White lesions


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White lesions

  1. 1. White lesions in oral cavity
  2. 2. White lesions in oral cavity .Def lesions appear as white patches in oral .cavity :-Causes of white lesions Increase in thickness of one or more of-1 .epithelial layers .Abnormal character of keratin-2 .Abnormal permeability of epithelium-3
  3. 3. :-Classification :-A) Keratotic White lesions .Focal (frictional) keratosis.1 .White sponge nevus.2 .Lichen planus.3 .Hairy leukoplakia.4 .Leukoplakia.5 .Candidal leukoplakia.6 .Discoid lupus erythromatosis.7 :-B) Non keratotic white lesions .Leukodema.1 .Candidiasis.2 .Mucosal burns.3
  4. 4. :-Focal (frictional) keratosis( 1 :-Etiology chronic rubbing of friction against an oral -1 . mucosa It represents a protective action against -2 low grade, long term trauma as . habitual lip or cheek biting
  5. 5. :-Clinically .Age: 5-6 decades .Sex: male>female Site: mandibular mucosa, cheek, palate, floor of the mouth, maxillary mucosa, tongue, buccal mucosa along occlusal .line, edentulous ridges Shape: focal keratosis clinically show outlined white patches, not indurated ,have no red .margin, painless
  6. 6. Histopathology hyperkeratosis or-1 .hyperparakeratosis thickening of granular cell-2 .layer acanthosis but the-3 individual cells are .normal a few chronic-4 inflammatory cells in adjacent connective .tissue
  7. 7. :-Diagnosis .Careful history taking. 1 .Careful examination. 2 Biopsy must be taken if no exact cause . 3 . is known :-Treatment Removal of the cause, the lesion may .disappear in 2-3 weeks
  8. 8. 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
  9. 9. :-Shape The mucosa appears thickened, folded, corrugated (velvety), with a spongy texture and a peculiar white opalescent .hue It is bilateral and symmetrical
  10. 10. :-Histopathology The epithelium is irregular,- 1 thickened, showing both hyperparakeratosis and .acanthosis The superficial epithelial cells fail-2 to take any stain (washed out (.appearance These vaculated cells may show-3 pyknotic nuclei The connective tissue show a mild-4 .inflammatory cell infiltration Intra-cellular and inter-cellular-5 .odema
  11. 11. .D.D .hereditary bengin epithelial dyskeratosis -1 (.Lichen planus (hypertrophic type-2 .Cheek biting-3 .Leukodema-4 :-Treatment .No specific treatment .Topical tetracycline
  12. 12. :-Lichen Planus :-Def It is a chronic inflammatory disease, not .infectious It is one of the most common dermatological disease to manifest itself in oral cavity, in which oral lesions precede .the skin lesions
  13. 13. :-Its importance relates to .its degree of frequency of occurrence - 1 its occasional similarity to other mucosal - 2 .diseases .its occasional painful nature- 3 .its possible connection to malignancy - 4
  14. 14. :-Etiology :-Unknown, it may be emotional stress, over work, trauma, (1 .infection, malnutrition .Psychosomatic in origin(2 :Auto-immune disease(3 the epithelial cells are the primary the * .target cells The mechanism of basal cell damage is * related to cell mediated immune process involving Langerhans cells, T.lymphocytes, Macrophages
  15. 15. ,Stimulus activate langerhans cells macrophages -attract T &lymphocytes stimulate them to produce Interleukin 2 Interleukin 1
  16. 16. .Interleukin 2 .T-cell activation T-cell proliferation Activated lymphocytes .toxic for basal cells Secrete Gamma interferon Gamma interferon induce keratinocytes to express .HLA-DR class 2 histocompatibility antigen .Lymphocytes normally express HLA-DR Linkage of these HLA-DR occur which result in inappropriate epithelial antigenic information .passed to lymphocytes So, self antigen may be recognized as foreign, by host T-lymphocytes resulting in auto immune .response
  17. 17. :-Clinically .Age: middle age, rare in children .Sex: male=female :-Site skin lesions: any where, bilateral, symmetrical ( 1 on flexor surface of wrist, inner aspect of .thighs, trunk, nails, vulvar mucosa ,Oral lesions: gingiva, cheek, lips, tongue( 2 .palate
  18. 18. :-Oral lesions :-Lichen planus has patterns in oral cavity .Reticular lichen planus- 1 .Hypertrophic lichen planus- 2 .Atrophic lichen planus- 3 .Erosive lichen planus- 4 .Bullous lichen planus- 5
  19. 19. :-Reticular Lichen planus .The most common type Site: posterior buccal mucosa bilaterally, lips, .palate, gingiva Shape: radiating white, velvety, thread like papules in a linear, annular or retiform .arrangement A tiny white elevated dots is present at the intersection of white lines known as (striae of (.wickham
  20. 20. :-Erosive Lichen Planus Site: posterior- inferior aspect of buccal mucosa adjacent to mandibular .molar teeth Shape: atrophic, erythematous areas with central ulceration, the periphery of atrophic regions is bordered by fine, white radiating .striae
  21. 21. :-Atrophic Lichen planus .Site: attached gingiva Shape: smooth red, poorly defined atrophic zones, at its margins there are whitish keratotic striae radiating peripherally and blending into .surrounding mucosa
  22. 22. :-Hypertrophic lichen planus Site: dorsum of tongue .and buccal mucosa Shape: well circumscribed white lesions (plaque like) which range from slightly elevated and smooth to slightly .irregular
  23. 23. :-Histopathology .Hyperorthokeratosis or hyperparakeratosis-1 .Variable degree of acanthosis-2 Destruction of basal cell layer of epithelium - 3 (hydropic degeneration) with vacuolization of .basal cell layer Rete process may be absent, hyperplastic or- 4 .saw-toothed shape .tearing between epithelium and C.T- 5 presence of colloid (civatte, hyaline, cytoid -6 bodies) as discrete eosinophilic ovoid bodies at .basal cell layer
  24. 24. Lichen planus
  25. 25. Atrophic Lichen Planus Erosive Lichen Planus
  26. 26. .D.D .candidiasis- 1 .leukoplakia-2 .squamous cell carcinoma-3 .drug eruption-4 .discoid lupus erythromatosis-5 :-N.B. Grinspan`s syndrome .Lichen planus .Diabetes mellitus . Vascular hypertension
  27. 27. :-Treatment .No specific systemic or local therapy (.Corticosteroids (topical, intralesional ,systemic .Antifungal therapy .Retinoids
  28. 28. :-Prognosis It is a benign lesion , it was not considered a premalignant condition But a large number of cases of epidermoid carcinoma .developing in oral lesions of lichen planus The majority of cases of cancer have .occurred in erosive and atrophic types
  29. 29. :-Hairy leukoplakia .:-Def It is an unusual white lesion with a hairy appearance or corrugated surface that occurred on the lateral border or .dorsum of tongue :-Etiology .In male homosexuals-1 .An opportunistic infection relates to Epstein-Barr virus-2 .It is related to AIDS patients-3 N.B. Viral particles are present and replicated within the epithelial cells of tongue. Human papilloma virus present in co-existence .with EBV
  30. 30. :-Clinically Site: lateral surface of tongue, dorsum of tongue, floor of mouth, .palate Shape: unilateral or bilateral surface which is folded or corrugated or (.papillary( hairy No associated symptoms unless it is superimposed .by candidal infection
  31. 31. :-Histopathology .Epithelial hyperplasia-1 .Marked hyperparakeratosis-2 Formation of keratotic surface- 3 .irregularities and ridges Spinous cell layers show-4 .koilocytosis Alterationas of nuclear chromatin in-5 .form of viral inclusions Candidal albicans hyphae extend-6 .into superficial epithelial layers No inflammatory cell infiltration in- 7 .C.T
  32. 32. :-Diagnosis Immunohistochemical staining technique ( 1 . using anti-viral antibodies Ultrastructural study using electron ( 2 .microscope .Southern blot hybridization procedure ( 3
  33. 33. .D.D .idiopathic leukoplakia-1 .leukoplakia associated with tobacoo use -2 .lichen planus-3 .chronic hyperplastic candidiasis-4 .frictional keratosis-5 keratotic reaction associated with -6 .electrochemical interactions
  34. 34. :-Treatment Acyclovir .Topical corticosteroids
  35. 35. (Candidiasis (Moniliasis .Def This is a term that encompasses a group of mucosal and cutaneous conditions with a common etiological agent .from the Candida genus of fungi :-Etiology .The causative organism is Candida Albicans :-The predisposing factors are .topical corticosteroids-1 .malabsorption , malnutrition-2 .poor oral hygiene-3 .xerostomia-4 .systemic antibiotic therapy-5 .Cancer chemotherapy-6 .AIDS- 7
  36. 36. :-Classification of Oral Candidiasis :A) Acute Candidiasis (.pseudomembranous (Thrush-1 (.atrophic (antibiotic sore mouth-2 :B) Chronic Candidiasis (atrophic (denture sore mouth & angular chelitis -1 hypertrophic (candidal leukoplakia &median -2 rhomboid glossitis & chronic multifocal (.candidiasis :C) Mucocutanous forms .localized-1 .familial-2 .syndrome-associated-3
  37. 37. Thrush
  38. 38. :-Laboratory findings remaval of a portion of the-1 .candidal plaque It is smeared on a-2 microscopic slide, macerated with 20% .potassium hydroxide Then examination for-3 .typical hyphae Culture identification and-4 quantification of organisms may be performed with a variety of media as blood agar or .cornmeal agar
  39. 39. :-Histopathology Histological section is stained with periodic acid Schiff reagent PAS will show presence of yeast cells and hyphae in the superficial and deeper layers of involved epithelium give bright magenta .color :-Histological features include .hyperparakeratosis-1 chronic inflammatory cell- 2 infiltration in CT collections of neutrophils (micro--3 .abscess) in parakeratin layer The candidal hyphae embedded-4 .in parakeratin layer
  40. 40. .D.D .slough associated with chemical burns-1 .traumatic ulcerations-2 .mucous patches of syphilis-3 .white keratotic lesions-4 :-Treatment .Nystatin( 1 .Imidazole agents(2 .Triazole agents(3
  41. 41. :-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
  42. 42. Site: buccal mucosa, labial mucosa, floor of .the mouth Shape: bilateral, symmetrical filmy opalescence mucosa become grayish white in late stage with .corrugated surface .Race: blacks > whites
  43. 43. :-Histopathology .The epithelium is acanthotic, parakeratotic -1 The enlarged cells in the superficial part of -2 stratum spinosum appear vacuolated because .they contain glycogen .The rete ridges are broad and enlarged -3
  44. 44. :-Diagnosis gentle stroking with a gauze pad will not remove -1 (it ( not rub off With stretching of buccal mucosa, the opaque -2 .changes will dissipate .D.D .leukoplakia-1 .white sponge nevus-2 .response to chronic cheek biting-3 :-Treatment .No treatment is necessary
  45. 45. :-Mucosal burns :-Chemical Burns Topical applications of chemicals as aspirin tablets which is used in self medication and held locally against a painful tooth and allowed to . dissolve slowly :-Thermal Burns Common in hard palatal mucosa caused by hot, .sticky food
  46. 46. :-Premalignant lesion It is a benign , morphologically altered tissue that has a greater than normal risk .of malignant transformation .Ex. 1-leukoplakia .erythroplakia-2 .sublingual keratosis-3 .candidal leukoplakia-4 .stomatitis nicotina-5
  47. 47. :-Premalignant condition It is a disease or patient habit that doesn`t necessarily alter the clinical appearance of local tissue but is associated with a greater than normal risk of precancerous lesion or cancer .development in that tissue .Ex. 1-Oral sub mucous fibrosis .Paterson-Kelly syndrome-2 .lichen planus-3 .Discoid lupus erythematosis-4
  48. 48. :-Leukoplakia .Def It is a white patch or plaque that cannot be characterized .clinically or pathologically as any other disease .It is a clinical term :-Etiology :-Exact etiology is unknown ,it may be .tobacco-1 .alcohol-2 .ultraviolet radiation-3 .trauma-4 .nutritional deficencies-5 micro-organisms (treponema pallidum , candida albicans ,-6 (.human papilloma virus
  49. 49. :-Clinically .Age: middle age 4-6 decades .Sex: male > female Site: Tongue, floor of mouth, buccal mucosa, .palate, lower lip, retro molar sites :-Shapes .mild ( thin ) leukoplakia-1 .Homogenous (thick) leukoplakia-2 .Granular or nodular leukoplakia-3 .Verrucous leukoplakia-4 .Proliferative verrucous leukoplakia-5 .Erythroleukoplakia or speckled leukoplakia- 6
  50. 50. Leukoplakia
  51. 51. Proliferative verrucous leukoplakia
  52. 52. Speckled Leukoplakia
  53. 53. :-Histopathology :-It varies as follow Hyperkeratosis: thickened keratin layer of-1 surface epithelium either hyperparakeratosis or .hyperorthokeratosis .Acanthosis: thickened spinous layer-2 Surface hyperkeratosis but show atrophy or -3 .thinning of surface epithelium
  54. 54. :-epithelial dysplasia - 4 It is a term to sum up various disturbances of epithelial :-growth as .drop-shaped epithelial ridges-1 .basal layer hyperplasia-2 .loss of basal cell polarity-3 .loss of normal stratification-4 .cellular pleomorphism-5 .nucleal pleomorphism and hyperchromatism-6 .increased nuclear/cytoplasm ratio-7 .loss of intercellular adherence-8 .individual cell keratinization-9 incrased normal and abnormal mitosis in shape, site,-10 .number
  55. 55. Epithelial dysplasia
  56. 56. Epithelial dysplasia is classified according to the :-severity as follow Mild: when alterations limited to basal and .parabasal layers Moderate: when alterations involve from basal .layer to midportion of spinous layer Severe: when alterations involve from basal layer .to a level above midpoint of epithelium
  57. 57. :-Carcinoma in situ .Def Dysplastic epithelial cells that extend from basal layer to surface of mucosa (Top-to.Bottom) changes (.It is called (intra-epithelial carcinoma
  58. 58. .D.D .frictional keratosis-1 .galvanic keratosis-2 .verrucous hyperplasia-3 .lichen planus-4 .leukodema-5 .white sponge nevus-6
  59. 59. :-Treatment Identification of the etiological factor-1 . discontinuation If no dysplastic changes are found, periodic -2 and careful follow-up is needed every 6 . months Removal of dysplastic changes : surgically,-3 .cryosurgery, electrodessication .In case of extensive lesions, grafting is needed- 4
  60. 60. :-Candidal Leukoplakia Age: adult :-Histopathology mitotic activity is 4 times higher than that of-1 .idiopathic leukoplakia heavly infiltration of surface epithelium with hyphae -2 .of Candida .chronic inflammatory cells are more numerous -3 Treatment: antifungal therapy may improve the .condition
  61. 61. :-Nicotinic Stomatitis .Def It is the most frequently leukoplakic lesion .of the palate :-Etiology .pipe and cigar smoking-1 .long term use of extremely hot beverges -2 .reverse smoking-3
  62. 62. :-Clinically .Age: more than 45 years .Sex: male > female .Site: palatal mucosa :-Shape Erythematous patches over time increase in keratinization ,opacification. Red dots are seen in posterior portion of .hard palate These dots are surrounded by white keratotic ring , these dots represent inflammation of ductal elements of underlying .minor salivary gland
  63. 63. :-Histopathology .epithelial hyperplasia-1 .acanthosis-2 .hyperkeratinization-3 chronic inflammatory cell-4 infiltration of sub epithelial .connective tissue minor salivary gland show-5 moderate degrees of .inflammation excretory ducts show-6 .squamous metaplasia
  64. 64. :-Treatment .Stop smoking-1 It is a completely reversible habit, the -2 palate return to normal within 1-2 weeks of .smoking cessation
  65. 65. :-Erythroplakia .Def It is a clinical term represents a red patch that can't be clinically or pathologically diagnosed as .any other condition :-Etiology Unknown, Some etiological factors as : tobacco, .alcohol ,nutritional defects, chronic irritation N.B. Erythroplakia is less common but more .dangerous than leukoplakia
  66. 66. :-Clinically .Age: 50-70 years .Sex: male > female Site: floor of mouth, retro molar area , .tongue, soft palate :-Shape homogenous: red-1 patch ,velvety ,well demarcated, soft .macule or papule spkeled: associated-2 .with focal white area
  67. 67. :-Histopathology of cases show 90% .severe dysplasia of cases show 50% invasive squamous .cell carcinoma of cases show 40% .carcinoma in situ
  68. 68. .D.D .atrophic candidiasis-1 .macular form of Kaposi sarcoma-2 .vascular malformation-3 .contact allergic reaction-4 .psoriasis-5
  69. 69. :-Treatment .careful examination-1 .biopsy taking is necessary-2 .surgical excision is necessary-3 post operative histopathological-4 .examination is necessary
  70. 70. Oral submucous fibrosis .Def It is a chronic , progressive, scarring high .precancerous condition of oral mucosa :-Etiology .chronic chewing of areca and betel nut-1 .general nutritional deficiency-2 hypersensitivity to various dietary constituents as -3 .spicy
  71. 71. :-Clinically .Race: North America, Pakistanis .Age: wide range, 20-40 years Site: buccal mucosa, retro molar area, soft .palate may extend into pharynx, esophagus Shape: White yellowish lesion, the oral mucosa loses its resilience and elasticity, the process progresses from lamina propria to underlying .musculature
  72. 72. :-Histopathology .hyperkeratosis with epithelial atrophy -1 .variable degrees of dysplastic changes -2 superficial portions of lamina propria are poorly -3 .vascularized and hyalinized submucosal deposition of extremely dense and -4 a vascular collagenous C.T. with variable .numbers of chronic inflammatory
  73. 73. .D.D .radiating related sub epithelial fibrosis-1 mucosal scarring secondary to thermal or-2 .chemical burn :-Treatment .stop the habit-1 .stretching exercises-2 .introlesional injection of corticosteroids -3 surgical excision of fibrous bands and sub-4 . mucosal placement of placental grafts
  74. 74. Paterson-Kelly syndrome. (:-(Plummer-Vinson Syndrome :-It Includes .glossitis-1 .hystrical dysphagia-2 .hypochromic microcytic anemia-3 :-Etiology .micro-organisms:Candida Albicans, Staph-1 .xerostomia-2 .nutritional deficiencies-3 .anamias-4 .mechanical trauma-5 .neurologic abnormalities-6
  75. 75. :-Clinically .Age: middle age 40-50 years .Sex: female .Site: soft palate, buccal mucosa Symptoms: pain, burning sensation, altered taste .and xerostomia Shape: lemon-tinted pallor skin, angular cheilosis, .smooth glazy painful tongue .koilonchia
  76. 76. :-Histopathology .atrophy of the epithelium-1 .complete absence of rete process -2 .hyalinization of lamina propria-3 .narrowing of blood vessels-4 :Treatment .replacement nutritional therapy-1 .identification of the cause and treat it -2 .high protein diet-3
  77. 77. Nevus .Def It is a congenital or developmental malformation of skin and mucosa leads to pigmented lesion composed of .nevus cells :-Nevus cell Origin : melanoblasts originates from neural crest cells in dorsal region of embryo and migrates to skin and mucous membrane along the course of peripheral .nerves : Shape .Oval, round or polygonal* (.Tend to make nests ( Theques* .Produce melanin in superficial areas of lesion*
  78. 78. :-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 the amount of melanin produced and the depth of .the lesion
  79. 79. :-Histopathology It is characterized by a benign unencapsulated proliferation of nevus cells which has a characteristic feature is that the superficial nevus cells tend to be organized into round aggregates (.(Theques :-There are 3 types .junctional nevus-1 .compound nevus-2 .intradermal nevus-3
  80. 80. :-junctional nevus- 1 Theques of vevus cells are found only along the basal cell .layer of epithelium, especially at tips of rete ridges It presents at junctional zone between epithelium and .C.T
  81. 81. :-Compound nevus-2 Groups of nevus cells proliferate to drop off into .underlying dermis or lamina propria Nevus cells present both along junctional area .and within underlying C.T
  82. 82. :-Intradermal (intramucosal) nevus-3 .Nevus cells are found only within underlying C.T
  83. 83. :-Oral Nevi The most common type is intramucosal * .nevus The lesion may or may not show some * .degree of melanin pigmentation
  84. 84. Malignant transformation of nevus (:-(dysplastic nevus :-Clinically .varies pigmentation-1 .irregular margins-2 .distorted surface architecture-3 :-Histopathology disorded proliferation of nevus cells at dermal- -1 .epidermal junction nuclear atypia as nuclear pleomorphism,-2 .hyperchromatism
  85. 85. :-Blue nevus .Def It is a benign proliferation of dermal melanocytes usually deep within .subepithelial connective tissue :-Types .common blue nevus-1 .cellular blue nevus-2
  86. 86. :-Common blue nevus-1 .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 branching dendritic extensions located within dermis. These cells align themselves parallel to .surface
  87. 87. :-Cellular blue nevus-2 .Site: buttock region .Age: 2-4 decades .Size: > 2cm Shape: slow-growing blue-black papule or .nodule :-Histopathology Wellcircumscribed ,highly cellular aggregation of plump,melanin producing spindle cells within dermis or submucosa , more typical pigmented dendritic spindle cells are seen at the periphery of the .lesion
  88. 88. .D.D .Kaposi sarcoma-1 .Haemangioma-2 .Early melanoma-3 :-Treatment .Conservative surgical excision