate is so high for OKCs)

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80
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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81
Q

Which cyst is assoicated with

Nevoid Basal Cell Carcinoma
Syndrome

?

A

Odontogenic Keratocyst
“OKC”

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82
Q

What is this histological finding?

A

Odontogenic
Keratocyst
OKC

stratified squamous epithelium which is 6 to 8 cells in
thickness

Keratin is noted in the cyst lumen (grossly appears as a
cream colored “cheesy” paste-like substance)

Epithelium lining is thin, friable and easily detached from the
FCT,

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83
Q

Nevoid Basal Cell Carcinoma
Syndrome

(Gorlin syndrome)

_modes of inheritanc_e

A

Autosomal dominant inheritance

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84
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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85
Q

Nevoid Basal Cell Carcinoma
Syndrome

Prognosis

A

■ Prognosis depends on progression of skin tumors

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86
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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87
Q

What is the Most common type of skin cancer?

A

Basal Cell Carcinoma
(BCC)

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88
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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89
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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90
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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91
Q

What is this histological finding?

A

Calcifying Odontogenic Cyst COC

 Masses of ghosts cells may fuse to form sheets of eosinophilic, amorphous, acellular material within the epithelium
 Calcification within the ghost cells is common and is why radiopacity is seen in radiographs
 if calcifications have not yet formed, lesion will appear radiolucent, not mixed radiolucent/radiopaque
 Areas of FCT adjacent to the epithelium may also show deposition of an eosinophilic material thought to be some sort of odontogenic matrix material (“dentinoid”) formed as a result of the epithelium’s inductive effects
on the adjacent mesenchymal tissue

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92
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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93
Q

Nasolabial Cyst

Treatment

A
  • Surgical Excision via intraoral approach,
  • usually do not recur ~ very low risk of occurrence
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94
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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95
Q

What is this clinical finding?

A

Nasolabial Cyst

the lesion raising the edge of the nose slightly

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96
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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97
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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98
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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99
Q

Most common non-odontogenic cyst of the oral cavity

A

Nasopalatine Duct Cyst

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100
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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101
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

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102
Q

Nasopalatine Duct Cyst

Treatment

A

✎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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103
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

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104
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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105
Q

What is this radiographic finding?

A

Median Palatine Cyst

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106
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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107
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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108
Q

Nasopalatine Duct Cyst

Treatment

A
  • surgical excision
  • recurrence is rare
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109
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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110
Q

Surgical Ciliated
Cyst of the Maxilla

Etiology

A

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

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111
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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112
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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113
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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114
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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115
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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116
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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117
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
appearance
where it would come up tothe edge of
the sinus

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118
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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119
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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120
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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121
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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122
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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123
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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124
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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125
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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126
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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127
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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128
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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129
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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130
Q

Stafne Bone Cyst

Etiology

A
  • Believed to be developmental in origin, but usually noted only in _adults_
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131
Q

Stafne Bone Cyst

Treatment

A
  • lesions in the posterior MD are usually pathognomonic
  • no further treatment is necessary
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132
Q

Dermoid Cyst

Treatment

A
  • surgical excision
  • recurrence is rare
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133
Q
A

Dermoid Cyst

a dome shaped
swelling
in the floor of the
mouth.

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

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134
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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135
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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136
Q

Epidermoid Cyst

Etiology

A
  • Often occur after _inflammation of a hair follicl_e
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137
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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138
Q

Epidermoid Cyst

Treatment

A

■ Treatment is excision

Recurrence is rare

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139
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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140
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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141
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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142
Q

What is the most common

developmental cyst of the neck?

A

Thyroglossal Duct Cyst

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143
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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144
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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145
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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146
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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147
Q

Branchial Cleft Cyst

Treatment

A

surgical excision, recurrence is rare

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148
Q

Oral Lymphoepithelial Cyst

Treatment

A
  • Surgical Excision
  • Reccurance is Rare
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149
Q

What is the spectrum of benign and malignant lesions

A
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150
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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151
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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152
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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153
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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154
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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155
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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156
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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157
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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158
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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159
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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160
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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161
Q
A

Peripheral
Ameloblastoma

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162
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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163
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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164
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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165
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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166
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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167
Q
A

Calcifying Epithelial Odontogenic Tumor(CEOT)

  • well‐circumscribed radiolucency with calcifications in lower anteriors
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168
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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169
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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170
Q

What is this clinical finding?

A

Adenomatoid odontogenic tumor

(AOT)

Swelling in maxillary vestibule

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171
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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172
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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173
Q

What is this radiographic finding?

A

Adenomatoid odontogenic tumor

(AOT)

Snowflake‐like calcifications within mixed, well‐circumscribed radiolucency

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174
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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175
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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176
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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177
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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178
Q

What is this radiographic finding?

A

Central odontogenic fibroma (COF)

  • well‐circumscribed radiolucency posterior to molar
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179
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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180
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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181
Q

What is this radiographic finding?

A

Odontogenic Myxoma

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182
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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183
Q

Adenomatoid odontogenic tumor

(AOT)

Treatment

A
  • Treatment is usually enucleation
  • recurrence is rare
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184
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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185
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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186
Q

Squamous Odontogenic Tumor

(SOT)

Treatment

A
  • Treatment is conservative local excision
  • Recurrence is rare
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187
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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188
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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189
Q

What is this radiographic finding?

A

Compound Odontoma

little teeth‐like structures blocking canine eruption

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190
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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191
Q

Case

A

Primordial
Odontogenic Tumor
(POT)

unilocular radiolucency

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192
Q

What is this radiographic finding?

A

Ameloblastic Fibroma
(AF)

1‐3 potential locules, no impacted tooth associated

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193
Q

Central odontogenic fibroma

(COF)

Treatment

A
  • Enucleation with curettage or excision
  • usually don’t recur
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194
Q

What is this radiographic finding?

A

Ameloblastic Fibro-odontoma (AFO)

  • well‐circumscribed radiolucency
  • corticated edge + calcification
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195
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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196
Q

What is this radiographic finding?

A

Ameloblastic Fibrosarcoma

in the mandible developed after two years from AF

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197
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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198
Q

What is this histological finding?

A

Odontogenic Myxoma

▪ Mimics the histology of dental pulp
Stellate, spindle, and round shaped cells set in a loose myxoid to
lightly collagenized stroma (if abundant mature collagen ‐
fibromyxoma)
▪ Abundant ground substance (mucopolysaccharide extracellular
matrix or GAGs)
Can see residual bone trabeculae and scattered rests of odontogenic
epithelium

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199
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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200
Q

Odontoma

Treatment

A

Simple excision or enucleation
Unlikely to recur

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201
Q

Primordial
Odontogenic Tumor
(POT)

Treatment

A
  • conservative excision/enucleation
  • So far no recurrence
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202
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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203
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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204
Q

What is this radiographic finding?

A

Chondrosarcoma

  • its consistent widening as opposed to seen in periodontitis and inflammatory disease
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205
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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206
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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207
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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208
Q

What is this clinical finding?

A

Osteosarcoma

▪ Swelling on left side of face
▪ Difficult opening

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209
Q

What is this clinical finding?

A

Osteosarcoma

  • See something in the operculum
  • Infection in third molar?
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210
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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211
Q

What is this radiographic finding?

A

Osteosarcoma

  • Classic sunburst pattern
  • Fuzzy appearance on outer edges of cortex
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212
Q

What is this radiographic finding?

A

Osteosarcoma

  • cloudy bone formation on surface of cortex on facial and lingual aspect
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213
Q

What is this clinical finding?

A

Osteosarcoma

a patient with swelling with side of face

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214
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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215
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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216
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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217
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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218
Q

What is this clinical finding?

A

Langerhans Cell
Disease

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

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219
Q

What is this clinical finding?

A

Langerhans Cell
Disease

we see lesions on maxilla

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220
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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221
Q

What are these clinical findings?

A

Langerhans Cell Disease

Torus and molar involvement

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222
Q

What is this clinical finding?

A

Eosinophilic
Granulations

Erythematous area

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223
Q

What is this radiographic finding?

A

▪ Child with disseminated form of Langerhans cell histiocytosis
Punched out radiolucency in the skull

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224
Q

What is this clinical finding?

A

▪ Child with bone loss surround the teeth
▪ Floating teeth

disseminated form

Langerhans cell histiocytosis

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225
Q

What is this radiographic finding?

A

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

disseminated form

Langerhans cell histiocytosis

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226
Q

What is this radiographic finding?

A

Eosinophilic granuloma

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227
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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228
Q

What is this radiographical finding?

A
  • Punched out radiolucency
  • Lytic radiolucency without cortication

MM

Multiple Myeloma

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229
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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230
Q

What is this radiographical finding?

A

Multiple Myeloma

▪ Radiolucency without sclerotic border

▪ Multiple and separated

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231
Q

What is this clinical finding

A

Swelling of gingiva

▪ Plasmacytoma

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232
Q

What is this gross finding?

A

Ewing Sarcoma

▪ Long bone

▪ Large expansion

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233
Q

What is this radiographical finding?

A

Ewing Sarcoma

  • an _expansion of tissu_e
  • Dissolution of bone in that area
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234
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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235
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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236
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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237
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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238
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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239
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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240
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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241
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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242
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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243
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 controloral ulcerations resolve
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244
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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245
Q

Which systemic disease has this oral manifestation?

A
  • we see the ulceration and hyperplastic tissue surrounding it.
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246
Q

Which systemic disease has this oral manifestation?

A

Crohn Disease

Nodular appearance of buccal mucosa

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247
Q

Which systemic disease has this oral manifestation?

A

Crohn Disease

we see more nodules

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248
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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249
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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250
Q

Oral Manifestations of which systemic disease?

A

Pyostomatitis
Vegetans

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251
Q

Oral Manifestations of which systemic disease?

A

Pyostomatitis
vegetans

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252
Q

Oral Manifestations of which systemic disease?

A

Pyostomatitis
vegetans

Snail track
appearance

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253
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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254
Q

Oral manifestation of which Systemic Disease?

A

Amyloidosis

Nodular “waxy” depositions in skin

deposition on the eyelid

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255
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

orange, red, yellow tinge

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256
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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257
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

macroglossia

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258
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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259
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

Submucosal amyloid deposit

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260
Q

Which systemic disease has this oral manifestation?

A

Amyloidosis

Amyloid deposition with ulceration and petechiae

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261
Q

Which systemic disease has these oral manifestations?

A

Amyloidosis

▪ different color compared to normal tongue with amyloid

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262
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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263
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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264
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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265
Q

Diabetes Mellitus

Type I

Definition

Demographics

Etiology

A

Definition

insulin‐dependent diabetes mellitus (IDDM)

Demographics

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

Etiology

Autoimmune disease

Thought to be possible viral infection as trigger to Islet cell antibody destruction of beta cells

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266
Q

Diabetes Mellitus

Type II

Definition

Demographics

Etiology

A

Definition

  • non‐insulin‐dependent diabetes mellitus (NIDDM)

Demographics

About 90% of cases

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

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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267
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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268
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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269
Q

Diabetes Mellitus, Oral Findings, are mostly found with what type and what are the?

A

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

  • 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 Caries
  • Benign migratory glossitis

Increased prevalence in type I

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270
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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271
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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272
Q

Oral Manifestation of which systemic disease ?

A

Hyperplastic gingiva (Gingival Hyperplasia)

Manifestation of different systemic disease such as

diabetes

  • Crohn’s disease*
  • anemia*
  • lymphoma*
  • vitamin deficiencies*
  • HIV*

It is also caused by inflammation. It can also be drug-induced, as a side effect of prescribed medications. Common medications that can cause this overgrowth include:

  • antiseizure drugs
  • immunosuppressants
  • calcium channel blockers
  • drugs used to treat high blood pressure and other heart-related conditions
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273
Q

Oral Manifestation of which systemic disease ?

A

Hyperplastic gingiva (Gingival Hyperplasia)

Manifestation of different systemic disease such as

diabetes

  • Crohn’s disease*
  • anemia*
  • lymphoma*
  • vitamin deficiencies*
  • HIV*
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274
Q

Oral Manifestation of which systemic disease ?

A

Diabetes Mellitus

Sialadenosis

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275
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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276
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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277
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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278
Q

Which systemic disease has this oral manifestation?

A

Hyperthyroidism

  • enlargement of the neck
  • characteristic stare
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279
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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280
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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281
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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282
Q

Which systemic disease has this oral manifestation?

A

Hypothyroidism

Macroglossia and crenation (scalloping)

of the lateral tongue

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283
Q

Before and after tx of which systemic disease?

A

hypothyroidism

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284
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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285
Q

An Oral Manifestaion of which systemic disease?

A

Hyperparathyroidism

in young children

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286
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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287
Q

Which systemic disease has this oral manifestation?

A

Pseudohypoparathyroidism

pulp chambers are very
elongated

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288
Q

Which systemic disease has this oral manifestation?

A

Pseudohypoparathyroidism

issues with eruption, no
pulp stones present

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289
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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290
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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291
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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292
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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293
Q

Hyperparathyroidism

Treatment

A

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

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294
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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295
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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296
Q

Pseudohypoparathyroidism

Management

A
  • Vitamin D and calcium supplements
  • Serum and urinary calcium are monitored
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297
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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298
Q

Acromegaly

Etiology

A

Etiology

▪ Usually due to a pituitary adenoma

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299
Q

Which systemic disease has these clinical manifestations?

A

Acromegaly

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300
Q

Which systemic disease manfiest like this?

A

Addison’s Disease

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301
Q

Which systemic disease manfiest like this?

A

Addison’s Disease

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302
Q

Which systemic disease is associated with this symptom?

A

Pellagra

Deficience in Vitamine B3 (Niacin)

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303
Q
A

Pellagra

Deficience in Vitamine B3 (Niacin)

Dermititis of the skin

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304
Q

Which systemic disease manifests like this?

A

Pellagra

Deficience in Vitamine B3 (Niacin)

erythema of the tongue

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305
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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306
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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307
Q

Which systemic diseaswe associated with these oral manifestations?

A

PLUMMER‐VINSON
SYNDROME

denuded tongue
and angular chelitis

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308
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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309
Q

Vitamin C

Deficiency

Known as

A

scurvy

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310
Q

Iron Deficiency
Anemia

Treatment

A

Treated with iron supplements, extreme cases with blood infusions

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311
Q

Which systemic disease manifests like this?

A

Pernicious Anemia

glossitis, denuded papillae

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312
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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313
Q

Which systemic disease has this oral manifestation?

A

Uremic Stomatitis

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314
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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315
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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316
Q

Which systemic disease has these oral manifestations?

A

Reiter’s Syndrome (Reactive arthritis)

This not actually a geogrpahic tongue!

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317
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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318
Q

Which systemic disease has these clinical manifestations

A

Infective Endocardiatios

Janeway lesions

These are Septic Emboli

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319
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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320
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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321
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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322
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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323
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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324
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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325
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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326
Q

Pernicious Anemia

Treatment

A
  • monthly IM injections of cyanocobalamin
  • cannot take ​B12 orally, you need injections
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327
Q

Pernicious Anemia

CLASSIC TRIAD

A

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

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328
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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329
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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330
Q

Reiter’s Syndrome (Reactive Arthritis)

Etiology

A

Etiology

  • Thought to be due to an abnormal immune response to the infection
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331
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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332
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.
How well did you know this?
1
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2
3
4
5
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333
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
4
5
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334
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)

How well did you know this?
1
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2
3
4
5
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335
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.

How well did you know this?
1
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2
3
4
5
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336
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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337
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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1
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2
3
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338
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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339
Q

Ranula

Definition

Associated with

Clinical features

Treatment

A

Definition: mucocele-like lesion that forms unilaterally on the floor of the mouth

associated with: the ducts of the sublingual & submandibular glands
• clinical features:

• treatment: surgical excision

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340
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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341
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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342
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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343
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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344
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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345
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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346
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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347
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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348
Q

Which systemic disease manifests radiographically like this?

A

Hypophosphatasia

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349
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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350
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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351
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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352
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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353
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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354
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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355
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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356
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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357
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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358
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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359
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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360
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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361
Q

What is this clinical finding?

A

Palatine Torus/Torus Palatinus

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362
Q

What is this clinical finding?

A

Palatine Torus/Torus Palatinus

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363
Q

What is this clinical finding?

A

Mandibular Torus:
Torus Mandibularis

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364
Q

What is this clinical finding?

A

Mandibular Torus:
Torus Mandibularis

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365
Q

What is this clinical finding?

A

Buccal Exostoses

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366
Q

What is this clinical finding?

A

Unencapsulated Lymphoid Aggregates

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367
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.

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368
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.

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369
Q

What is this clinical finding?

A

Fordyce Granules

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370
Q

What is this clinical finding?

A

Fordyce Granules

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371
Q

What is this clinical finding?

A

Fimbriated
fold/Plica
semiluminaris

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372
Q

What is this clinical finding?

A

Frenal tag

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373
Q

What is this clinical finding?

A

Sublingual Varices

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374
Q

What is this clinical finding?

A

Sublingual Varices

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375
Q

What is this clinical finding?

A

Sublingual Varices

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376
Q

What is this clinical finding?

A

Circumvallate papillae

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377
Q

What is this clinical finding?

A

Parotid Papillia (Stenson duct)

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378
Q

What is this clinical finding?

A

Parotid Papillia (Stenson duct)

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379
Q

What is this clinical finding?

A

Linea Alba

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380
Q

What is this clinical finding?

A

Leukoedema

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381
Q

What is this clinical finding?

A

Palatal Rugae

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382
Q

Irritation Fibromas

Etiology

Location

Treatment

A
  • AKA – Fibroma, Traumatic Fibroma
  • Occurs as a result of chronic trauma
  • Locations: buccal mucosa, tongue, lips, gingiva
  • 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
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383
Q

What is this clinical finding?

A

Irritation Fibromas

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384
Q

What is this clinical finding?

A

Irritation Fibromas

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385
Q

What is this clinical finding?

A

Chronic Hyperplastic Pulpitis (pulp polyp)

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386
Q
A

Giant Cell Fibroma

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387
Q

Chronic Hyperplastic Pulpitis

What is it?

Treatment?

A
  • AKA: pulp polyp
  • An e_xcessive proliferation of chronically inflamed dental pulp tissue_

Treatment: RCT or extraction of tooth

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388
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

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389
Q

What is this clinical finding?

A

Epulis Fissuratum

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390
Q

What is this clinical finding?

A

Inflammatory Papillary Hyperplasia of the Palate

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391
Q

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

A

Cowden Syndrome

Very rare!

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392
Q

Epulis Fissuratum

AKA

Cause

Treatment

A
  • AKA: denture-induced fibrous hyperplasia, fibrous inflammatory
  • Cause: ill-fitting denture

Treatment: surgical excision (scalpel vs CO2 laser -laser is better)
and reline then remake of denture

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393
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

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394
Q

What is this clinical finding?

A

Pyogenic Granuloma:

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395
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

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396
Q

Inflammatory Papillary Hyperplasia of the Palate

Majority occur with what disease?

Associated with what?

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)
  • Treatment:Treat underlying candidiasis, fix denture. These bumps can be removed, take electrosurgery loop, and scrape off the bumps – heals well
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397
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

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398
Q

What is this clinical finding?

A

Peripheral Giant Cell Granuloma

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399
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

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400
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
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401
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

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402
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
  • Location:
    • Most common - gingiva
    • Also occurs in other areas of the oral mucosa
  • Treatment: Excision and removal of irritant (eg calculus, overhanging restorations)
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403
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

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404
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
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405
Q

What is this clinical finding?

A

Hereditary Gingivofibromatosis

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406
Q
A

Infantile
Hemangioma

(“strawberry” hemangioma).

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

Neville Cr

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407
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

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408
Q

What is this clinical finding?

A

Capillary
Malformation (Low
flow)

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409
Q

What is this clinical finding?

A

Venous
malformation (low
flow)

Many pts can live with this without treatment

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410
Q

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

A

_Osler-Weber-Rendu
Syndrome
_

Hereditary hemorrhagic telangiectasia (HHT)

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411
Q

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

A

Sturge-Weber
Angiomatosis

Sturge-Weber syndrome

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412
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

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413
Q

What is this clinical finding?

A

Lymphangioma

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414
Q

What is this clinical finding?

A

Cystic Hygroma

a type of Lymphangioma

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415
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
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416
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

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417
Q

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

A

Multiple Endocrine
Neoplasia (MEN)
Syndrome

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418
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

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419
Q

What is this clinical finding?

A

neurofibroma

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420
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)
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421
Q

What is the clinical finding?

A

Schwannoma/ Neurilemoma

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422
Q

What is this clinical finding?

A

Schwannoma/ Neurilemoma

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423
Q

What is this clinical finding?

A

Granular Cell Tumor

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424
Q

What is this clinical finding?

A

Granular Cell Tumor

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425
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)

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426
Q

What is this clinical finding?

A

Congenital Epulis

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427
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

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428
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.

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429
Q

Lipoma

What is it?

Histologically?

Treatment?

A
  • What is it: Benign tumor of mature fat cells; Relatively rare
  • Histologically: a well-delineated tumor composed of mature fat cells with a thin capsule
  • Treatment: surgical excision,does not recur
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430
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

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431
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
  • 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
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432
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).

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433
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?

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434
Q

What is this clinical finding?

A

Leiomyosarcoma

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435
Q

Hereditary Gingivofibromatosis

What causes it?

How common?

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

Treatment

  • Need surgical (usually laser) treatment – just grows back, so have to get it done periodically
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436
Q

What are these clinical findings?

A

Rhabdomyosarcoma

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

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437
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,
  • Treatment: Typically will involute with time, Some cases don’t involute, so need to be removed
  • It is a vascular Anomaly
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438
Q

What is this clinical finding?

A

Fibrosarcoma

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439
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^

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440
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
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441
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
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442
Q
A

Acute myelogenous
leukemia
with
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
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443
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
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444
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

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445
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

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446
Q

Osler-Weber-Rendu
Syndrome

AKA

What is it ?

Type of Herditary and Etiology

What can it cause?

A

AKA

Hereditary Hemorrhagic Telangiectasia

What is it ?

disorder of development of the vasculature characterized by telangiectases and arteriovenous malformations in specific locations.

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

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447
Q

Lymphangioma

What is it?

Treatment

A

What is it?

• Benign tumor of lymphatic vessels

Treatment:

monitor, surgery if needed, recurrence common

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448
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

Increase risk of which cancer?

Increased risk for medullary thyroid cancer (prophylactic thyroidectomy)

Common board questions

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449
Q

Neurofibroma

What is it?

Treatment?

Mailgnancy?

A

What is it?

  • A benign tumor arising from peripheral nerve tissue

Treatment: surgical excision

Malignant transformation reported, but rare

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450
Q

Schwannoma/ Neurilemoma

What is it?

Treatment?

malignant
transformation ?

A

What is it?

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

• Treatment

• surgical excision

malignant
transformation

reported, but rare

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451
Q

Granular Cell Tumor

What is it?

Treatment?

A

What is it?

Benign tumor derived from
Schwann cells

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

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452
Q

Congenital Epulis

AKA

Cell resemble?

Cell origin?

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

• Treatment:Surgical excision, does not recur

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453
Q

Neuroectodermal tumor of infancy

Rate of development?

Treatment?

Origin?

A

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

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454
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%

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455
Q

Kaposi Sarcoma

Etiology

Types

Treatment

A

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

Treatment

  • Surgical excision, radiation therapy or systemic chemotherapy for multiple nonoral lesions, if it gets large, dose-radiation therapy!
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456
Q

What is this clinical finding?

A

PLEOMORPHIC ADENOMA

(MIXED TUMOR)

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457
Q

What is this clinical finding?

A

PLEOMORPHIC ADENOMA

Classic presentation: includes swelling in the parotid region

(MIXED TUMOR)

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458
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)

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459
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)

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460
Q

What is this clinical finding?

A

Untreated pleomorphic adenoma

slow growing, but can grow to enormous sizes

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461
Q

What is this clinical finding?

A

Canalicular Adenoma

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462
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.
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463
Q

What is this clinical finding?

A

Basal Cell Adenoma

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464
Q

What is this clinical finding?

A

PAPILLARY
CYSTADENOMA
LYMPHOMATOSUM
(WARTHIN TUMOR)

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465
Q

MUCOEPIDERMOID
CARCINOMA

Can be mistaken for

Histopahtology

A

 Most common malignancy of salivary glands
 Most common malignant SG tumor in children

 Can be mistaken for mucocele

Histopathology: note the cells growing into adjacent tissue, showing infiltration

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466
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

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467
Q

What is this clinical finding?

A

MUCOEPIDERMOID
CARCINOMA

468
Q

What is this clinical finding?

A

MUCOEPIDERMOID
CARCINOMA

Request all for biopsies!

469
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
470
Q

What is the clinical finding?

A

ACINIC CELL
ADENOCARCINOMA

471
Q

What is the clinical finding?

A

ACINIC CELL
ADENOCARCINOMA

blue‐ish tint

472
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.

473
Q

What is this clinical finding?

A

Adenoid Cystic Carcinoma

474
Q

What are these clinical findings?

A

Adenoid Cystic Carcinoma

475
Q

What are these clinical findings?

A

Adenoid Cystic Carcinoma

476
Q

What is this clinical presentation?

A

Polymorphous
Adenocarcinoma

477
Q

What is this clinical presentation?

A

Polymorphous
Adenocarcinoma

478
Q

What is this clinical finding?

A

Carcinoma Ex Pleomorphic
Adenoma

479
Q

PAPILLARY
CYSTADENOMA
LYMPHOMATOSUM
(WARTHIN TUMOR)

Etiology?

Treatment?

A
  • 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 ofsalivary gland elements early in development
  • Strong correlation with cigarette smoking
  • Treatment: surgical excision, responds very well to it
480
Q

MUCOEPIDERMOID
CARCINOMA

Treatment

Prognosis

Therapy by gene?

A

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)

481
Q

Adenoid Cystic Carcinoma

Growth rate

Treatment

Prognosis

A

Growth rate
 Usually a slowly growing mass

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

482
Q

Polymorphous
Adenocarcinoma

growth patterns

Treatment

A
  • 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
483
Q

Carcinoma Ex Pleomorphic
Adenoma

What is it?

Growth pattern

Treatment?

Prognosis

A

What is it? (benign tumors that have underwent malignant transformation‐ takes a lot time, 15 to 20 years)

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

484
Q

What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION

Lower lip

A

o Mucocele
o Mucoepidermoid Ca
o Pleomorphic Adenoma

485
Q

What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION

upper lip

A

o Canalicular Adenoma
o Salivary Duct Cyst*
o Pleomorphic Adenoma

486
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

487
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

488
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

489
Q

Mucocele

Definition

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

• treatment: surgical excision, removal of associated minor salivary glands
• may recur if don’t remove all associated injured minor salivary glands

490
Q

What is this clinical finding?

A

Mucocele

491
Q

What is this clinical finding?

A

Mucous Cyst

492
Q

What is this clinical finding?

A

Ranula

Notice how it’s unilateral

on the floor of the mouth

493
Q

What is this clinical finding?

A

Ranula

  • Notice how it’s unilateral*
  • on the floor of the mouth*
494
Q

Necrotizing Sialometaplasia

Definition

Predisposing factors

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

  • Treatment: no treatment, spontaneously resolves within 6 to 10 weeks
  • irrigating & debriding the area can reintroduce vascularity & help healing
495
Q

What is this clinical finding?

A

Necrotizing Sialometaplasia

496
Q

Sialolithiasis

Definition

Treatment

A

Definition: lith = stone ;; sialolith: a salivary gland stone

Treatment: promote passage of stone (massage, sialogogues, increase fluid intake) or surgical removal

497
Q

What is this clinical finding?

A

Sialolithiasis

498
Q

What is this clinical finding?

A

Sialolithiasis

Notice how it can appear radiographically as a well defined radioluecency

It doesn’t always appear radioapaque!

499
Q

What is this Radiographical finding?

A

Sialolithiasis

500
Q

What are these Radiographical findings?

A

Sialolithiasis

501
Q

What are these Radiographical & clinical findings?

A

Sialolithiasis

A, Minor salivary gland sialolith presenting
as a hard nodule in the upper lip.

B, A soft tissue radiograph of
the same lesion revealed a laminated calcified mass.

502
Q

Mucous Cyst

Definition

Clinical features

Treatment

A
  • Definition: a pseudocyst
  • clinically you CANNOT tell the difference between a mucocele & mucous cyst and histologic features same as mucocele but will see an epithelial linin

treatment: same as mucocele; surgical excision

503
Q

Sialadenitis

definition

causes:

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

• Treatment: antibiotics, rehydration, surgical drainage, or surgical removal of gland

504
Q

What is this clinical finding?

A

Sialadenitis

Acute: parotid papilla purulent discharge

505
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

506
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
507
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

508
Q

What is this clinical finding?

A

‐ Aphthous Ulcer of the tongue

‐ Aphthous ulcers can occur on specialized structures of the mouth

509
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

510
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

511
Q

How do we treat this?

A

‐ Repair sharp teeth/restorations
‐ Remove plaque
‐ Optimize lubrication

Ulcer

512
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

513
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

514
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

515
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

516
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
517
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
518
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
519
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
520
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
521
Q

What is this clinical finding?

A

Sialadenitis

Chronic: caused fibrosis

522
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
523
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

524
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
525
Q

RAS:

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

526
Q

Rx Topical
Treatments:
Corticosteroids

for

Ulcers/RAS

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

527
Q

What about
systemic
treatments – taking
pills to treat ulcers?

(for RAS/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

528
Q

What is the Mode of infection of HHV?

A

Primary infection → Latency → Reactivationn → Recurrent infection

529
Q

After the primary infection the HHV‐1/HSV1 stays in ————

A

Sensory ganglia

530
Q

After the primary infection the HHV‐2/HSV2 stays in ————

A

Sensory ganglia

531
Q

After the primary infection the HHV‐3/VZV stays in ————

A

Sensory ganglia (dorsal root ganglia)

532
Q

After the primary infection the HHV‐4/EBV stays in ————

A

B‐Lymphocytes

533
Q

After the primary infection the HHV‐5/CMV stays in ————

A

Myeloid cells, salivary gland cells, endothelium

534
Q

After the primary infection the HHV‐6 stays in ————

A

CD4+ T‐Lymphocytes

535
Q

After the primary infection the HHV‐7 stays in ————

A

CD4+ T‐Lymphocytes

536
Q

After the primary infection the HHV‐8 stays in ————

A
  • *B‐lymphocytes (latency)**, **endothelial cells (Kaposi
    sarcoma) **
537
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
).

538
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
539
Q

Who’s the typical group that will get primary herpetic gingivostomatitis?

A

 Children and young patients

540
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.

541
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
542
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

543
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.

544
Q

HSV‐ Histopathology

A

❏ Molding
❏ Margination
❏ Multinucleation
❏ Also Tzanck cells

545
Q

What is a
definitive diagnosis for HSV1 Herpes simplex

A

HSV‐ Cytology‐
Papanicolaou Stain
(PAP)

546
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.

547
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)
548
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

549
Q

Reccurent HSV-1 Latency place is ——–

A

trigeminal ganglion

550
Q

What are the Stages of recurrent Hsv-1?

A

Prodrome►papules►vesicles►ulcer►crust►heals►no scar

551
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

552
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

Punctuate ulceration
erythematous border, irregular shape, fixed mucosa, unilateral

553
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

554
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

555
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

Vesicle stage (unilateral)

556
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

crust → later
crust comes off and then
you’ll have
epithelialization
underneath

557
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

papule bc its
raised

558
Q

What is this infectious disease?

describe it

A

Recurrent HSV-1

healing stage cause
you might see this one day

559
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

560
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

561
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

562
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

563
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!**

564
Q

RECURRENT HERPES LABIALIS-RX TOPICAL/SYSTEMIC AGENTS

A

Topical like Acyclovir

or Acylovir + steroid combination

There are many OTC topical medications

565
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.

566
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

567
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)

568
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

569
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

570
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

571
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.

572
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.

573
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
574
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

575
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

576
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.
577
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
578
Q

What is this infectious diasese?

A

EBV mucocutaneous ulceration

Very rare

Photos from google

579
Q

Which disease has Stary sky pattern histopathology?

A

Burkitt
Lymphoma

caused by EBV

580
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.

581
Q

Kaposi sarcoma

Histopathology

A

Histopathology shows malignant endothelial cells proliferating.
There are tiny spaces. Extravasation of RBCs can be seen

582
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.

583
Q

What are HPV types that cause

Genital Benign Lesions?

A

6, 11, 16, 18

(condyloma – can be malignant)

584
Q

What are HPV types that cause

Non‐genital Benign Involving Mucosa?

A

6 & 11

585
Q

What are HPV types that cause

Non‐genital Benign Involving the Skin?

A

2 & 4

586
Q

What are HPV types that cause

Malignant & Potentially Malignant Disorders?

A

16, 18

587
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.
588
Q

HPV Genome
Organization

A

▪ LCR: long control region
▪ P97: promoter protein
▪ E1‐E7: early region genes
▪ L1,L2: late region genes

589
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)

590
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

591
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

592
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

593
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

In 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

594
Q

Most prevelant HPV TYPE?

A

HPV 16 = most prevalent

595
Q

What is the Prevalence of HPV
HIV + ?

A

Ppl w/ HIV+ and low CD4 T‐cells lvl = higher risk of
HPV
HPV 16+ higher if CD4 <200

596
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

597
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

598
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
599
Q

SQUAMOUS PAPILLOMA

What is it?

Treatment?

A

Benign proliferation of stratified squamous
epithelium resulting
► papillary, verruciform, rugose (ridged or wrinkled) mass
HPV types 6 + 11 – Low risk

▪ **should remove from mouth – but WOULD NOT submit for HPV typing

600
Q

What is this infectious diease?

A

SQUAMOUS PAPILLOMA

Benign Oral Low Risk HPV
Lesion

HPV 6+11
“finger‐like projections

601
Q

What is this infectious disease?

A

Oral Verruca Vulgaris
HPV 2,4,6
Also “finger‐like
projections”

remember it’s contagious

602
Q

Oral Verruca Vulgaris

What is it?

Contagious?

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

Soft, painless, usually pedunculated, exophytic lesions w/ numerous fingerlike projections (similar to squamous papilloma)
How to tell the difference? Under microscope

603
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

604
Q

What is this infectious disease?

A

(Multifocal) Epithelial
Hyperplasia/Heck’s
Disease

HPV 13,32
“Flat‐top papules”

605
Q

What is this infectious disease?

A

(Multifocal) Epithelial
Hyperplasia/Heck’s
Disease

HPV 13,32
“Flat‐top papules”

606
Q

Condyloma Acuminatum
(Venereal Wart)

What is it?

Contagious?

Transmission?

Apperance ?

A

HPV Types 6, 11condyloma 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)

▪ Characteristic clustering of multiple lesions

607
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

608
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!

609
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

610
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)

611
Q

Management of Oral HPV
Lesions

Solitary Lesions

A

‐ Usually appear exophytic and papillary
‐ Excision is warranted
‐ Consider possible recurrence

612
Q

Oral Molluscum
Contagiosum

Which viruse causes it?

Who get affected?

Treatment?

A

Poxvirus

▪ Florid cases seen in immunocompromised persons
▪ Children, young adults

Treatment

‐ Kids can have 6‐9mo and will go away

613
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

614
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

615
Q

What is this infectious disease?

A

Measles

*Characterized by Koplik’s spots

salts/grains

616
Q

HPV multiple lesions

Excision/Ablation

A

Excision/Ablation

▪ Scalpel
▪ Carbon dioxide laser – be cautious, don’t know what is burned away
▪ Electrosurgery

617
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.

618
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

619
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.

620
Q

HPV multiple lesions

Topical Therapy

A

▪ Podophyllin resin
▪ Imiquimod (extra‐oral use only)
▪ Cidofovir
▪ Interferon

621
Q

What is this infectious disease?

A

Rubella

caused by

Family: Togavirus; Genus: Rubivirus

Forchheimer sign (left)
Palatal petechiae (right)

(German Measles)

622
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

623
Q

Topical Imiquimod

A

▪ Induces cytokines + chemokines w/ resutlant anti‐virl (HPV) effects

Not FDA approved for oral warts

624
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%

625
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”

626
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

627
Q

Rubella
(German Measles)

Which viruse causes it?

How does it spread?

Clinical signs?

Assosited with what syndrome?

Is there a vaccine?

How it is diagnosed?

A

▪ Family: Togavirus; Genus: Rubivirus

▪ Respiratory droplets

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

628
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

629
Q

Mucosal/Oral infections, which are generally non‐invasive are
caused primarily by ——–

A

Candida albicans

630
Q

Dimorphism

of

Candida

Two forms?

A

SPORES‐ when they are in this form, they do NOT invade
HYPHAE‐ when they begin their invasion

631
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)

632
Q

What is this infectious disease?

A

Onychomycosis

a type of candidiasis

633
Q

What is this infectious disease?

A

Oral candidiasis

a type of candidiasis

634
Q

What is this infectious disease?

A

Esophageal Candidiasis

a type of candidiasis

635
Q

What is this infectious disease?

A

Vulvovaginitis

a type of candidiasis

636
Q

What is this infectious disease?

A

“Diaper Rash”

a type of candidiasis

637
Q

What is this infectious disease?

A

Intertrigo

a type of candidiasis

638
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

639
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

640
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

641
Q

What is this infectious disease?

A

PSEUDOMEMBRANOUS CANDIDIASIS

Severe dry mouth

This is severe disease

we would want to use systemic treatments/
intervention

642
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

643
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

TreatmentNystatin applied to intaglio surface of denture and wear denture and patient to remove denture at night

a subtype of Erythematous
Candidiasis

644
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

645
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

646
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
647
Q

What is this infectious disease?

A

HYPERPLASTIC CANDIDIASIS

648
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

649
Q

What is this infectious disease?

A

Chronic
Mucocutaneous
Candidiasis

Severe infection of mucosal surfaces, nails, and skin

650
Q

What is this infectious disease?

A

Mucocutaneous
Candidiasis

APECED

Autoimmune
Polyendocrinopathy
Candidiasis
Ectodermal
Dystrophy
Syndrome

Biopsy of the tonuge revealed SCC

651
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).

652
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.
653
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

654
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

655
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

656
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

657
Q

Which regions can Blastomycosis happen?

A

Eastern half of US which extends farther north

Seen in the wild

658
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

659
Q

What is this infectious disease?

A

Blastomycosis

660
Q

Chronic
Mucocutaneous
Candidiasis

is

at

increased

risk of what?

A

● Increased risk of squamous cell carcinoma

661
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

662
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

663
Q

What is Chronic Suppressive
Therapy for fungal diseases?

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

664
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

665
Q

What is the Most common systemic fungal infection in US?

A

Histoplasmosis

666
Q

What causes Histoplasmosis?

what is its mode of pathogensis ?

A

● Histoplasma capsulatum

Dimorphic (yeast at body temperature and mold in soil)

667
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)

668
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

669
Q

Blastomycosis

What is it?

What causes it?

What is its mode of pathogenesis?

A

Uncommon fungal infection

Blastomyces dermatitidis

Dimorphic

670
Q

Acute Blastomycosis resembles ———-

A

Acute‐ Resembles pneumonia

671
Q

ChronicBlastomycosis resembles ———-

A

Chronic Resembles tuberculosis

672
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

673
Q

Paracoccidio Mycosis

What is it?

What causes it?

A

A deep fungal infecion

causes by:

Paracoccidioidomycosis brasiliensis

674
Q

Which regions Paracoccidio Mycosis happen?

Another name for it?

A

● Brazil (South America)

● So another name for it is: South American blastomycosis

675
Q

Paracoccidio Mycosis is seen in the soil around ——- (name of an animal)

A

nine‐ringed armadillos

676
Q

Paracoccidio Mycosis presents intially as which infection?

A

Pulmonary infection

677
Q

What is infectious disease?

A

Paracoccidio Mycosis

looks like the three tail in Naruto lol

678
Q

what is this infection disease ?

A

Paracoccidioidomycosis

looks like strawberry gingiva but it is not

679
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)

680
Q

How is Paracoccidioidomycosis treated?

A

Trimethoprim/ sulfamethoxazole (mild‐moderate)

IV Amphotericin B (severe disease)

681
Q

What is Coccidiomycosis?

A

deep fungal infection that present as Pulmonary infection

682
Q

Coccidiomycosis is known as ——-

A

Valley Fever

683
Q

What are the two types of Coccidiomycosis ?

A
  • Coccidioides immitis
  • Coccidioides posadasii
684
Q

What is this infectious disease?

A

Coccidioidomycosis

685
Q

What is the mode of pathogenesis of Coccidiomycosis?

A

Dimorphic organism (spores and hyphae)

686
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)

687
Q

Cryptococcus

How common is it?

What causes it?

A

●Uncommon

● Cryptococcus neoformans

● Incidence increased due to AIDS epidemic in 1990s

● Pulmonary infection

● Meningitis

688
Q

Cryptococcus is seen in ————–

A

pigeon excrement (poo)

689
Q

Cryptococcus can cause what kind of infections?

A

● Pulmonary infection

● Meningitis ( after it spreads from the lungs to the brain. )

690
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

691
Q

▪ The most common cyst of the jaws

A

Periapical Cysts

692
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?

693
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

694
Q

How is Cryptococcus treated?

A

● Mild case: Fluconazole or Itraconazole

● Cryptococcal meningitis: amphotericin B + other antifungals

695
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
696
Q

Which infectious disease has fruting body in its histopathology?

A

Aspergillosis

Histopathology includes:

●Branching septate hyphae

● Acute angle branching

● “Fruiting body

697
Q

what is this infectious disease?

A

Aspergillosis

arrow points toward a violaceous‐ purple colour

698
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

699
Q

What is Aspergillosis and what causes it?

A
  • Saprobic (in an environment rich of oxygen)
  • it caused by Aspergillus flavus and Aspergillus fumigatus
700
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

701
Q

What is this infectious disease?

A

Necrotizing Periodontitis (NP)

o Bone loss of the periodontium seen

702
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

703
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

704
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

705
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

706
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

707
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

708
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?

709
Q

NOMA is also called as ————

A

cancrum oris

710
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

711
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

712
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

713
Q

What is this infectious disease?

A

NOMA

Development of NOMA from day 1 to day 15

714
Q

NOMA can affect who?

A

Children

Adults with debilitating disease

715
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

716
Q

What is this infectious disease?

A

NOMA

Development of NOMA from day 1 to day 15

717
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

718
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

719
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

720
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

721
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

722
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

723
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

724
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
725
Q

What causes Impetigo?

A

‐ Caused by:

o Staphylococcus aureus

o Streptococcal pyogenes

Damaged skin allows infection to enter

Usually affects kids

726
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

727
Q

What is this infectious disease?

A

Congenital Syphilis

‐ Hutchinson Incisors (left image)

‐ Mulberry molars (right image) - not part of the triad

728
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
729
Q

What is this infectious disease?

A

Secondary Syphilis

Mucous Patch

730
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

731
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

732
Q

What is this infectious disease?

A

Gonorrhea

looks like necrotizing gingivitis (NG) but fetor oris not present

733
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)

734
Q

What is this infectious disease?

A

Secondary Syphilis

Mucous Patch

735
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)

736
Q

How is Impetigo diagnosed and treated?

A

Diagnosis:

o Presumptive from clinical features

‐ Treatment:

o Topical mupirocin

o Systemic antibiotics

737
Q

What is this infectious disease?

A

‐ Tuberculosis

738
Q

What is this infectious disease?

A

‐ Tuberculosis

739
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

740
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

741
Q

What is Syphilis?

What causes it/

A
  • Chronic infection
  • caused by spirochete Treponema pallidum
742
Q

What are the three stages of Syphillis?

A

Three stages

  1. o Primary (chancre)
  2. o Secondary (rash)
  3. o Tertiary (gumma)
743
Q

What is this infectious disease?

A

TB

Ulceration (tongue ulceration most common)

744
Q

What is this infectious disease?

A

Miliary TB

compared to miliary seeds

745
Q

What is Differential Diagnosis for Primary Syphilis (Chancre)?

3

A
  1. SCC
  2. Fungal Ulcer
  3. Trumatic Ulcer
746
Q

Differential Diagnosis for teritiary syphillis “Gumma”

A

Differential Diagnosis:

  1. ▪ T‐cell Lymphoma
  2. ▪ Cocaine abuse
  3. ▪ Granulomatosis
  4. ▪ Polyangiitis
  5. ▪ Mucor
747
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

748
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

749
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

750
Q

What is Gonorrhea?

What causes it?

A

‐ a Sexually transmitted (F>M)

caused by

‐ Neisseria gonorrhoeae

751
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)

752
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)

753
Q

Gonorrhea can have coinfection

with what other infectious bacteria?

A

Chlamydia trachomatis

754
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

755
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

756
Q

What are the chance
active disease if you get infected with Primary TB

A

Only 5%-10% infections lead to active disease i

757
Q

“Secondary TB” reactivation

A
  • Leads to disseminated TB (miliary TB)
  • True, active TB
758
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

759
Q

What are the causes of secondary Tuberculosis?

A
  • Immunosuppressive medications
  • Diabetes
  • Old age
  • Crowded living conditions
  • AIDS
760
Q

What are the chance
active disease if you get infected with Primary TB

A

Only 5%-10% infections lead to active disease i

761
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
762
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

763
Q

What is this infectious disease?

A

Primary Oral TB

tongue ulceration

764
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

765
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)

766
Q

What is this infectious disease?

A

Scrofula

767
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

768
Q

What is Non‐Tuberculosis
Mycobacterial
Infection

A

Scrofula

769
Q

What causes scrofula?

A

Mycobacterium bovis

Infected milk leads to scrofula

RARE today as milk is pasteurized

770
Q

What is this infectious disease?

A

Leprosy

771
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
772
Q

Leprosy is also known as ———

A

Hansen disease

773
Q

What causes Leprosy?

A

Mycobacterium leprae

774
Q

What is this infectious disease?

A

Actinomycoses

it’s an external Sinus

775
Q

What causes Actinomycoses?

A

‐ Associated Bacteria:

o Actinomyces israelii
o Actinomyces viscosus

‐ Normal component of oral flora -gram positive anaerobic
bacteria

776
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

777
Q

What is this infectious disease?

A

Cat‐Scratch
Disease

778
Q

Differential Diagnosis to Actinomycoses

A

o Erysipelas

779
Q

What is Cat‐Scratch
Disease?

A

‐ Infectious disease which is seen in lymph nodes

780
Q

What causes Cat‐Scratch
Disease ?

A

‐ Causative organism:
o Bartonella henselae
‐ Previous contact with a cat (scratch or saliva)

781
Q

—– is the most COMMON cause of regional lymphadenopathy in children

(22,000 cases annually)

A

Cat Scratch Disease

782
Q

What are the Differential Diagnoses: of Cat Scratch Disease ?

A


o Swellings in the lymph node

o Unilateral swellings of the neck

783
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

784
Q

Ossifying Fibroma is a ———

A

Benign neoplasm

785
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%)

786
Q

What is Polystotic Fibrous dysplasia?

A

a Fibrous dysplasia involving more than one bone

787
Q

What is the Second most common type of Fibrous dysplasia?

A

Polystotic Fibrous dysplasia

788
Q

What is Craniofacial Fibrous dysplasia?

A

-a Fibrous dysplasia limited to Skull and Facial Bones...

789
Q

What is Mazabraud Syndrome

A

-Fibrous dysplasia with intramuscular myxomas

790
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

791
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

792
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.
793
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.

794
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.

795
Q

What is this trabecular pattern of the FD?

A

Cotton wool
appearance

Irregullary shaped and outlined radiopacities blending in with adjacent bone

796
Q

What is this trabecular pattern of the FD?

A

Peau d’orange

surface of an orange – the bone shows a “pitting” appearance.

797
Q

What is this trabecular pattern of the FD?

A

Ground Glass Pattern

it appears granular in nature. (Grainy)

798
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 the canal ►think of it as originiating from the bone itself

799
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.
800
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

801
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

802
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.

803
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.

804
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.

805
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

806
Q

What is this radiologic finding

A

Periapical COD

Sagital cross section of the anterior Mandible.
Mixed radiolucent/radiopaque area (green circle)

807
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)

808
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.

809
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).
810
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.

811
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

812
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
813
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
814
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

815
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
816
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.
817
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
818
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)

819
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.

820
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).

821
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.

822
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

823
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.

824
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.

825
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.

826
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.

827
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.

828
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.

829
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.

830
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.

831
Q

What are these two disease?

A

Sometimes, simple bone cysts should be differentiated from odontogenic keratocysts (OKCs)

832
Q

 CGCG should be differentiated from ————-

A

brown tumor.

833
Q

What is this disease?

A

central giant cell granuloma

CGCG

834
Q

What is this disease?

A

Aneurysmal Bone Cyst

835
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)

836
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)
837
Q

What is the Management of COD?

A
  • Typically, no treatment is required unless these regions show clinical/radiographic evidence of secondary infection
    • Ex if patient complain of some pain of that area –> we want to follow up that region
  • Surgery within the dense bone has a high risk of causing osteomyelitis
  • Patients should be seen regularlyfor preventive treatment
  • Want tooth supported rather than tissue supported RPD and CD
838
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 some larger or more clincally aggressive cases.
839
Q

What is this clinical presentation?

A

Leukemia

o Dilantin hyperplasia (drug induced gingival hyperplasia) –
fibrotic looking

o Has to an addition of thromocytopenia

840
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

841
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.

842
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

843
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)
844
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)
845
Q

What is this clinical presentation?

A

Cyclic Neutropenia

o Teeth floating in air

846
Q

What is this clinical presentation?

A

Cyclic Neutropenia
▪ Gingiva is most severely affected with periodontal bone loss and
tooth mobility

847
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

848
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

849
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

850
Q

What is this clinical presentation?

A

Hematoma

because of THROMBOCYTOPENIA or Trauma

851
Q

What is this clinical presentation?

A

Hematoma

because of THROMBOCYTOPENIA orTrauma

852
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

853
Q

What is this clinical presentation?

A

o hematoma

because of THROMBOCYTOPENIA or Trauma

854
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

855
Q

What is this clinical presentation?

A

Sickle Cell Anemia

Can see prominent trabeculae left, looks like steps on a ladder

856
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

857
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

858
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

859
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
860
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

861
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
862
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)
863
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

864
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.
865
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**
866
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

867
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

868
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

869
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

870
Q

What is this clinical presentation?

A

leukomia

Cause of infiltrate they has bone loss

871
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

872
Q

What is this clinical presentation?

A

Hodgkins lymphoma

873
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

874
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

875
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

876
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

877
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

878
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)
879
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
880
Q

What is this clinical presentation?

A

Multiple Myeloma

Pathological fracture

881
Q

What is this clinical presentation?

A

Multiple myeloma

882
Q

What is this clinical presentation?

A

Multiple Myloma

Punched out translucency in crest

883
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

884
Q

What is this histological presentation?

A

Plasma Cell Disorders

Clock face nucleaus

885
Q

What is this clinical presentation?

A

Plasma cell gingivitis

▪ Allergen causes mass infiltrate into gingival
▪ Benign
▪ Diet log to identify allergen, allergy testing

886
Q

Plasma cell gingivitis Treatment

A

▪ Diet log to identify allergen, allergy testing
▪ Ideally eliminate offending substance
Can manage with topical steroids

887
Q

What is this clinical presentation?

A

Plasma cell gingivitis

▪ Allergen causes mass infiltrate into gingival
▪ Benign

888
Q

What is this clinical finding?

A

Multiple Myeloma

Deposition of amyloid in soft tissues
o Can cause macroglossia if tongue is involved

889
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

890
Q

What is this clinical presentation?

A

Multiple Myeloma

891
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

892
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
893
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

894
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.

895
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

896
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

897
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

898
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)

899
Q

What is Polycythemia

A

▪ Increase in the number of circulating red blood cells

900
Q

People with chronic Polycythemia are at
increased risk of —— or ——-

A
  • *of MI or CVA (cerebral vascular accident or
    stroke) **
901
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
902
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

903
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

904
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

905
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)

906
Q

What is the treatment of

THROMBOCYTOPENIA?

A

▪ Treatment is usually platelet transfusion

907
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

908
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

909
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)
910
Q

What is Leukemia?

A

▪ Represents several types of malignancies derived from
hematopoietic stem cells

▪ ~ 2.5% of all cancers in USe

911
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

912
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

913
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.

914
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.

915
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

916
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
917
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

918
Q

What are the Clinical and radiological features

of

Multple Myeloma MM

A
  • Bones most commonly involved include vertebrae and ribs, skull
    • 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)
    • Due increased plasma cells ⇒ plasma cells makeantibodies ⇒ 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
919
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

920
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)
921
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

922
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
923
Q

What causes Myelodysplastic Syndrome?

A

– environmental

924
Q

What causes Megaloblastic Anemias
?

A

o Folic Acid def
o Vit B12 def (pernicious anemia)

925
Q

What causes Iron Deficiency anemia?

A
  • *menstruation, pregnancy, malabsorption diseases
    (eg. Celiac)**
926
Q

What causes Aplastic Anemia ?

A

– environmental, things like bensin

927
Q

What causes Thalassemia & Sickle Cell anemia ?

A

Genetic

928
Q

What causes Anemias of Chronic Disease?

A

inflammatory conditions, malignancy
– organ disease

929
Q

What causes Anemias of Chronic Renal Insufficiency?

A

low levels of
erythropoietin – organ disease

930
Q

What is the treatment for
Deficiency Anemias

B12 def?

A
  • 1mg IM injections weekly for 1‐2 months
  • Monitored for lifetime
931
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

932
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

933
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)

934
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

935
Q

Which ares alpha thalassemia is common?

A

Areas with a lot of malaria

936
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)

937
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
938
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)
939
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

940
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

941
Q

What is this clinical presentation?

A

Homogeneous leukoplakia.

○ Non-wipeable white patch

942
Q

What is this clinical presentation?

A

Speckled leukoplakia.

Non-homogenous leukoplakia

943
Q

What is this clinical presentation?

A

Homogeneous leukoplakia

○ Thickened leathery, White plaque
○ Well-demarcated, Deepened fissures
○ Non-wipeable white patch

944
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.

945
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
946
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Multifocal

947
Q

What is this clinical presentation?

A

Hairy Leukoplakia

corrugated white lesion on the lateral tongue.
• It only occurs on the lateral tongue

948
Q

What is this clinical presentation?

A

Hairy Leukoplakia

949
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

950
Q

What is this clinical presentation?

A

homogenous leukoplakia

Just
white color

951
Q

What is this clinical presentation?

A

Oral lichen planus

Lichen planus of the dorsum of the tongue

this is a hypertrophic form.

952
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Location
○ Gingiva (Frequent)
○ Buccal Mucosa
○ Palatal Mucosa

953
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

954
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

955
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

956
Q

What is this clinical presentation?

A

Oral lichen planus

on the buccal mucosa (most common site

reticular form.

957
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
958
Q

Hairy Leukoplakia

Etiology

A

Epstein–Barr virus seems to play an important role in the
pathogenesis.

959
Q

What is this clinical presentation?

pts takes allopurinol

A

Oral Lichenoid Drug
Reaction

960
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.

961
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

962
Q

What is this clinical presentation?

pts takes Thiazide Diuretic

A

Oral Lichenoid Drug
Reaction

963
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
964
Q

What is this clinical presentation?

A

Nicotinic Stomatitis

These papules represent inflamed minor salivary glands and their ductal orifices.

965
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
966
Q

What is this clinical presentation

A

Nicotine Stomatitis.

967
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)

968
Q

What is this clinical presentation?

A

Geographic tongue, localized lesion.

969
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
970
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

971
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

972
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

973
Q

Proliferative Verrucous Leukoplakia

Treatment

A

complete removal: excision, electrocautery, cryosurgery, or laber ablation

Lesions rarely regress despite therapy

974
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.

975
Q

What is this clinical presentation?

A

Leukoedema of the buccal mucosa.
Laskaris,

976
Q

What is this clinical presentation?

A

White Sponge Nevus

(Canon disease)

977
Q

What is this clinical presentation?

A

White Sponge Nevus

Diffuse, thickened white plaques
of the buccal mucosa

978
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Extensive papillary, white
lesion of the maxillary vestibule

979
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Large, exophytic, papillary
mass of the maxillary alveolar ridge.

980
Q
A

Traumatic Erythema /Traumatic Hematoma

on the lower lip.

981
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Large, exophytic, papillary
mass of the maxillary alveolar ridge.

982
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Early verrucous carcinoma of the buccal mucosa.

983
Q

What is this clinical presentation?

A

Geographic tongue: well-demarcated red patch on the tongue.

984
Q

What is this clinical presentation?

A

Median rhomboid glossitis.

a Chronic hyperplastic, erythematous candidiasis

985
Q

what is this clinical presentation?

A

Denture stomatitis.

986
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.

987
Q

What is this clinical presentation?

A

Erythroplakia

of the buccal mucosa

Well-demarcated erythematous patch or plaque with soft velvety texture

988
Q

What is this clinical presentation?

A

Erythroplakia of the buccal mucosa.

989
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

990
Q

What is this clinical presentation?

A

Erythroplakia

Firey red Well-demarcated patch or plaque with soft velvety texture

transformed into SCC

991
Q

Oral lichen planus

Treatment:

A
  • Incisional biopsy on non-keratinized, non-ulcerated mucosa

○ Asymptomatic → no tx
○ Symptomatic → 0.5mg/ml Dexamethasone Elixir.

992
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.

993
Q

What is this clinical presentation?

A

Erythroplakia.

Well-circumscribed red patch on the
posterior lateral hard and soft palate

994
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.

995
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

996
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Severe

997
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

998
Q

What is this clinical presentation?

A

Pemphigus vulgaris

PV Lesions can affect
virtually any mucosal
surface (oral, nasal,
ocular, pharyngeal,
esophageal, genital)

999
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

1000
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

1001
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Multiple erosions of the left
buccal mucosa and soft palate.

1002
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Large, irregularly shaped ulcerations
involving the floor of the mouth and ventral tongue.

1003
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

. Multiple erosions affecting the
marginal gingiva.

1004
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

1005
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

Oral Hygiene: Plaque
related gingival
inflammation
contributing to
continued VB
desquamative
gingivitis

1006
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

1007
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal

can
result in functional
blindness

1008
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

1009
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

1010
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
1011
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.

1012
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.
1013
Q

Nicotine Stomatitis.

Etiology

A

The elevated temperature, rather than the tobacco chemicals,
is responsible for this lesion.

1014
Q

Geographic tongue/
areata migrans

Etiology

A

The exact etiology remains unknown. It may be genetic.

1015
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
1016
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

1017
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.

1018
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
1019
Q

Verrucous Carcinoma

Treatment

A

○ Surgical Excision

○ Radiotherapy

1020
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

1021
Q

Median Rhomboid Glossitis

Treatment

A

No treatment is required.

1022
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

1023
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

1024
Q

Smokeless tobacco keratosis

Treatment:

A

typically resolves weeks after cessation

○ if persists 6+weeks -> biopsy to rule out dysplasia + SCC

1025
Q

What is this clinical finding?

A

Frictional keratosis

on the tongue

1026
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)

1027
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.

1028
Q

Mucous membrane pemphigoid

Etiology

A

Mucocutaneous autoimmune disease characterized by sub‐epithelial
blisters (bullae) which ruptures to form large, non‐healing ulcerations

1029
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**
1030
Q

PV and MMP

Biopsy

A

Option 1: take perilesional sample that has both intact and ulcerated epithelium
○ This is not easily achieved
● Option 2: 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
● Option 3: just collect a large punch of normal non‐ulcerated epithelium and submit for immunofluorescence
○ You will still get product even though it is not ulcerated

1031
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

1032
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.

1033
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

1034
Q

What is this clinical presentation?

A

SCC

arising from Actinic Cheilitis

1035
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.

1036
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. .

1037
Q

What is this clinical presentation?

A

Oral Melanoma

a highly malignant neoplasia, arising from melanocytes, the cells that produce the brownish pigment melanin.

1038
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.

1039
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.)

1040
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.

1041
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.

1042
Q

Actinic cheilitis

Etiology

A

due to chronic ultraviolet light exposure.

1043
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

1044
Q

What is this clinical presentation

A

Oral Melanoma

1045
Q

What is this clinical presentation

A

Oral Melanoma

1046
Q

What is this clinical presentation?

A

Traumatic

Granuloma

(traumatic ulcertaive granuloma)

1047
Q

What is this clinical presentation

A

Oral Melanoma

1048
Q

What is this clinical presentation?

A

Traumatic ulcer

Most often on tongue, lips, buccal mucosa

Any sites that may be injured by dentition

1049
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

1050
Q

What is this clinical presentation?

A

Traumatic ulcer

caused by sharp or puncturing food stuff

1051
Q

What is this clinical presentation?

A

Traumatic

Granuloma

1052
Q

What is this clinical presentation?

A

Traumatic Granuloma

( Traumatic Ulcerative Granuloma)

1053
Q

What is this clinical presentation?

A

Squamous cell carcinoma

on the buccal mucosa)

1054
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

1055
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).

1056
Q

What is this clinical presentation?

A

Graphite tattoo

Gray, black, or blue-ish macule

1057
Q

What is this clinical presentation?

A

Graphite tattoo

Most common location on the palate and gingiva

Gray, black, or blue-ish macule

1058
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

1059
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.

1060
Q

Oral Melanoma

Treatment

A
  • Surgical excision
  • Radiotherapy
  • Chemotherapy
1061
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
1062
Q

What is this clinical presentation?

A

Traumatic ulcer

Post-anaesthesia traumatic ulcer on lower lip.

1063
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

1064
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

1065
Q

SCC treatment

A

Early stage: Radiation and/or Surgical removal

Late stage : combination of surgery, radiation therapy, or chemotherapy

1066
Q

Graphite tattoo

Etiology

A

result from pencil lead that is traumatically implanted, usually during the elementary school years

1067
Q

Graphite tattoo

Treatment

A

If patient is concerned for cosmetic reasons ► then removal of lesion with autogenous graft

1068
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.

1069
Q

What is this clinical finding?

A

Hemangioma of Infancy

1070
Q

What is this clinical presentation?

A

Traumatic ulcer of the tongue.

1071
Q

Hemangioma of Infancy

Treatment

A

○ Because most hemangiomas of infancy undergo involution, management often consists of “watchful neglect.”

1072
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

1073
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

1074
Q

What is this clinical finding?

A

Xerostomia-related Caries

Or

Dry Mouth

. Extensive cervical caries of
mandibular dentition secondary to radiation-related xerostomia.

1075
Q

Necrotizing Sialadenometaplasia

Etiology

A

The cause is uncertain, although the hypothesis of ischemic
necrosis after vascular infarction seems acceptable.

1076
Q

Necrotizing Sialadenometaplasia

Treatment

A

No Treatment Needed

but we need to biopsy to rule out other diseases

1077
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.

1078
Q

Frictional Keratosis.

Differential Diagnosis

A

Leukoplakia

Linea alba

Chronic cheek chewing (bite injury)

Candidiasis

Oral Lichen planus

Squamous cell carcinoma

1079
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.

1080
Q

Frictional Keratosis

Etiology

A
  • Trauma from Sharp cusp & ortho appliance
  • Chronic mechanical irritation (chronic biting)
  • Masticatory function
  • Normal hyperplastic response
  • Dentures/missing teeth
1081
Q

Frictional Keratosis

Treatment

A
  • Remove the cauative factor that caused the trauma
  • observe large lesion regularly

excellent prognosis

1082
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)

1083
Q

What is the normal rate for Unstimulated Saliva
Production

A

300 ml/day
▪ Flow rate: mean 0.3 ml/min

1084
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

1085
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).

1086
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.
1087
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.

1088
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

1089
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

1090
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)

1091
Q

Severity of patients
with xerostomia using
objective measures

A
1092
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.

1093
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?
1094
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
1095
Q

What is this clinical presentation?

A

SJÖGREN’S SYNDROME

Dry Mouth

very severe
cervical disease & very dry lips

1096
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.

1097
Q

What is this clinical presentation?

A

Depapillated &
Fissured Tongue

SJÖGREN’S SYNDROME

1098
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.
1099
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)
1100
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

1101
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)
1102
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
1103
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).
1104
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

1105
Q

What is this clinical presentation?

A

SJÖGREN’S SYNDROME

Autoimmune exocrinopathy

Marked bilateral parotid gland enlargement in a patient with primary Sjögren syndrome

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)

1106
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

1107
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

1108
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

1109
Q

What is this clinical finding?

A

Angioedema

1110
Q

Urticaria

Etiology

A

❖ Medications ► causing rash
❖ Foods ► like peanuts
❖ Airborne allergens ► pollen
❖ Physical stimuli ► ex cold weather

1111
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)

1112
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.
1113
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.

1114
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.
1115
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

1116
Q

What is this clinical finding?

A

Exfoliative Cheilitis

caused by titanium implants and
some mercury in amalgam.

1117
Q

What is this clinical finding?

A

Perioral Dermatitis

Allergic Contact
Reactions‐ Non‐
Mucosal

erythematous
papules/vesicles
– papules ( raised) & vesicles
(actual blisters)

1118
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.

1119
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.

1120
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

1121
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

1122
Q

What is this clinical finding?

A

Orofacial
Granulomatosis

1123
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.)

1124
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

1125
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
.

1126
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.

1127
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.

1128
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. *
1129
Q

What is this clinical finding?

A

Granulomatosis with
Polyangiitis

Orally

We want to
biopsy to confirm because it Could be contact mucositis.

1130
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

1131
Q

What is this clinical finding?

A

Urticaria.

1132
Q

What is this clinical finding?

A

Erythema multiforme

1133
Q

What is this clinical finding?

A

* Erythema multiforme

1134
Q

What is this clinical finding?

A

‐ Orofacial granulomatosis.

We make sure there’s no tb, no fungal, no foreign material in the
granulomas

1135
Q

What is this clinical finding?

A

Sarcoidosis

*Erythemous papules (grey circle)
Asteroid bodies ( blue arrow)
Hilar lymph nodes (green circle)

1136
Q

What is this clinical finding?

A

Granulomatosis with polyangiitis

1137
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.

1138
Q

What is this clinical finding?

A

Sarcoidosis

1139
Q

What is this clinical finding?

A

angioedema

1140
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.

1141
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
1142
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

1143
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

1144
Q

Granulomatosis with
Polyangiitis

Treatment

A

First line: oral prednisone
❖ After remission immunosuppressive drugs:
❖ Methotrexate
❖ Cyclosporine
❖ Rituximab
❖ Treatment induces prolonged remission
❖ May have relapses

1145
Q

White wipeable plaque in the mouth

DDx

A

● pseudomembranous candidiasis
● Mucosal sloughing‐ Allergic Contact Stomatitis
● Food particles

1146
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

1147
Q

Exfoliative cheilitis

causes

A

Medications, lipsticks,
sunscreens, toothpaste
floss, cosmetics

1148
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

1149
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

1150
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)

1151
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

1152
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.

1153
Q

What is this clinical finding?

A

Sarcoidosis

large red nodule on the lower lip.

1154
Q

What is this clinical finding?

A

Urticaria

developed after bites from an imported fire ant.

1155
Q

What is this clinical finding?

A

Erythema multiforme

multiple erosions on the lips and tongue.

1156
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).

1157
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.

1158
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

1159
Q

Sarcoidosis
Etiology

A

Granulomatous disorder
❖ Multisystem
❖ Unknown cause

1160
Q

Granulomatosis with
Polyangiitis

Etiology

A

First line: oral prednisone
❖ After remission immunosuppressive drugs:
❖ Methotrexate
❖ Cyclosporine
❖ Rituximab
❖ Treatment induces prolonged remission
❖ May have relapses

1161
Q

Urticaria

DDX

A
  • erythema multiforme
  • morbilliform drug eruption
1162
Q

Cinnamon Contact
Stomatitis

DDx

A
  • Oral hairy leukoplakia
  • hyperplastic candidiasis
1163
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)

1164
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 )

1165
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.