Calcium Hydroxyapatite Deposition Disease


Calcium hydroxyapatite is the primary mineral of bone and teeth. Abnormal accumulation of this can occur in areas of tissue damage , in hypercalcemic or hyperparathyroid states, in chronic renal failure, hyperphosphatemia and in certain conditions of unknown cause.

Hydroxyapatite may be released from exposed bone and cause the acute synovitis occasionally seen in chronic stable osteoarthritis. Hydroxyapatite deposition is also an important factor in an extremely destructive chronic arthropathy of the elderly that occurs most often in knees and shoulder.

Joint destruction is associated with attenuation or rupture of supporting structures, leading to instability and deformity.

Progression tends to be painless, and synovial fluid white blood cells counts are usually less than 1000 cells/µL. Symptoms range from minimal to severe pain and disability .

Clinical Manifestations

Periarticular and articular deposits may coexist and be associated with acute and/or chronic damage to the joint capsule, tendons, bursa, or articular surfaces.

Most common sites of hydroxyapatite arein and/or around

  • Knees
  • Shoulders
  • Hips
  • Fingers.

There might be presentation with asymptomatic radiographic abnormalities, acute synovitis or tendonitis, and chronic destructive arthropathy.


Most patients with hydroxyapatite arthropathy are elderly.

30 to 50 percent of patients with osteoarthritis have hydroxyapatite microcrystals in their synovial fluid. Such crystals can frequently be identified in clinically stable osteoarthritis joints, but they are more likely to come to attention in persons experiencing acute or subacute worsening of joint pain and swelling.

Diagnosis depends on identification of crystals from synovial fluid or tissue. Individual crystals are very small, nonbirefringent, and can only be seen by electron microscopy.

Treatment

Treatment of hydroxyapatite arthritis is nonspecific.

Acute attacks of synovitis may be self-limiting, resolving in from days to several weeks.

Aspiration of effusions and the use of either nonsteroidal anti-inflammatory agents or oral colchicines for 2 weeks or of intraarticular injection of glucocorticoid salts appear to shorten the duration and intensity of symptoms.

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