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Crystal associated arthropathies
This document discusses various types of crystal-associated arthropathies including: - Monosodium urate monohydrate crystals which cause gout. Gout typically affects middle-aged males and causes painful inflammation in joints. - Calcium pyrophosphate dihydrate crystals which cause pseudogout/chondrocalcinosis. This tends to affect the elderly and can mimic many other joint diseases. - Calcium-containing crystals like hydroxyapatite which are associated with aging, osteoarthritis, and renal disease and can cause acute attacks of inflammation.
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Crystal associated arthropathies
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- 2. Crystalline particles injoint disease • Intrinsic • Monosodium urate monohydrate (Gout) • Calcium pyrophosphate dihydrate (Pseudogout) • Calcium phosphates • • Basic—hydroxyapatite, octacalcium phosphate, tricalcium phosphate • • Acidic—brushite, monetite • Calcium oxalate • Lipids • Cholesterol • Lipid liquid crystals • Charcot–Leyden (phospholipase) crystals • Cystine • Xanthine, hypoxanthine • Protein precipitates (e.g. cryoglobulins) • Extrinsic • Synthetic corticosteroids • Plant thorns (semicrystalloid cellulose), especially blackthorn, rose, dried palm fronds • Sea urchin spines (crystalline calcium carbonate) • Methylmethacrylate
- 3. COMMON DISEASES • Gout •Monosodium urate monohydrate • Pseudogout or Chondrocalcinosis • Calcium pyrophosphate dihydrate • Basic calcium phosphate • Hydroxyapatite • Calcium oxalate
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- 5. GOUT • Metabolic disease •↑ Body pool of urate • Hyperuricemia • Monosodium urate monohydrate deposition • Joints • Connective tissue • Kidney interstitium • Uric acid nephrolithiasis
- 6. GOUT • Affects:- • Middleaged to elderly males • Postmenopausal women • Precipitants:- • Purine rich foods • Alcohol intake • Trauma, surgery • Hypouricemic drugs • Serious illness – MI, stroke
- 7. GOUT RISK FACTORS •Primary:- • Hyperuricemia • Male sex • Hypertension • Obesity • Insulin resistance • Metabolic syndrome • Alcohol • Purine rich diet • ↓ uric acid excretion • Secondary:- • Diuretics • CKD • Osteoarthritis • Chronic renal failure • Lead poisoning (rare) • Ciclosporin (rare) • Myeloproliferative disorders (rare)
- 8. GOUT PHASES 1) Asymptomatichyperuricemia 2) Acute gout • Single peripheral joint – 50% podagra (big toe) • Midtarsal, ankle, knee, small hand joints, wrist, elbow • Swollen, red, hot, shiny, tender joint 3) Intercritical gout • Repeated attacks • Turns chronic by 10 years 4) Chronic tophaceous gout • Tophi – large crystal deposits • Irregular firm nodule • Joint deformity & damage • Associated – Uric acid stones, c/c urate nephropathy
- 10. GOUT • Diagnosis:- • Synovialfluid aspirate / tophi • Birefringent crystals – polarized light • Radiological:- • Soft tissue swelling • Cystic changes • Erosion of articular surfaces • Sclerotic margins
- 11. GOUT TREATMENT • ↓inflammation:- • NSAIDs • Colchicine low dose • Joint aspiration • Steroids – intra-articular, systemic • Icepacks • Long term:- • Lifestyle modification • Avoid alcohol • Avoid purine rich foods • Weight reduction • Urate lowering • Allopurinol, febuxostat • Uricosuric + Fluid intake + Alkalinization • Probenecid , sulfinpyrazone
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- 13. CPPD DEPOSITION • Elderly- •65-75 years = 10-15% • >85 years = 30-50% • Cause – uncertain • ↑ ATP degradation to adenosine+pyrophosphate • ↑ Extracellular pyrophosphate transport (genetic mutation) • Calcium pyrophosphate formed and deposited • Crystals phagocytosed (monocytes, macrophages, neutrophils) • Inflammation • Destruction
- 14. CPPD DEPOSITION • Associatedwith – • Aging • Disease-associated • Primary hyperparathyroidism • Hemochromatosis • Hypophosphatasia • Hypomagnesemia • Chronic gout • Postmeniscectomy • Gitelman's syndrome • Epiphyseal dysplasias
- 15. CPPD DEPOSITION CLINICAL •MC asymptomatic • A/c, sub a/c, c/c, a/c on c/c arthritis • Presentations mimic- • Gout – pseudogout • Osteoarthritis – atypical joints, age, progression • Neuropathic arthritis – severe destruction • Rheumatoid arthritis – symmetrical arthritis • Ankylosing spondylitis – IVD & lig flavum calcific, spine immobility • Spinal stenosis • Periarticular tophus-like nodule – very rare
- 16. CPPD DEPOSITION • Jointsinvolved- • MC knee • Wrist, shoulder, ankle, elbow, hand joints • Rarely TMJ, ligamentum flavum • Usually polyarticular • Mimic many others • Low grade fever • Precipitated by- • Trauma • Rapid ↓ serum calcium levels
- 17. CPPD DEPOSITION • Synovialfluid- • TC = 1000s to 100,000/mm3 • Definitive – • Rhomboid, square, rod-like crystals • Weak birefringent • Inside tissue fragments, clots, neutrophils • Radiographic- • Chondrocalcinosis • Punctate / linear opacities in cartilaginous tissue
- 18. CPPD DEPOSITION Rx •Acute • Joint aspiration • NSAIDs • Intra-articular steroids • Severe • Short course steroids • Anakinra – IL-1β antagonist • Prophylaxis • Daily low-dose colchicine • Advanced destruction • Joint replacement
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- 20. CA DEPOSITION • akaBasic calcium phosphate deposition disease • Deposition- • Dystrophic – damaged tissue • Metastatic – hypercalcemia • Unknown cause • CKD – hyperphosphatemia • Clinical course- • Recurrent acute attacks • Inflammation • Destructive arthropathy
- 21. CA DEPOSITION ASSOCIATIONS •Aging • Osteoarthritis • Hemorrhagic shoulder effusions in the elderly (Milwaukee shoulder) • Destructive arthropathy • Tendinitis, bursitis • Tumoral calcinosis (sporadic cases) • Disease-associated • Hyperparathyroidism • Milk-alkali syndrome • Renal failure/long-term dialysis • Connective tissue diseases (e.g., systemic sclerosis, idiopathicmyositis, SLE) • Heterotopic calcification after neurologic catastrophes (e.g., stroke, spinal cord injury) • Heredity • Bursitis, arthritis • Tumoral calcinosis • Fibrodysplasia ossificans progressiva
- 22. CA DEPOSITION • Periarticular/articulardeposits • Acute reversible inflammation • +/- chronic damage • Joint capsule, tendon, bursa, articular surface • Knee, shoulder, hip fingers • Presentations- • Asymptomatic radiographic changes • Acute synovitis, bursitis, tendinitis • Chronic destructive arthropathy
- 23. CA DEPOSITION • Synovialfluid- • Low TC <2000/mm3 • But dramatic symptoms • Crystal clumps • Individual crystals – electron micro, X-ray diffraction, IR spectroscopy • Crystal clumps – • 1-20 micrometre • Intra/extracellular • Nonbirefringent • Wright’s stain – purplish • Alizarin red – bright red • Radiographic- • Intra/peri-articular calcification • +/- erosive/destructive/hypertrophic changes
- 24. CA DEPOSITION Rx •Acute attacks- • May self limit by days to several weeks • Joint aspiration • NSAIDs • Colchicine • Intra/periarticular depot steroid • Renal failure- • Phosphate lowering agents • Severe destruction- • Joint replacement
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- 26. COD DISEASE • Primaryoxalosis- • Rare hereditary disorder • Enzyme defects • Hyperoxalemia – Ca oxalate crystal deposition • Nephrocalcinosis, renal failure, arthritis, periarthritis • Death by 20 years of age • Secondary- • Complication of ESRD • Pt on haemo/peritoneal dialysis • Ascorbic acid supplements • Visceral organs, blood vessels, bones, cartilages • Arthritis in CKD
- 27. COD DISEASE • Clinicalfeatures- • Mimics other crystal arthropathies • Rptd a/c attacks, later c/c • Bone, articular cartilage, synovium, periarticular tissues • Progressive joint destruction • Fingers, wrist, elbows, knees, ankles, feet • X-Ray- • Chondrocalcinosis, soft tissue calcification • Synovial fluid- • TC<2000/mm3 • Crystals- variable shape & birefringence • Characteristic- bipyramidal, strong birefringence • Alizarin red S stain positive
- 28. COD DISEASE • Treatment- •Medical mildly effective • Joint replacement in end-stage • Liver transplant for Primary oxalosis