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Oral Pathology > More diseaess-Kerr, Dry mouth > Flashcards

More diseaess-Kerr, Dry mouth Flashcards

1
Q

What is this clinical presentation?

A

Homogeneous leukoplakia

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

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2
Q

What is this clinical presentation?

A

Homogeneous leukoplakia.

○ Non-wipeable white patch

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3
Q

What is this clinical presentation?

A

homogenous leukoplakia

Just
white color

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4
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

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5
Q

What is this clinical presentation?

A

Speckled leukoplakia.

Non-homogenous leukoplakia

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6
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.

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7
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
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8
Q

What is this clinical presentation?

A

Hairy Leukoplakia

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

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9
Q

What is this clinical presentation?

A

Hairy Leukoplakia

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10
Q

Hairy Leukoplakia

Etiology

A

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

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11
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
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12
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

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13
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

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

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14
Q

What is this clinical presentation?

A

Proliferative Verrucous Leukoplakia

Multifocal

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15
Q

Proliferative Verrucous Leukoplakia

Treatment

A

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

Lesions rarely regress despite therapy

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16
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

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17
Q

What is this clinical presentation?

A

Oral lichen planus

on the buccal mucosa (most common site

reticular form.

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18
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

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19
Q

What is this clinical presentation?

A

Oral lichen planus

Lichen planus of the dorsum of the tongue

this is a hypertrophic form.

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20
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.

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21
Q

Oral lichen planus

Treatment:

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

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

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22
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

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23
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.

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24
Q

What is this clinical presentation?

pts takes Thiazide Diuretic

A

Oral Lichenoid Drug
Reaction

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25
Q

What is this clinical presentation?

pts takes allopurinol

A

Oral Lichenoid Drug
Reaction

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26
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
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27
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
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28
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.

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29
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
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30
Q

What is this clinical presentation?

A

Nicotinic Stomatitis

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

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31
Q

What is this clinical presentation

A

Nicotine Stomatitis.

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32
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.
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33
Q

Nicotine Stomatitis.

Etiology

A

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

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34
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)

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35
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
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36
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

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37
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

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38
Q

What is this clinical presentation?

A

Geographic tongue/
areata migrans

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39
Q

What is this clinical presentation?

A

Geographic tongue, localized lesion.

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40
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
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41
Q

Geographic tongue/
areata migrans

Etiology

A

The exact etiology remains unknown. It may be genetic.

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42
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.

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43
Q

What is this clinical presentation?

A

Leukoedema of the buccal mucosa.
Laskaris,

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44
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

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45
Q

What is this clinical presentation?

A

White Sponge Nevus

Diffuse, thickened white plaques
of the buccal mucosa

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46
Q

What is this clinical presentation?

A

White Sponge Nevus

(Canon disease)

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47
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.

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48
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Early verrucous carcinoma of the buccal mucosa.

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49
Q

What is this clinical presentation?

A

Verrucous Carcinoma

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

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50
Q

What is this clinical presentation?

A

Verrucous Carcinoma

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

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51
Q

What is this clinical presentation?

A

Verrucous Carcinoma

Extensive papillary, white
lesion of the maxillary vestibule

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52
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
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53
Q

Verrucous Carcinoma

Treatment

A

○ Surgical Excision

○ Radiotherapy

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54
Q
A

Traumatic Erythema /Traumatic Hematoma

on the lower lip.

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55
Q

What is this clinical presentation?

A

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

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56
Q

What is this clinical presentation?

A

Median rhomboid glossitis.

a Chronic hyperplastic, erythematous candidiasis

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57
Q

Median Rhomboid Glossitis

Treatment

A

No treatment is required.

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58
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

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59
Q

what is this clinical presentation?

A

Denture stomatitis.

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60
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

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61
Q

What is this clinical presentation?

A

Erythroplakia

of the buccal mucosa

Well-demarcated erythematous patch or plaque with soft velvety texture

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62
Q

What is this clinical presentation?

A

Erythroplakia of the buccal mucosa.

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63
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

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64
Q

What is this clinical presentation?

A

Erythroplakia

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

transformed into SCC

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65
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

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66
Q

What is this clinical presentation?

A

Erythroplakia.

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

67
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.

68
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

69
Q

What is this clinical presentation?

A

Smokeless tobacco keratosis/TOBACCO POUCH KERATOSIS

Tobacco Pouch Keratosis, Severe

70
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.

71
Q

Smokeless tobacco keratosis

Treatment:

A

typically resolves weeks after cessation

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

72
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

. Multiple erosions affecting the
marginal gingiva.

73
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

Multiple erosions of the left
buccal mucosa and soft palate.

74
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

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

75
Q

What is this clinical presentation?

A

Pemphigus Vulgaris.

76
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

77
Q

What is this clinical presentation?

A

Pemphigus vulgaris

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

78
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

79
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

80
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.

81
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)

82
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

83
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

SEVERE/HIGH RISK FORMS OF MMP
▪ Ocular
▪ Esophageal

can
result in functional
blindness

84
Q

What is this clinical presentation?

A

Mucous membrane pemphigoid

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

85
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

86
Q

Mucous membrane pemphigoid

Etiology

A

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

87
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**
88
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

89
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.

90
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

​

91
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

92
Q

Actinic cheilitis

Etiology

A

due to chronic ultraviolet light exposure.

93
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

94
Q

What is this clinical presentation?

A

SCC

arising from Actinic Cheilitis

95
Q

What is this clinical presentation?

A

Oral Melanoma

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

96
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.

97
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.)

98
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.

99
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. .

100
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.

101
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.

102
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

103
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.

104
Q

Oral Melanoma

Treatment

A
  • Surgical excision
  • Radiotherapy
  • Chemotherapy
105
Q

What is this clinical presentation

A

Oral Melanoma

106
Q

What is this clinical presentation

A

Oral Melanoma

107
Q

What is this clinical presentation

A

Oral Melanoma

108
Q

What is this clinical presentation?

A

Traumatic ulcer

caused by sharp or puncturing food stuff

109
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

110
Q

What is this clinical presentation?

A

Traumatic ulcer

Post-anaesthesia traumatic ulcer on lower lip.

111
Q

What is this clinical presentation?

A

Traumatic ulcer

Most often on tongue, lips, buccal mucosa

Any sites that may be injured by dentition

112
Q

What is this clinical presentation?

A

Traumatic

Granuloma

113
Q

What is this clinical presentation?

A

Traumatic

Granuloma

(traumatic ulcertaive granuloma)

114
Q

What is this clinical presentation?

A

Traumatic Granuloma

( Traumatic Ulcerative Granuloma)

115
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
116
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

117
Q

What is this clinical presentation?

A

Squamous cell carcinoma

on the buccal mucosa)

118
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

119
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).

120
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

121
Q

SCC treatment

A

Early stage: Radiation and/or Surgical removal

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

122
Q

What is this clinical presentation?

A

Graphite tattoo

Most common location on the palate and gingiva

Gray, black, or blue-ish macule

123
Q

What is this clinical presentation?

A

Graphite tattoo

Gray, black, or blue-ish macule

124
Q

Graphite tattoo

Treatment

A

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

125
Q

Graphite tattoo

Etiology

A

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

126
Q

What is this clinical presentation?

A

Traumatic ulcer of the tongue.

127
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.

128
Q

What is this clinical finding?

A

Hemangioma of Infancy

129
Q

Hemangioma of Infancy

Treatment

A

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

130
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

131
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

132
Q

Necrotizing Sialadenometaplasia

Etiology

A

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

133
Q

Necrotizing Sialadenometaplasia

Treatment

A

No Treatment Needed

but we need to biopsy to rule out other diseases

134
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.

135
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.

136
Q

Frictional Keratosis.

Differential Diagnosis

A

Leukoplakia

Linea alba

Chronic cheek chewing (bite injury)

Candidiasis

Oral Lichen planus

Squamous cell carcinoma

137
Q

What is this clinical finding?

A

Frictional keratosis

on the tongue

138
Q

Frictional Keratosis

Etiology

A
  • Trauma from Sharp cusp & ortho appliance
  • Chronic mechanical irritation (chronic biting)
  • Masticatory function
  • Normal hyperplastic response
  • Dentures/missing teeth
139
Q

Frictional Keratosis

Treatment

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

excellent prognosis

140
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.

141
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.
142
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

143
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

144
Q

What is this clinical finding?

A

Xerostomia-related Caries

Or

Dry Mouth

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

145
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)

146
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

147
Q

What is the normal rate for Unstimulated Saliva
Production

A

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

148
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).

149
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)

150
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.

151
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?
152
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
153
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

154
Q

Severity of patients
with xerostomia using
objective measures

A
155
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)
156
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).
157
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
158
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

159
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)

160
Q

What is this clinical presentation?

A

SJÖGREN’S SYNDROME

Dry Mouth

very severe
cervical disease & very dry lips

161
Q

What is this clinical presentation?

A

Depapillated &
Fissured Tongue

SJÖGREN’S SYNDROME

162
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.

163
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)
164
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.

Oral Pathology (23 decks)

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