Hydroxyapatite Deposition Disease
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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
Long head of the biceps Subscapularis
Short head of the biceps
Supraspinatus
Infraspinatus Subscapularis Teres minor
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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.
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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. 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.
Hydroxyapatite Deposition Disease 327
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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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OTHER SITES Around the hip, hydroxyapatite deposition may occur in the gluteal insertions into the greater trochanter and surrounding bursa. These calcifications may appear linear or cloud-like (Fig. 18-4). Calcification in the elbow occurs around the medial and lateral condyles of the humerus or in the triceps as it inserts into the olecranon (Fig. 18-5).
FIGURE 18-4 AP view of the hip demonstrating hydroxyapatite deposition into the gluteal insertions at the greater trochanter (arrow). The calcifications are both cloud-like and linear in their appearance.
FIGURE 18-5 Lateral view of the elbow demonstrating calcification in the common extensor tendon as it inserts into the lateral epicondyle.
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In the wrist, the most frequent deposition occurs in the flexor carpi ulnaris. This is observed as calcification adjacent to the pisiform. Calcification may also be seen volar to the radiocarpal joint in the flexor carpi radialis or adjacent to the distal ulna and ulna styloid in the extensor carpi ulnaris (Fig. 18-6). Tendinitis may cause adjacent bone osteoporosis (Fig. 18-7).
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FIGURE 18-6 A, Oblique view of the wrist demonstrating calcification volar to the radius and scaphoid (arrows), most likely in the flexor carpi radialis. B, Oblique view of the wrist demonstrating calcification adjacent to the triquetrum and distal to the ulna (arrow). This most likely is in the extensor carpi ulnaris.
FIGURE 18-7 Posteroanterior (PA) view of the wrist showing calcification in the soft tissue radial to the radial styloid (arrowhead). The bone adjacent to this calcification is reacting with osteoporosis (arrows).
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Perhaps the most painful hydroxyapatite deposition occurs in the neck in the longus colli muscle, which is the chief flexor of the cervical spine. The patient usually complains of tremendous pain on swallowing. Radiographically, one observes soft tissue swelling and amorphous calcification anterior to the C2 vertebral body just inferior to the body of the atlas (Fig. 18-8).
FIGURE 18-8 Lateral view of the upper cervical spine showing amorphous calcification inferior to the atlas and anterior to C2 lying in the longus colli muscle (arrow). There is adjacent soft tissue swelling.
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It is now recognized that hydroxyapatite can deposit intraarticularly. Both periarticular and intraarticular deposition can lead to an arthropathy (Fig. 18-9). Most of the time an osteoarthritic radiographic picture has been described as part of the arthropathy. However, a severely destructive arthropathy has also been described involving the hand as well as the shoulder.
FIGURE 18-9 Two digits showing intra- and periarticular deposition of hydroxyapatite crystals. There is loss of the joint space, as well as erosive changes (arrows).
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UNUSUAL MANIFESTATIONS Deposition of HADD in the fingers may present clinically with redness and swelling that may mimic fracture or infection (Fig. 18-10). HADD may be associated with erosion of adjacent cortical bone and on rare occasion, deposition of crystal in the underlying bone marrow can be seen that leads to a diagnostic concern for osseous neoplasm. This phenomenon is most common at: (1) the posterior aspect of the proximal femur at the insertion of the gluteus maximus, (2) the insertion of the pectoralis major tendon on the anterior humerus, and (3) the greater or lesser tuberosity of the proximal humerus (Fig. 18-11).
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FIGURE 18-10 A, PA view of the thumb shows hydroxyapatite crystals in the ulnar capsule of the interphalangeal joint (arrowhead). Coronal T1-weighted (B) and fat-suppressed T2-weighted (C) images of the thumb show medial interphalangeal joint capsular thickening (arrowhead) and pericapsular edema from crystal deposition that may be confused with trauma. This underscores the importance of comparing magnetic resonance images to available plain radiographs.
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FIGURE 18-11 AP (A) and axial (B) view of the right shoulder show calcification in the soft tissues (arrow) adjacent to a focal erosion of the anterior cortex of the proximal humerus (arrowhead). C, Axial CT shows calcification is in pectoralis major tendon. D, Axial fat-suppressed T1-weighted image following intravenous contrast administration shows no mass lesion. There is enhancement of the humeral cortical erosion (arrowhead) and adjacent soft tissues.
SUMMARY HADD is an extremely common disorder causing periarticular disease and only rarely causing intraarticular disease. The diagnosis is easily made by identifying calcification in the appropriate location. One must be careful to exclude an underlying systemic disease as the cause of this deposition.
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SUGGESTED READINGS Bonavita JA, Dalinka MK, Schumacher HR Jr: Hydroxyapatite deposition disease, Radiology 134:621–625, 1980. Dalinka MK, et al: Periarticular calcifications in association with intra-articular corticosteroid injections (IACI), Radiology 153:615–618, 1984. Dieppe PA, Doherty M, Macfarlane DG, et al: Apatite associated destructive arthritis, Br J Rheumatol 23:84– 91, 1984. Flemming DJ, Murphey MD, Shekitka KM, et al: Osseous involvement in calcific tendinitis: A retrospective review of 50 cases, AJR Am J Roentgenol 181:965–972, 2003. Halverson PB, Carrera GF, McCarty DJ: Milwaukee shoulder syndrome: Fifteen additional cases and a d escription of contributing factors, Arch Intern Med 150:677–682, 1990. Haun CL: Retropharyngeal tendinitis, AJR Am J Roentgenol 130:1137–1140, 1978. Holt PD, Keats TE: Calcific tendinitis: A review of the usual and unusual, Skeletal Radiol 22:1–9, 1993. McCarty DJ, Halverson PB, Carrera GF, et al: “Milwaukee shoulder”—association of microspheroids containing hydroxyapatite crystals, active collagenase, and neutral protease with rotator cuff defects. I. Clinical aspects, Arthritis Rheum 24:464–473, 1981. Pinals RS, Short CL: Calcific periarthritis involving multiple sites, Arthritis Rheum 9:566–574, 1966. Schumacher HR, Miller JL, Ludivico C, et al: Erosive arthritis associated with apatite crystal deposition, Arthritis Rheum 24:31–37, 1981.