STC Flashcards

1
Q

Irritation Fibromas

Composed of

Etiology

Clinical features ;Color

Location

Treatment

A
  • AKA – Fibroma, Traumatic Fibroma
  • Composed of dense, scar-like, fibrous connective tissue
  • Occurs as a result of chronic trauma
  • Clinical Features: Exophytic lesion
  • Usually less than a centimeter in diameter
  • Color: lighter pink than surrounding mucosa,the surface can be white sometimes bc it’s rubbing and bumping into other oral structures (like teeth), so they get surface keratinization
  • Locations: buccal mucosa, tongue, lips, gingiva
  • Very common; totally benign soft lesion
  • Treatment: You don’t have to remove them, but the surgical Tx = to excise them bc pts will stop biting them and they’ll heal and stop the irritation
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2
Q

What is this clinical finding?

A

Irritation Fibromas

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3
Q

What is this clinical finding?

A

Irritation Fibromas

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5
Q

What is this clinical finding?

A

Chronic Hyperplastic Pulpitis (pulp polyp)

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7
Q
A

Giant Cell Fibroma

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8
Q

Chronic Hyperplastic Pulpitis

What is it?

Location?

Age?

Clinical Appearance?

Treatment?

A

AKA: pulp polyp
• An e_xcessive proliferation of chronically inflamed dental pulp tissue_ – granulation tissue/ fibrous tissue with inflammatory cells (like a little fibroma that
occurs from pulp tissue​) ( benign soft tissue leasion)

• Location:
• Teeth with large, open carious lesions
• Primary or permanent molars
• Age: Children & young adults
Clinical Appearance: A red or pink nodule of soft tissue protruding from the
pulp chamber and fills the entire cavity of the tooth
Treatment: RCT or extraction of tooth

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10
Q

Giant Cell Fibroma

A
  • Very small form of fibrous tumour that show giant cells
  • Age: relatively rare in paediatric patients.
  • Clinically it is presented as a painless, sessile, or pedunculated growth which is usually confused with other fibrous lesions like irritation fibromas or Retrocuspid papilla
  • Location: Largely occur on lower gingivae and on palate\
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11
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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13
Q

What is this clinical finding?

A

Epulis Fissuratum

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14
Q

Cowden Syndrome

A
  • (multiple hamartoma and neoplasia syndrome)
  • Autosomal dominant disorder affecting multiple organ systems
  • • Caused by mutations in the phosphatase and tensin homolog gene (PTEN, a tumor suppressor gene)
  • • Oral and perioral findings include
  • *multiple papules on the lips and gingivae,**
  • papillomatosis (benign fibromatosis) of the buccal, palatal, faucial, and oropharyngeal
  • mucosae often producing a “cobblestone” effect, and the tongue may also present as pebbly or fissured.
  • Multiple papillomatous nodules (histologically inverted follicular keratoses or
  • trichilemmomas) are often present on the perioral, periorbital, and perinasal skin, the pinnae of the ears, and neck.
  • • These nodules are often accompanied by lipomas, hemangiomas, neuromas, vitiligo, café au lait spots, and acromelanosis .
  • • A variety of neoplastic changes occur in the organs exhibiting hamartomatous lesions,with an increased rate of breast and thyroid carcinoma and gastrointestinal malignancy.
  • Squamous cell carcinoma of the tongue and basal cell tumors of the perioral skin have also been reported.
  • Incredibly rare ( board loves it)
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15
Q

What is this clinical finding?

A

Inflammatory Papillary Hyperplasia of the Palate

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16
Q

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

A

Cowden Syndrome

Very rare!

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17
Q

Tuberous sclerosis complex

A

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

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19
Q

Epulis Fissuratum

AKA

Cause

Location

Clinical presentation

Composed of

Treatment

A

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

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20
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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22
Q

What is this clinical finding?

A

Pyogenic Granuloma:

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23
Q

Pyogenic Granuloma

Histology

A

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

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24
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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25
Q

Inflammatory Papillary Hyperplasia of the Palate

Majority occur with what disease?

Associated with what?

Clinical appearance

Treatment

A
  • Majority occur with denture stomatitis
  • Associated with a removable full or partial denture or orthodontic
  • appliance (Something you see in patients who wear denture all the time, don’t take it out, chronic denture wear)
  • Clinical Appearance: Palatal vault is covered by multiple erythematous papillary projections (fibrous connective tissue surfaced by epithelium) –(papillary but no papilla, instead it’s bumpy and bosselated)
    • Granular or cobblestone appearance
    • Erythema is usually due to superinfection with candida
  • Treatment:Treat underlying candidiasis, fix denture. These bumps can be removed, take electrosurgery loop, and scrape off the bumps – heals well
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26
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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27
Q

Peripheral Ossifying Fibroma

Histology

A
  • When sessile, when removing it, take scalpel blade and just cut into it
  • If has a little bone or cementum formation inside it, you can feel the bone with the scalpel
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29
Q

What is this clinical finding?

A

Peripheral Giant Cell Granuloma

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30
Q

Peripheral Giant Cell Granuloma

Histology

A

Giant cells inside the lesion

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31
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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32
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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33
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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34
Q

Pyogenic Granuloma

What is it?

Etiology

Assossiated with which demographics?

Location?

Treatment?

A
  • What is it? Reactive connective tissue hyperplasia - exuberant granulation tissue; Misnomer – not pyogenic and not a true granuloma
  • Etiology: Response to injury - calculus or overhang restoration
  • Assosiated with? Often occurs in pregnant women (“pregnancy tumor”), also associated with puberty
  • Treatment: Excision and removal of irritant (eg calculus, overhanging restorations)
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35
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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36
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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37
Q

What is this clinical finding?

A

Hereditary Gingivofibromatosis

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39
Q
A

Infantile
Hemangioma

(“strawberry” hemangioma).

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

Neville Cr

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40
Q

Pyogenic Granuloma

Clinical appearance

Location

Size

Developing rate

Age:

A
  • Clinical appearance
  • Usually ulcerated
  • Soft exophytic lesion, either sessile or pedunculated
  • Deep red to purple in color, bleeds easily
  • Location:
    • Most common – gingiva
    • Also occurs in other areas of the oral mucosa ( can happen anywhere)
  • Size: small to large (millimeters to centimeters)
  • Develop rapidly and then remain static
  • Age: Any age
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41
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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42
Q

What is this clinical finding?

A

Capillary
Malformation (Low
flow)

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43
Q

How to differentiate between

Venous
malformation (low
flow)

from

Arteriovenous or
arteriolar malformations
(High flow)

A

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

In other word, Venous lesion = Does not have pulse

Histopathologically they look different too

Treatment:

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

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

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44
Q

What is this clinical finding?

A

Venous
malformation (low
flow)

Many pts can live with this without treatment

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46
Q

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

A

Osler-Weber-Rendu
Syndrome

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48
Q

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

A

Sturge-Weber
Angiomatosis

Sturge-Weber syndrome

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49
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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51
Q

What is this clinical finding?

A

Lymphangioma

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52
Q

What is this clinical finding?

A

Cystic Hygroma

a type of Lymphangioma

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53
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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54
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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56
Q

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

A

Multiple Endocrine
Neoplasia (MEN)
Syndrome

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58
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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59
Q

What is this clinical finding?

A

neurofibroma

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60
Q

Peripheral Giant Cell Granuloma

​What is it?

Location?

Age?

Clinical appearance:

Radiographic finding?

A
  • What is it? Probably a reactive lesion due to local irritating factors (giant cells develop inside the lesion which is a benign soft tissue lesion)
  • Location: Gingiva, usually anterior to the molars
  • Age: Most frequently seen between 40-60 years old
  • Clinical appearance: dusky purple, sessile or pedunculated, smooth-surfaced, dome-shaped papule or nodule. Most lesions are less than 1.5 cm in diameter, though infrequently, may grow as large as 5 cm in greatest dimension
  • Radiographic Features: Usually none, but superficial destruction of the alveolar bone may occur
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61
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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63
Q

What is the clinical finding?

A

Schwannoma/ Neurilemoma

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64
Q

What is this clinical finding?

A

Schwannoma/ Neurilemoma

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65
Q

Schwannoma/ Neurilemoma

Histology

A

Antoni A and Antoni B.

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

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

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67
Q

What is this clinical finding?

A

Granular Cell Tumor

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68
Q

What is this clinical finding?

A

Granular Cell Tumor

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69
Q

Granular Cell Tumor

Histology

A

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

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70
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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71
Q

What is this clinical finding?

A

Congenital Epulis

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72
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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73
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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74
Q

Lipoma

What is it?

Location?

Cliniclly?

Histologically?

Treatment?

A
  • What is it: Benign tumor of mature fat cells; Relatively rare
  • Location:Won’t see on gingival tissue, will see on buccal mucosa, on the tongue, and floor of the mouth
  • Clinically appears as a yellowish mass surfaced by thin overlying epithelium, When you feel it, it’s soft
  • Histologically: a well-delineated tumor composed of mature fat cells with a thin capsule
  • Treatment: surgical excision,does not recur
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75
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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77
Q

Drug Induced Gingival
Enlargement

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

A
  • Phenytoin: (or Dilantin) – the drug that used to be given to every single
  • person that had seizures
  • Calcium-channel blockers
    • Nifedipine not as prescribed anymore
    • Dilitiazem still prescribe
    • Amlodipine: is prescribed as one of the first line therapy for hypertension (very commonly prescribed); it doesn’t typically cause gingival overgrowth except in some selected patients, usually
      those with pretty poor oral hygiene
  • Cyclosporine A (used for for bone marrow transplant, graft vs
    host disease, solid organ transplant)
    • Cyclosporine is universally recognized as causing gingival hyperplasia
    • Cyclosporine is largely replaced with Tacrolimus, which typically doesn’t cause gingival overgrowth
  • Cyclosporine A is largely replaced with Tacrolimus, which typically doesn’t cause gingival overgrowth
    Some drugs have more connective tissue component, others have more epithelial component
    Not all identical under the microscope
  • Cyclosporine provides more epithelial change, Dilantin causes more of a connective tissue change
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78
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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79
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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81
Q

What is this clinical finding?

A

Leiomyosarcoma

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82
Q

Hereditary Gingivofibromatosis

What causes it?

How common?

what effects on oral cavity?

Treatment?

A

What causes it?

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

How common?

  • Very rare

what effects on oral cavity?

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

Treatment

  • Need surgical (usually laser) treatment – just grows back, so have to get it done periodically
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84
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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85
Q

Infantile
Hemangioma

When do they appear?

Rate of Development

Clinical presentation

Treatment

A
  • When do they appear? They are rarely present at birth, infants are Born with this in place.
  • Rate of development: the tumor will demonstrate rapid development that occurs at a faster pace than the infant’s overall growth in the first few weeks of life,
  • Clinical presentation: Either superficial or deeper tumors
    • Superficial tumors of the skin appear raised and bosselated with a bright-red color (“strawberry” hemangioma); They are firm and rubbery to palpation, and the blood, cannot be evacuated by applying pressure.
    • Deeper tumors may appear only slightly raised with a bluish hue.
    • May be left with a pink or magenta macule in site where hemangioma occurred after its involute
  • Treatment: Typically will involute with time, Some cases don’t involute, so need to be removed
  • It is a vascular Anomaly
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86
Q

What is this clinical finding?

A

Fibrosarcoma

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88
Q

Capillary
Malformation
(Low
flow)

A
  • a type of vascular anomaly
  • CMs are commonly known as port wine stains.
  • They look like a pink, red or purple patch of skin
  • occur in 1 in 300 newborns.
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89
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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90
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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92
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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93
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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95
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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96
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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97
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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100
Q

Osler-Weber-Rendu
Syndrome

AKA

What is it and its clinical appearance

Type of Herditary and Etiology

What can it cause?

Location?

A

AKA

Hereditary Hemorrhagic Telangiectasia

What is it and its clinical appearance

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

Type of Herditary and Etiology

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

What can it cause?

• Can cause hemorrhage

Location?

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

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102
Q

Sturge-Weber
Angiomatosis

Sturge-Weber syndrome

A
  • Rare, non-hereditary developmental condition
  • Vascular proliferation involving tissues of the brain and face
  • Face: Unilateral distribution along one or more segments of the trigeminal nerve ( unilateral means don’t cross the midline) known as port wine stain/ nevus flammeus – they are deep-purple color.
    • Intracranial calcifications; neurological disorders
  • Intraoral involvement is common
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105
Q

Lymphangioma

What is it?

Types

Locations:

Treatment

A

What is it?

• Benign tumor of lymphatic vessels
Types

  • Microcystic
  • Mixed
  • Cystic hygroma (macrocystic)

Location

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

Treatment:

monitor, surgery if needed, recurrence common

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108
Q

Neuroma

AKA

What is it?

Clinical presentation

Location

A

AKA

  • traumatic neuroma

What is it?

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

Clinical presentation

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

Location

  • mental foramen area, tongue, lower lip
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110
Q

Multiple Endocrine Neoplasia (MEN) Syndrome

What is it?

Inhertiance type?

Which type is associated with multiple mucosal neruoma?

What other presentations?

Increase risk of which cancer?

A

What is it?

Group of rare conditions

Inhertiance type?

Autosomal dominant

Which type is associated with multiple mucosal neruoma?

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

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

Increase risk of which cancer?

Increased risk for medullary thyroid cancer (prophylactic thyroidectomy)

Common board questions

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112
Q

Neurofibroma

What is it?

Clinical presentation?

Location?

Treatment?

Mailgnancy?

A

What is it?

  • A benign tumor arising from peripheral nerve tissue

Clinical presentation:

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

Location:

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

Treatment: surgical excision

Malignant transformation reported, but rare

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115
Q

Neurofibromatosis syndrome

Most common form?

intheritance type?

Clinical presntation?

Malignant transformation?

A

Most common form?

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

intheritance type?

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

Clinical presentations:

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

Malignant transformation

  • reported in 5% of cases (neurofibrosarcoma)
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117
Q

Schwannoma/ Neurilemoma

What is it?

Age?

Location?

Clinical presentation?

Treatment?

malignant
transformation ?

A

What is it?

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

Age?

• Most common in young and middleaged
adults

Location?

• Most common intraoral location:
tongue

Clinical presentation?

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

• May present with pain

• Treatment

• surgical excision

malignant
transformation

reported, but rare

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121
Q

Granular Cell Tumor

What is it?

Location?

Age?

Treatment?

A

What is it?

Benign tumor derived from
Schwann cells

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

Clinical presentation?

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

Age:

40-60, rare in children

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

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125
Q

Congenital Epulis

AKA

Cell resemble?

Cell origin?

Clinical features & location

Treatment?

A

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

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

• Treatment:Surgical excision, does not recur

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127
Q

Neuroectodermal tumor of infancy

Location?

Rate of development?

Treatment?

Origin?

Clinical presentation?

A

Location?

Often occur as soft tissue mass largely in anterior maxilla

Rate of development?

So fast developing that it envelops and moves the teeth

Treatment?

Needs to be surgically excised

Origin?
Thought to be of neuroectodermal source

Clinical presentation?
Pigmented change in tissue

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131
Q

Lipoma vs Lipofibroma

A
  • Sometimes lipomas can be mixed with fibrous tissue, can be lipofibromous
  • Two lesions that look almost identical but one is lipoma, one is lipofibroma
  • Only difference is that one has fibrous tissue in it, no other difference
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132
Q

Benign Tumors of Muscle

A

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

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

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135
Q

Leiomyosarcoma

A
  • a type of rare cancer that grows in the smooth muscles.
  • So, so rare
  • Diseases that move rapidly, because they’re malignancies
  • You might see surface ulcerations, they’re moving so fast, they break through the epithelium
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137
Q

Rhabdomyosarcoma

A
  • is a type of sarcoma.
  • Rhabdomyosarcoma usually begins in muscles that are attached to bones and that help the body move, but it may begin in many places in the body
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138
Q

What is Sarcoma ?

A

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

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140
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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142
Q

Vascular Malignant Neoplasms

A

• Angiosarcoma

• Malignant tumor of blood vessels

• Lymphangiosarcoma

• Malignant tumor of lymphatic vessels

• Kaposi’s sarcoma

  • Malignant neoplasm associated with endothelial cells
  • Seen predominantly in poorly controlled HIV infected patient population (not exclusively)
  • Elderly people can develop Kaposi
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143
Q

Kaposi Sarcoma

Etiology

Types

Treatment

A

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

Types:

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

Treatment

  • Surgical excision, radiation therapy or systemic chemotherapy for multiple nonoral lesions, if it gets large, dose-radiation therapy!
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146
Q

Plasmacytoma in Multiple Myeloma

A

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

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149
Q

Lymphoma

A
  • Lymphoma is a general term for a complex group of heterogeneous lymphoreticular malignancies.
  • Lymphoma is the sixth most common malignancy and the second most common neoplasm of the head and neck after squamous cell carcinoma and accounts for 50-59% of head and neck neoplasms in children.
  • They constitute approximately 3-5% of all known malignancies and are generally divided into two morphologically distinct types: Hodgkin’s lymphoma (HL) and non-Hodgkin’s lymphoma (NHL).
  • These malignancies typically arise within the lymphatic tissues and can progress to extranodal disease as in NHL.
  • Cervical lymph node involvement can be present in any type of lymphoma.
  • HL extends by means of contiguous nodal spread whereas NHL tends to disseminate hematogenously and is typically a systemic diagnosis.
  • Within the head and neck, Waldeyer’s ring is the most common site of involvement, accounting for more than half of all extranodal head and neck lymphomas.
  • Oral involvement by lymphoma may represent a localized disease process but is more often part of a systemic process that secondarily involves the cervical lymph nodes.
  • Lymphoma arising within the oral cavity accounts for less than 5% of all oral malignancies, and approximately 85% of these lesions involve the pharyngeal tonsil and the palate
  • Extralymphatic sites include the salivary glands, paranasal sinuses, oral cavity, and larynx.
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150
Q

ADENOMA

A

benign tumor
of glandular origin

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151
Q

Characteristics of a Benign Tumor:

A

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

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152
Q

BENIGN SALIVARY GLAND
TUMORS

(list 3)

A

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

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153
Q

PLEOMORPHIC ADENOMA

(MIXED TUMOR)

A
  • This tumor comes in many forms/shapes
  • Most common salivary gland tumor
  • Painless, slowly growing, firm mass
  • Adults (30‐50 years old) ; slight female predilection
  • Sites:
    • 50% to 77% of parotid tumors (most commonly found in parotid-2/3rd to 3/4th of parotid tumors)
    • Minor SG: palate>upper lip>buccal mucosa> other site (most common intraoral site is the palate)
  • Malignant transformation possible in long standing lesions (about 5% cases) ‐> called Ca ex PA
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154
Q

What is this clinical finding?

A

PLEOMORPHIC ADENOMA

(MIXED TUMOR)

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155
Q

What is this clinical finding?

A

PLEOMORPHIC ADENOMA

Classic presentation: includes swelling in the parotid region

(MIXED TUMOR)

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156
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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157
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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158
Q

What is this clinical finding?

A

Untreated pleomorphic adenoma

slow growing, but can grow to enormous sizes

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159
Q

Pleomorphic adenoma
histology

A

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

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

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162
Q

What is this clinical finding?

A

Canalicular Adenoma

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163
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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164
Q

Basal Cell Adenoma

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

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

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165
Q

What is this clinical finding?

A

Basal Cell Adenoma

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167
Q

What is this clinical finding?

A

PAPILLARY
CYSTADENOMA
LYMPHOMATOSUM
(WARTHIN TUMOR)

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171
Q

MUCOEPIDERMOID
CARCINOMA

Charcterstics?

Location

Clinical appearance in minor gland

Can be mistaken for

Histopahtology

A

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

Locations
Palate, most common intraoral site
 Rare primary intrabony (jaws) tumors
 Most common in parotid
Minor SG: palate 2nd
Clinical appearance in minor gland: asymptomatic fluctuant swelling; blue or red colored
 Can be mistaken for mucocele
Histopathology: note the cells growing into adjacent tissue, showing infiltration

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172
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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173
Q

What is this clinical finding?

A

MUCOEPIDERMOID
CARCINOMA

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174
Q

What is this clinical finding?

A

MUCOEPIDERMOID
CARCINOMA

Request all for biopsies!

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175
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
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176
Q

Canalicular Adenoma

A
  • Almost exclusively in minor SG
  • Striking predilection for upper lip (>75%)
  • Nearly always occurs in older adults
  • Slowly growing, painless mass
  • One clue for visualization of soft tissue swellings is increased vascularity with blue‐ish tint in the area.
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177
Q

What is the clinical finding?

A

ACINIC CELL
ADENOCARCINOMA

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178
Q

What is the clinical finding?

A

ACINIC CELL
ADENOCARCINOMA

blue‐ish tint

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179
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.

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180
Q

Adenoid Cystic Carcinoma

A

High grade salivary gland malignancy ( very bad cancer to get)
 Adults
Palatal mass; ulcerations
 Spread through perineural invasion ‐ tumor wraps itself around nerves and spreads through perineural spaces
Grows slowly in the beginning and then picks up speed
Histology: Duct like proliferation with cystic spaces

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182
Q

What is this clinical finding?

A

Adenoid Cystic Carcinoma

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183
Q

What are these clinical findings?

A

Adenoid Cystic Carcinoma

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184
Q

What are these clinical findings?

A

Adenoid Cystic Carcinoma

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185
Q

Adenoid Cystic Carcinoma

A

Swiss cheese appearance, cribriform pattern (full of holes aka cystic spaces)

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186
Q

Perineural invasion Histology

A

Perineural invasion: nerve nuble in the
center and is wrapped by tumor

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188
Q

What is this clinical presentation?

A

Polymorphous
Adenocarcinoma

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189
Q

What is this clinical presentation?

A

Polymorphous
Adenocarcinoma

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191
Q

What is this clinical finding?

A

Carcinoma Ex Pleomorphic
Adenoma

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193
Q

PAPILLARY
CYSTADENOMA
LYMPHOMATOSUM
(WARTHIN TUMOR)

A
  • finger‐like projections, benign, cystic spaces, aggregates oflymphocytes)
  • Vast majority occur within the parotid gland
  • Very rare intraorally
  • Predominantly in men
  • Typically between 5th and 8th decades
  • Strong correlation with cigarette smoking
  • Most common SG tumor to occur bilaterally (bilateral parotid swelling), but can be unilateral
  • Etiology: Thought to arise within lymph nodes as a result of entrapment of
  • salivary gland elements early in development
  • Clinical Features:
    • swelling that has more subtle presentation
    • Doughy to cystic mass
    • In the inferior pole of the gland, adjacent and posterior to the angle of the mandible
  • Treatment: surgical excision, responds very well to it
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195
Q

Summary for benign
tumors

A

Encapsulated, freely movable, not fixed to underlying structure, not tender, patients do not complain of pain, slow growing
 There is one tumor of the ones discussed that does have a risk of malignant transformation (only 5% and will take many, many years) and that is Pleomorphic adenoma

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196
Q

MALIGNANT SALIVARY
GLAND TUMORS

List 5

A

 Mucoepidermoid carcinoma
 Acinic cell carcinoma
 Adenoid cystic carcinoma
 Carcinoma ex‐mixed tumor/malignant mixed tumor
 Polymorphous adenocarcinoma

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197
Q

CLINICAL FEATURES OF
ADENOCARCINOMAS
(malignant gland tumors)

A

 Infiltrative
 Fixed to underlying structures, not moveable
 Rapid or slow growth, depending on grade and type of malignant salivary
gland tumor
 Larger, rapidly growing lesions may cause pain and/or paresthesia
 Ulcerated overlying mucosa

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199
Q

MUCOEPIDERMOID
CARCINOMA

What are its compoenents?

Within jaw prognosis

Treatment

Prognosis

Therapy by gene?

A

What are its compoenents? Mixture of mucus‐producing cells and epidermoid or squamous cells

May arise within jaws from odontogenic epithelium of dentigerous cysts
• More common in the mandible than maxilla
• Molar‐ramus area

Treatment: Usually treated by surgical excision

Prognosis:

• Overall prognosis is fairly good
• 10% of patients die, due to local recurrence or metastasis
 Low‐grade tumors have good prognosis (>90% are cured)
 High‐grade tumors the prognosis is guarded (Only 30% survive)
Therapy by gene?

CRTC1–MAML2, CRTC3‐MAML2 gene fusions (targeted therapy)

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203
Q

ACINIC CELL
ADENOCARCINOMA

A
  •  Occurs predominantly in major SGs,
  •  Found in all age groups, peak incidence in 5th and 6th grade
  • No gender predilection
  • Malignancy with serous acinar differentiation
  • Most common in the parotid (since 90% serous acini)
  •  Variable microscopic appearance
  •  May even appear encapsulated, since it is SLOW growing
  • Better prognosis than salivary gland malignancies
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208
Q

Adenoid Cystic Carcinoma

Location

Growth rate

Clinical presentation

Treatment

Prognosis

A

Location:

 Approx. 50% occur within the minor SG ‐ palate most common site

Growth rate
 Usually a slowly growing mass

Clinical presentation
 Pain is a common and important early finding, occasionally occurring before there is noticeable swelling (described at annoying pain)
 Tendency to show perineural invasion, corresponds to pain

Treatment
 Excision usually the treatment of choice ‐ but edges of tumor may have perineural invasion and remain undetected ‐ makes tumor dangerous

Prognosis
 5‐year survival rate as high as 70% (maybe 90%)
 By 20 years, only 20% ‐ poor long term prognosis

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214
Q

Polymorphous
Adenocarcinoma

Location

Gender

Appearance

growth patterns

Treatment

A
  • Location:
  • Almost exclusively in the minor SG
  • 60% on the hard or soft palate
  • Gender”
  • 2/3rds in females
  • Appearance:
  • Tumor cells have deceptively uniform appearance
  • Growth patterns:
  • Different growth patterns – polymorphous
  • Perineural invasion ‐ common ‐ but considered low grade tumor
  • Treatment: Wide surgical excision; overall prognosis relatively good, with 80% cure rate
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217
Q

Carcinoma Ex Pleomorphic
Adenoma

What is it?

Mean age?

Growth pattern

Treatment?

Prognosis

A

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

Mean age about 15 years greater than benign counterpart

Growth patterns: Mass present for many years with recent rapid growth with associated pain or ulceration

Treatment: Best treated by wide excision, with local node dissection and radiation

Prognosis: guarded, with 50% local recurrence or metastases and dying Prognosis is case to case scenario, may transform to high grade tumor

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219
Q

What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION

Lower lip

A

o Mucocele
o Mucoepidermoid Ca
o Pleomorphic Adenoma

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220
Q

What are the FREQUENCY OF SALIVARY
GLAND TUMORS BY
LOCATION

upper lip

A

o Canalicular Adenoma
o Salivary Duct Cyst*
o Pleomorphic Adenoma

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221
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

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222
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

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223
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

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224
Q

Palatine Torus/Torus Palatinus

A
  • Tori are incredibly common, a normal of variant
  • Part of physical exam is to visualize as well as running index finger over the hard palate every time
  • Sometimes, torus palatinus is quite small and unnoticeable until you touch it (feel a hard bump and it’s just a bony growth)
  • Sometimes, they are pedunculated; Sometimes, they get so large they become traumatized; vascular supply on surface can sometimes form ulcerations and even get a little bone exposure.
  • If patient with history of use of bisphosphonates (bone modifying agents given to women who have osteoporosis or osteopenia and to prevent metastesis for certain cancers), he will remove that dead bone, and it will slowly heal. That’s one of the perils of having an enlarged palatine torus
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225
Q

What is this clinical finding?

A

Palatine Torus/Torus Palatinus

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226
Q

What is this clinical finding?

A

Palatine Torus/Torus Palatinus

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228
Q

What is this clinical finding?

A

Mandibular Torus:
Torus Mandibularis

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229
Q

What is this clinical finding?

A

Mandibular Torus:
Torus Mandibularis

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231
Q

What is this clinical finding?

A

Buccal Exostoses

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232
Q

Mandibular Torus: Torus Mandibularis

A
  • Sometimes pt’s tori are so large that the sublingual frenum gets stuck underneath
  • repeated irritation/trauma can create a little white rim on the tori
  • these tori are rock hard and may grow overtime, but we don’t really understand why people get them
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233
Q

What is this clinical finding?

A

Unencapsulated Lymphoid Aggregates

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234
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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236
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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238
Q

What is this clinical finding?

A

Fordyce Granules

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239
Q

What is this clinical finding?

A

Fordyce Granules

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240
Q

Buccal Exostoses

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

Why does it happen?

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

a variant of normal

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241
Q

What is this clinical finding?

A

Fimbriated
fold/Plica
semiluminaris

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243
Q

What is this clinical finding?

A

Frenal tag

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244
Q

Unencapsulated Lymphoid Aggregates

A
  • the lymphoid aggregates are part of the foliate papillae (they contain some taste buds as well).
  • This is lymphoid tissue -- when you get a cold or upper respiratory tract infection, sometimes these areas can become hyperplastic in response to infectioncan become a little enlarged.
  • These are usually bilateral.
  • a variant of normal
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245
Q

What is this clinical finding?

A

Sublingual Varices

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246
Q

What is this clinical finding?

A

Sublingual Varices

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247
Q

What is this clinical finding?

A

Sublingual Varices

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249
Q

What is this clinical finding?

A

Circumvallate papillae

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251
Q

What is this clinical finding?

A

Parotid Papillia (Stenson duct)

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252
Q

What is this clinical finding?

A

Parotid Papillia (Stenson duct)

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253
Q

What is Lymphoepithelial
cyst?

A

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

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

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254
Q

What is this clinical finding?

A

Linea Alba

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256
Q

What is this clinical finding?

A

Leukoedema

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257
Q

Fordyce Granules

A
  • Occurs on the buccal labial mucosa, retro molar pad and tonsillar area and lips
  • They are white or yellow ectopic sebaceous glands
  • They can be present in small or large quantity
  • Why do we have sebaceous glands in mouth? we dont know, evolutionary advantage? we don’t really understand.
  • a variant of normal
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258
Q

What is this clinical finding?

A

Palatal Rugae

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261
Q

Fimbriated
fold/Plica
semiluminaris

A
  • Some patients have more obvious fimbriated folds or plica semilunaris in their mouths than others
  • When you look at the ventral surface of the tongue, you’ll sometimes be able to pick these up.
  • These are duct opening from a series of salivary glands, minor glands, but they’re a little bit different than other minor glands in the mouth.
  • They produce more of a viscous type of saliva, and they are the glands of the Blandin and Nuhn
  • a variant of normal
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263
Q

What is a Frenal tag?

A
  • Frenal attachments are thin folds of mucous membrane with enclosed muscle fibers that attach the lips to the alveolar mucosa and underlying periosteum.
  • Most often, during the oral examination of the patient the dentist gives very little importance to the frenum, for assessing its morpholology and attachment.
  • Sometimes occur; essentially normal of varient
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265
Q

Sublingual Varices

A
  • Tortuous dilated vessels (enlarged engourged veins) on the ventral surface of the tongue, and sometimes stretch onto lateral border
  • Appears bluish purple in color
  • More prominent with increasing age; we don’t see it in younger pts.
  • Nothing to be concerned about, a variant of normal
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269
Q

Circumvallate papillae

A
  • Located in the posterior region of the tongue; dividing the body from the base
  • They are mushroom shaped and arranged in V-shape formation
  • Although they are usually not apparent in most patients, you may be able to visualize them in some
  • a variant of normal
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271
Q

Parotid Papillia (Stenson duct)

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

A normal of variant

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274
Q

Linea Alba

A

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

  • due to some friction In that area. (the buccal mucosa)
  • It varies in thickness and opacity
  • Can be seen in some patients who have bruxism
  • a variant of normal
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276
Q

Leukoedema

A
  • A bluish and white filmy opalescence of the mucosa is observed
  • In order to differentiate it from other white lesions à gently stretch the patient’s cheek forward and the leukoedema will disappear or partly fade and appears less apparent
  • It is commonly found in people of color and some smokers.
  • a variant of normal
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278
Q

Palatal Rugae

A
  • Raised ridges or folds
  • Located in the anterior palate on either side of the mid-palatine raphe behind the incisive papilla
  • They vary in number and size
  • May increase with age
  • a variant of normal
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279
Q

Inflammatory/Reactive Lesions of the Salivary Glands

List 5

A
  • mucocele/mucous cyst
  • ranula
  • necrotizing sialometaplasia
  • sialolithiasis
  • sialadentitis
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280
Q

Mucocele

Definition

Clinical features

Location

Histological features

Treatment

A

• definition: a lesion that forms when a salivary gland duct is severed & secretion spills into the adjacent CT
a pseudocyst (not lined by epithelium) — mucous builds up in the CT & causes a bump
• clinical features:

  • swelling in the tissue that may increase & decrease in size
  • may have a bluish hue, fluctuant on palpation — fluid filled, soft, compressible

location: lower lip most common site, but may form in any area where there are minor salivary glands

• histologic features:
- a cyst-like space in soft tissue
- lined by compressed granulation tissue
- lumen filled with mucin, foamy macrophages & inflammatory cells
• treatment: surgical excision, removal of associated minor salivary glands
• may recur if don’t remove all associated injured minor salivary glands

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281
Q

What is this clinical finding?

A

Mucocele

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283
Q

What is this clinical finding?

A

Mucous Cyst

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285
Q

What is this clinical finding?

A

Ranula

Notice how it’s unilateral

on the floor of the mouth

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286
Q

What is this clinical finding?

A

Ranula

  • Notice how it’s unilateral*
  • on the floor of the mouth*
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287
Q

Necrotizing Sialometaplasia

Definition

Predisposing factors

Clinical features

Histologic features

Treatment

A

• Definition: locally destructive inflammatory condition — looks malignant but is benign
• salivary gland ischemia — “heart attack of the palate”; blood flow is interrupted
• predisposing factors:
- local trauma
- palatal injection of local anesthesia
- previous surgery
- many are idiopathic..
• usually a clinical diagnosis based on history & how fast — palate uncommon for SCC
• clinical features:
- initially appears as a non-ulcerated swelling of the palate
- often associated with pain or paresthesia
- within 2-3 weeks, necrotic tissue sloughs off & becomes a crater-like ulcer
- patient may say: “a chunk of the roof of my mouth fell out”
• histologic features:
- necrosis of the salivary glands — coagulative necrosis (green circles in histology —>)
- salivary gland duct epithelium is replaced by squamous epithelium — appear as islands of squamous epithelium deep in the CT & resembles SCC (arrows in histology —>)
Treatment: no treatment, spontaneously resolves within 6 to 10 weeks
irrigating & debriding the area can reintroduce vascularity & help healing

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288
Q

What is this clinical finding?

A

Necrotizing Sialometaplasia

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289
Q

Sialolithiasis

Definition

Location

Origin

Clinical features

Radiological features

Histological features

Treatment

A

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

Location: occur in both major & minor salivary glands

• floor of the mouth is most common location (Wharton’s duct is a common place)

• often causes obstruction of the duct

Origin: arise from desposition of calcium salts around nidus of debris within the duct lumen

  • *clinical features:**- minor glands: hard yellowish structure in soft tissue
  • may be visible on a radiograph
  • recurrent swelling (due to the obstruction)
  • episodic pain & swelling during times of increased salivation
  • can be palpated if the stone is located toward the terminal portion of the duct
  • *Radiological features** : may be viewed as a radiopacity on an occlusal x-ray–well defined radiopacity
  • *Histological features-** concentric rings of calcification, color of it in stain depends on level of calcificatio
  • *Treatment**: promote passage of stone (massage, sialogogues, increase fluid intake) or surgical removal
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290
Q

What is this clinical finding?

A

Sialolithiasis

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291
Q

What is this clinical finding?

A

Sialolithiasis

Notice how it can appear radiographically as a well defined radiolucency

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292
Q

What is this Radiographical finding?

A

Sialolithiasis

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293
Q

Mucous Cyst

Definition

Clinical features

Histological features

Treatment

A

Definition: a pseudocyst
• microscopicallly appears as an epithelial lined cystic structure that is actually a dilated duct
clinically you CANNOT tell the difference between a mucocele & mucous cyst
• clinical features:
- same as a mucocele
• histologic features:
- same as mucocele but will see an epithelial lining (but actually a dilated duct)
treatment: same as mucocele; surgical excision

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294
Q

What is this clinical finding?

A

Sialadenitis

Acute: parotid papilla purulent discharge

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295
Q

What is this clinical finding?

A

Sialadenitis

Chronic: caused fibrosis

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296
Q

Summery

of inflmattory salivaory conditions

A

Mucocele

  • fluctuant swelling
  • bluish hue
  • lower lip most common

Ranula

  • fluctuant swelling
  • floor of mouth

Sialolithisis

• major glands: episodic pain &
swelling of affected gland
• minor glands: asymptomatic/
local swelling or tenderness
• if superficial - firm to palpation
& yellowish color

Necrotizing
Sialometaplasia

• initial painful swelling
• later necrotic ulcer
• posterior lateral hard
palate & soft palate

Sialadenitis

• painful swelling of
affected gland
• purulent discharge if
acute infection

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298
Q

Ranula

Definition

Associated with

Clinical features

Treatment

A

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

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307
Q

Sialadenitis

definition

causes:

clinical features:

histologic features:

Treatment:

A

definition: acute or chronic inflammation in major or minor salivary glands
• causes:
• obstruction of a salivary gland duct (sialolith)
• infection (mumps [viral], staph aureus [bacterial, most common], candida [fungal])
• decreased salivary flow (Sjogren’s, sarcoidosis)
• parotid gland = parotitis
• clinical features:
- acute: most common in parotid, swollen & painful gland, erythematous & warm overlying mucosa/skin, purulent discharge, low-grade fever
- chronic: caused by recurrent or persistent ductal obstruction, periodic swelling & pain
• histologic features:
- acute or chronic inflammatory cell infiltrate in the salivary gland
- in chronic cases = salivary gland replaced by fibrous CT & fat
- cells: acute = neutrophils ;; chronic = lymphocytes, plasma cells, macrophages
• Treatment: antibiotics, rehydration, surgical drainage, or surgical removal of gland

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308
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

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309
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

310
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
311
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
312
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

313
Q

How do we treat this?

A

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

Ulcer

314
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

315
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

316
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

317
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
318
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
319
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
320
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
321
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

322
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
323
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

324
Q

What is this clinical finding?

A

‐ Aphthous Ulcer of the tongue

‐ Aphthous ulcers can occur on specialized structures of the mouth

325
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

327
Q

Rx Topical
Treatments:
Corticosteroid
Rinse‐

A

‐ Dexamethasone elixir 0.5mg/5ml (ETOH base) or solution (H20 base)
‐ Indicated for difficult to reach lesions to obtain access to all of them
o Disp:600ml
o Label: swish with 5‐10 ml for 5 minutes up to 0.5mg/5mL 4x/day and
expectorate 00s preservalve.) May be used as suppressive therapy in
selected patients with close surveillance
o Prevent recurrences
‐ May buy an EXTRA DAY of healing time

dr. Kerr prefers the elixir

331
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
341
Q

Rx Topical
Treatments:
Corticosteroids

for

Ulcers

A

‐ Triamcinolone acetonide in Orabase 0.1% (intermediate)
o Disp: 5g tube Dental Past
o Label: apply a thin film over ulcer after meals and bedtime APOTHECON
o Do not use for more than 2 weeks

‐ Fluocinonide gel or ointment 0.05% (Potent)
o Disp: 15g tube
o Label: apply a thin film over
o Do not use for more than 2 weeks
‐ Clobetasol ointment 0.05% (Ultra potent)
o Disp: 15gtube Label: apply a thin film over ulcer bid

343
Q

Problem with topical tx

A

Topical Treatments
‐ Drug is easily washed away or rubbed off
‐ Topical anesthetics have a short‐lived effect
‐ Often difficult to apply due to location
‐ Cost may be a disincentive to buy OTC
‐ Once ulcers are established, these treatments are not as effective, therefore
abortive treatment early on is preferred

344
Q

What about
systemic
treatments – taking
pills to treat ulcers?

A

‐ Prednisone or systemic steroids were the one systemic treatment that Dr. Kerr
has has success with in practice

o 0.5 mg/kg of Prednisone would be prescribed for about 1 week

o Very successful in patients with frequent outbreaks of multiple canker
sores
‐ In some limited cases Dr. Kerr has seen some success with:
o Colchicine
o Pentoxifylline

345
Q
A
346
Q

What is this clinical presentation?

A

Homogeneous leukoplakia

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

347
Q

What is this clinical presentation?

A

Homogeneous leukoplakia.

○ Non-wipeable white patch

348
Q

What is this clinical presentation?

A

homogenous leukoplakia

Just
white color

349
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

350
Q

What is this clinical presentation?

A

Speckled leukoplakia.

Non-homogenous leukoplakia

353
Q

What is this clinical presentation?

A

Hairy Leukoplakia

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

354
Q

What is this clinical presentation?

A

Hairy Leukoplakia

357
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

358
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

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

359
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Multifocal

361
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

362
Q

What is this clinical presentation?

A

Oral lichen planus

on the buccal mucosa (most common site

reticular form.

363
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

364
Q

What is this clinical presentation?

A

Oral lichen planus

Lichen planus of the dorsum of the tongue

this is a hypertrophic form.

365
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.

366
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
367
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

368
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.

369
Q

What is this clinical presentation?

pts takes Thiazide Diuretic

A

Oral Lichenoid Drug
Reaction

370
Q

What is this clinical presentation?

pts takes allopurinol

A

Oral Lichenoid Drug
Reaction

372
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
374
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
375
Q

What is this clinical presentation?

A

Nicotinic Stomatitis

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

376
Q

What is this clinical presentation

A

Nicotine Stomatitis.

377
Q

Hairy Leukoplakia

Etiology

A

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

378
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
379
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)

380
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
381
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

382
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

383
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

384
Q

What is this clinical presentation?

A

Geographic tongue, localized lesion.

387
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.

388
Q

What is this clinical presentation?

A

Leukoedema of the buccal mucosa.
Laskaris,

390
Q

What is this clinical presentation?

A

White Sponge Nevus

Diffuse, thickened white plaques
of the buccal mucosa

391
Q

What is this clinical presentation?

A

White Sponge Nevus

(Canon disease)

392
Q

Proliferative Verrucous Leukoplakia

Treatment

A

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

Lesions rarely regress despite therapy

393
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Early verrucous carcinoma of the buccal mucosa.

394
Q

What is this clinical presentation?

A

Verrucous Carcinoma

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

395
Q

What is this clinical presentation?

A

Verrucous Carcinoma

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

396
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Extensive papillary, white
lesion of the maxillary vestibule

399
Q
A

Traumatic Erythema /Traumatic Hematoma

on the lower lip.

400
Q

What is this clinical presentation?

A

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

401
Q

What is this clinical presentation?

A

Median rhomboid glossitis.

a Chronic hyperplastic, erythematous candidiasis

404
Q

what is this clinical presentation?

A

Denture stomatitis.

405
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.

406
Q

What is this clinical presentation?

A

Erythroplakia

of the buccal mucosa

Well-demarcated erythematous patch or plaque with soft velvety texture

407
Q

What is this clinical presentation?

A

Erythroplakia of the buccal mucosa.

408
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

409
Q

What is this clinical presentation?

A

Erythroplakia

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

transformed into SCC

410
Q

Oral lichen planus

Treatment:

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

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

411
Q

What is this clinical presentation?

A

Erythroplakia.

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

412
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.

413
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

414
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Severe

415
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.

417
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

. Multiple erosions affecting the
marginal gingiva.

418
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Multiple erosions of the left
buccal mucosa and soft palate.

419
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

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

420
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

424
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
426
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.

430
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.
431
Q

Nicotine Stomatitis.

Etiology

A

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

438
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
439
Q

Geographic tongue/
areata migrans

Etiology

A

The exact etiology remains unknown. It may be genetic.

442
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

445
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.

450
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
451
Q

Verrucous Carcinoma

Treatment

A

○ Surgical Excision

○ Radiotherapy

455
Q

Median Rhomboid Glossitis

Treatment

A

No treatment is required.

456
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

458
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

463
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

469
Q

Smokeless tobacco keratosis

Treatment:

A

typically resolves weeks after cessation

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

470
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

471
Q

What is this clinical presentation?

A

Erythroplakia.

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

472
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.

473
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

474
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Severe

475
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.

477
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

. Multiple erosions affecting the
marginal gingiva.

478
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Multiple erosions of the left
buccal mucosa and soft palate.

479
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

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

480
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

481
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

482
Q

What is this clinical presentation?

A

Pemphigus vulgaris

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

483
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

484
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

487
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

488
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal

can
result in functional
blindness

489
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

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

490
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

493
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

494
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.

495
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

496
Q

Smokeless tobacco keratosis

Treatment:

A

typically resolves weeks after cessation

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

499
Q

What is this clinical presentation?

A

SCC

arising from Actinic Cheilitis

500
Q

What is this clinical presentation?

A

Oral Melanoma

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

501
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.

502
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.)

503
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.

504
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. .

505
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.

506
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.

510
Q

What is this clinical presentation

A

Oral Melanoma

511
Q

What is this clinical presentation

A

Oral Melanoma

512
Q

What is this clinical presentation

A

Oral Melanoma

513
Q

What is this clinical presentation?

A

Traumatic ulcer

caused by sharp or puncturing food stuff

514
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

515
Q

What is this clinical presentation?

A

Traumatic ulcer

Post-anaesthesia traumatic ulcer on lower lip.

516
Q

What is this clinical presentation?

A

Traumatic ulcer

Most often on tongue, lips, buccal mucosa

Any sites that may be injured by dentition

517
Q

What is this clinical presentation?

A

Traumatic

Granuloma

518
Q

What is this clinical presentation?

A

Traumatic

Granuloma

(traumatic ulcertaive granuloma)

519
Q

What is this clinical presentation?

A

Traumatic Granuloma

( Traumatic Ulcerative Granuloma)

522
Q

What is this clinical presentation?

A

Squamous cell carcinoma

on the buccal mucosa)

523
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

524
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).

526
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.

527
Q

What is this clinical presentation?

A

Graphite tattoo

Most common location on the palate and gingiva

Gray, black, or blue-ish macule

528
Q

What is this clinical presentation?

A

Graphite tattoo

Gray, black, or blue-ish macule

529
Q

Pemphigus vulgaris

Treatment

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)

531
Q

What is this clinical presentation?

A

Traumatic ulcer of the tongue.

532
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.

533
Q

What is this clinical finding?

A

Hemangioma of Infancy

536
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

538
Q

Mucous membrane pemphigoid

Etiology

A

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

539
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.

540
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.

541
Q

Frictional Keratosis.

Differential Diagnosis

A

Leukoplakia

Linea alba

Chronic cheek chewing (bite injury)

Candidiasis

Oral Lichen planus

Squamous cell carcinoma

542
Q

What is this clinical finding?

A

Frictional keratosis

on the tongue

543
Q

Frictional Keratosis

Etiology

A
  • Trauma from Sharp cusp & ortho appliance
  • Chronic mechanical irritation (chronic biting)
  • Masticatory function
  • Normal hyperplastic response
  • Dentures/missing teeth
544
Q

Frictional Keratosis

Treatment

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

excellent prognosis

545
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.

546
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.
547
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

548
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

549
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**
553
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

554
Q

Actinic cheilitis

Etiology

A

due to chronic ultraviolet light exposure.

555
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

559
Q

Severity of patients
with xerostomia using
objective measures

A
564
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)

565
Q

What is this clinical presentation?

A

SJÖGREN’S SYNDROME

Dry Mouth

very severe
cervical disease & very dry lips

566
Q

What is this clinical presentation?

A

Depapillated &
Fissured Tongue

SJÖGREN’S SYNDROME

567
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.

568
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)
569
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.
571
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

572
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.

573
Q

Oral Melanoma

Treatment

A
  • Surgical excision
  • Radiotherapy
  • Chemotherapy
584
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
585
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

589
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

590
Q

SCC treatment

A

Early stage: Radiation and/or Surgical removal

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

593
Q

Graphite tattoo

Treatment

A

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

594
Q

Graphite tattoo

Etiology

A

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

598
Q

Hemangioma of Infancy

Treatment

A

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

599
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

601
Q

Necrotizing Sialadenometaplasia

Etiology

A

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

602
Q

Necrotizing Sialadenometaplasia

Treatment

A

No Treatment Needed

but we need to biopsy to rule out other diseases

613
Q

What is this clinical finding?

A

Xerostomia-related Caries

Or

Dry Mouth

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

614
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)

615
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

616
Q

What is the normal rate for Unstimulated Saliva
Production

A

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

617
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).

618
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)

619
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.

620
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?
621
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
622
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

624
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)
625
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).
626
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
627
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

628
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

629
Q

What is this clinical presentation?

A

Erythroplakia.

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

630
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.

631
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

632
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Severe

633
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.

635
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

. Multiple erosions affecting the
marginal gingiva.

636
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Multiple erosions of the left
buccal mucosa and soft palate.

637
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

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

638
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

639
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

640
Q

What is this clinical presentation?

A

Pemphigus vulgaris

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

641
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

642
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

645
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

646
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal

can
result in functional
blindness

647
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

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

648
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

651
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

652
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.

653
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

654
Q

Smokeless tobacco keratosis

Treatment:

A

typically resolves weeks after cessation

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

657
Q

What is this clinical presentation?

A

SCC

arising from Actinic Cheilitis

658
Q

What is this clinical presentation?

A

Oral Melanoma

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

659
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.

660
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.)

661
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.

662
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. .

663
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.

664
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.

668
Q

What is this clinical presentation

A

Oral Melanoma

669
Q

What is this clinical presentation

A

Oral Melanoma

670
Q

What is this clinical presentation

A

Oral Melanoma

671
Q

What is this clinical presentation?

A

Traumatic ulcer

caused by sharp or puncturing food stuff

672
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

673
Q

What is this clinical presentation?

A

Traumatic ulcer

Post-anaesthesia traumatic ulcer on lower lip.

674
Q

What is this clinical presentation?

A

Traumatic ulcer

Most often on tongue, lips, buccal mucosa

Any sites that may be injured by dentition

675
Q

What is this clinical presentation?

A

Traumatic

Granuloma

676
Q

What is this clinical presentation?

A

Traumatic

Granuloma

(traumatic ulcertaive granuloma)

677
Q

What is this clinical presentation?

A

Traumatic Granuloma

( Traumatic Ulcerative Granuloma)

680
Q

What is this clinical presentation?

A

Squamous cell carcinoma

on the buccal mucosa)

681
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

682
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).

684
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.

685
Q

What is this clinical presentation?

A

Graphite tattoo

Most common location on the palate and gingiva

Gray, black, or blue-ish macule

686
Q

What is this clinical presentation?

A

Graphite tattoo

Gray, black, or blue-ish macule

687
Q

Pemphigus vulgaris

Treatment

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)

689
Q

What is this clinical presentation?

A

Traumatic ulcer of the tongue.

690
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.

691
Q

What is this clinical finding?

A

Hemangioma of Infancy

694
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

696
Q

Mucous membrane pemphigoid

Etiology

A

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

697
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.

698
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.

699
Q

Frictional Keratosis.

Differential Diagnosis

A

Leukoplakia

Linea alba

Chronic cheek chewing (bite injury)

Candidiasis

Oral Lichen planus

Squamous cell carcinoma

700
Q

What is this clinical finding?

A

Frictional keratosis

on the tongue

701
Q

Frictional Keratosis

Etiology

A
  • Trauma from Sharp cusp & ortho appliance
  • Chronic mechanical irritation (chronic biting)
  • Masticatory function
  • Normal hyperplastic response
  • Dentures/missing teeth
702
Q

Frictional Keratosis

Treatment

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

excellent prognosis

703
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.

704
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.
705
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

706
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

707
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**
711
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

712
Q

Actinic cheilitis

Etiology

A

due to chronic ultraviolet light exposure.

713
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

717
Q

Severity of patients
with xerostomia using
objective measures

A
722
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)

723
Q

What is this clinical presentation?

A

SJÖGREN’S SYNDROME

Dry Mouth

very severe
cervical disease & very dry lips

724
Q

What is this clinical presentation?

A

Depapillated &
Fissured Tongue

SJÖGREN’S SYNDROME

725
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.

726
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)
727
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.
729
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

730
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.

731
Q

Oral Melanoma

Treatment

A
  • Surgical excision
  • Radiotherapy
  • Chemotherapy
742
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
743
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

747
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

748
Q

SCC treatment

A

Early stage: Radiation and/or Surgical removal

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

751
Q

Graphite tattoo

Treatment

A

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

752
Q

Graphite tattoo

Etiology

A

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

756
Q

Hemangioma of Infancy

Treatment

A

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

757
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

759
Q

Necrotizing Sialadenometaplasia

Etiology

A

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

760
Q

Necrotizing Sialadenometaplasia

Treatment

A

No Treatment Needed

but we need to biopsy to rule out other diseases

771
Q

What is this clinical finding?

A

Xerostomia-related Caries

Or

Dry Mouth

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

772
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)

773
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

774
Q

What is the normal rate for Unstimulated Saliva
Production

A

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

775
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).

776
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)

777
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.

778
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?
779
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
780
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

782
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)
783
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).
784
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
785
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