The synovium lines joints and produces synovial fluid. It contains two cell types and secretes hyaluronic acid. Synovial fluid contains water, proteins, and nutrients. The two main types of crystal synovitis are gout caused by monosodium urate crystals typically in the big toe, and pseudogout caused by calcium pyrophosphate crystals usually in large joints like the knee. Both involve crystal deposition in the synovium and similar acute inflammatory attacks. Risk factors, investigations, and treatments aim to reduce crystal levels and attack frequency or progression. Complications can include joint damage and renal problems if untreated.

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.

5. 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.

6. 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.

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

8.  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.

9. FUNCTIONS OF SYNOVIAL FLUID
Hold joints together.
Lubrication.
Cushions.
Nourishes.

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

11. Gout

12. 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.

13. INCIDENCE
0.3/1000 population.

14. AGE
Men –after mid twenties.
Women –after menopause.

15. 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

16. 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.

17.  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.

18. 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.

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

21.  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.

22. INVESTIGATIONS
o 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.

23.  * 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.

24.  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.

25.  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.

27.  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.

29. 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.

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

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

32. 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.

33.  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.

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

35. PSEUDOGOUT(PYROPHOSPHATE
ARTHROPATHY)/ CHONDROCALCINOSIS

36.  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.

37. 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

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

39.  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.

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

41. 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.

42. DIFFERENTIAL DIAGNOSIS
 Acute gout
 Septic arthritis
 Osteoarthritis
 Rheumatoid arthritis

43.  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.

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

45. Thank
you