Calcifying Tendonitis
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Painter described calcification in the shoulder in 1907. Codman established that the calcification was within the tendons of the rotator cuff. Calcifying tendinitis of the shoulder is characterized by the presence of macroscopic deposits of hydroxyapatite (a crystalline calcium phosphate) in any tendon of the rotator cuff. [1] This article addresses only calcifying tendinitis as it occurs in the shoulder. (See also the Medscape Reference article Rotator Cuff Disease.)
Rebuzzi et al performed a retrospective study comparing arthroscopic surgery (22 cases) with low extracorporeal shockwave therapy (ESWT) (24 cases) in patients with calcific deposits in the supraspinatus tendon. The patients who underwent ESWT received an average of 3 treatment sessions with 1,500 impulses/session of 0.10-0.13 mJ/mm2. According to the UCLA rating system, the mean score for the arthroscopy group improved from 9.36 (±5.2) to 30.3 (±7.62) points after 24 months, with 81.81% reporting good or excellent results. In the ESWT group, the mean score after 24 months rose from 12.38 (±6.5) to 28.13 (±9.34) points, with 70.83% reporting good or excellent results. After 2 years of follow-up, no calcific deposits were present in 86.35% of the arthroscopy patients and in 58.33 % of the ESWT patients. [2]
However, Balke et al concluded in a study of 70 shoulders in 62 patients that although arthroscopy treatment had good clinical outcomes, the affected shoulder showed significantly lower clinical scores than healthy shoulders. [3] Ioppolo et al reported that ESWT was a legitimate intervention but found only limited evidence for the useful range of doses. [4] Barber and Cowden concluded that arthroscopic debridement resulted in good function and patient satisfaction. [5]
Lorbach et al evaluated preoperative deposit stage, postoperative deposit elimination, and preoperative ESWT on the treatment of tendinosis calcarea. Of 45 patients studied, the 24 patients who underwent ESWT before surgery did not show better results than those who did not receive ESWT. The authors concluded that arthroscopic removal of calcific deposits provides good clinical results for pain reduction, shoulder function, and patient satisfaction but that the type of calcific deposit and preoperative treatment with ESWT did not have any significant impact on the postoperative results. [6]
Adamietz et al studied 102 patients with 115 painful shoulder joints who underwent low-dose radiotherapy. Radiotherapy consisted of 2 series, with a total dose of 6.0 Gy. According to the authors, pain relief was achieved in 94 of 115 joints (82%) at a follow-up of a median of 18 months. They noted that low-dose radiotherapy showed the greatest benefit in patients with Farin type III calcification. [7]
A recent assessment of minimally invasive treatments conlcuded that shockwave therapy is safe and effective. However, ultrasound-guided needle therapy is safe but not necessarily more effective than subacromial corticosteroid injection. [8]
For excellent patient education resources, see eMedicineHealth’s patient education article Tendinitis.
Even supraspinatus tendons that are macroscopically normal contain minute amounts of calcium deposits. Degenerative tendons that have ruptured contain more calcium deposits, but it is not always in the form of calcium phosphate. The increase in calcium deposits is due to degenerative calcification. [9] In contrast, the calcium in tendons with radiographically visible calcification is in the form of crystalline hydroxyapatite. Calcifying tendinitis is a different condition from that of degenerative tendons in which there is a small increase in calcium content.
The diagnosis of calcifying tendinitis is made from imaging studies or from direct inspection of the affected tendon. Therefore, it is a description of a morphologic status. This condition may be an incidental finding in an asymptomatic shoulder, or it may be the cause of shoulder pain. [10] However, calcification may be found in a painful shoulder and yet not be the cause of pain. Indeed, considering that calcific deposits are found in 3-20% of painless shoulders and 7% of painful shoulders, the calcific deposit may not be the cause of shoulder pain in many cases.
The incidence of rotator cuff calcification without shoulder symptoms in the general population is 3-20% according to different reports. The highest incidence is in adults aged 30-50 years. [11] The incidence of symptomatic calcifying tendinitis appears to have declined in the last 20-30 years.
The supraspinatus tendon is affected most often. Calcification is observed with decreasing frequency in the infraspinatus, teres minor, and subscapularis tendons. More than one tendon may be involved. Women are affected slightly more frequently than are men (housewives and clerical workers account for most cases), and the right shoulder is affected slightly more often than the left is. Both shoulders can have or develop calcific deposits in 13-47% of subjects, and the calcific deposit usually is described as being approximately 1-2 cm proximal to the tendon insertion on the greater tuberosity.
The cause of calcifying tendinitis is not known. It is generally agreed that it is not caused by trauma, and it is rarely part of a systemic disease.
The pathophysiology of calcifying tendinitis is controversial. The early hypothesis of Codman and others was that the calcification is a consequence of age-related tendon degeneration; however, this is not supported by the following observations:
The peak incidence of calcifying tendinitis occurs at an earlier age than that of degeneration.
Calcifying tendinitis, in contrast to degenerative tendinopathy, may resolve, and the tendon heals spontaneously.
Calcifying tendinitis is rarely associated with tears of the rotator cuff.
The chemical composition of the calcium salts in degenerate tendons is different.
The calcific deposit of calcifying tendinitis consists of poorly crystallized hydroxyapatite.
Calcifying tendinitis appears to occur in viable, not necrotic, tissue, whereas dystrophic calcification appears to occur in necrotic tissue.
Uhthoff and Loehr proposed that calcifying tendinitis is a disease that progresses through correlating pathologic and clinical stages, as follows [12] :
Formative phase: As a consequence of an unknown trigger, a portion of the tendon undergoes fibrocartilaginous transformation, and calcification occurs in the transformed tissue. The deposit enlarges; the calcific deposit resembles chalk.
Resting phase: Once formed, the calcific deposit enters a resting period. The calcific deposit may or may not be painful. If large enough, the deposit may cause mechanical symptoms.
Resorptive phase: After a variable period, an inflammatory reaction may ensue. Vascular tissue develops at the periphery of the deposit. Macrophages and multinuclear giant cells absorb the deposit during this phase. The calcific deposit resembles toothpaste and occasionally leaks into the subacromial bursa, which may result in very painful symptoms.
Postcalcific phase: Once the calcific deposit has been resorbed, fibroblasts reconstitute the collagen pattern of the tendon.
Calcifying tendinitis is a morphologic condition. It may be discovered serendipitously by an imaging study and cause no symptoms. If and when this condition is symptomatic, calcifying tendinitis may present in the following 3 ways:
Chronic, relatively mild pain with intermittent flares, similar to shoulder impingement syndrome, is believed to indicate that the condition is in the formative phase.
Mechanical symptoms may arise from a large calcific deposit, which may block elevation of the shoulder.
More severe acute pain is attributed to the inflammatory response of the resorptive phase.
The pain commonly radiates from the point of the shoulder to the deltoid insertion and, less frequently, to the neck. It is often aggravated by elevation of the arm above shoulder level or by lying on the shoulder. Pain may waken the patient from sleep. Other complaints may be stiffness, snapping, catching, or weakness of the shoulder.
Patients with chronic or subacute symptoms may demonstrate loss of range of motion, a painful arc of motion from 70-110 º of forward elevation, or impingement signs. Catching or crepitus may be noted. In the acute phase, the pain may be so severe that only little movement is allowed, and the tenderness is very marked. Laboratory studies are not required for the diagnosis of calcifying tendinitis.
The indications for surgical treatment of calcifying tendinitis are progressive symptoms, failure of conservative care, interference with the activities of daily living, and the patient’s request.
The presence of local infection is a contraindication to invasive treatment. Allergies to medications contraindicate the use of the offending agents.
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Anthony H Woodward, MD Orthopedic Surgeon, Private Practice
Anthony H Woodward, MD is a member of the following medical societies: American Association of Orthopaedic Medicine, Oregon Medical Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Paul E Di Cesare, MD
Paul E Di Cesare, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American College of Surgeons
Disclosure: Nothing to disclose.
Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine; Clinical Professor of Surgery, Nova Southeastern School of Medicine
Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, Arkansas Medical Society, Florida Medical Association, Florida Orthopaedic Society
Disclosure: Nothing to disclose.
Jegan Krishnan, MBBS, FRACS, PhD Professor, Chair, Department of Orthopedic Surgery, Flinders University of South Australia; Senior Clinical Director of Orthopedic Surgery, Repatriation General Hospital; Private Practice, Orthopaedics SA, Flinders Private Hospital
Jegan Krishnan, MBBS, FRACS, PhD is a member of the following medical societies: Australian Medical Association, Australian Orthopaedic Association, Royal Australasian College of Surgeons
Disclosure: Nothing to disclose.
Calcifying Tendonitis
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