Synovium & crystal synovitis

1. SYNOVIUM & CRYSTAL SYNOVITIS

2. SYNOVIUM Differentiates from the mesenchymal tissue around the articular disc Clears the articular surface by the fifth month in utero .

3. HISTOLOGY Fatty, fibrofatty , or fibrous and contains type1 and 3 collagen. Two types of cells- type A- macrophages like phagocytic cells and type B- resemble fibroblasts. Responsible for the secretion of hyaluronic acid and protein.

4. Subsynovial tissue contains macrophages and fibroblasts and precursors of the synovial cells,which give rise to the new membrane after synovectomy . Rich in vascular plexus and lymphatics .

5. SYNOVIAL FLUID Clear viscous yellow fluid which does not clot on standing (no fibrinogen). Knee joint-0.5ml of fluid. Viscosity depends on conc of hyaluronic acid. Lowered in ageing,osteoarthritis,and trauma. 96% water and 4%solutes with a specific gravity of 1.010 and a ph of 7.3-7.6. Reduced in osteoarthritis and after trauma.

6. Proteins are present in lower conc than in plasma. Albumin is the major protein(2/3 rd ) and others are alpha2-macroglobulin,lipoproteins, and IgM .

7. In an inflamed synovium protein content increases. In severly inflamed joints protein is similar to that in serum. Clots due to significant increase in fibrinogen.

8. FUNCTIONS OF SYNOVIAL FLUID Hold joints together. Lubrication. Cushions. Nourishes.

9. CRYSTAL SYNOVITIS Mainly two types. Monosodium urate crystals- gout. Calcium pyrophosphate crystals- pseudogout .

10. Gout

11. GOUT(Monosodium urate arthropathy ) a/c or c/c. Sites- monoarticular , first metatarsophalangeal joint. Ankle,knee,wrist,fingers and elbow. Distal and lower extremity joints are involved more often.

12. I ncidence 0.3/1000 population.

13. Age Men –after mid twenties. Women –after menopause.

14. RISK FACTORS Male sex * Meat * Seafood * Alcohol (10 or more grams per day) * Diuretics * Obesity * Hypertension * Coronary heart disease * Diabetes mellitus * Chronic renal failure * High triglycerides

15. Pathology It affects both upper and lower limbs with acute attacks. Less often it presents with painful, tophaceous deposits (± discharge) in Heberden's and Bouchard's nodes. * Most patients with hyperuricaemia never develop gout and gouty patients may not have hyperuricaemia at presentation. * Patients can be over- excreters of uric acid, normo-excreters or under- excreters . * Most cases of primary gout are due to undersecretion . * Fewer than 10% are due to overproduction.

16. a/c- ingestion of microcrystals of urate by neutrophils and release lysosomal enzymes. Solubility of urate in body fluids increases deposits accumulate. Plasma uric acid level lowers and deposits go into solutions.

17. CLINICAL FEATURES Pain , swelling,tenderness and increased temp of the first metatarsophalangeal joint. Attacks can be provoked by surgery,trauma . Mild attacks resolve with in 2 days. More severe attacks take 7 to 10 days to resolve.

18. Two extremities. Obese,alcoholic with family history of gout and no tophi . Old,frail,taking thiazide diuretics and with tophi .

19. Tophi can occur in long standing cases of gout. 10% cases kidney may be affected. HTN and c/c renal failure. Renal stones can occur in 10% cases. Renal disease is the major cause of death in gout.

20. INVESTIGATIONS typical presentations such as inflammation of the first metatarsophalangeal joint (also known as podagra ) with hyperuricaemia . * Demonstration of monosodium urate (MSU) crystals in synovial fluid or tophi confirms the diagnosis of gout. * Since gout can present atypically examine all samples of synovial fluid aspirated from joints for MSU crystals, even if not inflamed at the time. * Gram staining and culture of synovial fluid should be done, even if MSU crystals are found, since gout and sepsis can co-exist. * Fasting glucose and lipids should be performed to rule out hyperglycaemia and hyperlipidaemia as gout is commonly associated with metabolic syndrome.

21. * Renal uric acid secretion (as detected by a 24-hour urine sample) helpful in diagnosis, in patients with a family history of young onset gout, patients whose first attack of gout was under the age of 25, and patients with renal stones. Such patients are likely to be over- excreters of uric acid.

22. Although a raised serum uric acid level is an important risk factor for gout, the use of serum uric acid as a diagnostic test is limited. It can be normal during acute gout, whilst patients with hyperuricaemia may never develop an attack. Studies suggest that the cut-off point above which a level can be considered raised is 360 µmol/l.

23. Radiographs may be useful in chronic gout, when punched out lesions, areas of sclerosis and, in the latter stages, tophi may be seen. The first lesions usually occur in and around the first metatarsophalangeal joint. CT scanning may be helpful in less accessible areas.

24. Urate crystals can be identified using polarising microscope and are found as needle-shaped crystals inside neutrophils . Distinguished from calcium pyrophosphate crystals – pleomorphic and show weak positive birefringes .

25. TREATMENT INDOMETHACIN(200mg/day). Ideally pt should have only one attack of gout. It can be achieved by xanthine oxidase inhibitor( allopurinol 300mg/day). Dose is according to serial plasma uric acid level. First 3 months add a small dose of indomethacin to prevent a/c attacks.

26. Aspiration of affected joint and intra- articular steroid injection terminates a/c attack.

27. In those are at risk of renal stones, necessary to ensure that they pass large amount of alkaline urine.

28. COMPLICATIONS Renal disease Renal colic . Chronic urate nephropathy results from widespread deposition of urate crystals in the interstitium of medulla and pyramids causing inflammation and fibrosis. End stage renal failure occurs in up to 25% of cases of untreated chronic tophaceous gout.

29. Gout patients who have a 24-hour urinary excretion of uric acid above 1100 mg have a 50% risk of developing urate and oxalate kidney stones. Those with a measured urate excretion greater than 800 mg per 24 hours may benefit from allopurinol prophylaxis to prevent urate nephropathy.

30. * Severe degenerative arthritis * Secondary infections * Recurrent painful episodes * Carpal tunnel syndrome (rare) * Nerve or spinal cord impingement

31. PSEUDOGOUT(Pyrophosphate arthropathy )/ chondrocalcinosis

32. Deposition of calcium pyrophosphate dihydrate . Pathology is similar to that of gout. Large joints-knee. Severe pain,swelling , low grade temp over 24-48hrs. Associated with hyperparathyroidism,haemochromatosis and gout.

33. PRECIPITATING FACTORS Dehydration Intercurrent illness Hyperparathyroidism Long-term use of steroids Hypothyroidism Any cause of arthritis Haemochromatosis Wilson's disease Acromegaly Dialysis Surgery or trauma

34. INVESTIGATION Crystals have got a characteristic appearance under polarising microscope with weak birefringes . Radiograph shows calcification in both fibro and hyaline cartilage.

35. Ultrasound may also be a useful diagnostic tool. Aspiration of the joint fluid: raised white cell count which is predominantly neutrophils . Glucose levels usually are normal. The joint fluid often looks purulent and septic arthritis must be excluded.

36. MANAGEMENT Joint aspiration and instillation of local steroid. Indomethacin and phenylbutazone to control a/c attacks $ prevent recurrence.

37. PROGNOSIS Acute attacks usually resolve within 10 days. Some patients develop progressive joint damage with functional limitation. Prognosis will also be dependent on any underlying cause.

38. DIFFERENTIAL DIAGNOSIS Acute gout Septic arthritis Osteoarthritis Rheumatoid arthritis

39. Hydroxyapatite crystals can seen ageing joints, synovial fluid or peritendonitis tissue. Can be stained by alizarin red 5. Whether they cause disease or result from a joint disease is not known. Some described in joints rapidly being destroyed.

40. In shoulder it is called milwaukee shoulder. It is due to discharge of the apatite crystal into the joints from the periarticular tissues.

41. Thank you