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Lupus erythematosus


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Muco-cutaneous lesion of Oral Cavity, Red lesion of Oral Cavity, Autoimmune disorder

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Lupus erythematosus

  1. 1. LUPUS ERYTHEMATOSUS Dr. Deepak K. Gupta
  2. 2. LUPUS ERYTHEMATOSUS • Lupus erythematosus (LE) may be seen in one of two well-recognized forms • Systemic (acute) lupus erythematosus (SLE) – profound impact it has on many organs • Discoid (chronic) lupus erythematosus (DLE) – chronic and localised skin lesions – involving the bridge of nose and adjacent cheeks – Without any systemic manifestations. – Rarely, discoid form may develop into disseminated form.
  3. 3. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) • Autoimmune disease characterized by autoantibodies, immune complex formation, and immune dysregulation resulting in damage to – Essentially any organ, including the kidney, – skin, – blood cells, – CNS • Natural history of this illness is unpredictable • Early diagnosis and careful treatment - improved the prognosis
  4. 4. Etiology • Specific cause of SLE remain undefined • Both cell mediated Immunity and Humoral mediated • Many factors, including genetics, hormones, and the environment • Tissue damage due to direct binding and/or immune complex deposition in tissues • Autoantibodies against DNA, other nuclear antigens, ribosomes, platelets, erythrocytes, leukocytes, and other tissue-specific antigen – result in widespread tissue damage
  5. 5. Clinical Features • Serious cutaneous-systemic disorder • Repeated remissions and exacerbations. • Peak age of onset: 30 years in females but about 40 years in males • Female predicted: 8 to 10 times more • Erythematous patches: Butterfly Rash – on the face which coalesce to form a roughly symmetrical pattern over the cheeks – and across the bridge of the nose
  6. 6. Clinical Features • neck, upper arms, shoulders and fingers may also be involved • Itching or burning sensations • Hyperpigmentation • severity is intensified by exposure to sunlight • Involvement of various organs, including the kidney and heart
  7. 7. Systemic Lupus Erythematosus (SLE)
  8. 8. Clinical Features • Kidney – fibrinoid thickening of glomerular capillaries – wire loops – Progressive thickening may lead to renal insufficiency • Heart: Libman-Sacks endocarditis – Involves valves, as well as fibrinoid degeneration of the epicardium and myocardium • Collagen diseases: widespread tissue involvement and the nature of the lesions have led to the inclusion of this disease • Rheumatic fever, • Rheumatoid arthritis, • Polyarteritis nodosa, • Scleroderma • Dermatomyositis
  9. 9. SLE: Clinical Feature
  10. 10. Oral Manifestations • 20–50% of cases of DLE, slightly more frequently in SLE • Oral mucosa may be involved prior to skin manifestation or later or even in its absence • Oral Lesions of SLE and DLE are similar in nature except in SLE there is more severity of – hyperemia, edema and extension of the lesions – tendency for bleeding, petechiae and superficial ulcerations
  11. 11. Oral Manifestations • It may be associated with oral candidiasis as well as xerostomia. • Diagnosis should not be based on oral findings alone – clinical findings frequently simulate other diseases, chiefly leukoplakia and lichen planus • Lesions usually affect the palate, buccal mucosa, and gingivae • Sometimes they appear as lichenoid reaction • It may also involve vermilion zone of the lower lip lupus cheilitis • Varying degrees of ulceration, pain, erythema, and hyperkeratosis may be present
  12. 12. Oral Manifestations
  13. 13. Chronic cutaneous lupus erythematosus
  14. 14. Histologic Features • Histologic features of SLE and DLE: similar • Just an increase of degree of certain of the findings in SLE occurs • Common findings are – hyperkeratosis with keratotic plugging, – atrophy of the rete pegs, – liquefaction, degeneration of the basal layer of cells, – perivascular infiltration of lymphocytes – Basophilic degeneration of collagen and elastic fibers, – Hyalinization, edema and fibrinoid change, particularly prominent immediately beneath the epithelium
  15. 15. Histologic Features Low-power: hyperparakeratosis with interface mucositis and perivascular inflammation. High-power: interface mucositis
  16. 16. Histologic Features • In SLE – degenerative features and collagen disturbance are usually more prominent – Inflammatory features less severe – Hydropic degeneration and liquefaction necrosis of the basal cell layer – subepithelial vesiculation or ulceration
  17. 17. Histologic Features: Direct Immunofluorescent Testing • Confirm a suspected diagnosis of LE • Detect the presence of immunoglobulins (IgG, IgM and IgA) at the epidermal-dermal junction or basement membrane zone of skin or oral mucosa of patient • 100 % systemic form and in nearly 75% with the discoid form • Incidence of complement C3 and of fibrinogen • Demonstrated in the uninvolved skin and mucosa of a significant percentage of patients with SLE
  18. 18. Laboratory Findings • Raised ESR and CRP : elevated in inflammation from any cause. • Serum protein electrophoresis : increased gammaglobulin and decreased albumin. • Routine blood counts: anemia and low platelet and white cell counts. • Routine blood chemistry which may reveal: – Kidney involvement: increases in serum blood urea nitrogen and creatinine – Liver function tests: AST, ALT, BUN, creatinine – Muscle involvement: Increased muscle enzymes (such as CPK)
  19. 19. Laboratory Findings: Specific • Commonly used blood tests in the diagnosis of SLE are • Antinuclear antibody test (ANA): autoantibodies to cell nuclei are present in the blood • Anti-DNA antibody test: antibodies to the genetic material in the cell • Anti-Sm antibody test: antibodies to Sm (ribonucleoprotein) found in the cell nucleus • Serum (blood) complement test: total level of a group of proteins which can be consumed in immune reactions • Complement proteins C3 and C4: examine specific levels
  20. 20. Laboratory Findings: Specific
  21. 21. Treatment • Careful and frequent clinical and laboratory evaluation – Decide adequate medical regimen – Provide prompt recognition and treatment of disease flare • Lifelong illness, and patients must be monitored indefinitely • high-risk disease: possibility of end-organ damage to any organ • Decreased quality of life
  22. 22. Treatment • Avoid excessive sunlight exposure • DLE – topical corticosteroids – If resistant to topical therapy: systemic antimalarial drugs or low-dose thalidomide, sulfones • SLE – nonsteroidal antiinflammatory drugs (NSAIDs) combined with antimalarial drugs, such as hydroxychloroquine – Severe, acute episodes: systemic corticosteroids combined with other immunosuppressive agents.
  23. 23. Prognosis • SLE patient prognosis is variable – 5-year survival rate: approx. 82% to 90%; – 20 years survival rate: 63% to 75% – Prognosis depends on which organs are affected and how frequently the disease is reactivated – Common cause of death is renal failure – Chronic immunosuppression also predisposes these patients to increased mortality – Prognosis is worse for men than for women • Transformation to SLE may be seen in approximately 5% of DLE patients – 50% of DLE patients - eventually resolves after several years
  24. 24. Refrences • Shafers, Oral Pathology 6th edition • Regezi: Oral Pathology: Clinical Pathologic Correlations, 5th ed • Essential of Oral Pathology and medicine 7th ed : Cawsons & odell • Color atlas of Oral Pathology: Nevile • Pathology of the Head and Neck: Antonio Cardesa, Pieter J. Slootweg • Essential of Oral Pathology : Swapan Kumar Purkait
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