White Lesions


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The presentation explain white lesions in oral cavity and the classification the demonstrate the etiology, histopathology, diagnosis and treatment for each one.

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White Lesions

  1. 1. White lesions in oral cavity
  3. 3. 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.
  4. 4. 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.
  5. 5. 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.
  6. 6. 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.
  7. 7. Histopathology1-hyperkeratosis orhyperparakeratosis.2-thickening of granular celllayer.3-acanthosis but theindividual cells arenormal.4-a few chronicinflammatory cells inadjacent connectivetissue.
  8. 8. 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.
  9. 9. 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.
  10. 10. Shape:- The mucosa appearsthickened, folded,corrugated (velvety), witha spongy texture and apeculiar white opalescenthue. It is bilateral andsymmetrical
  11. 11. 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.
  12. 12. D.D.1-hereditary bengin epithelial dyskeratosis.2-Lichen planus (hypertrophic type).3-Cheek biting.4-Leukodema.Treatment:-No specific treatment.Topical tetracycline.
  13. 13. 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.
  14. 14. 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.
  15. 15. 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.
  16. 16. Stimulus activate langerhans cells,macrophages Interleukin 1 attract T- lymphocytes & stimulate them to produce Interleukin 2
  17. 17. 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.
  18. 18. 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.
  19. 19. Oral lesions:-Lichen planus has patterns in oral cavity:- 1- Reticular lichen planus. 2- Hypertrophic lichen planus. 3- Atrophic lichen planus. 4- Erosive lichen planus. 5- Bullous lichen planus.
  20. 20. 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).
  21. 21. 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.
  22. 22. Atrophic Lichen planus:-Site: attached gingiva.Shape: smooth red,poorly definedatrophic zones, at itsmargins there arewhitish keratoticstriae radiatingperipherally andblending intosurrounding mucosa.
  23. 23. Hypertrophic lichen planus:-Site: dorsum of tongueand buccal mucosa.Shape: wellcircumscribed whitelesions (plaque like)which range fromslightly elevated andsmooth to slightlyirregular.
  24. 24. 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.
  25. 25. Lichen planus
  26. 26. Atrophic Lichen PlanusErosive Lichen Planus
  27. 27. D.D.1- candidiasis.2-leukoplakia.3-squamous cell carcinoma.4-drug eruption.5-discoid lupus erythromatosis.N.B. Grinspan`s syndrome:- Lichen planus. Diabetes mellitus. Vascular hypertension.
  28. 28. Treatment:-No specific systemic or local therapy.Corticosteroids (topical, intralesional ,systemic).Antifungal therapy.Retinoids.
  29. 29. 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 .
  30. 30. 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.
  31. 31. 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.
  32. 32. 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.
  33. 33. Diagnosis:-1) Immunohistochemical staining technique using anti-viral antibodies.2) Ultrastructural study using electron microscope.3) Southern blot hybridization procedure .
  34. 34. D.D.1-idiopathic leukoplakia.2-leukoplakia associated with tobacoo use.3-lichen planus.4-chronic hyperplastic candidiasis.5-frictional keratosis.6-keratotic reaction associated withelectrochemical interactions.
  35. 35. Treatment:-AcyclovirTopical corticosteroids.
  36. 36. 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.
  37. 37. Classification of Oral Candidiasis:-A) Acute Candidiasis: 1-pseudomembranous (Thrush). 2-atrophic (antibiotic sore mouth).B) Chronic Candidiasis: 1-atrophic (denture sore mouth & angular chelitis) 2-hypertrophic (candidal leukoplakia &median rhomboid glossitis & chronic multifocal candidiasis).C) Mucocutanous forms: 1-localized. 2-familial. 3-syndrome-associated.
  38. 38. Thrush
  39. 39. 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.
  40. 40. 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.
  41. 41. 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.
  42. 42. 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.
  43. 43. Site: buccal mucosa,labial mucosa, floor ofthe mouth.Shape: bilateral,symmetrical filmyopalescence mucosabecome grayish whitein late stage withcorrugated surface.Race: blacks > whites.
  44. 44. 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.
  45. 45. 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.
  46. 46. 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.
  47. 47. 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.
  48. 48. 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.
  49. 49. 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 ).
  50. 50. 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.
  51. 51. Leukoplakia
  52. 52. Proliferative verrucous leukoplakia
  53. 53. Speckled Leukoplakia
  54. 54. 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.
  55. 55. 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.
  56. 56. Epithelial dysplasia
  57. 57. 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.
  58. 58. 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).
  59. 59. D.D.1-frictional keratosis.2-galvanic keratosis.3-verrucous hyperplasia.4-lichen planus.5-leukodema.6-white sponge nevus.
  60. 60. 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.
  61. 61. 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.
  62. 62. 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.
  63. 63. 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.
  64. 64. 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.
  65. 65. Treatment:-1-Stop smoking.2-It is a completely reversible habit, thepalate return to normal within 1-2 weeksof smoking cessation.
  66. 66. 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.
  67. 67. 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.
  68. 68. Histopathology:-90% of cases showsevere dysplasia.50% of cases showinvasive squamouscell carcinoma.40% of cases showcarcinoma in situ.
  69. 69. D.D.1-atrophic candidiasis.2-macular form of Kaposi sarcoma.3-vascular malformation.4-contact allergic reaction.5-psoriasis.
  70. 70. Treatment:-1-careful examination.2-biopsy taking is necessary.3-surgical excision is necessary.4-post operative histopathologicalexamination is necessary.
  71. 71. 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.
  72. 72. 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.
  73. 73. 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.
  74. 74. 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.
  75. 75. Paterson-Kelly syndrome.(Plummer-Vinson Syndrome):-It Includes:- 1-glossitis. 2-hystrical dysphagia. 3-hypochromic microcytic anemia.Etiology:-1-micro-organisms:Candida Albicans, Staph.2-xerostomia.3-nutritional deficiencies.4-anamias.5-mechanical trauma.6-neurologic abnormalities.
  76. 76. Clinically:-Age: middle age 40-50 years.Sex: female.Site: soft palate, buccal mucosa.Symptoms: pain, burning sensation, altered tasteand xerostomia.Shape: lemon-tinted pallor skin, angular cheilosis,smooth glazy painful tongue .koilonchia.
  77. 77. 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.
  78. 78. 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.
  79. 79. 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.
  80. 80. 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.
  81. 81. 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.
  82. 82. 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.
  83. 83. 3-Intradermal (intramucosal) nevus:-Nevus cells are found only within underlying C.T.
  84. 84. Oral Nevi:-* The most common type is intramucosalnevus.* The lesion may or may not show somedegree of melanin pigmentation.
  85. 85. 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.
  86. 86. Blue nevus:-Def. It is a benign proliferation of dermalmelanocytes usually deep withinsubepithelial connective tissue.Types:-1-common blue nevus.2-cellular blue nevus.
  87. 87. 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.
  88. 88. 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.
  89. 89. D.D.1-Kaposi sarcoma.2-Haemangioma.3-Early melanoma.Treatment:-Conservative surgical excision.