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WHITE LESION OF ORAL MUCOSA
Dr. Samina
ORAL MUCOSA
DEFINITION It is defined as a moist lining of oral cavity
that communicates with the exterior.
Mucous membrane are also found lining other body cavities such as sinuses, GIT, uterus etc.
ORALMUCOSA
MasticatoryGINGIVA,
HARD PALATE
Lining Lips, cheeks, soft palate
SpecializedDorsum of
tongue
ORAL MUCOSA
The oral mucosa consists of two layers: an epithelium (stratified squamous epithelium) & an underlying layer of connective tissue, which is the lamina propria.
Beneath selected areas of the oral mucosa is a loose connective tissue, the submucosa
ORAL MUCOSA
The Epithelium Keratinization
(orthokeratinization) Parakeratinization Nonkeratinization
Orthokeratinized -- no nuclei presentParakeratinized -- pyknotic nuclei retained
keratinisation - organic process by which keratin is deposited in cells
KERATINIZED EPITHELIUM
Most of the oral mucosal surface is lined by nonkeratinized stratified squamous epithelium except gingiva, hard palate and dorsal surface of the tongue where the epithelium is keratinized
The keratinized cells have no nuclei and the cytoplasm is displaced by large numbers of keratin filaments
Keratinized epithelium is associated with masticatory function and have four layers of cells
MASTICATORY MUCOSA
Basal layer Spinous layer Granular layer Cornified layer
NONKERATINIZED EPITHELIUM Nonkeratinized epithelial cells in the superfecial
layers do not have keratin filaments in the cytoplasm
The surface cells also have nuclei
The stratum corneum and stratum granulosum layers are absent
This epithelium is associated with lining of the oral cavity
LAMINA PROPRIA Is the connective tissue layer immediately below
the epithelium. Can be divided into the papillary layer &
reticular layer.
In the papillary layer, finger-like projections of connective tissue extend into the deep surface of the epithelium.
An increase in the number & length of the papillae is seen in areas where mechanical adhesion between the epithelium & lamina propria is required (masticatory mucosa).
Oral Mucous Membrane
Oral Mucous Membrane
Epithelium
Lamina Propria
Submucosa
Periosteum
Bone
WHITE LESIONS Color of oral mucosa:
O.M is translucent & reflect s content of underlying tissue.
Normal color of oral mucosa is PINK but the intensity varies due to factors like; 1 -Thickness of O.M. 2 -Degree of keratinization 3 -Amount of vascularity & fibrous content in
C.T. 4 -Formation of pseudomembrain 5 -Pigmentation producing cells like
melanocytes
WHITE LESIONS
Color of different location of healthy oral mucosa: Masticatory mucosa= light pink Lining mucosa =reddish pink Palatoglossal arch =dusky red (due to
increase vasculrity.)
WHITE LESION
.It is a non specific term used to describe any abnormal area of o.m that on clinical examination appears whiter than surrounding tissue. It is usually slightly raised ,roughened or of different texture than adjacent normal mucosa.
WHITE LESIONS
REASON OF WHITE APPEARANCE: Increase thickness of epithelium with
increase production of keratin (hyperkeratosis) & production of abnormal keratin & imbibitions of fluid by upper layer of mucosa
Pseudomembrain; occur in coagulation of tissue surface e.g. burn
RED LESION
Refers to an area of reddened mucosa that may appear red and atrophic or exhibits granular, velvety texture.
These lesions may occur alone or in combination with white lesions. Such lesion may termed as a MIXED or RED & WHITE lesions
RED LESIONS
Reasons for appearance of red lesions: Dilated blood vessels Influx of new blood vessels Hemorrhage under epithelium Relatively thin outer epithelium
RED & WHITE LESIONSetiologic classification
1) NORMAL MUCOSAL VARIATION-Leukoedema- Fordyce granules ( sebaceous gland)- linea alba buccalis
2) GENITICALLY LINKED WHITE KERATOTIC LESION-oral genodermatoses-white sponge nevus-Hereditary benign intraepithelial dyskeratosis-Pachyonychia congenita (pachy=thick onyx=nail _abnormal thickening of Nail)
3) Post inflammatory white lesions-Traumatic keratosis-Mechanical trauma-thermal burn- chemical burn-radiation mucositis-reactive mucosal hyperplasia (stomatitis nicotina palati)
RED & WHITEetiologic classification
4) WHITE & RED LESIONS DUE TO INFECTIONS
-syphilis
-Measles (koplik,s spot)
-candidiasis
-Bacterial stomatitis
5) PREMALIGNANT LESIONS
-Leukoplakia
-Lichen planus
-Lichenoid reaction
-Erythroplakia
-Acitinic keratoses
-Discoid lupus erythmatosus
-Chronic hyperplasic candidiasis
6) PREMALIGNANT CONDITIONS
-Oral submucous fibrosis-Oral psoriasiform-Dyskeratosis congenita-Sydropenic dysphagia-Syphilitic glossitis
7) MISCELLANEOUS
White lesion of oral cavityNon- scrapable ( keratotic) Scrapable (non-keratotic )
Linea alba buccallis Chemical/thermal burn
Frictional/traumatic keratosis Pseudo membranous dandidiasis
Homogenous leukoplakia Syphilitic mucous patch
Reticular lichen planus Diphtheric patch
Chronic hyperplasic candidiasis
Dyskeratosis congenita
White sponge nevus
FORDYCE GRANULE ectopic collections of sebaceous glands
upper lip, buccal mucosa, gingiva, anterior pillars of fauces bilaterally symmetrical distribution 60-70% of adult population granules in upper lip increases during puberty; granules in buccal mucosa increases in later stages of life multiple, small, discrete, milia-like, yellowish stuctures; 1-2mm diameter occasionally form slightly raised confluent plaques
FORDYCES NODULE
LEKODEMA
more in blacks than whites possibly due to mucosal pigmentation in blacks making edematous changes more noticeable
variation of normal rather than disease more common and severe in smokers (?) diffused, gray-white, milky, opalescent mucosa folded surface, wrinkles or whitish streaks lesions do not rub off bilateral, may extend onto labial mucosa easy to diagnose: white appearance diminishes when
cheek is stretched
LEUKODEMAIncreased thickness of epithelium with striking intracellular edema of spinuos layer Vacuolated cells appear large and have stretched nuclei Parakeratinized epithelial surface Broad and elongated rete ridges Benign condition
Pachyonychia congenita
Autosomal dominant hereditary condition
Gross thickening of nails Palmoplanter kertosis Oral lesion – white opaque patches
on dorsum & lateral borders of tongue
& cheeks
Dyskeratosis congenita
Hereditary disorder with Male predilection
Abnormal pigmentation of skin, dystrophic nails & hyperkeratosis of mucous membrane
Severe gingivitis & periodontal destruction
Follicular keratosis(Darier`s disease) Autosomal dominant disorder Mutation in genes that encode an
intrcellular calcium pump – abnormal desmosomal organization
Multiple heavily keratinized papules on forehead, scalp & ears, become secondarily infected & foul smelling
Oral lesions – whitish coalescing papules on hard palate & gingiva
Histological features; hyperkeratosis, suprabasal cleft containing
acantholytic cells Large abnormally keratinized
squamous cells (Corps ronds) & smaller flattened
cells (grains) seen in the roof of cleft
Darier`s disease
FRICTIONAL /TRAUMATIC KERATOSIS
Defined as a white patch with a rough surface which is clearly related to a source of mechanical irritation & that will disappear over a time with removal of stimuli.
-a) linea alba buccalis:nonscrapable line present on buccal mucosa usually along plane of occlusion.b) chronic lip,cheek,tongue chewingc) Due to rough flanges of dentureManagement:
-removal of etiologic agent-symptomatic treatment
CHEMICAL BURNS & THERMAL BURNS
Chemical burns- Analgesics like aspirin, clove oil etc, Phenol ,silver nitrate ,conc. H2O2 ,RCT medicaments.
Thermal burns- Intake of hot food & beverages
D.Dx. Acute pseudomembranous candidiasis Gangrenous stomatitis
Treatment: 1) topical application of anasthetic agent like
benzocain/lignocain Gel( choline salicylate 8.7%,benzylkonium0.01% & lignocain Hcl 2%)
2) Topical application of steroids e.g. Triamcinolone acetonide oral past 1%.
3) Analgesics for sever pain.
NICOTINE STOMATITIS,STOMATITIS NICOTINA PALATINUS,SMOKER’S PALATE
This lesion is a reactive hyperplasia to the heat generated by the tobacco smoke that act as a chronic irritating agent.
Mostly seen in reverse/ chutta & pipe smokers & less in beedi. Cigarette smokers.
NICOTINIC STOMATITIS
C/F. Usually seen in males Generally asymptomatic e.g. No pain Palatal mucosa appear as a diffuse grayish white
surface or flat top nodules with red pin point areas situated in center of nodules.
Red pin point areas correspond to the inflamed orifices of minor salivary glands ducts.
D.DX. Palatal papillary hyperplasia Focal epithelial hyperplasia (Heck’s disease) Darier,s disease ( follicular keratosis )
Histopathological features
Hyperkeratosis & Acanthosis of palatal epithelium
Mild patchy chronic inflammation of sub epithelial connective tissues & mucous glands
Squamous metaplasia of excretory ductsTreatment The palate will return to normal usually
within 1 to 2 weeks of smoking cessation High risk areas should be examined closely
WHITE SPONG NEVUS It is a hereditary dyskeratotic hyperplasia
of the mucous membrane that shows an autosomal dominant inheritance pattern with irregular penetrance.
Mutation in genes coding for keratins 4 & 13
It is also known as white folded gingivostomatitis,Familial white folded hypertrophy of the
mucous membrane leukokeratosis oris, hereditary leukokerarosis , leukoderma exfoliativum
mucosa oris & nevus spongiosus albus mucosae.
Aetiopathogenesis: Basic defect lies in epithelial cell maturation &
desquamation. There is decreased shedding of keratin which leads to
white sponge nevus
C/F: Usually present at birth or early childhood There in no sex predilection. Involve O.M but other mucosal sites also e.g. nasal cavity ,
esophagus , larynx. Present as an asymptomatic gray white folded or
corrugated spongy mucosal lesion Mucosal lesions have a soft or spongy texture & white
opalescent hue. Few millimeters to several centimeters It is usually asymptomatic, but can become symptomatic if
secondary infection occur
WHITE SPONGE NEVUS
D.DX.-leukoedema ,leukoplakia ,traumatic keratosis,chemical burn,candidiasis, lichen planus, pachyonychia congenita , Darier’s disease & dyskeratosis congenita.
HISTOPATHOLOGICAL FEATURES:
Epithelial thickening showing both acanthosis & hyperkeratosis.
Mild inflammatory cell infiltrate is seen in sub mucosa.
TREATMENT:-If asymptomatic =no treatment-If symptomatic = tetracycline M/W & penicillin.
ORAL LICHEN PLANUS (OLP)
Derived from Greek literature Lichen=tree moss & planus=flat
Definition: Olp is a common chronic immunological
inflammatory mucocutanious disorder that varies in appearance from keratotic to erythematous & ulcerative
ETIOPATHOGENESIS: Exact etiology is unknown Olp is T cell mediated disorder in which there
is production of cytokines which leads to apoptosis.
C/F: Commonly affect 1-2% of population 25% occur on oral mucosa alone 35% occur on cutaneous surface alone 40% occur on both oral & cutaneous surfaces Female: male 2:1
ORAL LICHEN PLANUS
C/F: Characteristic appearance of white papules
that usually coalesce forming a network of lines that may intersect or crisscross each other forming various patterns.
SKIN INVOLVMENT: Lesion is itchy & violaceous to brown papules
frequently over flexor aspect of wrist or ankle . ALOPECIA-loss of hair when scalp is involved. ONYCHORRHEXIS longitudinal ridging & grooves ANONYCHIA permanent nail loss
ORAL LICHEN PLANUSC/F:
ORAL MANIFESTATION: Basic lesion is papule arranged in linear or annular
forms & criss crossing each other forming various pattern like annular & reticular forms.
Six types Reticular (a net work) , papular , plaque like (a small circumscribed area distinct from
surrounding surface in character & appearance) , erosive atrophic & bullous .
D.DX:1) Lichenoid drug reaction 2) Hyperplasic candidiasis3) Electrogalvanic white lesions 4) Lupus erythmatosis5) Frictional keratosis 6) Graft versus host reaction7) Leukoplakia
histopathology
Orthokeratosis / parakeratosis Reteriges may be absent or
hypertroplastic Pointed saw tooth shaped Destruction of basal cell layer Intense band like infiltrate of T-
lymphocytes immediately subjacent to epithelium
ORAL LICHEN PLANUS INVESTIGATIONS:
Dx. Achieved by clinical presentation Biopsy may be complementary .
COMPLICATION: It can developed into carcinoma(SCC)
specially erosive form.
MANAGEMENT: If asymptomatic then requires no specific
treatment except chlorhxidine M/W to stop secondary infection & follow up once three months.
If atrophic & ulcerative – Topical steroids (triamcinolone acetonoid
0.1%) Triamcinolone oral suspension 40-80 mg /day prednisolone 5-7 days
reducing to 5-10mg over 2-4-weeks Injection into site of prednisolone 10-20mg/ml
every 2-4 weeks Antifungal to stop candidiasis
-- Antihistamins--cyclosporines, Azathioprine Surgery:
Excision, laser , cryosurgery,
ORAL SUBMUCOUS FIBROSIS
OSF is a chronic, progressive, scarring, high risk precancerous condition of oral mucosa seen primarily in Indian subcontinent, South east Asia, Taiwan& China.
ORAL SUBMUCOUS FIBROSIS It is a chronic disease affecting any part of oral cavity. Role of Areca nuts (arecoline & tannin) in disturbing
homeostatic equilibrium between synthesis & degradation
of extracellular matrix activated inflammatory cells cytokines , growth factors fibrosis
collagen synthesis down regulating collagenase Copper in areca increases activity of enzym Lysyl
oxidase
Occasionally it is preceded & associated with vesicle formation & then followed by the hylinization of the lamina propria.
Later subepithelial & submucosal myofibrosis leads to stiffness of O.M.
ETIOPATHOGENESIS: Still unclear but it is believe to be multifactorial ; Chewing of betel nut is one of the most etiologic
factor Nutritional deficiency : anemia ,iron vitamins ,
proteins Genetic factors
C/F: Common age is 12-40 years Burning sensation , blanching of O.M. May involve buccal mucosa, retromolar area ,soft
palate,uvula & tongu
ORAL SUBMUCOUS FIBROSIS
C/F: Small & stiff tongue Blanched & leathery floor of the mouth Fibrotic & depigmented gingiva Rubbery soft palate & blenched atrophic tonsils Trismus ,impaired mouth movements (whistling, eating
blowing. Hearing loss due to stenosis of Eustachian tubes Dryness of mouth Dysphagia to solids
INVESTIGATIONS:Dx. Clinical finding Incisional biopsy Raised ESR
D.DX.: Scleroderma , anemia amyloidosis
Histopathology Submucosal deposition of dense & hypo
vascular collagenous connective tissue Variable number of inflammatory cellsEpithelial changes: Sub epithelial vesicles in early lesion Hyperkeratosis & marked epithelial
atrophy in older lesions Epithelial dysplasia in 10-15 % of cases Carcinoma in 6 % of cases
CONNECTIVE TISSUE-NORMAL MUCOSA
GRADE- III , OSMF
OSMF
TREATMENT1) HABIT CONTROL2) EXERCISE OR PHYSIOTHERAPY3) MEDICINES
Cortico steroids ( Dexamethasone & Betamethasone) Antioxident (Beta-Carotene, Zn sulfate, Curcumine, Mg,
Cu) Proteolytic enzymes ( Hyluronidase & placenta-extracts) Anticytokines (VB6, integrine) Newer drugs: Pentoxifylline ,interferon -γ( anti-fibrotic
cytokine), levamosol, lycopene
4) SURGICALSurgical relieving of fibrous bands with buccal
pad of fats covering the wound.
O.S.M.FTREATMENT: 1) HABIT CONTROL 2) EXERCISE OR PHYSIOTHERAPY:
Microwave Diathermy +Stretching exercises
3) MEDICINES: SYSTEMIC:
Iron supplements & vitamins. Antioxident capsule bid for 3 months ( Beta Carotene, Zn sulfate,
CURCUMIN, Mg, Cu) Immunomodulators: Levamisole 150mg OD for 3 days twice in a
month for 3 month TOPICAL: (corticosteroids)
Benzydamine 0.15% M/W Triamcenolone Gel or crushed Dexamethasone tablet in 20 ml
water as M/W. INTRLESIONAL INJECTIONS:
DEXAMETHASONE + HYLURONIDASE + LIGNOCANE multiple site once a week for 6 weeks
BETAMETHASONE +HYLURONIDASE +LIGNOCANE +PLACENTA EXTRACTS =3ML
Interferon gamma injection
4) SURGICAL: - in sever trismus or dysplastic changes but excision can result in contracture of
tissue.
PROGNOSIS:Is not good..
COMPLICATION: Can transformed into S.C.C. (7-14%) according to Cawson 25%
ORAL LEUKOPLAKIA
It is the most common precancerous lesion . DEFINITION:
It is often confusing & controversial. WHO definition :(1978) Leukoplakia is a white patch or
plaque that can not be characterized clinically or pathologically as any other disease.
ETIOPATHOGENESIS: 1) tobacco (smoke & smokeless form) 2) alcohol 3) viral infection –possibly Human Papilloma Virus 4) diabetes mellitus 5) candidiasis –may be primary cause or superinfaction 7) dietary factors – vitamin A,B12 ,C ,E
ORAL LEUKOPLAKIA
TYPES OF LEUKOPLAKIA 1) Homogeneous -2) Non-homogeneous Homogeneous L. appears white uniform , flat lesion that may exhibit
shallow cracks & has smooth , wrinkle or corrugated surface with consistent texture.
Non-homogeneous L. appears white or white & red (erythroleukoplakia) lesion that may be either irregularly flat , nodular or exophytic.
FEATURES ASSOCIATED WITH INCREASE MALIGNAT TRANSFORMATION:
Gender ; women seems to be at increase risk Long duration of leukoplakia Leukoplakia in non-smokers Location in floor of mouth & tongue Non-homogeneous type Presence of Candida albican Presence of epithelial dysplasia
ORAL LEUKOPLAKIA
DDX: from carcinoma, lichen planus, thrush INVESTIGATIONS:
TOLUDINE BLUE STAINING; clinically stains malignant lesions , but not normal mucosa. It also serves as a guide to biopsy
CYTOBRUSH TECHNIQUE ; BIOPSY
Incisional & excisional
D.DX. Chronic hyperplastic candidiasis Reticular lichen planus White sponge nevus
ORAL LEUKOPLAKIA
TREATMENT:1. General consideration- all possible white keratotic agent should be eliminated (sp. smoking)2.Topical antifungal- Clotrimazole cream thrice/day for a week. If reduction in size continue 1 month.3. NO RESPONSE: If less than 1 cm -Exicisional biopsy If more than 1 cm- Incisional boipsy
dysplasia absent - RETINOL-A ointment bid/1 month. dysplasia present
;total excision of lesion with graft ( follow up once in 6 months for 3 years)
If excision not possible A) Cap.Lycopene .4mg -8mg for 3 months B) Cap.Antioxidants with selenium bid 6 months C) topical Bleomycin 1% thrice /day for 15 days
LUPUS ERYTHEMATOSIS Collagen vascular /Connective tissue disease Autoimmune process Mostly females affected3 clinicopathological forms1) SLE, 2) CCLE, 3)
SCLE Systemic LE (SLE) multisystem disease Cutaneous + oral manifestations increase activity of B-lymphocytes abnormal funtion of T-lymphocytes
SLEClinical features kidneys, cardiac involmentOral lesions: 40% Palate, buccal mucosa & gingivae Lichenoid areas/ granulomatous
lesions Lupus cheilitis ( vermilion zone of
lower lip) Ulceration, pain erythema &
hyperkeratosis
Chronic Cutaneous LE
Skin lesions Discoid Lescaly erythematous distributed on sun-
exposed skin of head & neck Cutaneous atrophy & scarring hypo/ hyper
pigmentation
ORAL LESIONS Like Erosive lichen planus Ulcerated / atrophic central zone
surrounded by white fine , radiating striae Painful when exposed to acidic/ salty foods
Histopathological features
Hyperkeratosis Alternating atrophy & thickning of spinous
layer Degeneration of basal cell layer Subepithelial lymphocytic infilterationD/D Distinguished from LP by patchy deposits of PAS-positive material in basement membrane, subepithelial edema & perivascular
inflammatory infiltrate Direct Immunofluorescence study
Treatment Avoid sun exposure
NSAIDs + antimalarials Topical; steroidsPrognosis 5 yrs survival rate is 82%- 90% Most common cause of death is renal
failure
THANKS FOR LISTENING
