Presentation on theme: "1. White lesions of the oral mucosa"— Presentation transcript:
11. White lesions of the oral mucosa Differential Diagnosis of Oral and Maxillofacial lesions1. White lesions of the oral mucosa2. Solitary oral ulcer and fissures3. 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;
2White lesions of the oral mucosa Keratotic Lesions1. Leukoedema 2. Linea alba buccalis 3. Leukoplakia 4. Nicotinic stomatitis, snuff-dipper’s lesion 5. Benign migratory glossitis and mucositis 6. Lichen planus 7. Papilloma, verrucous vulgaris 8. white exophytic squamous cell carcinoma,Verrucous carcinoma 9. Hypertrophic candidiasis 10. White sponge nevus
4UlcersShort-term ulcersTraumatic ulcers (most)Recurrent aphthous ulcers (minor)Recurrent intraoral herpes simplex lesionsUlcers as result of odontogenic infectionUlcers with generalized mucositis or vesiculobullous diseaseUlcers secondary to systemic disease
5Persistent ulcersTraumatic ulcers (occasional)Ulcers from odontogenic infectionSquamous cell carcinomaChancreGummaUlcer secondary to systemic diseaseLow-grade mucoepidermoid tumorMetastatic tumor
6Normal 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).
9non-malignant variation of normal mucosa. Leukoedemanon-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).
12Leukoedema microscopic findings: increased thickness of epithelium. marked intracellular edema (ballooning)acanthosis: abnormal thickening of the spinous 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.
14leukoplakia, cheek-biting lesion, white sponge nevus. Treatment: LeukoedemaD.D.leukoplakia, cheek-biting lesion, white sponge nevus.Treatment:no treatment is required
15Linea alba buccalis usually on buccal mucosa near the occlusal plane. usually bilateral, may be related with occlusal trauma, therefore more prominent if patient has little overjet of molars and premolars.Microscopic findings:increased thickness of epithelium, or hyperorthokeratosis (hyperkeratosis without retention of nuclei).Treatment:no special treatment, to avoid bite injury, change the relationship of upper and lower teeth (new denture or orthodontic treatment)
17Leukoplakia 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.
18Leukoplakia Clinical 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.
26Hairy leukoplakia Special types of Leukoplakia AIDS patient: irregular surface like hair.acanthosis with marked hyperparakeratosis with 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).
30Lesion due to corroded amalgam fillings lingually in mandibular molars, similar with hairy leukoplakia
31D.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 located 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.
32D.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.
33White Sponge Nevus young, usually can be seen before puberty wide spread, usually whole oral cavityhas familial pattern
34D.D with lichen planusLichen 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 patternmay have skin lesion (leukoplakia : no skin lesion)
36Nicotinic stomatitis or smoker’s palate Nicotinic stomatitis or smoker’s palate, smoker’s keratosisman, pipe smokers.usually whole hard palate.reddish stomatitis changed to slightly opalescent then white.usually “red/pink dots/spots” as the centers of lesion indication inflammation of minor salivary glands.usually disappear after stopping pipe smoking.
38Snuff dipper’s lesion, Tobacco chewer’s lesion parboiled appearance of the white lesion, some are thick white plaquelesion 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.
43Black hairy tongue Caused by elongated filiform papillae. Other causes:(i) antibiotics (penicillin or tetracycline)(ii) mouthwashes (sodium perborate orchlorhexidine)(iii) iron preparations(iv) smoking(iv) some foodstuffs(v) herbs
45Geographic tongueBenign migratory glossitis and mucositis (Geographic tongue)1.psychological influences and suspected.2.irregularly shaped red patches and whitepatterns like map, on the dorsal , ventraland lateral surfaces of tongue.3.red patches: desquamated filiformpapillae: enlarge and regressive:changeevery week then completely disappear.
46Geographic tongue4.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
48Median rhomboid glossitis May be congenital ( persistence of the tuberculum 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 lamina propria.
49Lichen planus 1. Affecting 0.5-2.0% of the population 2. Mean age at onset: years3. A mild predilection for females4. Six forms: reticular, papular, plaque, atrophic, erosive, bullous5. Malignant transformation -- <1%6. Etiology: emotional stress oraberrant cellular immunity
50Lichen planus7. 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).
56Bullous Lichen PlanusIf severe liquefaction, then bullae formed;in very severe case, then disseminatederosions.
57D.D.1. White sponge nevus D.D.2. Geographic tongue White sponge nevus usually appears at birth (OLP : 70% after 40 yrs.)D.D.2. Geographic tongueGeographic tongue -- red center with a slightly raised white border: rapidly (in a few days) change site and shapeOLP , if change, take longer time
58D.D. 3. Leukoedema D.D. 4. Linea alba Leukoedema if has wrinkles, stretching test can be used to D.D. with Wickham’s striae.D.D. 4. Linea albaPatient sucking cheeks habit, then often has linea alba and mimic Wickham’s striae: asking about patient’s habit.
59D.D. 5. Lichenoid reactions History of taking drugs:a. systemic treatment with streptomycin, tetracycline, hypoglycemics, diuretics, indomethacine….b. dental restorative materials: dental gold, mercury, silver alloys.
63Squamous cell papilloma Features:1. exophytic, papillomatous shape,pedunculated with rough,cauliflower-like pebbly surface,deep cleft formation.2. In oral cavity, usually < 1 cm3. site: tongue (33%), palate, buccalmucosa, gingiva, lips,mandibular ridge, mouth floor
64Squamous cell papilloma 1. age: most 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.
65Verrucous hyperplasia Exophytic 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
71Verrucous hyperplasis *management:surgical removal microscopic findings: confined the final diagnosis.
72Verrucous carcinoma 1. an exophytic type of low-grade SCC. 2. features:1). most sites: mandibular labial and buccal vestibule and mucosa.2). older ages: average yrs.3). may be very large papillary mass or flat covered whole mucosa (sessile base).4). color depends on the amount of keratin: pink or white.5). may be moderately firm, but not so hard like invasive CA.
73Verrucous 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.
75Distinguishing histologic features between VH and V ca: s: VH, sharp varity; b: VH, blunt varity; c: V. ca
76Verruca vulgaris1. 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.
78D.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).
83Chronic 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
90CandidiasisManagement:a. discontinue broad spectrumantibiotics treatment, use more selective ones.b. anti-fungal therapy, ex. nystatin suspensionc. treatment of primary diseases.
91AIDS 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.
92Oral Candidiasis as the first manifestation of HIV Infection
93Submucous fibrosis 1. a fibroelastic change of the lamina propria. 2. epithelial atrophy: stiffness of theoral mucosa: trismus and inability toeat.3. etiology: unclear, strong irritatingfoods and vitamin B def., proteindef., betel nut chewing.Precancerous condition
94Submucous fibrosis 1.Clinical: 1). burning sensation: vesicles, ulcerations or recurrent stomatitis.2). stiffening of certain areas: difficultto opening the mouth and swallowing.3). like systemic sclerosis orscleroderma.4). mucosa: finally became blanched andopaque, fibrotic bands.5). age: usually yrs.
99Submucous fibrosis 2. Microscopic findings: severe atrophic, rete pegs disappeared, epithelial atypia, disappearance of fibroblasts, blood vessels obstructed or narrowed.3. Dense collagen bundles aggregation
100Submucous fibrosis3. Treatment:1).could be precancerous.2).systemic corticosteroidand local hydrocortisoneto alleviate pain.
101Sloughing Pseudomembranous Necrotic Lesions May be scraped off the mucosa with a tongue blade, leaving a raw bleeding surface.
102Plaque Plaque (material alba): *dental plaque is on the tooth surface, not easily been washed off with water.
103Chemical 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.
109ANUG 2. Predisposing factors are very important: (i). mainly due to decrease resistance to infection(ii).gingivitis and periodontitis: poor oral hygiene(iii). Stressthese lead to overgrowth of the normal flora or superinfection by anaerobic and fusiform bacilliand spirochete (should be P.i.).
110ANUG Differential diagnosis: 1.punched out defects of the inter-dental papillae: pathognomic for ANUG.2.diffuse gangrenous stomatitis: necrotic gangrenous process spread to oral mucosa except interdental papillae and marginal gingiva: systemic disorders??
111ANUGManagement:1.mainly aimed to : superinfection by anaerobic fusiform and spirochetes, poor oral hygiene (gingivitis and periodontitis), and low resistance to infection.
112ANUG (i). antibiotics (penicillin 500mg, q.i.d. >5days). (ii). careful scaling, curettement and debridment ( best 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 necessary.
117Yellow LesionsFordyce’s granules:a collection of sebaceous glands, covered by normal mucosa.clinically: small elevated granules, color from whitish yellow to yellow.
118Fordyce’s granules1. 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.% population may have, a benign lesions, patient cancer phobia.
121Lipoma1. 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).
122Lipoma4. in oral cavity: most on buccal mucosa 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.
124Lipoma1. 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.
125Epidermoid 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.
126Epidermoid and Dermoid Cysts 5. any ages, but mostly discovered in 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 fromdifferent germinal layers: bone,muscle, teeth etc.
129Oral 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 (scarformation).
130RAU 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.
131RAU and IRHS (ii). Sites: RAU: freely movable mucosa (non-keratinized): lips, buccal mucosa, tongue, mucobuccal fold, floor of the mouth, soft palate.IRHS: fixed mucosa (keratinized): hard palate, gingiva and alveolar ridge.
132RAU and IRHS 3. Management: a. in general, no treatment, heal after 1-2 weeks;b. some ones used:RAU: tetracycline mouthwash and cortisonein Orabase; analgesics (may be).IRHS: Vira-A or Zovirax cream (Acyclovir)
139Tuberculosis (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.
140TB 5. irregular, painful ulcer, became larger slowly 6. easily to have trauma then can be mistaken as traumatic ulcer or carcinoma7. sometimes without ulcer; if on gingival, then diffuse, hyperemic, nodular or papillary proliferation8. sometimes involved bone (maxilla or mandible) through hematogenous spread.
142Tubercles of epitheloid cells, Langhan’s giant cells, mononuclear cells in periphery
143Ulcers secondary to systemic disease Differential Diagnosis of UlcersUlcers secondary to systemic disease1. History of predisposing disease or history revealing information suggesting presence of disease.2. Example: Steven-Johnson syndrome (Erythema multiform).
144Erythema multiform1. involves lips with multiple red lesions (papule or bullae): rupture: raw, painful lesions2. other sites including skin lesions; before disease, may have HSV, taken drugs (antibiotics, contraceptives, barbiturates), post-radiation therapy ( i.e. ulcerative colitis patient).
145Ulcers from odontogenic infections 1. suspicion of ulcer on alveolar or palate2. digital pressure on alveolus or tooth elicits pus from ulcer3. trace sinus with gutta percha cone: x-rays to isolate involved teeth.
146RAU IRHS Recurrent aphthous ulcer: 1. yellowish ulcer, cm diameter, with narrow erythematous halo2. on loose mucosa surface.IRHSIntraoral recurrent herpes simplex:1. cluster of small punctuate ulcers (< 0.5cm)2. on bound mucosa.
147Traumatic ulcersHistory of trauma or presence of potential etiologic agent.
148Squamous cell carcinoma 1. high suspicion if patient is male over 40, heavy drinker or smoker2. no evidence of trauma or systemic disease; negative serologic findings3. risk factors involved: alcohol, betel quid chewing, smoking