white lesions
TRANSCRIPT
White lesions in oral cavityWhite lesions in oral cavity
White lesions in oral White lesions in oral cavitycavityDefDef..
lesions appear as white patches in orallesions appear as white patches in oral cavitycavity..
Causes of white lesionsCauses of white lesions-:-: 11--Increase in thickness of one or more ofIncrease in thickness of one or more of
epithelial layersepithelial layers.. 22--Abnormal character of keratinAbnormal character of keratin..
33--Abnormal permeability of epitheliumAbnormal permeability of epithelium..
ClassificationClassification-:-:A) Keratotic White lesionsA) Keratotic White lesions-:-:
11..Focal (frictional) keratosisFocal (frictional) keratosis.. 22..White sponge nevusWhite sponge nevus..
33..Lichen planusLichen planus.. 44..Hairy leukoplakiaHairy leukoplakia..
55..LeukoplakiaLeukoplakia.. 66..Candidal leukoplakiaCandidal leukoplakia..
77..Discoid lupus erythromatosisDiscoid lupus erythromatosis..
B) Non keratotic white lesionsB) Non keratotic white lesions-:-: 11..LeukodemaLeukodema.. 22..CandidiasisCandidiasis..
33..Mucosal burnsMucosal burns..
11 ) )Focal (frictional) Focal (frictional) keratosiskeratosis-:-:
EtiologyEtiology-:-:
11--chronic rubbing of friction against chronic rubbing of friction against an oral mucosaan oral mucosa..
22--It represents a protective action It represents a protective action against low grade, long term against low grade, long term trauma astrauma as
habitual lip or cheek bitinghabitual lip or cheek biting . .
ClinicallyClinically-:-:
AgeAge:: 5-6 decades 5-6 decades..
Sex:Sex: male>female male>female..
Site:Site: mandibular mucosa, mandibular mucosa, cheek, palate, floor of the cheek, palate, floor of the mouth, maxillary mucosa, mouth, maxillary mucosa, tongue, buccal mucosa tongue, buccal mucosa along occlusal line, along occlusal line, edentulous ridgesedentulous ridges..
Shape:Shape: focal keratosis focal keratosis clinically show outlined clinically show outlined white patches, not white patches, not indurated ,have no red indurated ,have no red margin, painlessmargin, painless..
HistopathologyHistopathology
11--hyperkeratosis or hyperkeratosis or hyperparakeratosishyperparakeratosis..
22--thickening of granular thickening of granular cell layercell layer..
33--acanthosis but the acanthosis but the individual cells are individual cells are normalnormal..
44--a few chronic a few chronic inflammatory cells in inflammatory cells in adjacent connective adjacent connective tissuetissue..
DiagnosisDiagnosis-:-:
11 . .Careful history takingCareful history taking..
22 . .Careful examinationCareful examination..
33 . .Biopsy must be taken if no exact Biopsy must be taken if no exact cause is knowncause is known..
TreatmentTreatment-:-:
Removal of the cause, the lesion Removal of the cause, the lesion maymay
disappear in 2-3 weeksdisappear in 2-3 weeks..
White sponge nevusWhite sponge nevus(familial white folded (familial white folded gingivostomatitis)gingivostomatitis)
EtiologyEtiology-:-:
It is a hereditary diseaseIt is a hereditary disease..
SiteSite-:-:
Cheek mucosa along occlusal line Cheek mucosa along occlusal line bilaterally, ventral surface of tongue, bilaterally, ventral surface of tongue, floor of mouth, esophagus, rectum, floor of mouth, esophagus, rectum, vagina,larynxvagina,larynx..
ShapeShape-:-:
The mucosa appears The mucosa appears thickened, folded, thickened, folded, corrugated (velvety), corrugated (velvety), with a spongy texture with a spongy texture and a peculiar white and a peculiar white opalescent hueopalescent hue..
It is bilateral and It is bilateral and symmetricalsymmetrical
HistopathologyHistopathology-:-:11 - -The epithelium is irregular, The epithelium is irregular,
thickened, showing both thickened, showing both hyperparakeratosis and hyperparakeratosis and acanthosisacanthosis..
22--The superficial epithelial cells The superficial epithelial cells
fail to take any stain (washed fail to take any stain (washed out appearance)out appearance)..
33--These vaculated cells may These vaculated cells may show pyknotic nucleishow pyknotic nuclei
44--The connective tissue show a The connective tissue show a mild inflammatory cell mild inflammatory cell infiltrationinfiltration..
55--Intra-cellular and inter-cellular Intra-cellular and inter-cellular odemaodema..
D.DD.D.. 11--hereditary bengin epithelial dyskeratosishereditary bengin epithelial dyskeratosis..
22--Lichen planus (hypertrophic type)Lichen planus (hypertrophic type)..
33--Cheek bitingCheek biting..
44--LeukodemaLeukodema..
TreatmentTreatment-:-: No specific treatmentNo specific treatment..
Topical tetracyclineTopical tetracycline..
Lichen PlanusLichen Planus-:-:
DefDef-:-: It is a chronic inflammatory disease, It is a chronic inflammatory disease,
not infectiousnot infectious..
It is one of the most common It is one of the most common dermatological disease to manifest dermatological disease to manifest itself in oral cavity, in which oral itself in oral cavity, in which oral lesions precede the skin lesionslesions precede the skin lesions..
Its importance relates toIts importance relates to-:-:
11 - -its degree of frequency of occurrenceits degree of frequency of occurrence..
22 - -its occasional similarity to other its occasional similarity to other mucosalmucosal
diseasesdiseases..
33 - -its occasional painful natureits occasional painful nature..
44 - -its possible connection to malignancyits possible connection to malignancy..
EtiologyEtiology-:-:Unknown, it may beUnknown, it may be-:-:
11))emotional stress, over work, emotional stress, over work, trauma, infection, malnutritiontrauma, infection, malnutrition..
22))Psychosomatic in originPsychosomatic in origin.. 33))Auto-immune diseaseAuto-immune disease::
* *the epithelial cells are the primary the epithelial cells are the primary the target cellsthe target cells..
* *The mechanism of basal cell damage The mechanism of basal cell damage is related to cell mediated immune is related to cell mediated immune process involving Langerhans cells, process involving Langerhans cells, T-lymphocytes, MacrophagesT-lymphocytes, Macrophages..
Stimulus activate langerhans Stimulus activate langerhans cellscells,,
macrophages Interleukin 1macrophages Interleukin 1
attract Tattract T--
lymphocyteslymphocytes& &
stimulate them tostimulate them to
produce Interleukin 2produce Interleukin 2
Interleukin 2 T-cell proliferationInterleukin 2 T-cell proliferation.. T-cell activationT-cell activation..
Activated lymphocytesActivated lymphocytes toxic for basal cellstoxic for basal cells..
Secrete GammaSecrete Gamma interferoninterferon
Gamma interferon induce keratinocytes to Gamma interferon induce keratinocytes to express HLA-DR class 2 histocompatibility express HLA-DR class 2 histocompatibility antigenantigen..Lymphocytes normally express HLA-DRLymphocytes normally express HLA-DR..Linkage of these HLA-DR occur which result in Linkage of these HLA-DR occur which result in inappropriate epithelial antigenic information inappropriate epithelial antigenic information passed to lymphocytespassed to lymphocytes..So, self antigen may be recognized as foreign, So, self antigen may be recognized as foreign, by host T-lymphocytes resulting in auto by host T-lymphocytes resulting in auto immune responseimmune response..
ClinicallyClinically-:-:Age:Age: middle age, rare in children middle age, rare in children..
Sex:Sex: male=female male=female..
SiteSite-:-: 11 ) )skin lesions: any where, bilateral, skin lesions: any where, bilateral,
symmetrical on flexor surface of wrist, symmetrical on flexor surface of wrist, inner aspect ofinner aspect of
thighs, trunk, nails, vulvar mucosathighs, trunk, nails, vulvar mucosa..
22 ) )Oral lesions: gingiva, cheek, lips, tongueOral lesions: gingiva, cheek, lips, tongue,,
palatepalate..
Oral lesionsOral lesions-:-:
Lichen planus has patterns in oral Lichen planus has patterns in oral cavitycavity-:-:
11 - -Reticular lichen planusReticular lichen planus..
22 - -Hypertrophic lichen planusHypertrophic lichen planus..
33 - -Atrophic lichen planusAtrophic lichen planus..
44 - -Erosive lichen planusErosive lichen planus..
55 - -Bullous lichen planusBullous lichen planus..
Reticular Lichen planusReticular Lichen planus-:-:The most common typeThe most common type..Site:Site: posterior buccal posterior buccal mucosa bilaterally, mucosa bilaterally, lips, palate, gingivalips, palate, gingiva..Shape:Shape: radiating white, radiating white, velvety, thread like velvety, thread like papules in a linear, papules in a linear, annular or retiform annular or retiform arrangementarrangement..
A tiny white elevated A tiny white elevated dots is present at the dots is present at the intersection of white intersection of white lines known as lines known as (striae (striae of wickham)of wickham)..
Erosive Lichen PlanusErosive Lichen Planus-:-:
Site:Site: posterior- inferior posterior- inferior aspect of buccal aspect of buccal mucosa adjacent to mucosa adjacent to mandibular molar mandibular molar teethteeth..Shape:Shape: atrophic, atrophic, erythematous areas erythematous areas with central ulceration, with central ulceration, the periphery of the periphery of atrophic regions is atrophic regions is bordered by fine, bordered by fine, white radiating striaewhite radiating striae..
Atrophic Lichen planusAtrophic Lichen planus-:-:
Site:Site: attached gingiva attached gingiva..Shape:Shape: smooth red, smooth red, poorly defined poorly defined atrophic zones, at atrophic zones, at its margins there its margins there are whitish keratotic are whitish keratotic striae radiating striae radiating peripherally and peripherally and blending into blending into surrounding surrounding mucosamucosa..
Hypertrophic lichen planusHypertrophic lichen planus-:-:
Site:Site: dorsum of dorsum of tongue and buccal tongue and buccal mucosamucosa..
Shape:Shape: well well circumscribed white circumscribed white lesions (plaque like) lesions (plaque like) which range from which range from slightly elevated slightly elevated and smooth to and smooth to slightly irregularslightly irregular..
HistopathologyHistopathology-:-:
11--Hyperorthokeratosis or hyperparakeratosisHyperorthokeratosis or hyperparakeratosis..22--Variable degree of acanthosisVariable degree of acanthosis..
33 - -Destruction of basal cell layer of epithelium Destruction of basal cell layer of epithelium (hydropic degeneration) with vacuolization (hydropic degeneration) with vacuolization of basal cell layerof basal cell layer..
44 - -Rete process may be absent, hyperplastic Rete process may be absent, hyperplastic or saw-toothed shapeor saw-toothed shape..
55 - -tearing between epithelium and C.Ttearing between epithelium and C.T..66--presence of colloid (civatte, hyaline, cytoid presence of colloid (civatte, hyaline, cytoid
bodies) as discrete eosinophilic ovoid bodies) as discrete eosinophilic ovoid bodies at basal cell layerbodies at basal cell layer..
Lichen planusLichen planus
Atrophic Lichen Atrophic Lichen PlanusPlanus
Erosive Lichen PlanusErosive Lichen Planus
D.DD.D..11 - -candidiasiscandidiasis..
22--leukoplakialeukoplakia..
33--squamous cell carcinomasquamous cell carcinoma..
44--drug eruptiondrug eruption..
55--discoid lupus erythromatosisdiscoid lupus erythromatosis..
N.B.N.B. Grinspan`s syndrome Grinspan`s syndrome-:-:
Lichen planusLichen planus..
Diabetes mellitusDiabetes mellitus..
Vascular hypertensionVascular hypertension . .
TreatmentTreatment-:-:
No specific systemic or local therapyNo specific systemic or local therapy..
Corticosteroids (topical, Corticosteroids (topical, intralesional ,systemic)intralesional ,systemic)..
Antifungal therapyAntifungal therapy..
RetinoidsRetinoids..
PrognosisPrognosis-:-:
It is a benign lesion , it was not It is a benign lesion , it was not considered a premalignant condition considered a premalignant condition But a large number of cases of But a large number of cases of epidermoid carcinoma developing in epidermoid carcinoma developing in oral lesions of lichen planusoral lesions of lichen planus..
The majority of cases of cancer have The majority of cases of cancer have occurred in erosive and atrophic typesoccurred in erosive and atrophic types. .
Hairy leukoplakiaHairy leukoplakia-:-:DefDef-:.-:.
It is an unusual white lesion with a hairy appearance or It is an unusual white lesion with a hairy appearance or corrugated surface that occurred on the lateral border corrugated surface that occurred on the lateral border or dorsum of tongueor dorsum of tongue..
EtiologyEtiology-:-:
11--In male homosexualsIn male homosexuals..22--An opportunistic infection relates to Epstein-Barr virusAn opportunistic infection relates to Epstein-Barr virus..
33--It is related to AIDS patientsIt is related to AIDS patients..
N.B.N.B. Viral particles are present and replicated within the Viral particles are present and replicated within the epithelial cells of tongue. Human papilloma virus epithelial cells of tongue. Human papilloma virus present in co-existence with EBVpresent in co-existence with EBV..
ClinicallyClinically-:-:
Site:Site: lateral surface of lateral surface of tongue, dorsum of tongue, dorsum of tongue, floor of tongue, floor of mouth, palatemouth, palate..
Shape:Shape: unilateral or unilateral or bilateral surface which bilateral surface which is folded or corrugated is folded or corrugated or papillary( hairy)or papillary( hairy)..
No associated No associated symptoms unless it is symptoms unless it is superimposed by superimposed by candidal infectioncandidal infection..
HistopathologyHistopathology-:-:11--Epithelial hyperplasiaEpithelial hyperplasia..
22--Marked hyperparakeratosisMarked hyperparakeratosis..
33 - -Formation of keratotic surface Formation of keratotic surface irregularities and ridgesirregularities and ridges..
44--Spinous cell layers show Spinous cell layers show koilocytosiskoilocytosis..
55--Alterationas of nuclear Alterationas of nuclear chromatin in form of viral chromatin in form of viral inclusionsinclusions..
66--Candidal albicans hyphae Candidal albicans hyphae extend into superficial extend into superficial epithelial layersepithelial layers..
77 - -No inflammatory cell infiltration No inflammatory cell infiltration in C.Tin C.T..
DiagnosisDiagnosis-:-:
11 ) )Immunohistochemical staining Immunohistochemical staining technique using anti-viral technique using anti-viral antibodiesantibodies..
22 ) )Ultrastructural study using electronUltrastructural study using electron
microscopemicroscope..
33 ) )Southern blot hybridization Southern blot hybridization procedureprocedure. .
D.DD.D..
11--idiopathic leukoplakiaidiopathic leukoplakia..
22--leukoplakia associated with tobacoo leukoplakia associated with tobacoo useuse..
33--lichen planuslichen planus..
44--chronic hyperplastic candidiasischronic hyperplastic candidiasis..
55--frictional keratosisfrictional keratosis..
66--keratotic reaction associated with keratotic reaction associated with electrochemical interactionselectrochemical interactions..
TreatmentTreatment-:-:
AcyclovirAcyclovir
Topical corticosteroidsTopical corticosteroids..
Candidiasis (Moniliasis)Candidiasis (Moniliasis)
DefDef.. This is a term that encompasses a group of mucosal This is a term that encompasses a group of mucosal
and cutaneous conditions with a common and cutaneous conditions with a common etiological agent from the Candida genus of fungietiological agent from the Candida genus of fungi..
EtiologyEtiology-:-: The causative organism is Candida AlbicansThe causative organism is Candida Albicans..The predisposing factors areThe predisposing factors are-:-:
11--topical corticosteroidstopical corticosteroids..22--malabsorption , malnutritionmalabsorption , malnutrition..
33--poor oral hygienepoor oral hygiene..44--xerostomiaxerostomia..
55--systemic antibiotic therapysystemic antibiotic therapy..66--Cancer chemotherapyCancer chemotherapy..
77 - -AIDSAIDS..
Classification of Oral Classification of Oral CandidiasisCandidiasis-:-:
A) Acute CandidiasisA) Acute Candidiasis:: 11--pseudomembranous (Thrush)pseudomembranous (Thrush)..
22--atrophic (antibiotic sore mouth)atrophic (antibiotic sore mouth)..B) Chronic CandidiasisB) Chronic Candidiasis::
11--atrophic (denture sore mouth & angular atrophic (denture sore mouth & angular chelitis)chelitis)
22--hypertrophic (candidal leukoplakia &medianhypertrophic (candidal leukoplakia &median rhomboid glossitis & chronic multifocalrhomboid glossitis & chronic multifocal
candidiasiscandidiasis.).)C) Mucocutanous formsC) Mucocutanous forms::
11--localizedlocalized.. 22--familialfamilial..
33--syndrome-associatedsyndrome-associated..
ThrushThrush
Laboratory findingsLaboratory findings-:-:
11--remaval of a portion of remaval of a portion of the candidal plaquethe candidal plaque..
22--It is smeared on a It is smeared on a microscopic slide, microscopic slide, macerated with 20% macerated with 20% potassium hydroxidepotassium hydroxide..
33--Then examination for Then examination for typical hyphaetypical hyphae..
44--Culture identification Culture identification and quantification of and quantification of organisms may be organisms may be performed with a performed with a variety of media as variety of media as blood agar or cornmeal blood agar or cornmeal agaragar..
HistopathologyHistopathology-:-:
Histological section is stained Histological section is stained with periodic acid Schiff with periodic acid Schiff reagent PAS will show reagent PAS will show presence of yeast cells and presence of yeast cells and hyphae in the superficial and hyphae in the superficial and deeper layers of involved deeper layers of involved epithelium give bright magenta epithelium give bright magenta colorcolor..
Histological features includeHistological features include-:-:11--hyperparakeratosishyperparakeratosis..
22 - -chronic inflammatory cell chronic inflammatory cell infiltration in CTinfiltration in CT
33--collections of neutrophils collections of neutrophils (micro-abscess) in parakeratin (micro-abscess) in parakeratin layerlayer..
44--The candidal hyphae embedded The candidal hyphae embedded in parakeratin layerin parakeratin layer..
D.DD.D..
11--slough associated with chemical burnsslough associated with chemical burns..22--traumatic ulcerationstraumatic ulcerations..
33--mucous patches of syphilismucous patches of syphilis..44--white keratotic lesionswhite keratotic lesions..
TreatmentTreatment-:-:
11 ) )NystatinNystatin..22))Imidazole agentsImidazole agents..
33))Triazole agentsTriazole agents..
LeukodemaLeukodema-:-:
DefDef.. It is an abnormality of the buccal mucosa ofIt is an abnormality of the buccal mucosa of
unknown causeunknown cause.. It may be considered as variation of the normal ratherIt may be considered as variation of the normal rather
than a diseasethan a disease..
EtiologyEtiology-:-:Causative factors as: smoking, alcohol, bacterial Causative factors as: smoking, alcohol, bacterial infectioninfection..
Site:Site: buccal mucosa, buccal mucosa, labial mucosa, floor labial mucosa, floor of the mouthof the mouth..
Shape:Shape: bilateral, bilateral, symmetrical filmy symmetrical filmy opalescence opalescence mucosa become mucosa become grayish white in grayish white in late stage with late stage with corrugated surfacecorrugated surface..
Race:Race: blacks > blacks > whiteswhites..
HistopathologyHistopathology-:-:
11--The epithelium is acanthotic, The epithelium is acanthotic, parakeratoticparakeratotic..
22--The enlarged cells in the superficial part The enlarged cells in the superficial part of stratum spinosum appear vacuolated of stratum spinosum appear vacuolated because they contain glycogenbecause they contain glycogen..
33--The rete ridges are broad and enlargedThe rete ridges are broad and enlarged..
DiagnosisDiagnosis-:-:11--gentle stroking with a gauze pad will not gentle stroking with a gauze pad will not
remove it ( not rub off )remove it ( not rub off )22--With stretching of buccal mucosa, the With stretching of buccal mucosa, the
opaque changes will dissipateopaque changes will dissipate..
D.DD.D..11--leukoplakialeukoplakia..
22--white sponge nevuswhite sponge nevus..33--response to chronic cheek bitingresponse to chronic cheek biting..
TreatmentTreatment-:-:No treatment is necessaryNo treatment is necessary..
Mucosal burnsMucosal burns-:-:Chemical BurnsChemical Burns-:-:
Topical applications of Topical applications of chemicals as aspirin chemicals as aspirin tablets which is used tablets which is used in self medication and in self medication and held locally against a held locally against a painful tooth and painful tooth and allowed to dissolve allowed to dissolve slowlyslowly . .
Thermal BurnsThermal Burns-:-:Common in hard palatal Common in hard palatal mucosa caused by mucosa caused by hot, sticky foodhot, sticky food..
Premalignant lesionPremalignant lesion-:-: It is a benign , morphologically altered It is a benign , morphologically altered
tissue that has a greater than normal tissue that has a greater than normal risk of malignant transformationrisk of malignant transformation..
Ex.Ex. 1-leukoplakia 1-leukoplakia.. 22--erythroplakiaerythroplakia..
33--sublingual keratosissublingual keratosis.. 44--candidal leukoplakiacandidal leukoplakia..
55--stomatitis nicotinastomatitis nicotina..
Premalignant conditionPremalignant condition-:-: It is a disease or patient habit that doesn`t It is a disease or patient habit that doesn`t
necessarily alter the clinical appearance of necessarily alter the clinical appearance of local tissue but is associated with a local tissue but is associated with a greater than normal risk of precancerous greater than normal risk of precancerous lesion or cancer development in that lesion or cancer development in that tissuetissue..
Ex.Ex. 1-Oral sub mucous fibrosis 1-Oral sub mucous fibrosis..
22--Paterson-Kelly syndromePaterson-Kelly syndrome..
33--lichen planuslichen planus..
44--Discoid lupus erythematosisDiscoid lupus erythematosis..
LeukoplakiaLeukoplakia-:-:DefDef..
It is a white patch or plaque that cannot be It is a white patch or plaque that cannot be characterized clinically or pathologically as any other characterized clinically or pathologically as any other diseasedisease..
It is a clinical termIt is a clinical term..
EtiologyEtiology-:-:Exact etiology is unknown ,it may beExact etiology is unknown ,it may be-:-:
11--tobaccotobacco..22--alcoholalcohol..
33--ultraviolet radiationultraviolet radiation..44--traumatrauma..
55--nutritional deficenciesnutritional deficencies..66--micro-organisms (treponema pallidum , candida micro-organisms (treponema pallidum , candida
albicans , human papilloma virus )albicans , human papilloma virus )..
ClinicallyClinically-:-:Age:Age: middle age 4-6 decades middle age 4-6 decades..Sex:Sex: male > female male > female..Site:Site: Tongue, floor of mouth, buccal mucosa, Tongue, floor of mouth, buccal mucosa, palate, lower lip, retro molar sitespalate, lower lip, retro molar sites..
ShapesShapes-:-:11--mild ( thin ) leukoplakiamild ( thin ) leukoplakia..
22--Homogenous (thick) leukoplakiaHomogenous (thick) leukoplakia..33--Granular or nodular leukoplakiaGranular or nodular leukoplakia..
44--Verrucous leukoplakiaVerrucous leukoplakia..55--Proliferative verrucous leukoplakiaProliferative verrucous leukoplakia..
66 - -Erythroleukoplakia or speckled Erythroleukoplakia or speckled leukoplakialeukoplakia..
LeukoplakiaLeukoplakia
Proliferative verrucous Proliferative verrucous leukoplakialeukoplakia
Speckled LeukoplakiaSpeckled Leukoplakia
HistopathologyHistopathology-:-:
It varies as followIt varies as follow-:-:11--Hyperkeratosis: thickened keratin layer of Hyperkeratosis: thickened keratin layer of
surface epithelium either surface epithelium either hyperparakeratosis or hyperorthokeratosishyperparakeratosis or hyperorthokeratosis..
22--Acanthosis: thickened spinous layerAcanthosis: thickened spinous layer..
33--Surface hyperkeratosis but show atrophy or Surface hyperkeratosis but show atrophy or thinning of surface epitheliumthinning of surface epithelium..
44 - -epithelial dysplasiaepithelial dysplasia-:-:
It is a term to sum up various disturbances of It is a term to sum up various disturbances of epithelial growth asepithelial growth as-:-:
11--drop-shaped epithelial ridgesdrop-shaped epithelial ridges..22--basal layer hyperplasiabasal layer hyperplasia..
33--loss of basal cell polarityloss of basal cell polarity..44--loss of normal stratificationloss of normal stratification..
55--cellular pleomorphismcellular pleomorphism..66--nucleal pleomorphism and hyperchromatismnucleal pleomorphism and hyperchromatism..
77--increased nuclear/cytoplasm ratioincreased nuclear/cytoplasm ratio..88--loss of intercellular adherenceloss of intercellular adherence..
99--individual cell keratinizationindividual cell keratinization..1010--incrased normal and abnormal mitosis in shape, site, incrased normal and abnormal mitosis in shape, site,
numbernumber..
Epithelial dysplasiaEpithelial dysplasia
Epithelial dysplasia is classified according to Epithelial dysplasia is classified according to the severity as followthe severity as follow-:-:
Mild:Mild: when alterations limited to basal and when alterations limited to basal and parabasal layersparabasal layers..
Moderate:Moderate: when alterations involve from basal when alterations involve from basal layer to midportion of spinous layerlayer to midportion of spinous layer..
Severe:Severe: when alterations involve from basal when alterations involve from basal layer to a level above midpoint of layer to a level above midpoint of epitheliumepithelium..
Carcinoma in situCarcinoma in situ-:-:
DefDef.. Dysplastic epithelial cells that extend Dysplastic epithelial cells that extend
from basal layer to surface of from basal layer to surface of mucosa (Top-to-Bottom) changesmucosa (Top-to-Bottom) changes..
It is called (intra-epithelial carcinoma)It is called (intra-epithelial carcinoma)..
D.DD.D..
11--frictional keratosisfrictional keratosis..
22--galvanic keratosisgalvanic keratosis..
33--verrucous hyperplasiaverrucous hyperplasia..
44--lichen planuslichen planus..
55--leukodemaleukodema..
66--white sponge nevuswhite sponge nevus..
TreatmentTreatment-:-:11--Identification of the etiological factorIdentification of the etiological factor
discontinuationdiscontinuation . .
22--If no dysplastic changes are found, periodicIf no dysplastic changes are found, periodic
and careful follow-up is needed every 6and careful follow-up is needed every 6
monthsmonths . .
33--Removal of dysplastic changes : surgically, Removal of dysplastic changes : surgically, cryosurgery, electrodessicationcryosurgery, electrodessication..
44 - -In case of extensive lesions, grafting is neededIn case of extensive lesions, grafting is needed..
Candidal LeukoplakiaCandidal Leukoplakia-:-:Age:Age: adult adult
HistopathologyHistopathology-:-:11--mitotic activity is 4 times higher than that of mitotic activity is 4 times higher than that of
idiopathic leukoplakiaidiopathic leukoplakia..22--heavly infiltration of surface epithelium with heavly infiltration of surface epithelium with
hyphae of Candidahyphae of Candida..33--chronic inflammatory cells are more chronic inflammatory cells are more
numerousnumerous..
Treatment:Treatment: antifungal therapy may improve antifungal therapy may improve the conditionthe condition..
Nicotinic StomatitisNicotinic Stomatitis-:-:DefDef..
It is the most frequently leukoplakic It is the most frequently leukoplakic lesion of the palatelesion of the palate..
EtiologyEtiology-:-:11--pipe and cigar smokingpipe and cigar smoking..
22--long term use of extremely hot long term use of extremely hot bevergesbeverges..
33--reverse smokingreverse smoking..
ClinicallyClinically-:-:Age:Age: more than 45 years more than 45 years..
Sex:Sex: male > female male > female..
Site:Site: palatal mucosa palatal mucosa..
ShapeShape-:-: Erythematous patches over Erythematous patches over
time increase in time increase in keratinization ,opacificationkeratinization ,opacification. Red dots are seen in . Red dots are seen in posterior portion of hard posterior portion of hard palatepalate..
These dots are surrounded by These dots are surrounded by white keratotic ring , these white keratotic ring , these dots represent dots represent inflammation of ductal inflammation of ductal elements of underlying elements of underlying minor salivary glandminor salivary gland..
HistopathologyHistopathology-:-:11--epithelial hyperplasiaepithelial hyperplasia..
22--acanthosisacanthosis..
33--hyperkeratinizationhyperkeratinization..
44--chronic inflammatory chronic inflammatory cell infiltration of sub cell infiltration of sub epithelial connective epithelial connective tissuetissue..
55--minor salivary gland minor salivary gland show moderate degrees show moderate degrees of inflammationof inflammation..
66--excretory ducts show excretory ducts show squamous metaplasiasquamous metaplasia..
TreatmentTreatment-:-:
11--Stop smokingStop smoking..
22--It is a completely reversible habit, It is a completely reversible habit, the palate return to normal within 1-the palate return to normal within 1-2 weeks of smoking cessation2 weeks of smoking cessation..
ErythroplakiaErythroplakia-:-:DefDef..
It is a clinical term represents a red patch It is a clinical term represents a red patch that can't be clinically or pathologically that can't be clinically or pathologically diagnosed as any other conditiondiagnosed as any other condition..
EtiologyEtiology-:-:Unknown, Some etiological factors as : Unknown, Some etiological factors as : tobacco, alcohol ,nutritional defects, tobacco, alcohol ,nutritional defects, chronic irritationchronic irritation..
N.B.N.B. Erythroplakia is less common but more Erythroplakia is less common but more dangerous than leukoplakiadangerous than leukoplakia..
ClinicallyClinically-:-:
Age:Age: 50-70 years 50-70 years..
Sex:Sex: male > female male > female..
Site:Site: floor of mouth, floor of mouth, retro molar area , retro molar area , tongue, soft palatetongue, soft palate..
ShapeShape-:-:11--homogenous: red homogenous: red
patch ,velvety ,well patch ,velvety ,well demarcated, soft demarcated, soft macule or papulemacule or papule..
22--spkeled: associated spkeled: associated with focal white with focal white areaarea..
HistopathologyHistopathology-:-:
90%90% of cases show of cases show severe dysplasiasevere dysplasia..
50%50% of cases show of cases show invasive squamous invasive squamous cell carcinomacell carcinoma..
40%40% of cases show of cases show carcinoma in situcarcinoma in situ..
D.DD.D..
11--atrophic candidiasisatrophic candidiasis..
22--macular form of Kaposi sarcomamacular form of Kaposi sarcoma..
33--vascular malformationvascular malformation..
44--contact allergic reactioncontact allergic reaction..
55--psoriasispsoriasis..
TreatmentTreatment-:-:
11--careful examinationcareful examination..
22--biopsy taking is necessarybiopsy taking is necessary..
33--surgical excision is necessarysurgical excision is necessary..
44--post operative histopathological post operative histopathological examination is necessaryexamination is necessary..
Oral submucous fibrosisOral submucous fibrosis
DefDef.. It is a chronic , progressive, scarring high It is a chronic , progressive, scarring high
precancerous condition of oral mucosaprecancerous condition of oral mucosa..
EtiologyEtiology-:-:11--chronic chewing of areca and betel nutchronic chewing of areca and betel nut..
22--general nutritional deficiencygeneral nutritional deficiency..33--hypersensitivity to various dietary hypersensitivity to various dietary
constituents as spicyconstituents as spicy..
ClinicallyClinically-:-:Race:Race: North America, Pakistanis North America, Pakistanis..
Age:Age: wide range, 20-40 years wide range, 20-40 years..
Site:Site: buccal mucosa, retro molar area, buccal mucosa, retro molar area, soft palate may extend into pharynx, soft palate may extend into pharynx, esophagusesophagus..
Shape:Shape: White yellowish lesion, the oral White yellowish lesion, the oral mucosa loses its resilience and elasticity, mucosa loses its resilience and elasticity, the process progresses from lamina the process progresses from lamina propria to underlying musculaturepropria to underlying musculature..
HistopathologyHistopathology-:-:11--hyperkeratosis with epithelial atrophyhyperkeratosis with epithelial atrophy..
22--variable degrees of dysplastic changesvariable degrees of dysplastic changes..
33--superficial portions of lamina propria are superficial portions of lamina propria are poorly vascularized and hyalinizedpoorly vascularized and hyalinized..
44--submucosal deposition of extremely submucosal deposition of extremely dense and a vascular collagenous C.T. dense and a vascular collagenous C.T. with variable numbers of chronic with variable numbers of chronic inflammatoryinflammatory..
D.DD.D..11--radiating related sub epithelial fibrosisradiating related sub epithelial fibrosis..
22--mucosal scarring secondary to thermal or mucosal scarring secondary to thermal or chemical burnchemical burn..
TreatmentTreatment-:-:11--stop the habitstop the habit..
22--stretching exercisesstretching exercises..33--introlesional injection of corticosteroidsintrolesional injection of corticosteroids..
44--surgical excision of fibrous bands and sub surgical excision of fibrous bands and sub mucosal placement of placental graftsmucosal placement of placental grafts . .
Paterson-Kelly syndrome.Paterson-Kelly syndrome.(Plummer-Vinson Syndrome)(Plummer-Vinson Syndrome)-:-:
It IncludesIt Includes-:-: 11--glossitisglossitis..
22--hystrical dysphagiahystrical dysphagia.. 33--hypochromic microcytic anemiahypochromic microcytic anemia..
EtiologyEtiology-:-:11--micro-organisms:Candida Albicans, Staphmicro-organisms:Candida Albicans, Staph..
22--xerostomiaxerostomia..33--nutritional deficienciesnutritional deficiencies..
44--anamiasanamias..55--mechanical traumamechanical trauma..
66--neurologic abnormalitiesneurologic abnormalities..
ClinicallyClinically-:-:
Age:Age: middle age 40-50 years middle age 40-50 years..
Sex:Sex: female female..
Site:Site: soft palate, buccal mucosa soft palate, buccal mucosa..
Symptoms: pain, burning sensation, altered Symptoms: pain, burning sensation, altered taste and xerostomiataste and xerostomia..
Shape:Shape: lemon-tinted pallor skin, angular lemon-tinted pallor skin, angular cheilosis, smooth glazy painful cheilosis, smooth glazy painful tongue .koilonchiatongue .koilonchia..
HistopathologyHistopathology-:-:11--atrophy of the epitheliumatrophy of the epithelium..
22--complete absence of rete processcomplete absence of rete process..33--hyalinization of lamina propriahyalinization of lamina propria..
44--narrowing of blood vesselsnarrowing of blood vessels..
TreatmentTreatment::11--replacement nutritional therapyreplacement nutritional therapy..
22--identification of the cause and treat identification of the cause and treat itit..
33--high protein diethigh protein diet..
NevusNevusDefDef..
It is a congenital or developmental malformation of It is a congenital or developmental malformation of skin and mucosa leads to pigmented lesion skin and mucosa leads to pigmented lesion composed of nevus cellscomposed of nevus cells..
Nevus cellNevus cell-:-:Origin : melanoblasts originates from neural crest Origin : melanoblasts originates from neural crest cells in dorsal region of embryo and migrates to cells in dorsal region of embryo and migrates to skin and mucous membrane along the course of skin and mucous membrane along the course of peripheral nervesperipheral nerves..
ShapeShape : :**Oval, round or polygonalOval, round or polygonal..
**Tend to make nests ( Theques)Tend to make nests ( Theques)..**Produce melanin in superficial areas of lesionProduce melanin in superficial areas of lesion..
ClinicallyClinically-:-:
AgeAge: childhood: childhood..Sex:Sex: female > male female > male..Race:Race: whites > blackes whites > blackes..SiteSite-:-:
In skin : in any site most common above waistIn skin : in any site most common above waist..Intra-orally: palate, buccal mucosa, labial Intra-orally: palate, buccal mucosa, labial mucosa, gingiva, alveolar mucosa, vermilionmucosa, gingiva, alveolar mucosa, vermilion..Colour: range from tan to black depending on Colour: range from tan to black depending on the amount of melanin produced and the the amount of melanin produced and the depth of the lesiondepth of the lesion..
HistopathologyHistopathology-:-:
It is characterized by a benign It is characterized by a benign unencapsulated proliferation of nevus cells unencapsulated proliferation of nevus cells which has a characteristic feature is that which has a characteristic feature is that the superficial nevus cells tend to be the superficial nevus cells tend to be organized into round aggregates (Theques)organized into round aggregates (Theques)..
There are 3 typesThere are 3 types-:-:11--junctional nevusjunctional nevus..22--compound nevuscompound nevus..
33--intradermal nevusintradermal nevus..
11 - -junctional nevusjunctional nevus-:-:
Theques of vevus cells are found only along the Theques of vevus cells are found only along the basal cell layer of epithelium, especially at tips basal cell layer of epithelium, especially at tips of rete ridgesof rete ridges..
It presents at junctional zone between epithelium It presents at junctional zone between epithelium and C.Tand C.T..
22--Compound nevusCompound nevus-:-:Groups of nevus cells proliferate to drop off Groups of nevus cells proliferate to drop off into underlying dermis or lamina propriainto underlying dermis or lamina propria..Nevus cells present both along junctional Nevus cells present both along junctional area and within underlying C.Tarea and within underlying C.T..
33--Intradermal (intramucosal) nevusIntradermal (intramucosal) nevus-:-:
Nevus cells are found only within Nevus cells are found only within underlying C.Tunderlying C.T..
Oral NeviOral Nevi-:-:
* *The most common type is The most common type is intramucosal nevusintramucosal nevus..
* *The lesion may or may not show The lesion may or may not show some degree of melanin some degree of melanin pigmentationpigmentation..
Malignant transformation of Malignant transformation of nevusnevus(dysplastic nevus)(dysplastic nevus)-:-:ClinicallyClinically-:-:
11--varies pigmentationvaries pigmentation..22--irregular marginsirregular margins..
33--distorted surface architecturedistorted surface architecture..
HistopathologyHistopathology-:-:11--disorded proliferation of nevus cells at disorded proliferation of nevus cells at
dermal-epidermal junctiondermal-epidermal junction..22--nuclear atypia as nuclear pleomorphism, nuclear atypia as nuclear pleomorphism,
hyperchromatismhyperchromatism..
Blue nevusBlue nevus-:-:
DefDef.. It is a benign proliferation of dermal It is a benign proliferation of dermal
melanocytes usually deep within melanocytes usually deep within subepithelial connective tissuesubepithelial connective tissue..
TypesTypes-:-:11--common blue nevuscommon blue nevus..
22--cellular blue nevuscellular blue nevus..
11--Common blue nevusCommon blue nevus-:-:Site:Site: dorsa of hands, feet, palate dorsa of hands, feet, palate..Age:Age: children children..Sex:Sex: female female..ShapeShape: macular lesion, blue or black: macular lesion, blue or black..Size:Size: < 1cm < 1cm..HistopathologyHistopathology-:-:
It is composed of collection of It is composed of collection of elongated, slender melanocytes with elongated, slender melanocytes with branching dendritic extensions branching dendritic extensions located within dermis. These cells located within dermis. These cells align themselves parallel to surfacealign themselves parallel to surface..
22--Cellular blue nevusCellular blue nevus-:-:Site:Site: buttock region buttock region..
Age:Age: 2-4 decades 2-4 decades..
Size:Size: > 2cm > 2cm..
Shape:Shape: slow-growing blue-black papule slow-growing blue-black papule or noduleor nodule..
HistopathologyHistopathology-:-:
Wellcircumscribed ,highly cellular Wellcircumscribed ,highly cellular aggregation of plump,melanin aggregation of plump,melanin producing spindle cells within dermis producing spindle cells within dermis or submucosa , more typical or submucosa , more typical pigmented dendritic spindle cells are pigmented dendritic spindle cells are seen at the periphery of the lesionseen at the periphery of the lesion..
D.DD.D..
11--Kaposi sarcomaKaposi sarcoma..
22--HaemangiomaHaemangioma..
33--Early melanomaEarly melanoma..
TreatmentTreatment-:-:
Conservative surgical excisionConservative surgical excision..