Hydroxyapatite Deposition Disease




Hydroxyapatite deposition disease (HADD) is an extremely common disorder causing periarticular disease in the form of tendinitis or bursitis. Only rarely does it cause true articular disease. Calcium hydroxyapatite deposits in muscles, capsules, bursae, and tendon sheaths. Although this deposition is associated with many systemic diseases, such as collagen vascular diseases, renal osteodystrophy, hypervitaminosis D, and milk-alkali syndrome, in many patients it occurs idiopathically with no underlying systemic problem. The radiographic findings are as follows:



  • 1.

    Periarticular calcification



    • A.

      Early deposition is linear and poorly defined, often blending with the soft tissues


    • B.

      With time this calcification becomes denser, homogeneous, well delineated, and circular



  • 2.

    Soft tissue swelling


  • 3.

    Normal adjacent joint and bone


  • 4.

    Occasional joint effusion


  • 5.

    Occasional osteoporosis, occasional reactive sclerosis, uncommon erosion or scalloping of adjacent bone


  • 6.

    Single joint distribution; occasionally multiple joints may be involved either at the same time (33 percent of patients) or successively (67 percent of patients)


  • 7.

    Distribution in shoulder, hip, wrist, elbow, and neck, in decreasing order of frequency



Shoulder


The shoulder is the most common site of calcific tendinitis or bursitis. Calcium hydroxyapatite is said to be observed in 40 percent of the shoulders radiographed for shoulder pain. It usually locates first in a tendon. The actual tendon location can be identified by changes in rotation of the humerus on the radiograph ( Fig. 18-1 ). Fifty-two percent of the calcific tendinitis occurs in the supraspinatus tendon, which can be seen in profile over the greater tuberosity on external rotation. Internal rotation of the humerus profiles the posterior aspect of the head on at the lateral aspect of the radiograph and the anterior head medially. Calcification in the infraspinatus tendon profiles posteriorly on internal rotation. Calcification of the teres minor also profiles posteriorly on internal rotation, but it is inferior to the infraspinatus calcification. Calcification in the subscapularis profiles anteriorly on internal rotation. Calcification of the long head of the biceps is seen on the superior aspect of the glenoid; that of the short head of the biceps is seen on the tip of the coracoid. Rotation does not change the location of calcification in the biceps.




Figure 18-1


Locations of hydroxyapatite deposits in specific tendons as observed on anteroposterior (AP) view of the shoulder in ( A ) external rotation and ( B ) internal rotation.


Calcification in the rotator cuff area may eventually rupture into the bursa ( Fig. 18-2 ). In some patients this has led to a secondary severe destructive arthropathy. The result of this particular sequence of events has been labeled the “Milwaukee shoulder” ( Fig. 18-3 ).




Figure 18-2


AP view of the shoulder showing a large amorphous calcific deposit in the supraspinatus. The lateral aspect of the concretion is less distinct ( arrows ) indicating extension into the subacromial-subdeltoid bursa. The humeral head is inferiorly subluxed because of deltoid atony associated with acute bursal disease.



Figure 18-3


Patient with “Milwaukee shoulder.” A, AP view of the shoulder shows destruction of the superomedial aspect of the humeral head and osteophyte formation in the glenohumeral joint. Faint calcification is visible in the periphery of the distended subacromial-subdeltoid bursa ( arrow ) and axillary recess ( arrowhead ). B, Axial computed tomography (CT) shows flattened appearance of the humeral articular surface and calcification at the periphery of the distended bursa and joint ( arrows ).

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Jan 26, 2019 | Posted by in RHEUMATOLOGY | Comments Off on Hydroxyapatite Deposition Disease

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