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GI 2 Pathology--Chapt 16 and 17 > Chapter 16--Oral Cavity > Flashcards

Chapter 16--Oral Cavity Flashcards

1
Q

Caries (Tooth decay)

A
  • rfocal tooth degradation due to mineral dissolution (enamel and dentin); it occurs through acids released by oral bacteria during sugar fermentation
  • most common reason for tooth loss before age 35
  • Before was more common in industrialized countries bc of increased refined sugar consumption, but now more common in developing nations (more processed foods)
  • Decreased incidence in industrialized countries bc of oral hygiene and fluoridation of water (fluoride incorporates into crystalline structure of enamel forming fluorapetite which makes teeth resistance to degradation by bacterial acids)
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2
Q

Gingivitis

A
  • soft tissue inflammation of the squamous mucosa and soft tissues around teeth with erythema, edema, bleeding and gingival degeneration
  • Inadequate oral hygiene leads to accumulation of dental plaque (sticky, colorless biofilm of bacteria, salivary proteins, and desquamated epithelial cells) with subsequent mineralization (tartar/calculus); plaque bacteria causes caries, and plaque buildup below the gum line leads to gingivitis
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3
Q

Periodontitis

A
  • Inflammation of tooth-supporting structures (e.g., periodontal ligaments, alveolar bone, and cementum); can progress to complete destruction of the periodontal ligament (attachment of teeth to alveolar bone) and alveolar bone with tooth loss
  • poor oral hygiene–change in oral flora
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4
Q

Facultative gram-positive colonization of typical plaque vs. periodontitis-associated plaque (differences)

A
  • periodontitis associated plaque contains anaerobic and microaerophilic gram-negative flora
  • Aggregatibacter (actinobacillus) actinomycetemcomitans
  • porphyromonas gingivitis
  • prevotella intermedia
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5
Q

Periodontal disease and presentation (systemic vs. in isolation)

A
  • typically presents in isolation but can also occur in several systemic diseases, especially those affecting immunologic function
  • Periodontal disease can also underlie (cause) systemic diseases (infective endocarditis and brain abscesses)
  • associated with AIDS, leukemia, Crohn’s disease, diabetes, down syndrome, sarcoidosis, syndromes associated with neutrophil defect
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6
Q

Recap: Diseases of the oral cavity

A
  • Caries
  • Gingivitis
  • Periodontitis
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7
Q

Inflammatory and Reactive Lesions of the oral cavity

A

1) Aphthous Ulcers (Canker Sores)

2) Fibrous Proliferative Lesions–all benign!!

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8
Q

Aphthous Ulcers (Canker Sores)

A
  • affects unto 40% of Americans
  • can have familial predilection
  • most common–first 2 decades of life
  • recurrent ulcers associated with pure, IBD, and Behcet disease
  • single or multiple painful, shallow, hyperemic ulcerations initially infiltrated by mononuclear inflammatory cells
  • secondary bacterial infection recruits neutrophils
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9
Q

Fibrous Proliferative Lesions–what is it and the 4 types:

A
  • benign reactive lesions, usually cured by surgical excision:
    1) Traumatic/ Irritation fibromas
    2) Pyogenic granulomas
    3) Peripheral ossifying fibromas
    4) Peripheral giant cell granulomas
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10
Q

Traumatic/ Irritation fibromas

A
  • occur on the buccal mucosa along the “bite line” of gingiva
  • submucosal nodules of fibrous connective tissue/mass covered by squamous mucosa
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11
Q

Pyogenic granulomas

A
  • rapidly growing, highly vascular lesions similar to granulation tissue
  • common in children or during pregnancy
  • can regress (especially after pregnancy)
  • undergo fibrous maturation or develop into peripheral ossifying fibromas
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12
Q

Peripheral ossifying fibromas–cause, prognosis and treatment

A
  • can arise from pyogenic granulomas but most have unknown etiologies
  • 15-20% recurrence rate, surgical excision to periosteum is Tx of choice
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13
Q

Infections of the oral mucosa–how does it resist infection and how does infection occur?

A
  • resists by competitive suppression from low-virulence commensal organisms, high levels of IgA, the antibacterial properties of saliva and dilution from ingested food and liquids
  • Alteration in these defenses (due to immunodeficiency or antibiotic therapy) contributes to infections
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14
Q

Infection of the oral mucosa—names of types of infections

A
  • Herpes Simplex Virus
  • Oral Candidiasis (Thrush)
  • Deep fungal Infections
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15
Q

Herpes Simplex Virus infections (HSV1 and HSV2)

A
  • classically cause cold sores with minimal morbidity
  • 10-20% of primary infections present as acute herpetic gingivostomatitis with diffuse oral vesicles and ulceration, lymphadenopathy and fever
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16
Q

Morphology of HSV

A
  • Lesions consist of vesicles, large bullae, or shallow ulcerations
  • Histo: intracellular and intercellular edema (acantholysis), eosinophilic intranuclear inclusions and multinucleate giant cells (visualized by microscopic exam of vesicular fluid–Tzank test)
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17
Q

Morphology of HSV–healing and reactivation

A
  • Vesicles heal spontaneously in 3-4 weeks but virus treks along regional nerves and becomes dormant in local ganglia
  • Reactivation (driven by trauma, infection or immune suppression) occurs with crops of small vesicles that clear in 4-6 days
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18
Q

Most common fungal infection of the oral cavity? Where is it found?

A
  • Candida albicans

- Found in the normal oral flora in half the population

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19
Q

How does oral candidiasis present?

A

-can present as erythematous or hyperplastic lesions but classically manifests as superficial gray-white inflammatory membranes made of fibrinosuppurative exudates containing fungus

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20
Q

oral candidiasis occurs in the setting of? (aka cause)

A
  • broad-spectrum antibiotics
  • diabetes
  • neutropenia
  • immunodeficiency
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21
Q

Deep fungal infections–6

A
  • Histoplasmosis
  • blastomycosis
  • coccidiodomycosis
  • cryptococcosis
  • zygomycosis
  • Aspergillosis
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22
Q

Where do deep fungal infections occur? What increases the risk of developing deep fungal infections?

A
  • have predilection for the oral cavity and head and neck region
  • Immunocompromise increases risk
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23
Q

Oral manifestations of Systemic Disease–Hairy Leukoplakia

A
  • distinctive oral lesion seen in immunocompromised patients (80% are HIV infected)
  • Caused by Epstein-Barr virus (EBV)
  • white patches of hyperkeratosis on tongue lateral borders
  • superimposed candidal infections can augment the hariness
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24
Q

Systemic diseases that are INFECTIOUS that also have oral manifestations (5):

A
  • Scarlet fever
  • Measles
  • Infectious mononucleosis
  • Diptheria
  • HIV
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25
Q

Scarlet fever–associated oral changes

A

-Fiery red tongue with prominent papillae (raspberry tongue); white-coated tongue through which hyperemic papillae project (strawberry tongue)

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26
Q

Measles–associated oral changes

A
  • Spotty enanthema in the oral cavity often precedes the skin rash
  • Ulcerations on the buccal mucosa about Stenson duct produce Koplik spots
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27
Q

Infectious mononucleosis–associated oral changes

A
  • Acute pharyngitis and tonsillitis that may cause coating with a gray-white exudative membrane
  • Enlargement of lymph nodes in the neck, palatal petechiae
28
Q

Diphtheria–associated oral changes

A

-Characteristic dirty white, fibrinosuppurative, tough, inflammatory membrane over the tonsils and retropharynx

29
Q

HIV–associated oral changes

A
  • Predisposition to opportunistic oral infections–especially HSV, Candida, and other fungi
  • Oral lesions of Kaposi sarcoma and hairy leukoplakia
30
Q

Systemic diseases that are Dermatologic that have associated oral changes (4):

A
  • Lichen planus
  • Pemphigus
  • Bullous pemphigoid
  • Erythema multiforme
31
Q

Lichen planes–associated oral changes

A
  • Reticulate, lacelike, white keratotic lesions that sometimes ulcerate and rarely form bullae
  • seen in more than 50% of patients with cutaneous lichen plants
  • rarely the sole manifestation
32
Q

Pemphigus–associated oral changes

A

-Vesicles and bullae prone to rupture, leaving hyperemic erosions covered with exudates

33
Q

Bullous pemphigoid–associated oral changes

A

-Oral lesions (mucous membrane pemphigoid) resemble those of pemphigus but can be differentiated histologically

34
Q

Erythema multiforme–associated oral changes

A
  • Maculopapular, vesiculobullous eruption that sometimes follows an infection elsewhere, ingestion of drugs, development of cancer or a collagen vascular disease
  • called Stevens-Johnson syndrome when there is widespread mucosa and skin involvement
35
Q

Systemic diseases that are HEMATOLOGIC that have associated oral changes (3)

A
  • Pancytopenia
  • Leukemia
  • Monocytic leukemia
36
Q

Pancytopenia (agranulocytosis, aplastic anemia)–associated oral changes

A
  • Severe oral infections in the form of gingivitis, pharyngitis, tonsillitis
  • may extend to produce cellulitis of the neck (Ludwig angina)
37
Q

Leukemia–associated oral changes

A

-With depletion of functioning neutrophils, oral lesions may appear like those in pancytopenia

38
Q

Monocytic leukemia–associated oral changes

A

-Leukemic infiltration and enlargement of the gingivae, often with accompanying periodontitis

39
Q

Miscellaneous systemic diseases that have associated oral changes (4)

A
  • Melanotic pigmentation
  • Phenytoin (Dilantin) ingestion
  • Pregnancy
  • Rendu-Osler-Weber syndrome
40
Q

Melanotic pigmentation–associated oral changes

A

-May appear in Addision disease, hemochromatosis, fibrous dysplasia of bone (Albright syndrome) and Peutz-Jeghers syndrome (gastrointestinal polyposis)

41
Q

Phenytoin (Dilantin) ingestion–associated oral changes

A

-Striking fibrous enlargement of gingivae

42
Q

Pregnancy–associated oral changes

A

-A friable, red, pyogenic granuloma protruding from the gingiva (“pregnancy tumor”)

43
Q

Rendu-Osler-Weber syndrome–associated oral changes

A
  • Autosomal dominant

- Multiple congenital aneurysmal telangiectasias beneath mucosal surfaces of oral cavity and lips

44
Q

Precancerous and Cancerous lesions of the oral cavity

A
  • Leukoplakia and Erythroplakia

- Squamous Cell carcinoma

45
Q

Most common antecedent of Leukoplakia and Erythroplakia is?

A

-Tobacco use!

46
Q

Leukoplakia

A
  • white plaque on the oral mucosa that cannot be removed by scraping and cannot be classified as another disease entity
  • vary from begign epithelial thickenings to highly atypical dysplasia verging on carcinoma-in-situ
  • occurs in 3%; 5-25% are premalignant so until proved otherwise, should be considered precancerous!
47
Q

Erythroplakia

A
  • red velvety, relatively flat lesion
  • less common than leukoplakia but more ominous because epithelium is markedly atypical and has greater risk of malignant transformation
48
Q

Squamous cell carcinoma–epidemiology

A
  • 95% of oral cancers
  • 5 year survival is 50% varying dependent on stage–early stage=80%, late stage=20%
  • high rate of second primaries (3-7%) suggests “field cancerization” due to diffuse mucosal exposure to carcinogens
49
Q

SCC pathogenesis

A
  • Multifactorial
  • Tobacco and alcohol=common associations, especially in oral cavity but 70% of oropharyngeal cancers harbor ontogenetic variant of HPV, esp HPV 16!!
  • Patients with HPV positive tumors do better than those without!!
50
Q

Other risk factors (besides HPV) associated with SCC

A
  • Familial associations related to genomic instability
  • Radiation
  • Betel nut and paan chewing (India and Asia)
51
Q

Molecular Biology of SCC–multistage process; is heterogenous, but what is the general pathway?

A
  • 1) p16 inactivation–> loss of inhibitor of CDK and progression to hyperplasia/hyperkeratosis—more common in HPV associated SCC!
  • 2) p53 mutations lead to progression to dysplasia and can occur in both HPV- and smoking associated SCC
  • 3) Gross genomic alterations and/or deletions (4q, 6p, 8p, 11q, 13q, or 14q)–typically occur late in progression to malignancy
  • 4) Cyclin D1 over expression causes constitutively active cell cycle progression and typically occurs late in progression to cancer
52
Q

Morphology of squamous cell carcinoma–where in the mouth does it most commonly occur?

A

-VENTRAL tongue, mouth floor, lower lip, soft palate, and gingiva

53
Q

Morphology of squamous cell carcinoma–what do lesions look like?

A

-Can be raised, firm, ulcerated or verrucous

54
Q

Morphology of squamous cell carcinoma–Histology

A
  • typical squamous cell carcinomas of variable differentiation
  • degree of differentiation does not predict clinical behavior!
  • doesnt need to progress to full-thickness SCC in situ before invading underlying storm
  • Local infiltration precedes metastasis
55
Q

Favored local infiltration sites of squamous cell carcinoma

A
  • Cervical lymph nodes
  • Lungs
  • Liver
  • Bones
56
Q

Odontogenic Cysts and Tumors–what are they?

A
  • Epithelium-lined cysts in mandible and maxilla derive from odontogenic remnants
  • may be developmental or inflammatory
57
Q

Odontogenic Cysts and Tumors–types (3):

A
  • 1) Dentigerous cysts
  • 2) Odontogenic keratocyst (OKC)
  • 3) Periodical cysts
58
Q

Dentigerous cysts–where does it originate? Associated with? histology? Treatment?

A
  • originate near crowns of unerupted teeth and may result from dental follicle degeneration
  • most often associated with impacted third molars
  • uniocular lesions lined by stratified squamous epithelium with associated chronic inflammation
  • complete removal is curative!!
59
Q

Odontogenic keratocysts (OKC)

A
  • potentially aggressive
  • Tx requires complete resection (recurrence rates of 60% for partial resection)
  • most commonly occur in posterior mandible of males 10-40 yrs and are unilocular or multilocular lesions typically lined by parakeratinized stratified squamous epithelium
60
Q

Patients with multiple OKCs should be evaluated for?

A

-Nevoid basal cell carcinoma syndrome (Gorlin syndrome) related to PTCH tumor-suppressor gene mutations

61
Q

Periapical cysts

A
  • inflammatory lesions found at tooth apices
  • develop from long-standing pulpitis due to caries or tooth trauma
  • Persistent chronic inflammation leads to granulation tissue and proliferation of quiescent rests of odotogenic epithelium
62
Q

Odontogenic Tumors

A
  • diverse histology and clinical behavior

- Some are true neoplasms (both benign and malignant); others are hemartomas

63
Q

Odontogenic tumors–list of tumors (2)

A

1) Ameloblastoma

2) Odontoma

64
Q

Ameloblastoma

A
  • true neoplasm arising from odontogenic epithelium and showing NO ectomesenchymal differentiation
  • Typically cystic, slow growing, and locally invasive but often has indolent course!
65
Q

Odontoma

A
  • Most common odnotogeic tumor!

- most likely a hamartoma arising from epithelium with extensive enamel and dentin deposition

GI 2 Pathology--Chapt 16 and 17 (14 decks)

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