VesiculobullousVesiculobullous
diseasesdiseases
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
PEMPHGOIDPEMPHGOID
ERYTEMA MULTIFORME...
CLASSIFICATION OF VESICULOBULLOUSCLASSIFICATION OF VESICULOBULLOUS
DISEASESDISEASES
VESICLE&BULLAVESICLE&BULLA
A clear flu...
CLASSIFICATION OF VESICULOBULLOUSCLASSIFICATION OF VESICULOBULLOUS
DISEASESDISEASES
CLASSIFICATIONCLASSIFICATION
INTRA EPI...
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
Autoimmune disease.Autoimmune disease.
Common in Ashkenazi and Mediterranean jews .Co...
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
CLINICAL FEATURES:CLINICAL FEATURES:
Painful ulcers or bulla are formed which are flu...
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
Some time the ulcers are joined together to make aSome time the ulcers are joined tog...
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
PATHOGENESIS:PATHOGENESIS:
It is an autoimmune diseaseIt is an autoimmune disease
The...
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
The epithelial damage is directly proportion toThe epithelial damage is directly prop...
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
HISTOPATHOLOGY:HISTOPATHOLOGY:
Intra epithelial vesicles or bulla and cleft like spac...
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
histologyhistology
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
histologyhistology
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
tazank cellstazank cells
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
immunoflorecenceimmunoflorecence
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
DIFFRENTIAL DIAGNOSIS:DIFFRENTIAL DIAGNOSIS:
PempegiodPempegiod
Erthema multiformeErt...
PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
TREATMENT:TREATMENT:
High mortality rates previouslyHigh mortality rates previously
I...
PEMPHGOIDPEMPHGOID
PEMPHGOIDPEMPHGOID
Mucous membrane pemphigoidMucous membrane pemphigoid
(cicatricial) CIKA-TRI-CIAL(cicatricial) CIKA-TRI-...
PEMPHGOIDPEMPHGOID
PATHOLOGYPATHOLOGY
Autoimmune diseaseAutoimmune disease
Not life threateningNot life threatening
Elderl...
PEMPHGOIDPEMPHGOID
PEMPHGOIDPEMPHGOID
CLINICAL FEATURES(MMP)CLINICAL FEATURES(MMP)
Oral mucosa is the first site- lesions are rarelyOral muco...
PEMPHGOIDPEMPHGOID
occular involvementoccular involvement
PEMPHGOIDPEMPHGOID
CASCADEOF EVENTSCASCADEOF EVENTS
Antibody antigen complexAntibody antigen complex
↓↓
Complement activat...
PEMPHGOIDPEMPHGOID
PEMPHGOIDPEMPHGOID
MANAGEMENTMANAGEMENT
Confirm diagnosisConfirm diagnosis
Topical corticosteroidsTopical corticosteroids
...
ERYTEMAERYTEMA
MULTIFORMEMULTIFORME
ERYTEMA MULTIFORMEERYTEMA MULTIFORME
Mucocutaneous diseaseMucocutaneous disease
Males adolosents , young adults areMales a...
ERYTEMA MULTIFORMEERYTEMA MULTIFORME
AETIOLOGY /PATHOLOGYAETIOLOGY /PATHOLOGY
Unclear aetiology and pathogenesisUnclear ae...
ERYTEMA MULTIFORMEERYTEMA MULTIFORME
CLINICAL FEATURESCLINICAL FEATURES
Prodomal signs:Prodomal signs:
Upper respiratory i...
ERYTEMA MULTIFORMEERYTEMA MULTIFORME
Signs during the disease:Signs during the disease:
Red macules – 1cm or more in diame...
ERYTEMA MULTIFORMEERYTEMA MULTIFORME
ERYTEMA MULTIFORMEERYTEMA MULTIFORME
HISTOPATHOLOGYHISTOPATHOLOGY
Necrosis of the kertinocytesNecrosis of the kertinocytes...
ERYTEMA MULTIFORMEERYTEMA MULTIFORME
ERYTEMA MULTIFORMEERYTEMA MULTIFORME
MANAGEMENTMANAGEMENT
No specific treatment required , if HSV inf..No specific treatme...
EPIDERMOLYSISEPIDERMOLYSIS
BULLOSABULLOSA
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
Definition:Definition:
A large group of clinically similarA large group of clin...
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
MAJOR CATEGORIES OF EPIDERMOLYSIS BULLOSAMAJOR CATEGORIES OF EPIDERMOLYSIS BULL...
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
HEREDITARY TYPES:HEREDITARY TYPES:
Congenital absence of componentsCongenital a...
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
CLINICAL FEATURESCLINICAL FEATURES
1.1.Epidermolysis Bullosa SimplexEpidermolys...
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
2.2. Junctional Epidermolysis BullosaJunctional Epidermolysis Bullosa
Severe fo...
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
3.3. Dystrophic Epidermolysis BullosaDystrophic Epidermolysis Bullosa
Both auto...
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
Epidermolysis Bullosa AcquisitaEpidermolysis Bullosa Acquisita
Non-hereditary f...
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
HISTOPATHOLOGYHISTOPATHOLOGY
Simplex type exhibits zone of cleavageSimplex type...
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
MANAGEMENTMANAGEMENT
No specific treatment available for hereditaryNo specific ...
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Vesiculobullous diseases

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Vesiculobullous diseases

  1. 1. VesiculobullousVesiculobullous diseasesdiseases PEMPHIGUS VULGARISPEMPHIGUS VULGARIS PEMPHGOIDPEMPHGOID ERYTEMA MULTIFORMEERYTEMA MULTIFORME EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA LUPUS ERYTHEMATOSISLUPUS ERYTHEMATOSIS Dr.khurram zafarDr.khurram zafar
  2. 2. CLASSIFICATION OF VESICULOBULLOUSCLASSIFICATION OF VESICULOBULLOUS DISEASESDISEASES VESICLE&BULLAVESICLE&BULLA A clear fluid lesion just below theA clear fluid lesion just below the epithelium which ruptures to form an ulcer,epithelium which ruptures to form an ulcer, if this is smaller than 5mm then it is aif this is smaller than 5mm then it is a vesicle ,if larger than 5mm than it is a bullavesicle ,if larger than 5mm than it is a bulla
  3. 3. CLASSIFICATION OF VESICULOBULLOUSCLASSIFICATION OF VESICULOBULLOUS DISEASESDISEASES CLASSIFICATIONCLASSIFICATION INTRA EPITHELIAL VESICLESINTRA EPITHELIAL VESICLES: The lesion is formed: The lesion is formed within the epitheliumwithin the epithelium Acantholytic vesicles :Acantholytic vesicles : This is because of the breakThis is because of the break down of specialized attachments called thedown of specialized attachments called the desmosomesdesmosomes Nonacantholytic vesiclesNonacantholytic vesicles: It is usually in the viral: It is usually in the viral infections because of the death or the rupture of theinfections because of the death or the rupture of the group of cells.group of cells. SUB EPITHELIAL VESICLESSUB EPITHELIAL VESICLES: Lesions formed between the: Lesions formed between the epithelium and the lamina propria eg:epithelium and the lamina propria eg: Erthyma multifomeErthyma multifome PhempegoidPhempegoid Dermatitis herpetiformisDermatitis herpetiformis Epidermolysis bullosaEpidermolysis bullosa
  4. 4. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS Autoimmune disease.Autoimmune disease. Common in Ashkenazi and Mediterranean jews .Common in Ashkenazi and Mediterranean jews . Middle aged females.Middle aged females. Other variants are:Other variants are: Pemphius VegitansPemphius Vegitans Pemphigus Foliaceus & ErthematosusPemphigus Foliaceus & Erthematosus Paraneoplastic pemphigus.Paraneoplastic pemphigus.
  5. 5. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS CLINICAL FEATURES:CLINICAL FEATURES: Painful ulcers or bulla are formed which are fluidPainful ulcers or bulla are formed which are fluid filled.filled. They can be formed any where in the oral cavity .They can be formed any where in the oral cavity . The bulla is rapidly ruptured leaving a collapsed roofThe bulla is rapidly ruptured leaving a collapsed roof of grayish membrane with a red ulcerated base.Theof grayish membrane with a red ulcerated base.The ulcer may look like an apthous ulcer or may be largeulcer may look like an apthous ulcer or may be large map shaped.map shaped. Nikolsky sign is positive.Nikolsky sign is positive. C/F con…dC/F con…d
  6. 6. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS Some time the ulcers are joined together to make aSome time the ulcers are joined together to make a confluence this condition is very painful.confluence this condition is very painful. It has a variable course might involve skin,It has a variable course might involve skin, oesophagus, cervix.oesophagus, cervix. Protein/fluid,electrolyte and weight loss /secondaryProtein/fluid,electrolyte and weight loss /secondary infections.infections. Fatal if untreated.Fatal if untreated.
  7. 7. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
  8. 8. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS PATHOGENESIS:PATHOGENESIS: It is an autoimmune diseaseIt is an autoimmune disease There are circulating antibodies of type IgG.There are circulating antibodies of type IgG. These antibodies are reactive against theThese antibodies are reactive against the desmosomes or the tonofilament complex.desmosomes or the tonofilament complex. There destruction or disruption of theseThere destruction or disruption of these tonofilament complex ,resulting in the loss oftonofilament complex ,resulting in the loss of attachment from cell to cellattachment from cell to cell path.cont…dpath.cont…d
  9. 9. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS The epithelial damage is directly proportion toThe epithelial damage is directly proportion to the number of the circulating antibobies.the number of the circulating antibobies. The tonofilament or desmosomes are disruptedThe tonofilament or desmosomes are disrupted by a proteolytic enzyme which is released byby a proteolytic enzyme which is released by these antibodies .these antibodies . The cell to cell break down also takes placeThe cell to cell break down also takes place through a complement system but this processthrough a complement system but this process is not clearly understood .is not clearly understood .
  10. 10. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS
  11. 11. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS HISTOPATHOLOGY:HISTOPATHOLOGY: Intra epithelial vesicles or bulla and cleft like spacesIntra epithelial vesicles or bulla and cleft like spaces are produced by acantolysisare produced by acantolysis These changes are in the stratum spinosum or theThese changes are in the stratum spinosum or the prickle cell layerprickle cell layer The basal cell remain attach to the lamina propriaThe basal cell remain attach to the lamina propria and project into the bulla like tombstones.and project into the bulla like tombstones. Inflammatory cells are very scanty howeverInflammatory cells are very scanty however eosinophils may be seen.eosinophils may be seen. Acantholytic statum spinosum cells occur singly orAcantholytic statum spinosum cells occur singly or are in the forms of clumps lying freely within theare in the forms of clumps lying freely within the blister fluid. These cell loose there polyhedralblister fluid. These cell loose there polyhedral morphology rather they are small rounded andmorphology rather they are small rounded and contain hyper chromatic nuclei called the TAZANKcontain hyper chromatic nuclei called the TAZANK CELLS.CELLS.
  12. 12. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS histologyhistology
  13. 13. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS histologyhistology
  14. 14. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS tazank cellstazank cells
  15. 15. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS immunoflorecenceimmunoflorecence
  16. 16. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS DIFFRENTIAL DIAGNOSIS:DIFFRENTIAL DIAGNOSIS: PempegiodPempegiod Erthema multiformeErthema multiforme Bullous lichen plannusBullous lichen plannus
  17. 17. PEMPHIGUS VULGARISPEMPHIGUS VULGARIS TREATMENT:TREATMENT: High mortality rates previouslyHigh mortality rates previously Introduction of systemic corticosteroidsIntroduction of systemic corticosteroids like prednisolone in stable cases.like prednisolone in stable cases. Prednisolone plus azathioprinePrednisolone plus azathioprine methotrexate and cyclophospamide inmethotrexate and cyclophospamide in progressed or advance cases.progressed or advance cases.
  18. 18. PEMPHGOIDPEMPHGOID
  19. 19. PEMPHGOIDPEMPHGOID Mucous membrane pemphigoidMucous membrane pemphigoid (cicatricial) CIKA-TRI-CIAL(cicatricial) CIKA-TRI-CIAL Bullous pemphigoidBullous pemphigoid
  20. 20. PEMPHGOIDPEMPHGOID PATHOLOGYPATHOLOGY Autoimmune diseaseAutoimmune disease Not life threateningNot life threatening Elderly females above 60 yrs of ageElderly females above 60 yrs of age Loss of attachment and separation of full thicknessLoss of attachment and separation of full thickness epithelium from the lamina propria.epithelium from the lamina propria. Alteration of rete pegsAlteration of rete pegs Epithelium forms the roof of the blistersEpithelium forms the roof of the blisters Auto antibodies are formed against theAuto antibodies are formed against the hemidesmosomes (BPAG-1,230kd;BPAG-2; 180kd.hemidesmosomes (BPAG-1,230kd;BPAG-2; 180kd. InflammatoryInflammatory cells(lymphocytes,neutrophils,eosinophils)are seencells(lymphocytes,neutrophils,eosinophils)are seen in the later stagesin the later stages
  21. 21. PEMPHGOIDPEMPHGOID
  22. 22. PEMPHGOIDPEMPHGOID CLINICAL FEATURES(MMP)CLINICAL FEATURES(MMP) Oral mucosa is the first site- lesions are rarelyOral mucosa is the first site- lesions are rarely wide spreadwide spread Subepithelial bullae, ruptured in the later stages.Subepithelial bullae, ruptured in the later stages. Bleeding in the bullae – bleeding blistersBleeding in the bullae – bleeding blisters Slow progress, skin involvement absent or rareSlow progress, skin involvement absent or rare Involvement of eyes, nose larynx, pharynx andInvolvement of eyes, nose larynx, pharynx and osephaghusosephaghus Nikolsky sign is positiveNikolsky sign is positive
  23. 23. PEMPHGOIDPEMPHGOID occular involvementoccular involvement
  24. 24. PEMPHGOIDPEMPHGOID CASCADEOF EVENTSCASCADEOF EVENTS Antibody antigen complexAntibody antigen complex ↓↓ Complement activationComplement activation ↓↓ Neutrophils & Eosinophils recruitedNeutrophils & Eosinophils recruited ↓↓ Release of proteases by the recruited cellsRelease of proteases by the recruited cells ↓↓ Sub epithelial blister formationSub epithelial blister formation
  25. 25. PEMPHGOIDPEMPHGOID
  26. 26. PEMPHGOIDPEMPHGOID MANAGEMENTMANAGEMENT Confirm diagnosisConfirm diagnosis Topical corticosteroidsTopical corticosteroids Ocular involvement –systemic steroids.Ocular involvement –systemic steroids.
  27. 27. ERYTEMAERYTEMA MULTIFORMEMULTIFORME
  28. 28. ERYTEMA MULTIFORMEERYTEMA MULTIFORME Mucocutaneous diseaseMucocutaneous disease Males adolosents , young adults areMales adolosents , young adults are affected moreaffected more
  29. 29. ERYTEMA MULTIFORMEERYTEMA MULTIFORME AETIOLOGY /PATHOLOGYAETIOLOGY /PATHOLOGY Unclear aetiology and pathogenesisUnclear aetiology and pathogenesis Infections like HSV can trigger thisInfections like HSV can trigger this diseasedisease Drugs like Sulphonamides ,barbituratesDrugs like Sulphonamides ,barbiturates Suggested cause is also given as to aSuggested cause is also given as to a type III hypersensitivity reactiontype III hypersensitivity reaction
  30. 30. ERYTEMA MULTIFORMEERYTEMA MULTIFORME CLINICAL FEATURESCLINICAL FEATURES Prodomal signs:Prodomal signs: Upper respiratory infectionUpper respiratory infection Headache and malaiseHeadache and malaise Nausea and arthralgiaNausea and arthralgia C/Fcont…dC/Fcont…d
  31. 31. ERYTEMA MULTIFORMEERYTEMA MULTIFORME Signs during the disease:Signs during the disease: Red macules – 1cm or more in diameter withRed macules – 1cm or more in diameter with cyanotic centercyanotic center Lips grossly swollen ,split crusted bleedingLips grossly swollen ,split crusted bleeding Widespread fibrin covered erosions andWidespread fibrin covered erosions and erythema in the mouth.erythema in the mouth. Mild feverMild fever Conjunctivitis may be associatedConjunctivitis may be associated Attacks recur at the intervals of several monthsAttacks recur at the intervals of several months Usually self limiting.Usually self limiting.
  32. 32. ERYTEMA MULTIFORMEERYTEMA MULTIFORME
  33. 33. ERYTEMA MULTIFORMEERYTEMA MULTIFORME HISTOPATHOLOGYHISTOPATHOLOGY Necrosis of the kertinocytesNecrosis of the kertinocytes Inter & intra cellular odema.Inter & intra cellular odema. Subepithelial blisters are commonSubepithelial blisters are common Infiltration of inflammatory cells.Infiltration of inflammatory cells.
  34. 34. ERYTEMA MULTIFORMEERYTEMA MULTIFORME
  35. 35. ERYTEMA MULTIFORMEERYTEMA MULTIFORME MANAGEMENTMANAGEMENT No specific treatment required , if HSV inf..No specific treatment required , if HSV inf.. acycoviracycovir Systemic steroids may give relief to theSystemic steroids may give relief to the fever.fever. In severe cases antibiotics are used toIn severe cases antibiotics are used to prevent ant secondary infections.prevent ant secondary infections. Symptomatic –analgesics, antipyretics,Symptomatic –analgesics, antipyretics, antihistamines.antihistamines.
  36. 36. EPIDERMOLYSISEPIDERMOLYSIS BULLOSABULLOSA
  37. 37. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA Definition:Definition: A large group of clinically similarA large group of clinically similar desquamating disease processes of thedesquamating disease processes of the skin and mucosa that have in common theskin and mucosa that have in common the separation of the epithelium from theseparation of the epithelium from the underlying connective tissue and theunderlying connective tissue and the formation of large blisters that frequentlyformation of large blisters that frequently result in extensive and often immobilizingresult in extensive and often immobilizing scar formation.scar formation.
  38. 38. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA MAJOR CATEGORIES OF EPIDERMOLYSIS BULLOSAMAJOR CATEGORIES OF EPIDERMOLYSIS BULLOSA TypeType Genetic PatternGenetic Pattern Separation LevelSeparation LevelDefec. StructureDefec. Structure HereditaryHereditary SimplexSimplex Autosomal dominant IntraepithelialAutosomal dominant Intraepithelial linking proteinslinking proteins JunctionalJunctional autosomal recessive lamina lucidaautosomal recessive lamina lucida anchoring filamentsanchoring filaments DystrophicDystrophic autosomal dominant sublamina densaautosomal dominant sublamina densa type VII collagentype VII collagen AcquiredAcquired AcquisitaAcquisita None/autoimmune sublamina densaNone/autoimmune sublamina densa type VII collagentype VII collagen
  39. 39. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA HEREDITARY TYPES:HEREDITARY TYPES: Congenital absence of componentsCongenital absence of components ACQUIRED TYPES:ACQUIRED TYPES: Autoantibodies (IgG; sometimes IgA) toAutoantibodies (IgG; sometimes IgA) to type VII collagen.type VII collagen.
  40. 40. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
  41. 41. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA CLINICAL FEATURESCLINICAL FEATURES 1.1.Epidermolysis Bullosa SimplexEpidermolysis Bullosa Simplex Mild form; autosomal dominantMild form; autosomal dominant Sites of trauma/frictionSites of trauma/friction Involve hands, feet and neck; occ. kneesInvolve hands, feet and neck; occ. knees and elbowsand elbows Teeth not affected; intraoral blisters seenTeeth not affected; intraoral blisters seen Appears during infancyAppears during infancy
  42. 42. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
  43. 43. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA 2.2. Junctional Epidermolysis BullosaJunctional Epidermolysis Bullosa Severe form; autosomal recessiveSevere form; autosomal recessive Haemorrhagic blisters; loss of nails, largeHaemorrhagic blisters; loss of nails, large blisters of face, trunk and extremitiesblisters of face, trunk and extremities Generalized scarring and atrophyGeneralized scarring and atrophy Intraorally-haemorrhagic blisters of palate,Intraorally-haemorrhagic blisters of palate, perioral and perinasal areasperioral and perinasal areas Erupted teeth exhibit hypoplastic and severelyErupted teeth exhibit hypoplastic and severely pitted enamel prone to cariespitted enamel prone to caries
  44. 44. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA 3.3. Dystrophic Epidermolysis BullosaDystrophic Epidermolysis Bullosa Both autosomal dominant and recessive; recessive isBoth autosomal dominant and recessive; recessive is severesevere Lesions are birth; arise at pressure sitesLesions are birth; arise at pressure sites Blisters rupture leaving painful ulcers which heal withBlisters rupture leaving painful ulcers which heal with large scars that undergo contractures, leading to loss oflarge scars that undergo contractures, leading to loss of motility and claw-like hands (Mitten Deformity)motility and claw-like hands (Mitten Deformity) Teeth exhibit delayed eruption and enamel hypoplasiaTeeth exhibit delayed eruption and enamel hypoplasia with rapid caries developmentwith rapid caries development Scarring around mouth leads to diminished opening,Scarring around mouth leads to diminished opening, ankyloglossiaankyloglossia
  45. 45. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA Epidermolysis Bullosa AcquisitaEpidermolysis Bullosa Acquisita Non-hereditary form; appears in adulthoodNon-hereditary form; appears in adulthood Clinically resembles autosomal dominantClinically resembles autosomal dominant type of JEB-type VII collagentype of JEB-type VII collagen Trauma/friction induced blisters of knees,Trauma/friction induced blisters of knees, elbows, hands and feet- heal with scarselbows, hands and feet- heal with scars Intraoral blisters rare- when present sameIntraoral blisters rare- when present same picture same picture as JEBpicture same picture as JEB
  46. 46. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA HISTOPATHOLOGYHISTOPATHOLOGY Simplex type exhibits zone of cleavageSimplex type exhibits zone of cleavage (intra-epithelial) above basal cell layer.(intra-epithelial) above basal cell layer. Remaining types have sub-epithelialRemaining types have sub-epithelial separationseparation
  47. 47. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA
  48. 48. EPIDERMOLYSIS BULLOSAEPIDERMOLYSIS BULLOSA MANAGEMENTMANAGEMENT No specific treatment available for hereditaryNo specific treatment available for hereditary typestypes Acquired form maybe treated withAcquired form maybe treated with corticosteroids and immuno-suppressantscorticosteroids and immuno-suppressants Maintenance of pt’s nutritional and oral hygieneMaintenance of pt’s nutritional and oral hygiene statusstatus Wound healing techniquesWound healing techniques Prevention of infectionsPrevention of infections Systemic use of Phenytoin (also acts as aSystemic use of Phenytoin (also acts as a collagenase inhibitor)collagenase inhibitor)
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