ORAL DIAGNOSIS Pathology and Diagnosis pt 1 Flashcards Preview

m 2 > ORAL DIAGNOSIS Pathology and Diagnosis pt 1 > Flashcards

Flashcards in ORAL DIAGNOSIS Pathology and Diagnosis pt 1 Deck (322)
Loading flashcards...
1
Q

what percent of cleft lips are unilateral, and what percent are bilateral?

A

80% unilateral, 20% bilateral

2
Q

cleft lips are caused by a defect between the ___ process and ___ process

A

medial nasal process and maxillary process

3
Q

what is the occurrence of cleft lip?

A

1/1000 births, but varies with race

4
Q

cleft palates result from a lack of fusions between ___

A

palatal shelves

5
Q

what is the occurrence of cleft palate?

A

1/2000 births

6
Q

what percent of patients affected by cleft lip/palate have cleft lip only, cleft palate only, and both?

A
  • cleft lip only 25%
  • cleft palate only 25%
  • cleft lip and palate 50%
7
Q

___ are invaginations at the commissures or near the midline

A

lip pits

8
Q

what are fordyce granules? where are they commonly seen?

A
  • ectopic sebaceous glands

- buccal mucosa or lip

9
Q

___ is a bilateral opacification of the buccal mucosa

A

leukoedema

10
Q

is leukoedema common? what is the clinical significance?

A
  • common

- no significance

11
Q

what are the causes of macroglossia?

A
  • congenital hyperplasia/hypertrophy
  • tumors (lymphangioma, vascular malformation, neurofibroma, multiple granular cell tumors, salivary gland tumors, endocrine abnormality)
  • acromegaly, cretinism
  • infections obstructing lymphatics
  • beckwith-wiedemann syndrome
  • exophthalmos, gigantism
  • amyloidosis
12
Q

what is lingual thyroid? what part of the tongue is it located?

A

thyroid tissue mass located at the midline tongue base

13
Q

what is lingual thyroid caused by?

A
  • incomplete descent of thyroid anlage

- may be patients only thyroid

14
Q

thyroglossal tract cyst is a ___ swelling secondary to ___

A
  • midline neck swelling

- cystic change of remnants of thyroid tissue

15
Q

thyroglossal tract cysts are located along the ___ of thyroid descent

A

embryonic path

16
Q

what are two other names for geographic tongue?

A

benign migratory glossitis and erythema migrans

17
Q

geographic tongue is common and affects ___% of the population

A

2%

18
Q

what is the cause of geographic tongue?

A

unknown

19
Q

how does geographic tongue appear?

A

white annular lesions surrounding atrophic red central zones that migrate with time

20
Q

is geographic tongue symptomatic?

A

occasionally (mild pain or burning)

21
Q

what is the treatment for geographic tongue?

A

none necessary

22
Q

fissured tongue is common and affects ___% of the population

A

3%

23
Q

is fissured tongue symptomatic?

A

usually not

24
Q

fissured tongue is a component of melkersson-rosenthal syndrome. what are the other two components?

A

granulomatous cheilitis and facial paralysis

25
Q

what are the two types of hemangiomas?

A

congenital and vascular malformation

26
Q

describe congenital hemangiomas

A
  • focal proliferation of capillaries
  • most lesions undergo involution
  • persistent lesions are excised
27
Q

describe hemangiomas that result from vascular malformations

A
  • persistent malformation of capillaries, veins, and arteries
  • exhibits a thrill (palpate a pulse) and bruit (hear a pulse)
28
Q

what is sturge-weber syndrome?

A
  • type of vascular malformation (hemangioma)
  • aka encephalotrigeminal angiomatosis
  • lesions involve skin along one of the branches of the trigeminal nerve
  • the leptomeninges of the cerebral cortex may be involved by the malformations, leading to mental retardation and seizures
29
Q

___ is a congenital focal proliferation of lymphatic channels

A

lymphangioma

30
Q

when a lymphangioma occurs in the neck, it is termed ___

A

hygroma colli

31
Q

exostoses are excessive ___ bone growth of unknown cause

A

cortical

32
Q

what are the types of exostoses?

A

buccal exostoses, torus palatinus, torus mandibularis

33
Q

___ is a developmental soft tissue cyst that presents as a mass in the midline floor of the mouth if above the mylohyoid muscle, or in upper neck if below mylohyoid muscle

A

dermoid cyst

34
Q

___ is a developmental soft tissue epithelial cyst within the lymph nodes of the neck

A

branchial cyst

35
Q

___ is a developmental soft tissue cyst within lymphoid tissue that is the oral counterpart of the branchial cyst of the neck

A

oral lymphoepithelial cyst

36
Q

where are oral lymphoepithelial cysts commonly found?

A

soft palate, oral floor, or lateral tongue

37
Q

a stafne (static) defect is a diagnostic radiolucency of the mandible secondary to ___

A

invagination of the lingual surface of the jaw

38
Q

where are stafne defects typically located?

A

posterior mandible below the mandibular canal

39
Q

a nasopalatine duct (canal) cyst is a lucency, often heart shaped, in the nasopalatine canal. what is it caused by?

A

cystification of nasopalatine duct remnants

40
Q

a ___ is a clinical term denoting any pathologic radiolucency between the maxillary cuspid and the lateral incisor

A

globulomaxillary lesion

41
Q

why is histopathologic analysis required for the definitive diagnosis of a globulomaxillary lesion?

A

it is present between the maxillary cuspid and lateral incisor, and many other lesions occur in this location and therefore radiolucency in this location represents a wide array of inflammatory lesions, odontogenic cysts and tumors, and nonodontogenic bone diseases

42
Q

___ is a radiolucent dead space (no epithelial lining) in the mandible of teenagers

A

traumatic (simple) bone cyst

43
Q

are traumatic bone cysts associated with trauma?

A

some, but not all

44
Q

___ is a lucency in the jaw that contains hematopoietic bone marrow, often in an extraction site

A

focal osteoporotic marrow defect

45
Q

___ is a common white lesion caused by chronic friction on mucosa

A

focal (frictional) hyperkeratosis

46
Q

how is focal (frictional) hyperkeratosis differentiated from idiopathic leukoplakia?

A

the cause of focal hyperkeratosis is known

47
Q

___ is a type of frictional hyperkeratosis that appears as a linear white line in the buccal mucosa

A

linea alba

48
Q

traumatic ulcers are very common. chronic ulcers mimic ___ and ___

A

oral cancer and chronic infectious ulcers

49
Q

chemical burns usually manifest as ___

A

ulcers

50
Q

chemical burns may be caused by what?

A

aspirin, hydrogen peroxide, silver nitrate, phenol, or other agents

51
Q

___ is a white change in the palate caused by smoking

A

nicotine stomatitis

52
Q

what are the red dots in the white lesions of nicotine stomatitis?

A

inflamed salivary duct orifices

53
Q

is nicotine stomatitis considered premalignant?

A

not unless it is related to reverse smoking

54
Q

___ is caused by the traumatic implantation of amalgam particles into mucosa

A

amalgam tattoo

55
Q

what is the most common oral pigmented lesion?

A

amalgam tattoo

56
Q

___ is caused by a chemical in tobacco smoke that stimulates melanin production

A

smoking-associated melanosis

57
Q

is smoking-associated melanosis reversible?

A

yes, if smoking is discontinued

58
Q

where is smoking-associated melanosis typically seen?

A

anterior gingiva

59
Q

___ is the most common melanotic lesion

A

melanotic macule

60
Q

what is melanotic macule caused by?

A

may be postinflammatory, syndrome-associated (primarily peutz-jeghers syndrome [freckles and benign intestinal polyps]), or idiopathic

61
Q

what are the most common causes of drug-induced pigmentation?

A
  • minocycline
  • chloroquine
  • cyclophosphamide
  • azidothymidine (zidovudine)
62
Q

what is hairy tongue?

A

elongation of filiform papillae (cosmetic significance only)

63
Q

what are the causes of hairy tongue?

A

extended use of antibiotics, corticosteroids, and hydrogen peroxide

64
Q

what is dentifrice-associated slough?

A

superficial chemical burn of buccal mucosa caused by some dentifrices

65
Q

oral infections are ___, ___, or ___ in nature

A

viral, bacterial, or fungal

66
Q

what are the most commonly encountered infections caused by (either viral, bacterial, or fungal)?

A

viral, usually herpes simplex virus

67
Q

clinical presentations of viral infections depends on viral type. how do the following typically present:
herpes, HPV, epstein-barr (EBV)

A
  • herpes = mucosal ulceration preceded by vesicles
  • HPV induces a verruciform (warty) lesion
  • EBV causes a white lesion (hairy leukoplakia)
68
Q

most bacterial and fungal infections manifest as ___

A

chronic ulcers

69
Q

the fungus candida albicans can cause either ___ or ___ lesions

A

white or red

70
Q

primary HSV infections are predominantly in what population?

A

children

71
Q

HSV infections are severe in which population?

A

immunocompromised patients

72
Q

secondary disease of HSV infections is ___ and is triggered by ___

A
  • reactivating of latent virus in the trigeminal ganglion

- sunlight, stress, or immunosuppression

73
Q

HSV lesion on the finger is called ___

A

herpetic whitlow

74
Q

in HSV infections, ___ in epithelial cells are diagnostic when taken in clinical context

A

intranuclear viral inclusions

75
Q

what is varicella (chickenpox)?

A
  • self limiting childhood disease caused by varicella-zoster virus (VZV)
  • oral lesions are uncommon
76
Q

which disease represents reactivation of latent VZV?

A

herpes zoster

77
Q

the latent varicella zoster virus is believed to reside where?

A

the dorsal root and trigeminal ganglia

78
Q

hand foot and mouth disease and herpangina are infections caused by which virus?

A

coxsackievirus

79
Q

are coxsackievirus infections self limiting? what population do they affect?

A

self limiting childhood systemic infections, usually endemic

80
Q

what are the typical lesion sites for hand foot and mouth disease? what about herpangina?

A
  • hand foot and mouth disease…guess…….hands, feet, and mouth
  • herpangina = posterior oral cavity
81
Q

measles are also called ___

A

rubeola

82
Q

___ is a self-limiting childhood systemic infection caused by measles virus

A

measles (rubeola)

83
Q

what are the presenting signs of measles?

A

fever, malaise, and skin rash

84
Q

in measles (rubeola), what precedes the skin rash?

A

punctuate buccal mucosa ulcers (koplik’s spots)

85
Q

what are the 3 HPV infections?

A
  • papillomas
  • condyloma acuminatum (genital warts)
  • focal epithelial hyperplasia (heck’s disease)
86
Q

describe papillomas

A
  • benign epithelial proliferations (pedunculated or sessile) of little significance
  • most, if not all, caused by HPV
  • include verruca vulgaris (wart), which are more prevalent in HIV positive patients
87
Q

describe condyloma acuminatum (genital warts)

A
  • caused by HPV 6 and 11
  • oral lesions acquired by oral-genital contact
  • broad-based verruciform lesion
88
Q

describe focal epithelial hyperplasia (heck’s disease)

A
  • most common in certain ethnic groups (native americans, inuits, and central americans)
  • multiple, small, dome-shaped warts on oral mucosa
  • caused by HPV 13 and 32
89
Q

hairy leukoplakia is a result of which virus?

A

epstein barr

90
Q

describe hairy leukoplakia

A
  • opportunistic infection resulting in white patch or patches of the lateral tongue
  • almost all associated with HIV (may be a pre-AIDS sign)
  • occurrence is decreasing with use of new AIDS drugs
91
Q

T or F:

hairy leukoplakia is frequently seen in normal healthy patients

A
  • false
  • almost all cases are associated with HIV
  • infrequently seen in patients with other immunosuppressed states
92
Q

how is hairy leukoplakia diagnosed?

A

biopsy specimen showing intranuclear viral inclusions

93
Q

what are the malignancies associated with EBV?

A
  • burkitt’s lymphoma and nasopharyngeal carcinoma

- EBV has an etiologic role in these two malignancies

94
Q

what are the oral complications of AIDS?

A
  • herpes simplex and herpes zoster
  • EBV-associated hairy leukoplakia
  • cytomegalovirus
  • HPV associated warts
  • tuberculosis
  • histoplasmosis
  • candidiasis
  • neoplasms
  • kaposi’s sarcoma (HHV 8)
  • high grade lymphomas
  • severe aphthous ulcers
  • xerostomia
  • gingivitis and periodontal disease
95
Q

why are acute bacterial infections uncommon in oral mucosa?

A
  • owing to the protective effects (immunologic and physical) that saliva provides the stratified squamous epithelium lining the mouth
  • chronic bacterial infections are also uncommon, probably for the same reasons
96
Q

what type of bacterial infections can sometimes appear in the oral mucosa after deep trauma or surgery?

A
  • acute pustular staphylococcal infections

- treated with appropriate antibiotics and surgical techniques

97
Q

syphilis is a bacterial infections caused by contact with patients infected with which bacteria?

A

treponema pallidum

98
Q

what are the primary, secondary, and tertiary lesions of syphilis?

A
  • primary lesion is a chancre
  • secondary lesions are oral mucous patches, condyloma latum, and maculopapular rash
  • tertiary lesions are gummas, and have central nervous system involvement, and cardiovascular involvement
99
Q

congenital syphilis is an in utero infection that causes ___

A

hutchinson’s triad (notched incisors, deafness, and ocular keratitis)

100
Q

tuberculosis is a bacterial infection caused by inhalation of which bacteria?

A

mycobacterium tuberculosis

101
Q

in tuberculosis infections, how do oral lesions present?

A
  • nonhealing chronic ulcers

- appear after lung infection

102
Q

why is the incidence of tuberculosis increasing?

A

overcrowding, debilitation, and AIDS

103
Q

tuberculosis causes caseating granulomas with ___ cells

A

multinucleated giant cells (langerhan’s giant cells)

104
Q

how is tuberculosis treated?

A

multidrug therapy (isoniazid, rifampin, and ethambutol

105
Q

gonorrhea is a sexually transmitted disease caused by ___

A

neisseria gonorrhoeae

106
Q

what is the oral manifestation of gonorrhea?

A

oral pharyngitis (rarely seen)

107
Q

actinomycosis is caused by which opportunistic bacterium found in the oral flora of many patients?

A

actinomyces israelii

108
Q

in patients with actinomycosis, ___ may follow dental surgery

A

chronic jaw infection

109
Q

in patients with actinomycosis, head and neck infections are called ___

A

cervicofacial actinomycosis

110
Q

how is actinomycosis treated?

A

long-term, high-dose penicillin

111
Q

scarlet fever is a systemic infection caused by some strains of which bacteria?

A

group A streptococci

112
Q

what are the manifestations of scarlet fever?

A
  • strep throat (pharyngitis, fever, and malaise)
  • rash caused by erythrogenic toxin
  • strawberry tongue (white coated tongue with red, inflamed fungiform papillae)
113
Q

how is scarlet fever treated?

A

penicillin to prevent complications of rheumatic fever

114
Q

what are considered “deep” fungi?

A

histoplasmosis, coccidioidomycosis, blastomycosis, and cryptococcosis

115
Q

histoplasmosis is endemic to ___, and coccidioidomycosis is endemic to ___

A
  • US midwest

- US west (san joaquin valley fever)

116
Q

deep fungal infections of the lung may lead to what oral manifestations?

A
  • oral chronic granulomatous ulcers secondary to oral implantation of microorganisms
  • oral lesions must be differentiated from oral cancer and chronic traumatic ulcers
117
Q

what are opportunistic fungi?

A
  • candidiasis (thrush, moniliasis)

- aspergillosis, mucormycosis, rhizopus

118
Q

candidiasis is caused by ___

A

c. albicans (part of normal flora)

119
Q

candidiasis is a predisposing factor for ___

A

fungal overgrowth

120
Q

how do acute and chronic candidiasis lesions present?

A
  • acute lesions are white, which represent the fungal colonies growing in mucosa (removal leaves raw, bleeding surface)
  • chronic lesions are erythematous
121
Q

what are the specific types of chronic candidiasis?

A

denture sore mouth, angular cheilitis, and median rhomboid glossitis

122
Q

what is are the treatment options for candidiasis?

A
  • topical treatment: nystatin, clotrimazole

- systemic treatment: fluconazole, itraconazole, caspofungin

123
Q

what are the predisposing factors for candidiasis?

A

immune deficiency, endocrine abnormality, diabetes mellitus, pregnancy, hypoparathyroidism, hypoadrenalism, stress, prolonged antibiotic therapy, prolonged corticosteroid therapy, chemotherapy for malignancies, xerostomia, poor oral hygiene

124
Q

aspergillosis, mucormycosis, and rhizopus are infections caused by organisms that are found throughout the ___

A

environment

125
Q

which patients are at risk of aspergillosis, mucormycosis, and/or rhizopus?

A

patients who are medically debilitated or immunocompromised

126
Q

how do aspergillosis, mucormycosis, and rhizopus lesions of the head and neck present?

A

appear as destructive ulcerations in the paranasal sinuses or nasal cavity

127
Q

how are aspergillosis, mucormycosis, and rhizopus infections treated?

A

intense antifungal therapy is indicated, along with controlling the contributing condition

128
Q

describe aphthous ulcers

A
  • recurrent painful ulcers (not preceded by vesicles)
  • unknown cause, probably related to focal immune defect
  • appear on nonkeratinized oral mucosa (unattached)
  • may be seen in association with some systemic diseases
129
Q

what are the 3 types of aphthous ulcers?

A

minor, major, herpetiform

130
Q

describe minor aphthous ulcers

A
  • one to several painful oval ulcers <0.5cm
  • most common type
  • duration of 7-10 days
131
Q

describe major aphthous ulcers

A
  • up to 10 deep crateriform ulcers >0.5cm
  • very painful and may be debilitating
  • may take several weeks to heal
132
Q

describe herpetiform aphthous ulcers

A
  • recurrent crops of minor aphthae
  • painful, take 1-2 weeks to heal
  • may be found on any mucosal surface
  • same cause as other aphthae (not viral)
133
Q

___ is a multisystem disease believed to represent immune dysfunction in which vasculitis is a prominent feature

A

behcet’s syndrome

134
Q

what are the features of behcet’s syndrome?

A
  • oral and genital aphthous-type ulcers
  • conjunctivitis
  • uveitis (inflammation of the layers of the eye)
  • arthritis
  • headache
  • other CNS manifestations
135
Q

how is behcet’s syndrome treated?

A

corticosteroids and other immunosuppressive drugs

136
Q

erythema multiforme is a self limiting ___ reaction that affects skin or mucosa or both

A

hypersensitivity

137
Q

erythema multiforme minor is associated with ___

A

secondary herpes simplex hypersensitivity

138
Q

erythema multiforme major is also called ___, and is often triggered by ___

A
  • stevens-johnson syndrome

- often triggered by drugs

139
Q

oral lesions that result from drug reactions and contact allergies include ___

A

vesicular, ulcerative, erythematous, and lichenoid

140
Q

acquired angioedema is a specific type of ___

A

allergic reaction

141
Q

acquired angioedema is precipitated by ___ and mediated by ___

A
  • drugs or food (shellfish, nuts)

- mast cell release of IgE

142
Q

acquired angioedema results in characteristic ___

A

soft, diffuse swelling of lips, neck, or face

143
Q

hereditary angioedema is a rare form of acquired angioedema that is a ___ trait

A

autosomal dominant

144
Q

what is wegener’s granulomatosis?

A

destructive granulomatous lesions with necrotizing vasculitis of unknown cause

145
Q

wegener’s granulomatosis affects ___

A

upper respiratory tract, lungs, and kidneys

146
Q

what is the diagnosis of wegener’s granulomatosis based on?

A

biopsy and demonstration of antineutrophil cytoplasmic antibodies

147
Q

how is wegener’s granulomatosis treated?

A
  • cyclophosphamide and corticosteroids or rituximab

- prognosis is good

148
Q

midline granuloma is a destructive necrotizing midfacial phenomenon that clinically mimics lesions of ___

A

wegener’s granylomatosis

149
Q

most midline granuloma cases represent ___

A

peripheral T-cell lymphomas of the upper respiratory tract or mouth (perforation of the hard palate may be seen)

150
Q

how is midline granuloma treated?

A
  • radiation

- good prognosis when treated early

151
Q

lichen planus is a common mucocutaneous disease that affects ___% of adults

A

1-2%

152
Q

what is lichen planus caused by?

A
  • T lymphocytes target and destroy basal keratinocytes

- reason for this immunologically mediated phenomenon is unknown

153
Q

describe the microscopy of lichen planus

A
  • hyperkeratosis
  • lymphocytes infiltrate at epithelial-connective tissue interface
  • basal zone vacuolation secondary to basal keratinocyte destruction
  • epithelium may exhibit a “saw tooth” pattern as it remodels after basal cell damage
154
Q

describe the oral lesions of lichen planus

A

bilateral on the buccal mucosa, although tongue and gingival lesions exhibit white (hyperkeratotic) lines

155
Q

what are the clinical types of lichen planus?

A
  • reticular: lesions consist of interlacing lines (wickham’s striae)
  • erosive: same presentation as reticular, but ulceration also present
  • erythematous or atrophic: lesions predominantly red
  • plaque: lesions predominantly plaque-like
156
Q

describe the cutaneous lesions of lichen planus

A
  • characteristically purple puritic papules on lower legs and arms
  • respond to corticosteroids
  • erosive form may have slightly increased risk for malignant change
157
Q

lupus erythematosus is an autoimmune disease that occurs in either ___ or ___ forms

A

discoid or systemic

158
Q

describe the discoid (chronic) form of lupus erythematosus

A
  • affects skin (especially face and scalp) or oral mucosa (buccal mucosa, gingiva, vermillion)
  • usually affects middle aged adults, especially women
  • lesions are erythematous; oral lesions mimic erosive lichen planus
  • no systemic signs or symptoms; rarely progresses to systemic form
159
Q

how is discoid lupus erythematosus treated?

A

corticosteroids and other drugs

160
Q

describe the systemic (acute) type of lupus erythematosus

A
  • multiple organ involvement (heart, kidney, joints, skin, oral)
  • classic sign: butterfly rash over bridge of the nose
  • autoantibodies directed against nuclear and cytoplasmic antigens
161
Q

how is systemic lupus erythematosus treated?

A

corticosteroids and other immunosuppressive drugs

162
Q

___ is an autoimmune, multiorgan disease of adults, especially women, in which fibrosis of tissues eventually leads to organ dysfunction

A

scleroderma

163
Q

scleroderma may occur concomitantly with other autoimmune diseases, such as ___

A

lupus erythematosus, rheumatoid arthritis, dermatomyositis, and sjogren’s syndrome

164
Q

describe the cutaneous changes seen in scleroderma patients

A

induration and rigidity, atrophy, and telangiectasias

165
Q

describe the oral changes seen in scleroderma patients

A

restriction of orifice, uniform widening of periodontal membrane, and bony resorption of posterior margin of the mandibular ramus

166
Q

___ is an autoimmune, mucocutaneous disease in which antibodies are directed against desmosomal protein (desmoglein 3)

A

pemphigus vulgaris

167
Q

how does pemphigus vulgaris manifest?

A

multiple, painful ulcers preceded by bullae that form within the epithelium

168
Q

what is a positive nikolsky’s sign? what immunologic disease is it sometimes present with?

A
  • formation of blister with rubbing or pressure

- pemphigus vulgaris and mucous membrane pemphigoid

169
Q

in pemphigus vulgaris, how often do oral lesions precede skin lesions?

A

about half the time

170
Q

what can happen if pemphigus vulgaris is untreated?

A

it runs a progressive clinical course and may be fatal if untreated

171
Q

how is pemphigus vulgaris treated?

A

systemic corticosteroids or other immunosuppressive drugs

172
Q

___ is a persistent, autoimmune disease of mucous membranes in which antibodies are directed against basement membrane antigens (laminin 5, BP180)

A

mucous membrane pemphigoid

173
Q

what patient population does mucous membrane pemphigoid affect?

A

older adults, typically >50 years old

174
Q

how does mucous membrane pemphigoid present?

A

multiple, painful ulcers preceded by bullae that form below the epithelium at the basement membrane

175
Q

where are mucous membrane pemphigoid lesions commonly found?

A

may be found in any region, especially and sometimes exclusively in the attached gingiva

176
Q

if untreated, what can ocular lesions associated with mucous membrane pemphigoid lead to?

A

blindness

177
Q

what is the management for mucous membrane pemphigoid?

A

corticosteroids

178
Q

patients with idiopathic leukoplakia, proliferative verrucous leukoplakia, erythroplakia, actinic cheilitis, oral submucous fibrosis, and smokeless tobacco-associated white lesions are at risk for the development of ___

A

squamous cell carcinoma

179
Q

___ is a white or opaque oral mucosa lesion that does not rub off and is not clinically diagnostic for any other white lesion

A

idiopathic leukoplakia

180
Q

what is the cause of idiopathic leukoplakia? what age population does it affect?

A
  • cause is unknown, although tobacco and alcohol may be contributing factors
  • biopsy is mandatory because diagnosis cannot be made clinically
  • > 40 years old
181
Q

what percent of benign idiopathic leukoplakia lesions transform to squamous cell carcinoma?

A

5-15%

182
Q

what is the treatment for idiopathic leukoplakia? is recurrence common?

A
  • excision

- recurrence is common

183
Q

what are the high risk sites for malignant transformation of idiopathic leukoplakia?

A

floor of mouth and tongue

184
Q

what are the different stages of idiopathic leukoplakia?

A
  • hyperkeratosis 80%
  • dysplasia 12%
  • in situ carcinoma 3%
  • squamous cell carcinoma 5%
185
Q

proliferative verrucous leukoplakia is a high-risk form of ___, with an unknown cause, although some are associated with which forms of HPV?

A
  • leukoplakia

- 16 and 18

186
Q

describe proliferative verrucous leukoplakia lesions

A
  • recurrent or persistent and usually multiple

- may start with a flat profile but progress to broad-based, wartlike (verruciform) lesions

187
Q

proliferative verrucous leukoplakia has a high risk of malignant transformation to ___ or ___

A

verrucous carcinoma or squamous cell carcinoma

188
Q

___ is a high-risk, idiopathic red patch of mucosa with an unknown cause, although some are tobacco related

A

erythroplakia (erythroplasia)

189
Q

most erythroplakia lesions represent ___ or ___

A

dysplasia or malignancy

190
Q

is erythroplakia more or less common than idiopathic leukoplakia?

A

much less common

191
Q

is a biopsy mandatory for erythroplakia?

A

yes

192
Q

erythroplakia usually occurs in what age population?

A

50-70 years old

193
Q

what are the high risk sites for erythroplakia?

A

floor of mouth, tongue, retromolar area

194
Q

describe the microscopy of erythroplakia

A
  • mild to moderate dysplasia 10%
  • severe dysplasia/carcinoma in situ 40%
  • squamous cell carcinoma 50%
195
Q

what is the cause of actinic (solar) cheilitis?

A

ultraviolet light, especially UVB, 2900-3200nm

196
Q

describe the presentation/progression of actinic (solar) cheilitis

A
  • the lower lip shows epithelial atrophy and focal keratosis
  • upper lip is minimally affected because it is more protected from UV light
  • the junction of the vermillion and skin becomes indistinct
  • may progress to squamous cell carcinoma
197
Q

oral submucous fibrosis is irreversible mucosal change thought to be due to hypersensitivity to ___, especially ___

A

dietary substances, especially betel nut

198
Q

describe the presentation/progression of oral submucous fibrosis

A
  • mucosa becomes opaque secondary to submucosal scarring

- may progress to squamous cell carcinoma

199
Q

why is smokeless tobacco-associated white lesion not idiopathic leukoplakia?

A
  • because the cause is known (white mucosal change from direct effects of smokeless tobacco and additives) and the lesion is clinically diagnostic
  • however, it could be classified under a more generic designation of leukoplakia or white patch
200
Q

where are smokeless tobacco-associated white lesions located?

A

labial and buccal vestibules where tobacco is held

201
Q

smokeless tobacco-associated white lesions may cause ___. is malignant transformation common?

A
  • focal periodontal destruction, tooth abrasion, or hypertension
  • malignant transformation is rare
202
Q

melanomas manifest as abnormally pigmented surface lesions that start at the junction of the ___ and ___

A

epithelium and submucosa

203
Q

___ is a well-differentiated, slow growing form of carcinoma that infrequently metastasizes and exhibits a broad-based verruciform architecture

A

verrucous carcinoma

204
Q

what are the etiological factors of verrucous carcinoma?

A

tobacco and/or HPV 16 and 18

205
Q

how is verrucous carcinoma treated?

A
  • surgical excision

- good prognosis

206
Q

squamous cell carcinoma is caused by ___

A

mutation, amplification, or inactivation of oncogenes and tumor suppressor genes

207
Q

what are some causes of genetic alterations seen in squamous cell carcinoma?

A

tobacco and heredity

208
Q

there is an increased incidence of oropharyngeal (including tonsillar) squamous cell carcinoma, many of which are associated with detection of ___

A

oncogenic HPV infection (HPV 16 a d 18)

209
Q

patients with ___ syndrome are at an increased risk of oral cancer

A

plummer-vinson syndrome (mucosal atrophy, dysphagia, and iron-deficiency anemia)

210
Q

what are the clinical features of squamous cell carcinoma?

A
  • may manifest as chronic, nonhealing ulcer, red or white patch, or mass
  • most commonly seen in posterior-lateral tongue and floor of mouth
211
Q

what is the prognosis based on for patients with squamous cell carcinoma?

A
  • clinical stage is more important than microscopic classification in determining prognosis
  • stage I (<2cm) is good
  • stage II (2-4cm) and no neck disease is fair
  • stage III and IV metastasis found in neck is poor
  • overall 5-year survival is 45-50%; with neck metastasis, 25%
212
Q

what is the treatment for squamous cell carcinoma?

A
  • surgical excision of primary
  • neck dissection with positive nodes or large primary lesion
  • radiotherapy
  • combination surgery and radiotherapy
  • radiotherapy combined with chemotherapy
213
Q

what is the most common skin cancer?

A

basal cell carcinoma

214
Q

describe basal cell carcinoma

A
  • low-grade, rarely metastasizes

- usually in sun-damaged skin; rare in mucosa

215
Q

how does basal cell carcinoma manifest?

A

nonhealing, indurated chronic ulcer

216
Q

how is basal cell carcinoma treated? what is the prognosis?

A
  • surgery

- very excellent prognosis

217
Q

oral melanoma is a malignancy of ___

A

melanocytes

218
Q

what are the high risk sites for oral melanoma?

A

palate and gingiva

219
Q

what population is oral melanoma more common in?

A

almost always in adults; rarely in children

220
Q

what are the survival rates for oral melanoma?

A
  • oral mucosa lesions 5-year survival rate is <20%

- skin lesions 5-year survival rate is >65%

221
Q

some oral melanoma lesions have prolonged ___ phase preceding vertical (invasive) growth

A

in situ

222
Q

connective tissue tumors manifest as ___. overlying epithelium is generally intact, unless ___

A
  • masses (lumps or bumps) within the submucosa

- ulceration occurs because of trauma to the lesion

223
Q

what are the two groups of benign connective tissue tumors?

A

reactive or neoplastic

224
Q

what are the types of benign fibrous reactive connective tissue lesions?

A

peripheral fibroma, generalized gingival hyperplasia, focal fibrous hyperplasia, denture-induced fibrous hyperplasia

225
Q

what is a peripheral fibroma?

A
  • fibrous reactive connective tissue lesion
  • fibrous hyperplasia of the gingiva
  • caused by trauma or chronic irritation
226
Q

what is generalized gingival hyperplasia?

A
  • fibrous reactive connective tissue lesion

- fibrous hyperplasia caused by local factors and modified by systemic conditions

227
Q

what are the drugs that can contribute to generalized gingival hyperplasia?

A
  • phenytoin (dilantin) for seizures
  • cyclosporine (immunosuppressant)
  • nifedipine (calcium channel blocker)
228
Q

what is focal fibrous hyperplasia?

A
  • fibrous reactive connective tissue lesion
  • fibrous hyperplasia or oral mucosa
  • caused by chronic trauma or chronic irritation
229
Q

focal fibrous hyperplasia is also called ___

A

traumatic fibroma, irritation fibroma, and hyperplastic scar

230
Q

what is denture-induced fibrous hyperplasia?

A
  • fibrous reactive connective tissue lesion
  • fibrous hyperplasia associated with ill-fitting dentures
  • usually seen in anterior labial vestibules
  • no malignant potential
231
Q

what is papillary hyperplasia (palatal papillomatosis) of the palate?

A

another type of fibrous hyperplasia associated with ill-fitting dentures

232
Q

what is a traumatic neuroma?

A
  • neural reactive connective tissue lesion
  • entangled submucosal mass of neural tissue and scar
  • caused by injury to nerve
  • most commonly seen at mental foramen in oral cavity
233
Q

what is a pyogenic granuloma?

A
  • vascular reactive connective tissue lesion
  • hyperplasia of capillaries and fibroblasts
  • caused by trauma or chronic irritation
  • common in gingiva but can be seen anywhere there is mucosal (or skin) trauma
234
Q

what are the types of neoplastic benign connective tissue lesions?

A
  • fibrous = nodular fasciitis and fibromatosis
  • neural = granular cell tumor, schwannoma (neurilemoma), neurofibroma, mucosal neuromas of multiple endocrine neoplasia 2B
  • muscle = leiomyoma and rhabdomyoma
  • fat = lipoma
235
Q

describe nodular fasciitis

A
  • fibrous neoplastic connective tissue lesion
  • rare submucosal proliferation of fibroblasts
  • reactive lesion that exhibits rapid growth
  • treated with surgical excision, rare recurrence
236
Q

describe fibromatosis

A
  • fibrous neoplastic connective tissue lesion
  • although benign, this troublesome fibroblastic neoplasm is locally aggressive and infiltrative
  • difficult to eradicate and often recurs
  • behavior similar to low-grade fibrosarcoma
237
Q

describe granular cell tumor

A
  • neural neoplastic connective tissue lesion
  • benign, nonrecurring submucosal neoplasm of schwann’s cells
  • tumor cells have granular or grainy cytoplasm
  • overlying epithelium may exhibit pseudoepitheliomatous hyperplasia (microscopically mimics carcinoma)
238
Q

what location are granular cell tumors most common?

A

tongue

239
Q

describe the infant counterpart of granular cell tumors

A
  • congenital granular cell tumor (congenital epulis)
  • occurs on gingiva only as pedunculated mass
  • no pseudoepitheliomatous hyperplasia
  • surgical excision, no recurrence
240
Q

describe a schwannoma

A
  • neural neoplastic connective tissue lesion
  • aka neurilemoma
  • benign neoplasm of schwann’s cells
  • any site, tongue favored
  • solitary; not syndrome-related
241
Q

describe a neurofibroma

A
  • neural neoplastic connective tissue lesion
  • benign neoplasm of schwann’s cells and perineural fibroblasts
  • any site, especially tongue and buccal mucosa
  • solitary to simple
  • syndrome of neurofibromatosis 1
242
Q

what is syndrome of neurofibromatosis 1?

A
  • multiple neurofibromas
  • six of more cafe au lait macules (each >1.5 cm diameter)
  • axillary freckling (crowe’s sign) and iris freckling (lisch spots)
  • malignant transformation of neurofibromas occurs in 5-15% of patients
243
Q

describe mucosal neuromas of multiple endocrine neoplasia 2B

A
  • neural neoplastic connective tissue lesion

- autosomal dominant inheritance

244
Q

what are the syndrome components of mucosal neuromas of multiple endocrine neoplasia 2B?

A
  • oral mucosal neuromas (hamartomas)
  • medullary carcinoma of the thyroid
  • pheochromocytoma of the adrenal gland
245
Q

what is a leiomyoma?

A
  • neoplastic connective tissue lesion

- rare, benign neoplasm of smooth muscle origin

246
Q

what is a rhabdomyoma?

A
  • neoplastic connective tissue lesion

- very rare, benign neoplasm of skeletal muscle origin

247
Q

what is a lipoma?

A
  • neoplastic connective tissue lesion
  • uncommon benign neoplasm of fat cell origin
  • buccal mucosa is characteristic site
248
Q

what is a fibrosarcoma?

A

rare sarcoma (malignant) showing microscopic evidence of fibroblast differentiation

249
Q

what is a neurosarcoma?

A
  • malignant peripheral nerve sheath tumor
  • rare sarcoma showing microscopic evidence of neural differentiation
  • may arise from preexisting neurofibroma or de novo (no preexisting lesion)
250
Q

what is kaposi’s sarcoma?

A
  • malignant vascular proliferation of endothelial cells
  • HHV 8 has etiologic role
  • most commonly seen as a complication of AIDS; incidence markedly reduced by new antiretroviral therapies
  • may also be seen as endemic african type or classic mediterranean type
251
Q

what is a leiomyosarcoma?

A

rare sarcoma (malignant) showing microscopic evidence of smooth muscle differentiation

252
Q

what is a rhabdomyosarcoma?

A

rare sarcoma (malignant) showing microscopic evidence of skeletal muscle differentiation

253
Q

what is a liposarcoma?

A

rare sarcoma (malignant) showing microscopic evidence of fat cell differentiation

254
Q

___ is a recurring submucosal nodule of saliva (often bluish in color) resulting from escape from duct of salivary gland

A

mucous extravasation phenomenon

255
Q

what are mucous extravasation phenomena caused by?

A

traumatic severance of salivary excretory duct

256
Q

where are mucous extravasation phenomena common?

A

lower lip (rare in upper lip) and buccal mucosa

257
Q

do mucous extravasation phenomena recur?

A

not if the contributing gland is removed

258
Q

___ is a submucosal nodule (often bluish in color) resulting from blockage of salivary duct by a salivary stone (sialolith)

A

mucous retention cyst

259
Q

where are mucous retention cysts most common?

A

floor of mouth, palate, buccal mucosa, and upper lip (rare in lower lip)

260
Q

a mucous retention cyst is known as a ___ when occurring in the floor of the mouth

A

ranula

261
Q

___ is a chronic ulcer of the palate secondary to ischemic necrosis of palatal salivary glands

A

necrotizing sialometaplasia

262
Q

necrotizing sialometaplasia is believed to be triggered by ___

A

trauma, surgery, or local anesthesia

263
Q

what is the treatment for necrotizing sialometaplasia?

A

heals in 6-10 weeks without treatment

264
Q

necrotizing sialometaplasia mimics ___ clinically and microscopically

A

carcinoma (squamous metaplasia of ducts)

265
Q

___ is a common insignificant incidental finding in a panoramic image that may represent blockage of the sinus salivary gland or focal fluid accumulation of sinus mucosa

A

maxillary sinus retention cyst (pseudocyst)

266
Q

what is the treatment for maxillary sinus retention cyst (pseudocyst)

A

lesions are asymptomatic and require no treatment

267
Q

what are the potential causes of infectious sialadenitis (salivary gland infections)?

A
  • acute or chronic

- viral or bacterial

268
Q

describe infectious sialadenitis due to viral infections

A
  • mumps is an acute viral infection usually of the parotid glands
  • cytomegalovirus infections are chronic and may be seen in immunosuppressed patients or (rarely) in infants via transplacental infection
269
Q

describe infectious sialadenitis due to bacterial infections

A
  • bacterial infections usually occur when salivary flow is reduced or impeded, especially in major glands, allowing bacterial overgrowth
  • staphylococci and streptococci are the usual infecting agents
270
Q

___ is a chronic granulomatous disease of unknown cause, although bacteria (possibly mycobacteria) are suspected

A

sarcoidosis

271
Q

sarcoidosis is primarily a ___ disease

A

pulmonary disease, although many other organs may be affected, including salivary glands and mucosa

272
Q

in sarcoidosis, ___ cause organ nodularity and loss of parenchyma

A

granulomas (macrophage infiltrates)

273
Q

how is sarcoidosis diagnosed?

A
  • biopsy, radiographic studies, and laboratory tests
  • serum chemistry for hypercalcemia and elevated angiotensin-converting enzyme
  • chest films for pulmonary involvement
  • radiographs for bone involvement
274
Q

how is sarcoidosis treated?

A

corticosteroids and other immunomodulating drugs

275
Q

bilateral parotid enlargement is associated with several ___ and ___ conditions. how do they feel to palpation?

A
  • systemic and metabolic

- soft

276
Q

what are the metabolic conditions associated with bilateral parotid enlargement?

A

chronic alcoholism, dietary deficiencies, obesity, diabetes mellitus, hypertension, hyperlipidemia, and sjogren’s syndrome

277
Q

___ is a chronic lymphocyte-mediated autoimmune disease affecting exocrine glands and other organ systems

A

sjogren’s syndrome

278
Q

primary sjogren’s syndrome consists of ___ and ___

A

keratoconjunctivitis sicca (dry eyes) and xerostomia

279
Q

secondary sjogren’s syndrome consists of ___ in addition to ___

A

dry eyes and mouth in addition to another autoimmune disease, often rheumatoid arthritis

280
Q

how is sjogren’s syndrome diagnosed?

A
  • assessment of salivary function (usually labial salivary gland biopsy)
  • assessment of decrease in lacrimal function (schirmer test)
  • laboratory tests for autoantibodies (rheumatoid factor, antinuclear antibodies, sjogren’s syndrome A and B)
281
Q

what is the cause and treatment of sjogren’s syndrome?

A
  • cause is unknown

- symptoms are treated

282
Q

patients with sjogren’s syndrome are at risk for ___

A

lymphoma

283
Q

what are the dental complications of sjogren’s syndrome?

A

cervical caries associated with xerostomia

284
Q

what is the most common benign salivary gland tumor (major and minor glands)

A

mixed tumor (pleomorphic adenoma)

285
Q

mixed tumor (pleomorphic adenomas) are a mixture of more than one cell type (___) in many patterns (___)

A
  • epithelial and connective tissue elements

- pleomorphic

286
Q

what is the most common site for mixed tumor (pleomorphic adenoma) minor gland lesions?

A

palate

287
Q

do mixed tumors (pleomorphic adenomas) recur?

A

occasional recurrence associated with incomplete or poorly formed tumor capsule

288
Q

___ are benign salivary tumors composed of a single cell type

A

monomorphic adenomas

289
Q

what are the types of monomorphic adenomas?

A

basal cell adenoma, canalicular adenoma, myoepitheliomas, and oncocytic tumors (oncocytes stain bright pink because of abundant mitochondrial proteins)

290
Q

how are monomorphic adenomas treated?

A

surgical excision with infrequent recurrences

291
Q

___ is an oncocytic tumor that also contains lymphoid tissue

A

warthin’s tumor

292
Q

what location and population is warthin’s tumor most commonly found?

A
  • parotid of older men

- occasionally bilateral

293
Q

what is the most common salivary malignancy in both minor and major glands?

A

mucoepidermoid carcinoma

294
Q

what is the most common intraoral site for mucoepidermoid carcinoma?

A

palate

295
Q

mucoepidermoid carcinoma is composed of what cell types?

A

mucous and epithelial cells

296
Q

describe metastasis of mucoepidermoid carcinoma

A
  • microscopic low grade lesions rarely metastasize and have excellent prognosis
  • microscopic high grade lesions frequently metastasize and have a fair prognosis
297
Q

___ is the second most common salivary gland malignancy (rare in major glands)

A

polymorphous low grade adenocarcinoma

298
Q

what is the most common site for polymorphous low grade adenocarcinoma?

A

palate

299
Q

what is the treatment and prognosis for polymorphous low grade adenocarcinoma?

A

low grade malignancy has a good prognosis after surgical excision

300
Q

adenoid cystic carcinoma is a ___ salivary malignancy and the ___ is the most common site

A
  • high grade

- palate

301
Q

what is the microscopic pattern of adenoid cystic carcinoma?

A

cribriform or “swiss cheese” microscopic pattern

302
Q

adenoid cystic carcinomas can spread through ___ spaces

A

perineural

303
Q

what is the 5-year survival rate for adenoid cystic carcinoma?

A
  • 70%

- 15 year survival rate is 10%

304
Q

all lymphoid neoplasms are ___

A

malignant

305
Q

hodgkin’s lymphoma is characterized by ___ cells

A
  • reed-sternberg cells

- rare in the oral cavity

306
Q

non hodgkins lymphoma is a malignancy of one of the cells making up lymphoid tissue. the microscopic classification of the various types of lymphomas currently follows the ___ classification

A

revised european-american lymphoma classification

307
Q

most lymphomas are ___ cell type

A
  • B-cell type

- T-cell lymphomas are very rare in the mouth

308
Q

lymphoma behavior patterns range from indolent to highly aggressive. most head and neck tumors start in ___ or in ___. most common intraoral sites are ___.

A
  • lymph nodes or in mucosa-assocaited lymphoid tissues (MALT)
  • tonsils and palate
309
Q

bone involvement, especially in Burkitt’s lymphoma, often results in ___

A

swelling, pain, tooth mobility, and lip parasthesia

310
Q

AIDS-associated lymphomas are typically high-grade ___-cell tumors

A

B-cell

311
Q

what is the treatment for lymphomas?

A
  • dependent on lymphoma classification and stage
  • radiation is used for localized disease
  • chemotherapy is used for extensive disease
  • chemoradiotherapy is also used
  • some indolent low-grade lymphomas, known to respond poorly to therapeutic regimens, are not treated
312
Q

___ represents a monoclonal neoplastic expansion of immunoglobulin-secreting B cells (plasma cells) in what could be termed a monoclonal gammopathy

A

multiple myeloma or plasma cell myeloma

313
Q

what are the radiographic characteristics of multiple myeloma (plasma cell myeloma)?

A

multiple punched out bone lucencies (solitary plasmacytoma invariably becomes multiple myeloma) in patients older than 50 years

314
Q

some of the clinical features of ___ include abnormal immunoglobulin protein peak (M protein) on serum electrophoresis and urinary monoclonal light chains (bence-jones protein)

A

multiple myeloma (plasma cell myeloma)

315
Q

what are the signs and symptoms of multiple myeloma?

A
  • pain, swelling, and numbness

- anemia, bleeding, infection, and fracture associated with extensive marrow involvement

316
Q

how is multiple myeloma treated? prognosis?

A
  • chemotherapy

- poor prognosis

317
Q

a form of amyloidosis occurs in ___% of patients with multiple myelosis

A

10%

318
Q

amyloidosis that occurs in 10% of patients with multiple myelosis is due to what?

A

formation of complex proteins in which immunoglobulin light chains are precursors

319
Q

amyoloidosis that occurs in patients with multiple myelosis results in amyloid protein that is deposited in various organs and can leads to organ dysfunction. which organs are commonly affected?

A

kidney, heart, GI tract, liver, and spleen

320
Q

how do amyloid proteins (amyloidosis) present microscopically?

A

amyloid proteins react with Congo red stain producing a green birefringence in polarized light

321
Q

secondary amyloidosis can develop in patients with ___

A

chronic diseases such as rheumatoid arthritis, chronic osteomyelitis, and chronic renal failure

322
Q

single organ or localized amyloidosis may be seen where in the mouth?

A

tongue