Hydroxyapatite deposition disease

Last revised by Rohit Sharma on 3 Jan 2023

Hydroxyapatite crystal deposition disease (HADD) or calcium apatite deposition disease (CADD) is a disease of uncertain etiology characterized by periarticular and intra-articular calcium deposits.

The shoulder is the most frequently involved site with classic calcific tendinitis presentation.  

Calcium apatite crystal deposition disease is most commonly found in middle-aged individuals.

Localized pain is one of the primary manifestations of the disease, associated with swelling, tenderness, and variable limitation of joint motion. Often asymptomatic.

The exact etiology has not been described; however, it is believed that calcific deposits begin to accumulate in damaged tendons (secondary to trauma) via fibrocartilaginous metaplasia 6.

The disease is characterized by calcific crystal deposition in the periarticular soft tissues, especially in the tendons (best recognized as calcific tendinitis).

Most frequently it involves the shoulder joint, where crystal deposition occurs in the supraspinatus tendon, but the disease can also affect numerous other sites. Calcific periarthritis or enthesitis would be the most appropriate term for this condition, as it occurs most commonly in the bony attachment of tendons near the joints 1.

This process can affect other tendons of the body, such as the gluteus medius tendon, or along the femur, as well as at various sites of tendinous attachments (e.g. elbow, wrist, hand, knee, ankle, foot, and spine) 2.

Calcifications of varying sizes and shapes can involve the para-articular tendons, bursae, and capsule. The disease can be mono- or polyarticular.

The appearance will vary based on the calcific stage, broken into the formative, resting and resorptive phases. The formative and resting phases will appear as round-to-ovoid calcification in the soft tissue with well-defined borders. The resorptive phase will appear ill-defined with a comet tail-like appearance. The resorptive phase may mimic a periosteal reaction  6.

It appears as homogeneous, round-to-ovoid calcification in the soft tissue with well-defined or ill-defined margins. The most characteristic lesions are seen in the shoulder with supraspinatus and biceps tendon involvement, adjacent to the greater tubercle and the glenoid tubercle, respectively, where these tendons attach.

Deposits within the infraspinatus and teres minor tendons are not uncommon and can be seen adjacent to the greater tuberosity on internal rotation or axillary views 1

Treatment is chiefly conservative, including NSAIDs, local heat application, and physiotherapy. Local corticosteroid injections may also be of benefit. 

Surgical removal of calcifications may be appropriate for cases refractory to other attempts of conservative treatment.

Ultrasound ablation may prove to be of short-term benefit in particular cases. However, its long-term benefit has not yet been demonstrated 3.

When intra-articular, calcium apatite crystals can cause joint destruction. Any joint can be involved; the shoulder is most commonly affected, resulting in Milwaukee shoulder 4. 

Early studies suggested the periarticular calcific deposits seen in this condition were of hydroxyapatite 7, however more recent analysis has shown deposits contain carbonate apatite and no evidence of hydroxyapatite 8,9, suggesting that the term hydroxyapatite deposition disease is a misnomer.

The differential diagnosis of joint pain with calcification is extensive and occurs in many conditions such as:

Another consideration for a calcific opacity in proximity to a joint (typically knee, elbow, etc.) would be a loose body from an osteochondritis dissecans (OCD) donor site. Therefore, radiographic findings, a thorough history, as well as physical examination, appropriate lab tests and additional imaging modalities, should be utilized to identify the most likely etiology 5.

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