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
  2. 2. Prof .Dr.Amal M. El DeebPROF.OF ORAL PATHOLOGYFACULTY OF DENTISTRY,UMM ALQURRA UNIVERSITY,MAKKA,SA
  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.

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