Prof .Dr.Amal M. El DeebPROF.OF ORAL PATHOLOGYFACULTY OF DENTISTRY,UMM ALQURRA UNIVERSITY,MAKKA,SA
White lesions in oral cavityDef. lesions appear as white patches in oral cavity.Causes of white lesions:- 1-Increase in thickness of one or more of epithelial layers. 2-Abnormal character of keratin. 3-Abnormal permeability of epithelium.
Classification:-A) Keratotic White lesions:- 1.Focal (frictional) keratosis. 2.White sponge nevus. 3.Lichen planus. 4.Hairy leukoplakia. 5.Leukoplakia. 6.Candidal leukoplakia. 7.Discoid lupus erythromatosis.B) Non keratotic white lesions:- 1.Leukodema. 2.Candidiasis. 3.Mucosal burns.
1) Focal (frictional) keratosis:-Etiology:- 1-chronic rubbing of friction against an oral mucosa. 2-It represents a protective action against low grade, long term trauma as habitual lip or cheek biting.
Clinically:-Age: 5-6 decades.Sex: male>female.Site: mandibular mucosa, cheek,palate, floor of the mouth,maxillary mucosa, tongue,buccal mucosa along occlusalline, edentulous ridges.Shape: focal keratosis clinicallyshow outlined white patches,not indurated ,have no redmargin, painless.
Histopathology1-hyperkeratosis orhyperparakeratosis.2-thickening of granular celllayer.3-acanthosis but theindividual cells arenormal.4-a few chronicinflammatory cells inadjacent connectivetissue.
Diagnosis:- 1. Careful history taking. 2. Careful examination. 3. Biopsy must be taken if no exact cause is known.Treatment:- Removal of the cause, the lesion may disappear in 2-3 weeks.
White sponge nevus(familial white folded gingivostomatitis) Etiology:- It is a hereditary disease. Site:- Cheek mucosa along occlusal line bilaterally, ventral surface of tongue, floor of mouth, esophagus, rectum, vagina,larynx.
Shape:- The mucosa appearsthickened, folded,corrugated (velvety), witha spongy texture and apeculiar white opalescenthue. It is bilateral andsymmetrical
Histopathology:-1- The epithelium is irregular,thickened, showing bothhyperparakeratosis andacanthosis.2-The superficial epithelial cells failto take any stain (washed outappearance).3-These vaculated cells may showpyknotic nuclei4-The connective tissue show a mildinflammatory cell infiltration.5-Intra-cellular and inter-cellularodema.
Lichen Planus:-Def:- It is a chronic inflammatory disease, notinfectious. It is one of the most commondermatological disease to manifest itself inoral cavity, in which oral lesions precedethe skin lesions.
Its importance relates to:-1- its degree of frequency of occurrence.2- its occasional similarity to other mucosal diseases.3- its occasional painful nature.4- its possible connection to malignancy.
Etiology:-Unknown, it may be:- 1)emotional stress, over work, trauma,infection, malnutrition. 2)Psychosomatic in origin. 3)Auto-immune disease:* the epithelial cells are the primary thetarget cells.* The mechanism of basal cell damage isrelated to cell mediated immune processinvolving Langerhans cells, T-lymphocytes,Macrophages.
Stimulus activate langerhans cells,macrophages Interleukin 1 attract T- lymphocytes & stimulate them to produce Interleukin 2
Interleukin 2 T-cell proliferation. T-cell activation.Activated lymphocytes toxic for basal cells. Secrete Gamma interferonGamma interferon induce keratinocytes to expressHLA-DR class 2 histocompatibility antigen.Lymphocytes normally express HLA-DR.Linkage of these HLA-DR occur which result ininappropriate epithelial antigenic informationpassed to lymphocytes.So, self antigen may be recognized as foreign, byhost T-lymphocytes resulting in auto immuneresponse.
Clinically:-Age: middle age, rare in children.Sex: male=female.Site:- 1) skin lesions: any where, bilateral, symmetrical on flexor surface of wrist, inner aspect of thighs, trunk, nails, vulvar mucosa. 2) Oral lesions: gingiva, cheek, lips, tongue, palate.
Reticular Lichen planus:-The most common type.Site: posterior buccalmucosa bilaterally, lips,palate, gingiva.Shape: radiating white,velvety, thread likepapules in a linear,annular or retiformarrangement. A tiny white elevated dotsis present at theintersection of white linesknown as (striae ofwickham).
Erosive Lichen Planus:-Site: posterior- inferioraspect of buccal mucosaadjacent to mandibularmolar teeth.Shape: atrophic,erythematous areas withcentral ulceration, theperiphery of atrophicregions is bordered byfine, white radiatingstriae.
Atrophic Lichen planus:-Site: attached gingiva.Shape: smooth red,poorly definedatrophic zones, at itsmargins there arewhitish keratoticstriae radiatingperipherally andblending intosurrounding mucosa.
Hypertrophic lichen planus:-Site: dorsum of tongueand buccal mucosa.Shape: wellcircumscribed whitelesions (plaque like)which range fromslightly elevated andsmooth to slightlyirregular.
Histopathology:-1-Hyperorthokeratosis or hyperparakeratosis.2-Variable degree of acanthosis.3- Destruction of basal cell layer of epithelium(hydropic degeneration) with vacuolization ofbasal cell layer.4- Rete process may be absent, hyperplastic orsaw-toothed shape.5- tearing between epithelium and C.T.6-presence of colloid (civatte, hyaline, cytoidbodies) as discrete eosinophilic ovoid bodies atbasal cell layer.
Treatment:-No specific systemic or local therapy.Corticosteroids (topical, intralesional ,systemic).Antifungal therapy.Retinoids.
Prognosis:-It is a benign lesion , it was not considereda premalignant condition But a largenumber of cases of epidermoid carcinomadeveloping in oral lesions of lichen planus.The majority of cases of cancer haveoccurred in erosive and atrophic types .
Hairy leukoplakia:-Def.:- It is an unusual white lesion with a hairy appearance orcorrugated surface that occurred on the lateral border ordorsum of tongue.Etiology:-1-In male homosexuals.2-An opportunistic infection relates to Epstein-Barr virus.3-It is related to AIDS patients.N.B. Viral particles are present and replicated within the epithelialcells of tongue. Human papilloma virus present in co-existencewith EBV.
Clinically:-Site: lateral surface oftongue, dorsum oftongue, floor of mouth,palate.Shape: unilateral or bilateralsurface which is folded orcorrugated or papillary(hairy). No associated symptomsunless it is superimposedby candidal infection.
Histopathology:-1-Epithelial hyperplasia.2-Marked hyperparakeratosis.3- Formation of keratotic surfaceirregularities and ridges.4-Spinous cell layers showkoilocytosis.5-Alterationas of nuclear chromatin inform of viral inclusions.6-Candidal albicans hyphae extendinto superficial epithelial layers.7- No inflammatory cell infiltration inC.T.
Diagnosis:-1) Immunohistochemical staining technique using anti-viral antibodies.2) Ultrastructural study using electron microscope.3) Southern blot hybridization procedure .
Candidiasis (Moniliasis)Def. This is a term that encompasses a group of mucosal andcutaneous conditions with a common etiological agentfrom the Candida genus of fungi.Etiology:-The causative organism is Candida Albicans.The predisposing factors are:-1-topical corticosteroids.2-malabsorption , malnutrition.3-poor oral hygiene.4-xerostomia.5-systemic antibiotic therapy.6-Cancer chemotherapy.7- AIDS.
Laboratory findings:-1-remaval of a portion ofthe candidal plaque.2-It is smeared on amicroscopic slide,macerated with 20%potassium hydroxide.3-Then examination fortypical hyphae.4-Culture identification andquantification oforganisms may beperformed with a varietyof media as blood agar orcornmeal agar.
Histopathology:-Histological section is stained withperiodic acid Schiff reagent PASwill show presence of yeast cellsand hyphae in the superficialand deeper layers of involvedepithelium give bright magentacolor.Histological features include:-1-hyperparakeratosis.2- chronic inflammatory cellinfiltration in CT3-collections of neutrophils (micro-abscess) in parakeratin layer.4-The candidal hyphae embeddedin parakeratin layer.
D.D.1-slough associated with chemical burns.2-traumatic ulcerations.3-mucous patches of syphilis.4-white keratotic lesions.Treatment:-1) Nystatin.2)Imidazole agents.3)Triazole agents.
Leukodema:-Def. It is an abnormality of the buccal mucosa of unknown cause. It may be considered as variation of the normal rather than a disease.Etiology:-Causative factors as: smoking, alcohol, bacterial infection.
Histopathology:-1-The epithelium is acanthotic, parakeratotic.2-The enlarged cells in the superficial part ofstratum spinosum appear vacuolated becausethey contain glycogen.3-The rete ridges are broad and enlarged.
Diagnosis:-1-gentle stroking with a gauze pad will not removeit ( not rub off )2-With stretching of buccal mucosa, the opaquechanges will dissipate.D.D.1-leukoplakia.2-white sponge nevus.3-response to chronic cheek biting.Treatment:-No treatment is necessary.
Mucosal burns:-Chemical Burns:-Topical applications ofchemicals as aspirintablets which is used inself medication and heldlocally against a painfultooth and allowed todissolve slowly.Thermal Burns:-Common in hard palatalmucosa caused by hot,sticky food.
Premalignant lesion:- It is a benign , morphologically alteredtissue that has a greater than normal riskof malignant transformation.Ex. 1-leukoplakia. 2-erythroplakia. 3-sublingual keratosis. 4-candidal leukoplakia. 5-stomatitis nicotina.
Premalignant condition:- It is a disease or patient habit that doesn`tnecessarily alter the clinical appearance of localtissue but is associated with a greater thannormal risk of precancerous lesion or cancerdevelopment in that tissue.Ex. 1-Oral sub mucous fibrosis. 2-Paterson-Kelly syndrome. 3-lichen planus. 4-Discoid lupus erythematosis.
Leukoplakia:-Def. It is a white patch or plaque that cannot be characterizedclinically or pathologically as any other disease. It is a clinical term.Etiology:-Exact etiology is unknown ,it may be:-1-tobacco.2-alcohol.3-ultraviolet radiation.4-trauma.5-nutritional deficencies.6-micro-organisms (treponema pallidum , candida albicans ,human papilloma virus ).
Clinically:-Age: middle age 4-6 decades.Sex: male > female.Site: Tongue, floor of mouth, buccal mucosa,palate, lower lip, retro molar sites.Shapes:-1-mild ( thin ) leukoplakia.2-Homogenous (thick) leukoplakia.3-Granular or nodular leukoplakia.4-Verrucous leukoplakia.5-Proliferative verrucous leukoplakia.6- Erythroleukoplakia or speckled leukoplakia.
Histopathology:-It varies as follow:-1-Hyperkeratosis: thickened keratin layer ofsurface epithelium either hyperparakeratosis orhyperorthokeratosis.2-Acanthosis: thickened spinous layer.3-Surface hyperkeratosis but show atrophy orthinning of surface epithelium.
4- epithelial dysplasia:-It is a term to sum up various disturbances of epithelialgrowth as:-1-drop-shaped epithelial ridges.2-basal layer hyperplasia.3-loss of basal cell polarity.4-loss of normal stratification.5-cellular pleomorphism.6-nucleal pleomorphism and hyperchromatism.7-increased nuclear/cytoplasm ratio.8-loss of intercellular adherence.9-individual cell keratinization.10-incrased normal and abnormal mitosis in shape, site,number.
Epithelial dysplasia is classified according to theseverity as follow:-Mild: when alterations limited to basal andparabasal layers.Moderate: when alterations involve from basallayer to midportion of spinous layer.Severe: when alterations involve from basal layerto a level above midpoint of epithelium.
Carcinoma in situ:-Def. Dysplastic epithelial cells that extend frombasal layer to surface of mucosa (Top-to-Bottom) changes. It is called (intra-epithelial carcinoma).
Treatment:-1-Identification of the etiological factor discontinuation.2-If no dysplastic changes are found, periodic and careful follow-up is needed every 6 months.3-Removal of dysplastic changes : surgically,cryosurgery, electrodessication.4- In case of extensive lesions, grafting is needed.
Candidal Leukoplakia:-Age: adultHistopathology:-1-mitotic activity is 4 times higher than that ofidiopathic leukoplakia.2-heavly infiltration of surface epithelium with hyphaeof Candida.3-chronic inflammatory cells are more numerous.Treatment: antifungal therapy may improve thecondition.
Nicotinic Stomatitis:-Def. It is the most frequently leukoplakic lesionof the palate.Etiology:-1-pipe and cigar smoking.2-long term use of extremely hot beverges.3-reverse smoking.
Clinically:-Age: more than 45 years.Sex: male > female.Site: palatal mucosa.Shape:- Erythematous patches over timeincrease in keratinization,opacification. Red dots areseen in posterior portion ofhard palate.These dots are surrounded bywhite keratotic ring , thesedots represent inflammation ofductal elements of underlyingminor salivary gland.
Histopathology:-1-epithelial hyperplasia.2-acanthosis.3-hyperkeratinization.4-chronic inflammatory cellinfiltration of sub epithelialconnective tissue.5-minor salivary gland showmoderate degrees ofinflammation.6-excretory ducts showsquamous metaplasia.
Treatment:-1-Stop smoking.2-It is a completely reversible habit, thepalate return to normal within 1-2 weeksof smoking cessation.
Erythroplakia:-Def. It is a clinical term represents a red patch thatcant be clinically or pathologically diagnosed asany other condition.Etiology:-Unknown, Some etiological factors as : tobacco,alcohol ,nutritional defects, chronic irritation.N.B. Erythroplakia is less common but moredangerous than leukoplakia.
Clinically:-Age: 50-70 years.Sex: male > female.Site: floor of mouth,retro molar area ,tongue, soft palate.Shape:-1-homogenous: redpatch ,velvety ,welldemarcated, softmacule or papule.2-spkeled: associatedwith focal white area.
Histopathology:-90% of cases showsevere dysplasia.50% of cases showinvasive squamouscell carcinoma.40% of cases showcarcinoma in situ.
D.D.1-atrophic candidiasis.2-macular form of Kaposi sarcoma.3-vascular malformation.4-contact allergic reaction.5-psoriasis.
Treatment:-1-careful examination.2-biopsy taking is necessary.3-surgical excision is necessary.4-post operative histopathologicalexamination is necessary.
Oral submucous fibrosisDef. It is a chronic , progressive, scarring highprecancerous condition of oral mucosa.Etiology:-1-chronic chewing of areca and betel nut.2-general nutritional deficiency.3-hypersensitivity to various dietary constituentsas spicy.
Clinically:-Race: North America, Pakistanis.Age: wide range, 20-40 years.Site: buccal mucosa, retro molar area, softpalate may extend into pharynx, esophagus.Shape: White yellowish lesion, the oral mucosaloses its resilience and elasticity, the processprogresses from lamina propria to underlyingmusculature.
Histopathology:-1-hyperkeratosis with epithelial atrophy.2-variable degrees of dysplastic changes.3-superficial portions of lamina propria are poorlyvascularized and hyalinized.4-submucosal deposition of extremely dense anda vascular collagenous C.T. with variablenumbers of chronic inflammatory.
D.D.1-radiating related sub epithelial fibrosis.2-mucosal scarring secondary to thermal orchemical burn.Treatment:-1-stop the habit.2-stretching exercises.3-introlesional injection of corticosteroids.4-surgical excision of fibrous bands and submucosal placement of placental grafts.
Histopathology:-1-atrophy of the epithelium.2-complete absence of rete process.3-hyalinization of lamina propria.4-narrowing of blood vessels.Treatment:1-replacement nutritional therapy.2-identification of the cause and treat it.3-high protein diet.
NevusDef. It is a congenital or developmental malformation of skinand mucosa leads to pigmented lesion composed ofnevus cells.Nevus cell:-Origin : melanoblasts originates from neural crest cells indorsal region of embryo and migrates to skin andmucous membrane along the course of peripheralnerves.Shape:*Oval, round or polygonal.*Tend to make nests ( Theques).*Produce melanin in superficial areas of lesion.
Clinically:-Age: childhood.Sex: female > male.Race: whites > blackes.Site:-In skin : in any site most common above waist.Intra-orally: palate, buccal mucosa, labial mucosa,gingiva, alveolar mucosa, vermilion.Colour: range from tan to black depending on theamount of melanin produced and the depth ofthe lesion.
Histopathology:-It is characterized by a benign unencapsulatedproliferation of nevus cells which has acharacteristic feature is that the superficialnevus cells tend to be organized into roundaggregates (Theques).There are 3 types:-1-junctional nevus.2-compound nevus.3-intradermal nevus.
1- junctional nevus:-Theques of vevus cells are found only along the basal celllayer of epithelium, especially at tips of rete ridges.It presents at junctional zone between epithelium andC.T.
2-Compound nevus:-Groups of nevus cells proliferate to drop off intounderlying dermis or lamina propria.Nevus cells present both along junctional area andwithin underlying C.T.
3-Intradermal (intramucosal) nevus:-Nevus cells are found only within underlying C.T.
Oral Nevi:-* The most common type is intramucosalnevus.* The lesion may or may not show somedegree of melanin pigmentation.
Malignant transformation of nevus(dysplastic nevus):-Clinically:-1-varies pigmentation.2-irregular margins.3-distorted surface architecture.Histopathology:-1-disorded proliferation of nevus cells at dermal-epidermal junction.2-nuclear atypia as nuclear pleomorphism,hyperchromatism.
Blue nevus:-Def. It is a benign proliferation of dermalmelanocytes usually deep withinsubepithelial connective tissue.Types:-1-common blue nevus.2-cellular blue nevus.
1-Common blue nevus:-Site: dorsa of hands, feet, palate.Age: children.Sex: female.Shape: macular lesion, blue or black.Size: < 1cm.Histopathology:-It is composed of collection of elongated,slender melanocytes with branchingdendritic extensions located within dermis.These cells align themselves parallel tosurface.
2-Cellular blue nevus:-Site: buttock region.Age: 2-4 decades.Size: > 2cm.Shape: slow-growing blue-black papule ornodule.Histopathology:-Wellcircumscribed ,highly cellularaggregation of plump,melanin producingspindle cells within dermis or submucosa ,more typical pigmented dendritic spindlecells are seen at the periphery of thelesion.