Most pathologic calcification in the body is calcium hydroxyapatite, which is also the most abundant form of calcium in bone. Calcium hydroxyapatite deposition disease refers to calcific tendinitis, periarticular hydroxyapatite deposition, and hydroxyapatite-induced arthritis. No one really knows why hydroxyapatite deposition occurs.
The calcium is deposited in tendons around the joint.
The most common location for hydroxyapatite deposition is the shoulder. The longus coli muscle is also a favorite location for examiners. Hydroxyapatite deposition disease occurs most commonly in middle-aged persons and slightly more often in men.
The disease can be divided into several clinical and radiographic phases, originally described for the shoulder. The first is the silent phase and is characterized by calcium hydroxyapatite is completely contained within the tendon. Patients have minimal symptoms in this phase. On radiographs, the calcium is sharply defined and circumscribed. This is the case shown above. The calcium (pink arrows) is well defined on radiographs. On MRI, we can see that the calcium is confined to the tendon.
This is followed by the mechanical phase, which is characterized by liquefaction and enlargement of the calcium within the tendon, leading to increased pressure and bursitis. Patients present with impingement-like symptoms at this stage. Radiographs show less well defined calcium.
Rupture of the liquefied and enlarging calcium leads to complete or partial rupture of the calcium either into the bursa or under the bursa. Patients present with recurrent bouts of bursitis. Radiographs will show calcium in a linear fashion. The calcium may also disappear altogether.
We finally arrive at adhesive periarthritis, which is characterized by adhesive bursitis with chunks of calcium deposits within a destroyed rotator cuff. Clinically, this phase is characterized by pain and limited range of motion.
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