White lesions ppt

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White lesions ppt

  1. 1. Red and white lesions of the oral mucosa
  2. 2. .Hereditary white lesions  Leukodema  White sponge nevus  Hereditary benign intraepithelial dyskeratosis  Darrier’s disease
  3. 3. Reactive/inflammatory white lesions      Frictional (Traumatic) keratosis Chemical injuries of the oral mucosa Actinic keratosis (cheilitis) Smokeless tobacco-induced keratosis Nicotine stomatitis
  4. 4. Infectious white lesions and white :and red lesions    Oral hairy leukoplakia Candidiasis Mucous patches
  5. 5. Idiopathic "TRUE" leukoplakia
  6. 6. Erythroplakia
  7. 7.  Oral lichen planus  Lichenoid reactions
  8. 8. Lupus erythematosus (systemic )and discoid
  9. 9. :Miscellaneous lesions  Oral submucous fibrosis.  Skin graft.
  10. 10. :Hereditary White Lesions  Leukoedema: Leukoedema is a common mucosal alteration that represents a variation of the normal condition rather than a true pathologic change.
  11. 11. : Features  Faint, white, diffuse, and filmy appearance  Numerous surface folds resulting in wrinkling of the mucosa.  It cannot be scraped off  It disappears or fades upon stretching the mucosa.  Microscopic examination reveals thickening of the epithelium, with significant intracellular edema of the stratum spinosum. The surface of the epithelium may demonstrate a thickened layer of parakeratin.
  12. 12. Leukoedema
  13. 13. Treatment  No treatment is indicated, no malignant change has been reported.
  14. 14. :White Sponge Nevus  The disease usually involves the oral mucosa and (less frequently) the mucous membranes of the nose, esophagus, genitalia, and rectum.  The lesions may be present at birth or may first manifest or become more intense at puberty.
  15. 15. :Features  Bilateral symmetric white, soft, “spongy”, or velvety thick plaques of the buccal mucosa.  Other sites in the oral cavity may be involved, including the ventral surface of the tongue, floor of the mouth, labial mucosa, soft palate, and alveolar mucosa.  Asymptomatic and does not exhibit tendencies toward malignant change.  Histopathologic features are epithelial thickening, parakeratosis, a peculiar perinuclear condensation of the cytoplasm, and vacuolization of the suprabasal layer of keratinocytes
  16. 16. :White Sponge Nevus
  17. 17. :Treatment  No treatment is indicated for this benign and asymptomatic condition.
  18. 18. Hereditary Benign Intraepithelial :Dyskeratosis 1- Oral Lesions:  Thick, corrugated, asymptomatic, white “spongy” plaques involving the buccal and labial mucosa.  Other intraoral sites include the floor of the mouth, the lateral tongue, the gingiva, and the palate.  Detected in the first year of life and gradually increase in intensity until the teens.
  19. 19. 2- Eye Lesions  Thick, gelatinous, foamy, and opaque plaques form adjacent to the cornea.  The plaques may exhibit seasonal prominence, with many patients reporting more-pronounced lesions in the Spring and regression during the Summer months.  Blindness due to corneal vascularization may occur.
  20. 20. Histopathologic Features:  Epithelium exhibits marked parakeratin production with thickening of the stratum spinosum and the presence of numerous dyskeratotic cells (eosinophilic cells that resemble epithelial pearls).
  21. 21.  Treatment:  No treatment is required for the oral lesions. For evaluation and treatment of the ocular lesions, the patient should be referred to an ophthalmologist.
  22. 22. Darrier’s Disease: (Keratosis (Follicularis  A genetic disorder characterized by a persistent eruption of hyperkeratotic papules.
  23. 23. :Pathology  Fissures (lacunae) appear due to acantholysis above the basal layer. They later extend irregularly.  Small groups of cells around the lacunae become separated from their neighbours, enlarge and present a darkly staining nucleus surrounded by clear cytoplasm and a glistening ring simulating a membrane. These corps ronds are cells showing premature partial keratinization (dyskeratosis); they give rise to the grains, small cells with shrunken cytoplasm, seen in the upper layers of the epidermis.
  24. 24.  Skin Lesions: A firm, rather greasy, harsh papule, which is skin coloured, yellow-brown or brown. Coalescence of the papules produces irregular warty plaques or papillomatous masses, which in the flexures, become vegetating and malodorous.
  25. 25.  Oral Lesions: White umbilicate or cobblestone papules on the palate, tongue, buccal mucosa, epiglottis, pharyngeal wall, vulva, oesophagus or rectum may occur, as may hypertrophy of gums. Confluence of the papules may form patches simulating leukoplakia. Blockage of the salivary glands may be associated
  26. 26. Nail Lesions: Characteristic nail changes are seen:  Broad, white, longitudinal bands;  Broad, slightly translucent, red, longitudinal bands;  A sandwich of red and white longitudinal bands, often with a V-shaped nick at the free margin of the nail.
  27. 27. :Ear Lesions  The external auditory meatus may be blocked by accumulated keratotic debris
  28. 28. Reactive and Inflammatory White Lesions: Frictional Keratosis
  29. 29. :Cheek Chewing
  30. 30. Chemical Injuries of the Oral :Mucosa
  31. 31. (:Actinic Keratosis (Cheilitis
  32. 32. Smokeless Tobacco-lnduced :Keratosis
  33. 33. :Nicotine Stomatitis
  34. 34. Infectious White Lesions and White and Red Lesions Oral Hairy Leukoplakia:  Corrugated white lesion  Usually occurs on the lateral or ventral surfaces of the tongue  In patients with severe immunodeficiency. The most common disease associated with oral hairy leukoplakia is HIV infection.  Epstein-Barr virus (EBV( is the causative agent
  35. 35. :Histopathology  Hyperparakeratosis with an irregular surface,  Acanthosis with superficial edema,  Koilocytic cells (virally affected "balloon" cells) in the spinous layer. The characteristic microscopic feature is the presence of homogeneous viral nuclear inclusions with a residual rim of normal chromatin.  Demonstrating the presence of EBV through in situ hybridization, electron microscopy, or polymerase chain reaction
  36. 36. :Treatment and Prognosis  The condition usually disappears when antiviral medications such as zidovudine, or acyclovir are used in the treatment of the HIV infection .
  37. 37. Oral Candidosis  Because Candida are normal oral inhabitants, thrush and other forms of oral candidiasis may be classified as specific endogenous infections.
  38. 38. Important predisposing factors for oral candidosis – Immunodeficiency (e.g. diabetes mellitus or AIDS) or immunosuppression (including steroid inhalers, cancer chemotherapy, and radiotherapy). – Poor oral hygiene – Pregnancy – Anaemia – Suppression of the normal oral flora by antibacterial drugs – Xerostomia – Haematologic malignancies
  39. 39. :Spectrum of oral candidosis Acute candidosis  Thrush (acute pseudomembranous candidosis).  Acute antibiotic stomatitis (acute atrophic or erythematous) Chronic candidosis  Denture-induced stomatitis  Chronic hyperplastic candidosis (candidal leukoplakia)  Median rhomboid glossitis  Chronic mucocutaneous candidosis  Erythematous candidosis Angular stomatitis (common to all types of oral candidosis).
  40. 40. Acute Pseudomembranous (Candidosis (Thrush Clinical Features:  Painless, soft, friable, and creamy plaques on the mucosa.  Can be easily wiped off, to expose an erythematous mucosa or shallow ulceration.  Their extent varies from isolated small flecks to widespread confluent plaques.  Angular stomatitis is frequently associated as it is with any form of intra-oral candidosis.  Sometimes a prodrome of bad taste or loss of taste sensation precedes the appearance of the lesions.
  41. 41. Pathology  A Gram-stained smear shows large masses of tangled hyphae, detached epithelial cells and leucocytes.  Biopsy shows hyperplastic epithelium infiltrated by inflammatory oedema and cells, predominantly neutrophils.  Staining with PAS shows many candidal hyphae growing down through the epithelial cells to the junction of the plaque with the spinous cell layer.
  42. 42. Management  Control of any local cause such as topical antibiotic treatment .  Nystatin or amphotericin lozenges (topical antifungals) should allow the oral microflora to return to normal.  Failure of response to topical antifungals suggests immune deficiency.  In immunodeficient patients as in HIV infection, candidosis may respond to fluoconazole or itraconazole.
  43. 43. :Acute Antibiotic Stomatitis  Overuse or topical oral use of antibiotics, especially tetracycline, suppressing normal competing oral flora.  Clinically, the whole mucosa is red and sore. Flecks of thrush may be present.  Resolution may follow withdrawal of the antibiotic but is accelerated by topical antifungal treatment.
  44. 44.  Generalized candidal erythema which is clinically similar, can also be a consequence of xerostomia which promotes candidal infection.  It is a typical complication of Sjogren's syndrome.  Nystatin suspension or miconazole gel held in the mouth is usually effective.
  45. 45. :Denture-induced Stomatitis  Asymptomatic erythema sharply limited to the area of mucosa occluded by a wellfitting upper denture or even an orthodontic plate.  Similar inflammation is not seen under the more mobile lower denture which allows a relatively free flow of saliva beneath it.  Angular stomatitis is frequently associated and may form the chief complaint.
  46. 46. :Pathology  Gram-stained smears show candidal hyphae and some yeast forms which have proliferated in the interface between denture base and mucosa.  Histologically, there is typically mild acanthosis with prominent blood vessels superficially and a mild chronic inflammatory infiltrate. The inflammation is probably a response to enzymes such as phospholipases produced by the fungus
  47. 47. :Treatment  Denture cleansing .Cleansers can be divided into groups according to their primary components: alkaline peroxides, hypochlorites, acids, disinfectants, and enzymes .Yeast lytic enzymes and proteolytic enzymes are the most effective against the infection.  Denture soak solution containing benzoic acid completely eradicates C albicans from the denture surface as it is taken up into the acrylic resin and eliminates the organism from the internal surface of the prosthesis.  A protease-containing denture soak also effectively removes denture plaque, especially when combined with brushing.  An oral rinse containing 0.12% chlorhexidine gluconate results in complete elimination of the presence of C albicans on the acrylic resin surface of the denture and in reduction of palatal inflammation .  Diet: High-sucrose diets should be avoided.
  48. 48. . Median Rhomboid Glossitis  Erythematous patches of atrophic papillae located in the central area of the dorsum of the tongue are considered a form of chronic atrophic candidiasis.
  49. 49. :Chronic Hyperplastic Candidiasis  Candidal leukoplakia is considered a chronic form of oral candidiasis in which firm white leathery plaques are detected on the cheeks, lips, palate, and tongue.  Mycelial invasion of the deeper layers of the mucosa and skin occurs, causing a prolifertive response of host tissue.  The differentiation of candidal leukoplakia from other forms of leukoplakia is based on finding periodic acid-Schiff (PAS)-positive hyphae in leukoplakic lesions.
  50. 50. Chronic Mucocutaneous :Candidiasis  Persistent infection with Candida usually occurs as a result of a defect in cellmediated immunity or may be associated with iron deficiency. Hyperplastic mucocutaneous lesions, localized granulomas, and adherent white plaques on affected mucous membranes are the prominent lesions that identify chronic mucocutaneous candidiasis (CMC).
  51. 51. Two categories of CMC have been described: (1( Syndrome-associated CMC (further categorized as either familial or chronic). (2( Localized and diffuse CMC.
  52. 52. Candidiasis endocrinopathy )syndrome (CES  A rare autosomal recessive disorder characterized by an onset of CMC during infancy or early childhood, associated with the appearance of hypoparathyroidism, hypoadrenocorticism and other endocrine anomalies  Patients develop persistent oral candidiasis and hyperplastic infections of the nail folds at an early age.
  53. 53. Chronic candidiasis associated with thymoma  The other syndrome-associated form , which appears with other autoimmune abnormalities such as myasthenia gravis.
  54. 54. Localized and diffuse CMC  Localized CMC is a variant associated with chronic oral candidiasis and lesions of the skin and nails.  The diffuse variant is characterized by randomly occurring cases of severe mucocutaneous candidiasis with widespread skin involvement and development of Candida granulomas.
  55. 55. Management Both oral and cutaneous lesions of CMC can be controlled by the continuous use of systemic antifungal drugs. Once treatment is discontinued, the lesions rapidly reappear.
  56. 56. :Erythematous Candidosis  This term applies to red mucosal macules due to Candida albicans infection in HIV – positive patients. Favoured sites, in order of frequency, are the hard palate, dorsum of the tongue and soft palate. Treatment with intraconazole is usually effective.
  57. 57. :Angular Stomatitis  Angular stomatitis is typically caused by leakage of Candida- infected saliva at the angles of the mouth. It can be seen in infantile thrush ,in denture wearers or in association with chronic hyperplastic candidosis. It is a characteristic sign of candidal infection.
  58. 58. :Treatment of Oral Candidiasis Treatment of underlying predisposing factors (if possible) Antifungal Drugs     Antifungal antibiotics nystatin and amphotericin B. Imidazole derivatives (clotrimazole, miconazole) are available for topical use (cream, oral gel). Systemic therapy includes the use of any one of these three: ketoconazole, itraconazole, and fluconazole. Fluconazole and amphotericin B may be used intravenously for the treatment of the resistant lesions of CMC and systemic candidiasis.
  59. 59.  Patients for whom predisposing factors such as xerostomia and immunodeficiency cannot be eliminated may need either continuous or repeated treatment to prevent recurrences.  The consumption of yogurt two to three times per week and improved oral hygiene can also help.
  60. 60. :Idiopathic “TRUE” Leukoplakia  Leukoplakia is a white oral precancerous lesion with a recognizable risk for malignant transformation.  Leukoplakia is currently defined as “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease”.
  61. 61. Etiology  A number of locally acting etiologic agents, including tobacco, alcohol, candidiasis, electrogalvanic reactions, sunlight and (possibly) herpes simplex and papilloma viruses, have been implicated as causative factors for leukoplakia.  Alcohol consumption alone is not associated with an increased risk of developing leukoplakia, but alcohol is thought to serve as a promoter that exhibits a strong synergistic effect with tobacco.
  62. 62. :Clinical Features More frequently found in men Can occur on any mucosal surface Infrequently causes discomfort or pain. Causes change in physical characteristics of tissues.  Prevalence increases rapidly with age.  Approximately 70% of oral leukoplakia lesions are found on the buccal mucosa, vermilion border of the lower lip, and gingiva.  Lesions of the tongue and the floor of the mouth account for more than 90% of cases that show dysplasia or carcinoma.    
  63. 63. Subtypes  Homogeneous leukoplakia welldefined white patch, that is slightly elevated and that has a fissured, wrinkled, or corrugated surface. On palpation, these lesions may feel leathery to “dry, or cracked mud-like”.
  64. 64.  Nodular (speckled) leukoplakia the name refers to a mixed red-and– white lesion in which keratotic white nodules or patches are distributed over an atrophic erythematous background. This type of leukoplakia is associated with a higher malignant transformation rate.
  65. 65. Nodular (speckled) leukoplakia
  66. 66. Verrucous leukoplakia  Thick white lesions with papillary surfaces .  Usually heavily keratinized  Most often seen in older adults in the sixth to eighth decades of life.  Some of these lesions may exhibit an exophytic growth pattern.
  67. 67. Proliferative verrucous leukoplakia Extensive papillary or verrucoid white plaques that tend to slowly involve multiple mucosal sites in the oral cavity and to transform into squamous cell carcinomas over a period of many years.
  68. 68. :Histopathologic Features  Parakeratosis or orthokeratosis or both, alternately.  The epithelium ranges from thinner than normal (atrophic) to much thicker (acanthotic)  Most leukoplakias show no dysplastic changes  A minority display a range of dysplasia from mild to severe and treatment is planned partly on this basis.  An inflammatory reaction of lymphocytes and plasma cells is often present in the underlying connective tissue.
  69. 69. :Diagnosis and Management  If a leukoplakia lesion disappears spontaneously or through the elimination of an irritant, no further testing is indicated.  For the persistent lesion, the definitive diagnosis is established by tissue biopsy.  Adjunctive methods as vital staining with toluidine blue and cytobrush are helpful in selecting the most appropriate spot for biopsy .
  70. 70.  Toluidine blue staining uses a 1% aqueous solution of the dye which stains dysplastic and malignant cells and resists washing away by rinsing with 1% acetic acid .  Cytobrush technique utilizes a brush with firm bristles that obtains individual cells from the full thickness of epithelium for cytologic examination .
  71. 71.  Definitive treatment involves surgical excision although cryosurgery and laser ablation are often preferred because of their precision and rapid healing.
  72. 72. :Prognosis  Clinical signs of malignant transformation of leukoplakia include : Ulceration , erythroplasia , bleeding , induration and lymphadenopathy  After surgical removal long-term monitoring of the lesion site is important since recurrences are frequent and because additional leukoplakias may develop.
  73. 73. Erythroplakia  “Bright red velvety plaque or patch which cannot be characterized clinically or histopathologically as being due to any other condition”.
  74. 74. Erythroplakia
  75. 75. :Clinical Features  Erythroplakia occurs predominantly in older men, in the sixth and seventh decades of life.  Erythroplakias are more commonly seen on the floor of the mouth, the ventral tongue, the soft palate, and the tonsillar fauces, all prime areas for the development of carcinoma. Multiple lesions may be present.  Almost all of the lesions are asymptomatic.
  76. 76. :Histopathologic Features  80 to 90% of cases of erythroplakia are histopathologically severe epithelial dysplasia, carcinoma in situ, or invasive carcinoma.
  77. 77. :Differential Diagnosis  In view of the clinical significance of erythroplakia, its differentiation from other red inflammatory lesions of the oral mucosa is critical.  Clinically similar lesions may include erythematous candidiasis, areas of mechanical irritation, denture stomatitis, vascular lesions, and a variety of nonspecific inflammatory lesions
  78. 78. :Lichen Planus  Lichen planus is a common chronic inflammatory disease of skin and mucous membranes. It mainly affects patients of middle age or over. Oral lesions have characteristic appearances and distribution
  79. 79. :Aetiology  The predominantly T-lymphocyte infiltrate suggests cell-mediated immunological damage to the epithelium
  80. 80. :Clinical Features Skin Lesions:  Pruritic, polyangular, planar papules and plaques , 2 to 4 mm in diameter, with angular borders, a violaceous color, and a distinct sheen in cross-lighting.  Usually symmetrically distributed most commonly on the flexor surfaces of the wrists, legs, trunk. The face is rarely involved during the acute phase.  New papules may appear at sites of minor skin injury (Koebner’s phenomenon).  Lesions may coalesce or change over time becoming hyperpigmented, atrophic hyperkeratotic (hypertrophic LP) or vesiculobullous.  If the scalp is affected,there is patchy scarring alopecia
  81. 81. Nail Lesions:  Nails are involved in up to 10% of cases. Findings vary in intensity with nail bed discoloration ,longitudinal ridging and lateral thinning and complete loss of the nail matrix and nail with scarring of the proximal nail fold onto the nail bed.
  82. 82. :Oral Lesions     The reticular form Atrophic lichen planus Erosive lesions Bullous lesions  Atrophic or erosive lichen planus involving the gingivae results in desquamative gingivitis
  83. 83. :Histopathologic Features  Three features are considered essential for the histopathologic diagnosis of lichen planus:  (1) Areas of hyperparakeratosis or hyperorthokeratosis.  (2) “liquefaction degeneration” or necrosis of the basal cell layer which is often replaced by an eosinophilic band.  (3) A dense subepithelial band of lymphocytes. This linear sub-basilar lymphocytic infiltration is composed largely of T cells
  84. 84.  Isolated epithelial cells, shrunken with eosinophilic cytoplasm and one or more pyknotic nuclear fragments (Civatte bodies), are often scattered within the epithelium and superficial lamina propria. These represent cells that have undergone apoptosis.
  85. 85. :Treatment  Asymptomatic lesions require no treatment.  Topical high-potency corticosteroids, as pastes or as gels.  Erosive lesions may respond to oral dapsone or cyclosporine rinses.  Systemic steroids : Prednisone tablets with dosages varying between 40 and 80 mg daily  Intralesional injection of corticosteroid may be used in lesions resistant to topical and systemic therapy triamcinolone acetonide ampules are used (weekly regimen).  Systemically administered dapsone, hydroxychloroquine, azathioprine and cyclosporine may help in cases resistant to corticosteroids  Drug combinations could also be used.
  86. 86. Lichenoid Reactions  This term is given to lichen planus-like lesions caused by either systemic drug treatment or those where the histological picture is not completely diagnostic.  Oral lichenoid reactions are most frequently responses to restorative materials, either amalgam or polymeric. Lesions are localized to mucosa in contact, not just close to, restorations.  Lichenoid reactions are treated in exactly the same way as lichen planus with withdrawal of drug(s) if possible or removal of restoration.
  87. 87. :Lupus Erythematosus  Lupus erythematosus is an autoimmune connective tissue disease which has two main forms namely systemic and discoid. Either can give rise to oral lesions which may appear similar to those of oral lichen planus
  88. 88. Systemic Lupus Erythematosus  Has varied effects. Any organ system can be affected. A great variety of autoantibodies, particularly antinuclear, is produced. Pathological features of systemic lupus erythematosus: Macroscopic:  Pleurisy.  Pericarditis.  Libman-sacks endocarditis.  Lymphadenopathy.  Splenomegaly.  May be none.
  89. 89. Microscopic:  Immunoglobulins and complement at the dermo-epidermal junction in skin lesions (90%) and uninvolved skin (60%).  Haematoxylin bodies in the endocardium, renal glomeruli and elsewhere.  Periarterial fibrosis of the spleen.  Wire loop lesions in the kidneys.
  90. 90. immunoglobulin & complement deposits at basement membrane :zone & nuclei of epithelial cells
  91. 91. :Discoid Lupus  A skin disease with mucocutaneous lesions indistinguishable clinically from those of systemic lupus. These may be associated with arthralgias but rarely, significant autoantibody production
  92. 92. Clinical Features: :A) Skin Lesions Cutaneous features of systemic lupus erythematosus.  Butterfly rash.  Facial oedema.  Subacute cutaneous LE.  Chronic discoid LE.  Scarring DLE alopecia  Non-scarring alopecia  Photosensitivity  Raynaud’s phenomenon  Chronic urticaria  Cutaneous vasculitis
  93. 93. :Histopathologic Features  Liquefaction degeneration of basal cell layer.  Degenerative changes in the connective tissue (hyalinization, oedema,..).  Lupus erythematosus shows more irregular patterns of acanthosis and lacks the band-like distribution of lymphocytes in the papillary corium of lichen planus.  The inflammatory infiltrate may have a perivascular distribution.
  94. 94. : Management  Oral lesions of discoid lupus erythematosus may respond in some degree to topical corticosteroids.  Oral lesions in acute systemic lupus erythematosus may not respond to doses of corticosteroids adequate to control systemic effects of the disease. Under such circumstances, palliative treatment is needed until disease activity decreases.
  95. 95. Miscellaneous Lesions: Oral Submucous Fibrosis  A slowly progressive chronic fibrotic disease of the oral cavity and oropharynx, characterized by fibroelastic change and inflammation of the mucosa, leading to a progressive inability to open the mouth, swallow, or speak.
  96. 96.  These reactions may be the result of either direct stimulation from exogenous antigens like Areca alkaloids or changes in tissue antigenicity that may lead to an autoimmune response.  It occurs almost exclusively in the Indian subcontinent.  The inflammatory response releases cytokines and growth factorsthat promote fibrosis by inducing the proliferation of fibroblasts, up-regulating collagen synthesis and down-regulating collagenase production.
  97. 97. :Etiology  General nutritional and vitamin deficiencies and hypersensitivity to certain dietary constituents such as chili peppers, chewing tobacco, habitual use of betel and its constituents (Areca catechu).
  98. 98. :Clinical Features  The disease first presents with a burning sensation of the mouth, particularly during consumption of spicy foods.  Often accompanied by the formation of vesicles or ulcerations and by excessive salivation or xerostomia and altered taste sensations.  Gradually, patients develop a stiffening of the mucosa, with a dramatic reduction in mouth opening and with difficulty in swallowing and speaking.  The mucosa appears blanched and opaque with the appearance of fibrotic bands that can easily be palpated.  Usually involves the buccal mucosa, soft palate, posterior pharynx, lips, and tongue.
  99. 99. :Histologic Features  Severely atrophic epithelium with complete loss of rete ridges.  Varying degrees of epithelial atypia may be present.  The underlying lamina propria exhibits severe hyalinization, with homogenization of collagen. Cellular elements and blood vessels are greatly reduced.
  100. 100. :Treatment and Prognosis  Oral submucous fibrosis is regarded as a premalignant condition.  Oral submucous fibrosis is very resistant to treatment.  Submucosal injected steroids and hyaluronidase, are some of the agents that have been used.  In severe cases surgical intervention is the only treatment but the fibrous bands and other symptoms often recur within a few months to a few years.
  101. 101. :Skin Grafts  A skin graft may be placed in the mouth to cover a raw area left after excision of a lesion.  Skin grafts typically appear sharply demarcated smooth and paler than the surrounding mucosa and occasionally contain hairs . Grafts on the dorsum of the tongue may become corrugated and less easy to differentiate from leukoplakia.

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