GOUT

Males 20: Females 1

Deposition of monosodium urate monohydrate crystals in minute clumps in connective tissue and cartilage

Remain inert for months, then maybe due to local trauma, they are dispersed into the joint and surrounding tissues where they excite an acute inflammatory reaction. Crystals may be phagocytosed by synovial cells and macrophages or float free in the joint. 

In time, urate deposits can build up in joints, periarticular tissues, tendons and bursae, resulting in tophi. (MTPJ, achilles tendon, olecranon bursa). These may ulcerate the skin and destroy cartilage and bone.

Primary          95% is an inherited overproduction or undersecretion of uric acid.
                      Attacks can be induced by alcohol, diuretics and salicylates.

Secondary     Increased uric acid production (Myeloproliferative) or undersecretion
                       (CRF)

Present with severe joint pain that may be spontaneous or after a trigger. MTP joint, ankle and fingers are the most common. Looks like a septic joint.

Uric acid levels not diagnostic.(Even if high).

Need to see NEGATIVELY birefringent urate crystals under polarized microscopy.

Chronic gout can produce joint erosions, esp. in the fingers. Tophi are seen on X-ray as punched-out cysts or deep erosions in the periarticular end of bones. These are larger and further always from the joint than RA.

Renal stones may occur.

Treat acute attacks with rest and NSAID’s. 

Colchicine can be used, may cause diarrhoea.

Can aspirate and inject hydrocortisone.

Prevent by avoiding alcohol, diuretics and aspirin. 

Can use Allopurinol. (Xanthine oxidase inhibitor). 

Tophi that ulcerate need curettage and are left open till they heal.

CALCIUM PYROPHOSPHATE DIHYDRATE DEPOSITION

CPPD encompasses 3 overlapping conditions:

• Chondrocalcinosis (Calcific material in cartilage)
• Pseudogout 
• Chronic pyrophosphate arthropathy

CPPD crystal deposition can occur in:

• Hyperparathyroidism
• Haemochromatosis (Cirrhosis, diabetes, bronze skin, joint pain and stiffness, CPPD common in MCP joints).
• Familial
• Local change due to aging.
• Alkaptonuria (Homogentisic acid in the urine, dark pigmentation in the tissues
  (Ochronosis) and CPPD. See calcification and disc narrowing and spinal osteoporosis. Large joints involved late.)

Pyrophosphate in abnormal cartilage combines with calcium, and enucliation occurs on collagen fibers. Tophi form, seen as amorphous deposits in the cartilage. More pronounced in fibrocartilage, such as menisci, TFC (triangular fibrocartilage in wrist), discs and symphysis. May also occur in periarticular tissues. Crystals may be extruded into the joint where they incite an inflammatory reaction similar to gout. The presence of CPPD crystals seems to result in the development of OA in joints not usually prone to this (Ankle, elbow).

Asymptomatic chondrocalcinosis is common in the menisci. May be associated with OA, cause and effect are unknown.

Pseudogout can be differentiated from gout, as it usually occurs in larger joints, has moderate pain and chondrocalcinosis is often seen on X-ray. See weakly POSITIVE birefringent crystals under polarized light.

Degenerative changes in pyrophosphate arthropathy are similar to OA.

Treatment involves rest and NSAID’s.

Aspiration and steroids may help.

HA CRYSTAL DEPOSITION

Dystrophic calcification occurs in diseased tissues.

Metastatic calcification occurs when Calcium and phosphate levels rise.

The HA crystals are deposited around chondrocytes in cartilage and in tendons and ligaments.

Grow by accretion, and can then be seen on X-ray. 

May be surrounded by an acute vascular reaction and inflammation. 

Crystal shedding into joints may give synovitis.

Acutely there is periarticular tenderness and significant local pain that subsides over weeks or months

Chronically the deposits may cause a destructive arthropathy.

Treat with rest and NSAID’s. A cortisone injection may help.