lupus erythematosis

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  • 1.SMIJAL

2. Auto immune disorder characterised by tissuedestruction due to the deposition of auto antibody andimmune complexes with in it. Production of antinuclear antibody hallmark 3. Specific cause undefined. Researchers suggest that genetics, hormonesand environment contribute to the immunedisregulation in lupus. 4. Age of onset: 30 years in females &40 years inmales. Skin lesions : fixed erythematous lesions thathave a butterfly configuration over the cheeks& across the bridge of nose. Also affect neck,shoulders,upper arm &fingers. Produce itching & burning sensation & areas ofhaemorrhage which is intensified by sunlight. 5. Female to male prevalence ratio : 2:1 before puberty & 4:1 afterpuberty. Extensive loss of hair from scalp. Kidney : fibrinoid thickening of glomerular capillaries. Heart : fibrinoid degeneration of epicardium and myocardium &atypical endocarditis. SLE included under category of collagen desease. 6. Shows white hyperkeratotic plaque like areas &resemble lichen planus. Hyperemia,edema and extention of lesion is moreprominent in SLE than DLE. Bleeding, petechiae, & superfitial ulcerations arepresent , which are surrounded by a red halo. Vermilion border of lip is affected-lupus cheilitis. Xerostomia , altered taste sensation , chronicperiodontal desease etc are also reported. In some cases lesions under go malignanttransformation. 7. Collagen disturbance & degenerative features areprominent. Atrophy with hyperkeratinisation of the oralepithelium. Liquifactive degeneration of the basal cell layer. Lymphatic infiltration & fibrinoid degeneration ofthe collagen fibers Edema of sub epithelial CT with vasculardilatations. 8. Specific test was established with the discoveryof LE cell inclusion by Hargraves and hisassociates. Test : add blood serum from a person undersuspicion to the buffy coat of normal blood. If the patient is suffering from SLE , typical LEcells will develop. 9. Systemic steroid therapy. 10. Chronic , scarring ,atrophy producing ,photosensitive dermatosis. Not associated with autoantibody production. 11. Occurs in genetically predisposed individuals. Heat shock protein is induced in thekeratinocyte due to UV light exposure or stress& this protein act as target for T cell mediatedepidermal cell toxicity. 12. Occurs in third & fourth decades of life. More common in women. Common sites : oral mucous membrane, chest,back & extremities. Skin lesions of DLE also present a butterflydistribution over the molar region & across thenose. 13. On forceful removal of covering scale ,neumerous carpet track extensions of thepialo sebacious channels appear. Skin lesions enlarge at the periphery &epidermoid or basal cell carcinoma maydevelop from these lesions. Involvement of scalp with lose hair is alsocommon. 14. Reported in 20 -50 % cases of DLE. Begins as erythematous areas ,with outinduration & typically with white spots.superfitial, painful ulceration occur withbleeding. No scale formation on skin. Seen in buccal mucosa,tongue,palate &vermilion border of the lip. Tongue : atrophy of papillae & fissuring areseen. 15. Hyper ortho or parakeratinisation of the surfaceepithelium. Atrophied epithelium. Few lesions exhibit keratin plugging & achanthosis. Basophilic degeneration of the collagen. Inflammatory cell infiltration till CT. Vasculitis absent. 16. scleroderma/dermatosclerosis/hide bounddisease. Systemic CT disease charecterised byvasomotor disturbances, fibrosis, subsequentatrophy of the skin, SC tissue, muscles &internal organs with associated immunologicdisorder. 17. Blood circulation insufficiency in tissue due toabnormalities in arterioles & blood capillariescause replacement of the normal CT by thedense collagen bundles & result in fibrosis orsclerosis of the tissue. Genetic factors are also involved.(HLA B8,HLADR3,HLA DR5,HLA DR52M,HLA DQB2). Apoptosis and generation of free radicals arealso involved. 18. Age: common in 30 to 50 years of age. Sex: female to male ratio is 3-6:1. Begins on the face, hands, or trunk. Typical indurated oedema of the skin,neuralgia, paresthesia, arthritis, joint pain etcare present. Erythema present. 19. Skin: yellow , gray , or ivory white waxyappearance. Brown pigmentation of the skin is present as alate manifestation. Calcinosis cutis is seen in the affected area. Eyes become narrow. Skin becomes hardened & atrophied. So thatwrinkles do not form. It gives a mask - like appearance of face.Monalisa face. 20. restriction of muscle movements results infibrosis. Finally internal organs like GI tract, heart,lungs & kidney become affected by fibrosis. Crest syndrome is variant of systemic sclerosis.It includes the following components. 1.calcinosis.2. Raynauds phenomenon. 3.esophageal dysfunction. 4.scleroductyly. 5.tielangiectasia. 21. 1.localised/circumscribedscleroderma/morphea. One or more welldefined ,slightly elevated or depressedcutaneous patches . Lesions occur on the sidesof the chest & and the thighs. 2.generalised/diffuse form/linearscleroderma . Occur as linear bands or ribbonson the face. 22. Monalisa face.* Multiple telangiectatic spots on the facial skin & loss of facial esthetics and expression.* Pinched appearance of the face-mouse facies.* Trismus & restricted movements of the TMJ.* Pain, clicking sound & crepitations in TMJ.* Pursed lips & fish mouth.* Xerostomia due to atrophy of SG.* Trigeminal neuralgia. 23. Chicken tongue. Loosened teeth. Weakness of hands, decreasad TMJ mobility,decreased salivary secretion, decreased mouthopening etc lead to poor oral hygiene. 24. Widening & thickening of PDL space. Bone resorption at condyle or ramus ofmandible. Osteomyelitis. 25. Atrophied oral epithelium with flattening of reteridges. Thickening & hyalinisation of the collagen fibres inthe CT with atrophy of minor SGs. BVs become scanty & its lumen become narrow dueto perivascular fibrosis. PDL thickness increased due to increased synthesisof collagen & oxytalin fibres. Sweat glands, sebacious glands, & hair folliclesabsent. 26. No specific treatment.Systemic steroid therapy produces partialremission.


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