WenChen Wang
1. White lesions of the oral mucosa
2. Solitary oral ulcer and fissures
3. Yellow conditions of the oral mucosa
王文岑 高雄醫學大學 牙醫學系 高醫大附設醫院 S 棟 2 樓 口腔病理影像診斷科
07-3208284; [email protected]
Differential Diagnosis of Oral and Maxillofacial lesions
WenChen Wang
White lesions of the oral mucosa
Keratotic Lesions 1. Leukoedema
2. Linea alba buccalis3. Leukoplakia4. Nicotinic stomatitis, snuff-dipper’s lesion5. Benign migratory glossitis and mucositis6. Lichen planus7. Papilloma, verrucous vulgaris8. white exophytic squamous cell carcinoma,
Verrucous carcinoma9. Hypertrophic candidiasis10. White sponge nevus
WenChen Wang
Sloughing, pseudomembranous, necrotic lesions
Plaque Traumatic ulcer Pyogenic granuloma Chemical burns ANUG Candidasis
WenChen Wang
Short-term ulcers Traumatic ulcers (most) Recurrent aphthous ulcers (minor) Recurrent intraoral herpes simplex lesi
ons Ulcers as result of odontogenic infectio
n Ulcers with generalized mucositis or ve
siculobullous disease Ulcers secondary to systemic disease
Ulcers
WenChen Wang
Persistent ulcers Traumatic ulcers (occasional) Ulcers from odontogenic infection Squamous cell carcinoma Chancre Gumma Ulcer secondary to systemic disease Low-grade mucoepidermoid tumor Metastatic tumor
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Normal Color of Oral Mucosa
1). dark pink (reddish) to very pale (almost white).
2). thickness of epithelium, degree of keratinizationA). thicker epithelium: more keratinized, more fibrous and
less vascular subepithelial connective tissue--color is whiter; hard palate, fixed gingival, dorsal surface of the tongue.
B). darker pink or more reddish in color: less keratin, more vascular tissues; vestibule, floor of the mouth, ventral surface of the tongue, retromolar regions.
C). normal variations pigmentations.
D). substances in the blood, i.e. hemoglobin level polycythemia (red, cherry red) anemia (pale).
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Healthy oral mucosa
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Healthy oral mucosa
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Leukoedema non-malignant variation of normal
mucosa. most often at buccal mucosa, but also
other sites (labial mucosa, soft palate). most often seen adults > 40 yrs. clinical features:
early stage: firmly opalescence; later stage: definite grayish white cast
with coarsely wrinkle surface which cannot be removed with a tongue blade, but will disappear on stretching.
(if injury: red eroded area, mimic cheek biting).
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Leukoedema
WenChen Wang
Leukoedema
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Leukoedema
microscopic findings: increased thickness of epithelium. marked intracellular edema (ballooning) acanthosis: abnormal thickening of the spin
ous layer (may be severe with elongation, thickening, blunting, and confluence of the rete pegs or may consist only of their elongation).
parakeratosis: hyperkeratosis with retention of nuclei.
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Leukoedema
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Leukoedema
D.D. leukoplakia, cheek-biting le
sion, white sponge nevus.
Treatment: no treatment is required
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Linea alba buccalis usually on buccal mucosa near the occlusal pl
ane. usually bilateral, may be related with occlusal t
rauma, therefore more prominent if patient has little overjet of molars and premolars.
Microscopic findings: increased thickness of epithelium, or hyperort
hokeratosis (hyperkeratosis without retention of nuclei).
Treatment: no special treatment, to avoid bite injury, cha
nge the relationship of upper and lower teeth (new denture or orthodontic treatment)
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Linear alba
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Leukoplakia White patch keratotic change occurring on mucous
membranes. usually caused by chronic irritation.
important etiologic factors including:
smoking, cold temperature, hot and/or spicy foods, alcohol, betel nut and /or tabacoo chewing, occlusal trauma, sharp edges of prostheses or teeth, actinic radiation.
WenChen Wang
LeukoplakiaClinical features: asymptomatic, old age group (40–70 yrs).most happened at: tongue, floor of the mouth, lower lip, commissures, palate, mucobuccal fold, alveolar ridge, retromolar area, buccal mucosa.
D.D.first R/O lesions of sloughing pseudomembranous types.easy to scrap off or not? if not, lesions are keratotic and need to D.D. with many white lesions.
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Homogeneous thick leukoplakia
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Leukoplakia
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Speckled leukoplakia
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Non-homogeneous thick leukoplakia
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Verrucous leukoplakia
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Verrucous leukoplakia
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Verrucous leukoplakia
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Hairy leukoplakia Special types of Leukoplakia
Hairy leukoplakia AIDS patient: irregular surface like hair. acanthosis with marked hyperparakeratosis wi
th formation of ridged and keratin projections, areas of ballooning cells and little or no inflammation in the connective tissue.
Ballooning changes = koilocytes: enlarged cells, some with enlarged nuclei with perinuclear halos, others are pyknotic nuclei.
(papilloma-like virus) ,(EM: EB virus), (Immunofluorescence staining for EB virus capsid antigens).
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EB 病毒感染引起
毛狀白斑(Hairy leukopla
kia)
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Hairy Leukoplakia on margin of tongue in a homosexual man
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Koilocytes: Hairy leukoplakia
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Lesion due to corroded amalgam fillings lingually in mandibular molars, similar with h
airy leukoplakia
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D.D. of hairy leukoplakia in AIDS
1. lesions due to restorative materials: corroded amalgam fillings, white lesions will disappear within a few weeks after fillings are replaced by plastic material.
2. leukoplakia: a. idiopathic leukoplakia: often locate
d on tongue (inferior surface), usually middle-aged women, extensive and smooth surface.
b. tobacco-associated leukoplakia: border of tongue, well-defined, smooth surface, regress after stop smoking.
WenChen Wang
D.D. of hairy leukoplakia in AIDS
3. lichen planus: border of the tongue, rare (reticular type).
4. chronic hyperplastic candidiasis: labial commissures extending to the buccal mucosa, disappear after fungi-static treatment.
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White Sponge Nevus
young, usually can be seen before puberty wide spread, usually whole oral cavity has familial pattern
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D.D with lichen planus
Lichen planus usually involve several lesions, leukoplakia is more often a solitary lesion.
may have Wickham’s striae: fine grayish white lines arranged in a lace-like pattern
may have skin lesion (leukoplakia : no skin lesion)
WenChen Wang
Lichen planus
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Nicotinic stomatitis or smoker’s palate
Nicotinic stomatitis or smoker’s palate, smoker’s keratosis
man, pipe smokers. usually whole hard palate. reddish stomatitis changed to slightly
opalescent then white. usually “red/pink dots/spots” as the c
enters of lesion indication inflammation of minor salivary glands.
usually disappear after stopping pipe smoking.
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Stomatitis nicotina palati
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Snuff dipper’s lesion, Tobacco chewer’s lesion
parboiled appearance of the white lesion, some are thick white plaque
lesion depends on where the tobacco was contact with the mucosa.
usually on the mandibular vestibule (both the incisors and the molar regions).
if change the habit, then most lesions will completely disappear.
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Tobacco chewer’s lesion
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Hairy Tongue
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White hairy tongue
1.elongation of the filiform papillae: increased retention of keratin.
2.male more than female.
3.depends on foods, the color can be different.
4.treated by tongue brushing.
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Black Hairy Tongue
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Black hairy tongue Caused by elongated filiform papillae.
Other causes:
(i) antibiotics (penicillin or tetracycline)
(ii) mouthwashes (sodium perborate or
chlorhexidine)
(iii) iron preparations
(iv) smoking
(iv) some foodstuffs
(v) herbs
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Geographic Tongue
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Geographic tongue Benign migratory glossitis and mucositis (Ge
ographic tongue) 1.psychological influences and suspected. 2.irregularly shaped red patches and white
patterns like map, on the dorsal , ventral and lateral surfaces of tongue. 3.red patches: desquamated filiform papillae: enlarge and regressive:change every week then completely disappear.
WenChen Wang
Geographic tongue
4.generally asymptomatic, sometimes burning sensation, tenderness and pain.
5. treated with : a. bland diet; b. coating the lesion with triamcinolone in Orabase, if symptoms occur
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Median rhomboid glossitis
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Median rhomboid glossitis May be congenital ( persistence of the tuberc
ulum impair) or may be associated with candidal infection. Smoking may predispose to the candidosis.
There is: (i) absence of filiform papillae. (ii) epithelial hyperplasia and acanthosis. (iii) chronic inflammatory infiltrate in the lami
na propria.
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Lichen planus
1. Affecting 0.5-2.0% of the population
2. Mean age at onset: 30-50 years
3. A mild predilection for females
4. Six forms: reticular, papular, plaque, atrophic, erosive, bullous
5. Malignant transformation -- <1%
6. Etiology: emotional stress or
aberrant cellular immunity
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Lichen planus
7. sites: mostly at buccal mucosa (85%), others including gingiva, tongue, palate, floor of the mouth, vermillion border, (skin: small flat papules/ulceration may fuse together).
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Reticular lichen planus (Wickham’s striae)
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Erosive lichen planus
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Plaque type lichen planus
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Erosive lichen planusDesquamative gingivitis
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Lichen planus
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Bullous Lichen Planus
If severe liquefaction, then bullae formed;in very severe case, then disseminated erosions.
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D.D.1. White sponge nevus
White sponge nevus usually appears at birth (OLP : 70% after 40 yrs.)
D.D.2. Geographic tongue
Geographic tongue -- red center with a slightly raised white border: rapidly (in a few days) change site and shape OLP , if change, take longer time
WenChen Wang
D.D. 3. LeukoedemaLeukoedema if has wrinkles, stretching test
can be used to D.D. with Wickham’s striae.
D.D. 4. Linea alba Patient sucking cheeks habit, then oft
en has linea alba and mimic Wickham’s striae: asking about patient’s habit.
WenChen Wang
D.D. 5. Lichenoid reactionsHistory of taking drugs:
a. systemic treatment with streptomycin, tetracycline, hypoglycemics, diuretics, indomethacine….
b. dental restorative materials: dental gold, mercury, silver alloys.
WenChen Wang
Papules Lichen Planus
WenChen Wang
no treatment jf no discomfort, examined periodically.clinical discomfort ( i.e. burning , tenderness, soreness of oral mucosa): topical steroidsevere cases: systemic administration of sedative and cortisone.
Management: OLP
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Squamous cell papilloma, papilloma
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Squamous cell papillomaFeatures: 1. exophytic, papillomatous shape, pedunculated with rough, cauliflower-like pebbly surface, deep cleft formation. 2. In oral cavity, usually < 1 cm
3. site: tongue (33%), palate, buccal mucosa, gingiva, lips, mandibular ridge, mouth floor
WenChen Wang
Squamous cell papilloma
1. age: most 21-50 yrs (<40yrs)2. Not usually in oral cavity, 3. malignant
change: very rare (no dysplastic changes)
4. color (depends on whether chronic irritation)hyperkeratosis or not white or pink.
WenChen Wang
Verrucous hyperplasiaExophytic mass (a proliferative epithelial lesion), like papilloma.
Precancerous lesionEpithelial hyperplastic fold towards mucosa surface.
If malignant change: towards underlying connective tissue
(some scholars believe: VH =CA).Betel nut chewing habit in Taiwan
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Verrucous hyperplasis
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Verrucous hyperplasis
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Verrucous hyperplasis
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Verrucous hyperplasis
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Verrucous hyperplasis
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Verrucous hyperplasis
*management:surgical removal. microscopic findings: confined the final diagnosis.
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Verrucous carcinoma1. an exophytic type of low-grade SCC. 2. features: 1). most sites: mandibular labial and bu
ccal vestibule and mucosa. 2). older ages: average 60-70 yrs. 3). may be very large papillary mass or fl
at covered whole mucosa (sessile base). 4). color depends on the amount of kerat
in: pink or white. 5). may be moderately firm, but not so h
ard like invasive CA.
WenChen Wang
Verrucous carcinoma
3. Management: 1). wide excision:5-yr survival rates as high
as 75%. 2). followed-up carefully: a tendency for
multifocal tumors to develop after excision. 3). radiation: not very successful due to
low grade tumor, on the contrary, radiation may induce malignancy.
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Verrucous Ca.
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Distinguishing histologic features between VH and V ca:
s: VH, sharp varity; b: VH, blunt varity; c: V. ca
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Verruca vulgaris
1. exophytic growth of the epithelium: very common lesion of the skin, rare in the oral cavity. Induced by HPV.
2. features:site: skin, vermillion border, rarely
on labial or buccal mucosa or tongue.
WenChen Wang
Verruca vulgaris (common wart)
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D.D. with papilloma and verrucous vulgaris
verrucous vulgaris: usually on skin, rarely in the oral cavity.
…sessile base vs. pedunculated (papilloma).
…round eosinophilic bodies in the cells ( in prickle cell layer and granular cell layer) : viral inclusion bodies( not seen in papilloma).
WenChen Wangverrucous vulgaris
Squamous cell papilloma
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Squamous cell carcinoma
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Squamous cell carcinoma
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Oral Candidiasis Moniliasis, candidosis Classification
A. Acute pseudomembranous (Thrush)
B. Acute atrophic (antibiotic sore mouth)
C. Chronic atrophic (denture-associated
stomatitis)
D. Chronic hyperplastic (chronic
mucocutaneous candidosis; candidal
leukoplakia)
WenChen Wang
Chronic candidiasis
if low grade infection by Candida albicans:
due to long term irritation: ( i.e. tobacco smoking) increase keratin production and retention hyperkeratosis, like leukoplakia can not be scraped off
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Chronic Mucocutaneous Candidiasis
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Acute pseudomembranus typecandidiasis
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Acute pseudomembranus typecandidiasis
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erythematous cndidiasis
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Factors predisposing to oral candidiasis
1. Systemic factors: physiologic old age, infancy, pregnancy
2. Endocrine disorders: diabetes mellitus, hypothyroidism
3. Nutritional deficiencies: iron, foliate, or vitamin B12 deficiency
4. Malignancies: acute leukemia, agranulocytosis, 5. Immune defects, immuosuppression, AIDS, thy
mic aplasia, corticosteroids
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Candida Albicans
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Candidiasis
Management: a. discontinue broad spectrum antibiotics treatment, use more s
elective ones. b. anti-fungal therapy, ex. nystatin
suspension c. treatment of primary diseases.
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AIDS
1. Pseudomembranous cadidiasis,
2. Erythematous candidiasis: lesion on the tongue: along the mid-line and the filiform papilla atrophic.
3. If esophageal candidiasis: may be AIDS.
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Oral Candidiasis as the first manifestation of HIV Infection
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Submucous fibrosis
1. a fibroelastic change of the lamina propria. 2. epithelial atrophy: stiffness of the oral mucosa: trismus and inability to
eat. 3. etiology: unclear, strong irritating foods and vitamin B def., protein def., betel nut chewing.Precancerous condition
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Submucous fibrosis1.Clinical: 1). burning sensation: vesicles, ulcerations or recurrent stomatitis. 2). stiffening of certain areas: difficult to opening the mouth and swallowing. 3). like systemic sclerosis or scleroderma. 4). mucosa: finally became blanched and opaque, fibrotic bands. 5). age: usually 20-40 yrs.
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Submucous fibrosis
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Submucous fibrosis
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Submucous fibrosis
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Submucous fibrosis
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2. Microscopic findings: severe atrophic, rete
pegs disappeared, epithelial atypia, disappearance of fibroblasts, blood vessels obstructed or narrowed.
3. Dense collagen bundles aggregation
Submucous fibrosis
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Submucous fibrosis
3. Treatment:
1).could be precancerous. 2).systemic corticosteroid and local hydrocortisone to alleviate pain.
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Sloughing Pseudomembranous Necrotic Lesions
May be scraped off the mucosa with a tongue blade, leaving a raw bleeding surface.
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PlaquePlaque (material alba): *dental plaque is on the
tooth surface, not easily been washed off with water.
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Chemical burns
Chemical burns:1. some analgesics put in the oral cavity:
mucosal lesions: aspirin burn etc. or causatic agents (phenol, silver nitrate) used by dentist.
2. diagnosis: history.3. treatment: protective coating: Orabase,
bland diet; systemic analgesics.
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chemical burn
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chemical burn
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chemical burn
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ANUG
Acute Necrotizing Ulcerative Gingivitis (ANUG, Vincent’s infection, Trench mouth)
1.inflammatory disorder of gingiva, necrotic ulcerative destruction of the free gingiva, crest and inter-dental papillae.
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ANUG
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ANUG2. Predisposing factors are very important:(i). mainly due to decrease resistance to infe
ction(ii).gingivitis and periodontitis: poor oral hyg
iene (iii). Stress these lead to overgrowth of the normal fl
ora or superinfection by anaerobic and fusiform bacilli
and spirochete (should be P.i.).
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ANUG
Differential diagnosis: 1.punched out defects of the inter-de
ntal papillae: pathognomic for ANUG. 2.diffuse gangrenous stomatitis: nec
rotic gangrenous process spread to oral mucosa except interdental papillae and marginal gingiva: systemic disorders??
WenChen Wang
ANUG
Management: 1.mainly aimed to : superinfection b
y anaerobic fusiform and spirochetes, poor oral hygiene (gingivitis and periodontitis), and low resistance to infection.
WenChen Wang
ANUG
(i). antibiotics (penicillin 500mg, q.i.d. >5days).
(ii). careful scaling, curettement and debridment ( best 24-48 hrs after antibiotics treatment).
(iii). oral rinsing with a solution of 3% H2O2
in saline (1:3), 12x daily. (iv). recontouring of the gingiva if necessa
ry.
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Candidiasis
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Angular cheilitis
Predisposing factors: decreased vertical dimension of dentures, anemia, vitamin B deficiencies
Infection with Candida albicans, other microorganisms
Treatment: eliminate predisposing factors, antifungal ointment (nystatin)
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Angular cheilitis
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Angular cheilitis
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Yellow Lesions
Fordyce’s granules: a collection of sebaceous glands, covered by normal mucosa. clinically: small elevated granules, color from whitish yellow to yellow.
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Fordyce’s granules
1. in oral cavity: buccal mucosa (usually bilateral), retromolar pad, labial mucosa.
2. usually no ulceration, looks like cheese.
3. histological features: like normal sebaceous glands of skin.
4. 50-80% population may have, a benign lesions, patient cancer phobia.
WenChen WangFordyce’s granule
WenChen WangFordyce’s granule
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Lipoma
1. the most common benign neoplasms, but rarely in oral cavity.
2. mature fat cells under skin tissue.
3. usually after 40 yrs., peak at 50 yrs (middle age).
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Lipoma 4. in oral cavity: most on buccal muco
sa and mucobuccal fold, then tongue, floor of the mouth and lips.
5. usually yellow color, but many shapes: sessile, pedunculated; usually smooth surface, no-ulcerated (except with trauma).
6. palpation: nontender, soft, felling like cheese.
7. usually single lesion.
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Lipoma
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Lipoma1. Microscopic findings: mature fat cells
within a connective tissue capsule, fibrous stroma divided into lobules, blood vessels in the septa.
2. Treatment: excision for large lesion, no treatment for small lesions.
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Epidermoid and Dermoid Cysts
1. a kinds of developmental anomalies. Cystic teratoma comes from germinal epithelium.
2. any place in the body, not usually in the oral cavity.
3. if in the oral cavity: patient may have swelling of his/her floor of the mouth.
4. at head and neck: most at floor of the mouth, then at submaxillary and submental areas.
WenChen Wang
Epidermoid and Dermoid Cysts5. any ages, but mostly discovered in 15-3
5 yrs. old, nontender, various sizes, non-fixed, if no trauma: smooth surface.
6. histology classification depends on cystic contents:
(i). epidermoid cyst: fluid, keratin, non- specific structures. (ii). dermoid cyst: sebaceous materials, keratin. (iii). Teratoma: many elements from different germinal layers: bone, muscle, teeth etc.
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Epidermoid cysts
Dermoid Cysts
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Epidermoid and Dermoid Cysts
Differential diagnosis: ranula, thyroglossal duct cyst, cystic h
ygroma, brachial cleft cyst, cellulitis, tumors, fat masses.
Thyroglossal duct cyst
WenChen Wang
Oral Ulcers and Fissures
Recurrent aphthous ulcer (canker sore) (RAU) and Intraoral recurrent ulcer of herpes simplex (IRHS)
Both are: (i). easy recurrent painful ulcer (superficial), each time lasts 1-2 wks; (ii). usually have tender LAP (iii). spontaneous heal, no sequelae (scar formation).
WenChen Wang
RAU and IRHS
Differences: (i). Etiology:RAU: psychic, allergic, microbial, traumatic,
endocrine, hereditary and autoimmune mechanisms.
IRHS: HSV infection, may be subclinical infection, virus became latent in nerve endings or ganglions reactivation epithelial cells lesions.
WenChen Wang
RAU and IRHS
(ii). Sites:RAU: freely movable mucosa (non-keratini
zed): lips, buccal mucosa, tongue, mucobuccal fold, floor of the mouth, soft palate.
IRHS: fixed mucosa (keratinized): hard palate, gingiva and alveolar ridge.
WenChen Wang
RAU and IRHS
3. Management: a. in general, no treatment, heal after 1-2 wee
ks; b. some ones used:RAU: tetracycline mouthwash and cortisone in Orabase; analgesics (may be).IRHS: Vira-A or Zovirax cream (Acyclovir)
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Minor type of Recurrent aphthous ulcer
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Major recurrent aphthous ulcer
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Herpetiform recurrent aphthous ulcer
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Primary herpetic gingivostomatitisPrimary herpetic gingivostomatitis
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Recurrent herpes labialis
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Herpetiform recurrent aphthous ulcer
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Tuberculosis (TB)
1. infectious organisms: Mycobacterium tuberculosis.
2. at oral cavity: uncommon, if any, rarely are primary lesion,
but secondary to pulmonary lesions.3. pulmonary lesion: sputum to small injury site
of mucosa tissue, or through hematogenous spread to submucosa then proliferation to ulceration.
4. mostly at tongue then palate, lips, buccal mucosa, gingiva, frenula.
WenChen Wang
TB
5. irregular, painful ulcer, became larger slowly
6. easily to have trauma then can be mistaken as traumatic ulcer or carcinoma
7. sometimes without ulcer; if on gingival, then diffuse, hyperemic, nodular or papillary proliferation
8. sometimes involved bone (maxilla or mandible) through hematogenous spread.
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Tubercurosis
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Tubercles of epitheloid cells, Langhan’s giant cells, mononuclear cells in periphery
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Ulcers secondary to systemic disease
1. History of predisposing disease or history revealing information suggesting presence of disease.
2. Example: Steven-Johnson syndrome (Erythema multiform).
Differential Diagnosis of Ulcers
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Erythema multiform
1. involves lips with multiple red lesions (papule or bullae): rupture: raw, painful lesions
2. other sites including skin lesions; before disease, may have HSV, taken drugs (antibiotics, contraceptives, barbiturates), post-radiation therapy ( i.e. ulcerative colitis patient).
WenChen Wang
Ulcers from odontogenic infections
Ulcers from odontogenic infections: 1. suspicion of ulcer on alveolar or pala
te 2. digital pressure on alveolus or tooth
elicits pus from ulcer 3. trace sinus with gutta percha cone:
x-rays to isolate involved teeth.
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RAU Recurrent aphthous ulcer: 1. yellowish ulcer, 0.5-2 cm diameter,
with narrow erythematous halo 2. on loose mucosa surface.
IRHSIntraoral recurrent herpes simplex: 1. cluster of small punctuate ulcers
(< 0.5cm) 2. on bound mucosa.
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Traumatic ulcers
History of trauma or presence of potential etiologic agent.
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Squamous cell carcinoma
1. high suspicion if patient is male over 40, heavy drinker or smoker
2. no evidence of trauma or systemic disease; negative serologic findings
3. risk factors involved: alcohol, betel quid chewing, smoking
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Squamous cell carcinoma
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Squamous cell carcinoma
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民國九十七年台灣地區十大癌症死因 死亡原因 每十萬人口 死亡人數
死亡率 1 肺癌 33.8 7,771 2 肝癌 33.3 7,651
3 結腸直腸癌 18.5 4,266 4 女性乳癌 13.5 1,541 5 胃癌 10.0 2,292 6 口腔癌 9.6 2,218 7 攝護腺癌 7.7 892 8 子宮頸癌 6.2 710 9 食道癌 6.2 1,433 10 胰臟癌 5.9 1,364
台灣地區民國 97 年有 38913 人死於癌症,平均每 13 分半就有 1 人死於癌症
98.6.1798.6.17 公佈公佈
WenChen Wang
民國九十七年男性與女性十大癌症死因
男性 女性 1 肝癌 1 肺癌 2 肺癌 2 肝癌 3 結腸直腸癌 3 結腸直腸癌 4 口腔癌 4 女性乳癌 5 胃癌 5 胃癌 6 食道癌 6 子宮頸癌 7 攝護腺癌 7 胰臟癌 8 胰臟癌 8 卵巢癌 9 鼻咽癌 9 白血病10 非何杰金淋巴癌 10 非何杰金淋巴癌 口腔癌男性死亡 2,079 人
98.6.1798.6.17 公佈公佈
WenChen Wang資料來源 :行政院衛生署 製圖:王文岑
台灣口腔癌死亡人數統計