4.6 Calcifying tendinitis

Periarticular calcification of the shoulder is frequently an incidental radiographic finding in asymptomatic patients. Some patients may have mild symptoms and a few will present with severe pain when these calcifications are undergoing resorption. The condition of formation and subsequent resorption of rotator cuff calcification is usually referred to as calcific or calcifying tendinitis. Although calcification may occur in the degenerate torn rotator cuff as a secondary process, the calcium deposition associated with calcifying tendinitis is transitory and does not lead to permanent damage of the involved shoulder.

Estimates as to the incidence of rotator cuff calcification in the general population vary considerably with age and type of sample. Estimates vary between 2.7–8% of the population, but many of these are asymptomatic.

The distribution of calcific deposits within the rotator cuff has been well documented by several authors. Calcification within the supraspinatus is more likely to become symptomatic, probably because of subacromial impingement of the swollen area of tendon. Calcification is found in supraspinatus in 74–82% of symptomatic cases.

Calcifying tendinitis seems to be a disease of middle age with a peak incidence in the fifth decade, but rarely presents in the elderly. Therefore calcification must be self-limiting. In Bosworth’s series almost 10% of deposits vanished in 3 years of follow-up.

Most authors found a higher incidence of calcification in females with an incidence range of 57–77%. The right shoulder is involved slightly more frequently and 13–24% of cases are bilateral. Although there have been reports of an association between periarticular shoulder calcification and calcification around the hip there is no evidence of any association of calcifying tendinitis with any systemic disorder of calcium metabolism or medical conditions such as diabetes or gout. With regard to the rotator cuff itself, there is no correlation between significant rotator cuff disease and calcifying tendinitis although partial cuff tears occasionally occur when a calcific deposit bursts into the subacromial bursa.

Although cuff tears are not associated with calcifying tendinitis, the edges of a torn degenerate cuff may show some calcification radiographically. This has a characteristic stippled appearance and should be considered a separate condition with a clinical course which reflects that of the underlying cuff disease.

Various classification systems for calcifying tendinitis have been proposed. In general, anatomical and radiological classifications have not been very helpful in directing management. Bosworth classified the deposits according to their size and thought that large deposits were more likely to become symptomatic. Deposits have also been classified by the quality of their radiographic appearance. DePalma classified the condition by the duration of symptoms at presentation into acute, subacute, and chronic forms. These probably represent different stages in the evolution of the disease process and the distinction between acute and chronic presentations does help plan initial management.

Macroscopically the calcium deposits seen in calcifying tendinitis are usually encapsulated in the substance of the tendon and have a chalky white appearance (Figure 4.6.1) or sometimes a more liquid consistency like toothpaste when incised. Histologically, the deposits are multifocal and are separated by areas of fibrocartilage that are usually avascular. The tendon surrounding the deposits is frequently abnormal, showing evidence of fibrillation and thinning. Under the electron microscope the calcium deposits appear as vesicle-like structures containing crystalline material. Chemical analysis has shown the crystals to consist of hydroxyapatite. Frequently there is a cellular reaction around the calcium deposits that may have a granulomatous appearance due to the presence of multinucleated giant cells. The deposits are often infiltrated by macrophages, polymorphs, and fibroblasts. Crystalline particles are often seen in the cytoplasmic vacuoles of the macrophages and giant cells indicating active phagocytosis of the calcified deposits. There is also frequently evidence of repair with fibroblasts and new capillary formation in the adjacent tendon.

The pathogenesis of these findings is unclear. Codman originally proposed that calcification occurred within a degenerate cuff, and there is experimental evidence to support a link between degeneration, mechanical disruption, and subsequent calcification of the tendon in rabbits. The self-resolving nature of the disease and the epidemiology observed in humans is, however, against a mechanical cause. An attractive theory of cyclical changes within an initially macroscopically normal tendon has been advanced by Uhthoff and Sarkar. They have suggested that the site of calcification initially undergoes transformation into fibrocartilage. Calcium crystals are then deposited in matrix vesicles that eventually coalesce to form deposits that gradually replace the fibrocartilage. After a variable resting period, spontaneous resorption of calcium occurs as vascular channels grow into the deposit and macrophages start to phagocytose the material. Phagocytosis is accompanied by the laying down of granulation tissue that is eventually remodelled to form normal tendon, thereby completing the cycle. The aetiology of the initiating fibrocartilagenous transformation in this cycle remains unexplained but tissue hypoxia might provide the initiating stimulus.

The initial formation of calcium deposits rarely causes significant symptoms. However, patients may be aware of vague discomfort in the shoulder for many months before an acute attack. This mild clinical presentation is referred to as chronic calcifying tendinitis. The pain is frequently referred over the outer aspect of the upper arm, particularly over the deltoid insertion. Patients frequently exhibit tenderness over the cuff insertion at the site of the deposit and may have a decreased range of elevation due to pain. A large deposit in the supraspinatus tendon can cause symptoms of subacromial impingement and patients may exhibit a painful arc and have a positive impingement signs.

The acute phase of calcifying tendinitis is usually very painful and associated with the resorption of the deposits. The clinical picture in many ways resembles that of a septic arthritis or acute gout. Patients complain of severe night pain and rest pain, and hold the affected shoulder in adduction and internal rotation. The patient resists any attempt at moving the shoulder and any movement elicited is likely to be scapulothoracic in origin. The shoulder is generally tender and warm to touch. The source of the severe pain in this acute condition is probably from within the tendon itself since there is little evidence of acute bursal inflammation either macroscopically or histologically. At surgery the calcified material often squirts out when incised and has a more liquid consistency than in the chronic situation. The probable mechanism of acute pain is therefore increased intratendinous pressure resulting from inflammation around the resorbing deposit. A more ill-defined fluffy appearance on radiograph, indicative of resorption, has been described in the acute situation.

Deposits are usually easily seen on radiographs in the subacute or chronic phase (Figure 4.6.2). In the acute phase the calcification may be very difficult to visualize radiographically because of its diffuse nature. Acute calcifying tendinitis can, however, usually be distinguished clinically from other causes of severe shoulder pain. Magnetic resonance imaging is unhelpful as the calcified deposit and the tendon give the same dark signal. The white cell count and sedimentation rate are normal in calcifying tendinitis and frequently elevated in infection. Serum urate may be elevated in acute gout. In cases of doubt the glenohumeral joint should be aspirated to exclude an effusion.

The main priority in acute cases is pain relief. Opiate analgesia as well as anti-inflammatory medication is usually required. A subacromial injection of long-acting local anaesthetic (e.g. bupivicaine) is usually of benefit and some authors have advocated needling or barbottage of the deposit under ultrasound control following local anaesthetic infiltration to relieve pressure within the painful tendon, accompanied by lavage of the subacromial space.

Corticosteroids have an effect on reducing vascular proliferation and macrophage activity, so they may contribute to a prolongation of the resorption process despite providing transient symptomatic relief. In a comparison between steroid injection and local anaesthetic injection alone no significant difference in outcome was observed in one study. Therefore the use of corticosteroid is not recommended.

Cases of chronic or subacute disease usually respond to conservative measures consisting of local therapy including heat, ultrasound, and local anaesthetic injections into the subacromial bursa. Physiotherapy is useful in maintaining the range of motion of the glenohumeral joint. In resistant cases surgery is probably the most dependable way of dealing with large symptomatic deposits. The most commonly accepted indications for surgery are constant pain that interferes with the activities of daily living, and a failure to improve after 3 months of conservative treatment.

Surgical removal of calcium deposits gives good results in most series. Gschwend reported good or excellent results in 25 of 28 cases and DePalma reported 96% good results but the time taken to recover from surgery was quite long. Only 53% had recovered by 6 weeks and a further 30% took 10 weeks. At operation the question arises whether to perform an acromioplasty. Vebostad reported on 43 cases in which one of three procedures had been carried out: arthroscopic excision of the deposit, excision of the deposit, and acromioplasty alone. There was no difference in the results between the three groups with 80% having good or excellent results.

Arthroscopic techniques are now the gold standard for excision of calcific deposits with 90% success rates in many studies. However, arthroscopic excision of the deposit is technically demanding. Visualization of the deposit may be difficult and good preoperative localization is helpful with plain films or ultrasound either preoperatively or intraoperatively. Probing the tendon with a needle at the site of the radiographic deposits may produce an exudate that can aid operative localization. The deposit is debrided with a synovial resector and debris removed with suction.

The needling and subsequent irrigation and aspiration of chronic and subacute calcific deposits under radiographic control has been described. This technique is most useful when there is radiographic evidence of resorption of calcium (diffuse calcification) and is less effective at breaking up the hard chalky substance of a large well-defined lesion. Overall 75% of patients treated with this method were improved at a minimum of 1-year follow-up. This technique has also been reported under ultrasonic guidance, thereby avoiding the use of radiographic screening.

Another minimally invasive approach that has recently been reported is the use of a lithotripter to provide high-energy extracorporeal shock waves to calcifications within the rotator cuff. However, the technique appears to be less effective than barbottage or arthroscopic excision, often requires multiple treatments, and patients don’t like it. Time will tell whether it may provide a useful alternative to surgery in the future for patients with well-localized deposits.

Most patients with calcifying tendinitis will have minimal symptoms and can be treated conservatively. The spontaneous resolution of the condition makes the evaluation of the various popular operative and non-operative treatments difficult. Patients who present with acute symptoms in the resorbing phase of the condition will have a good result if treated symptomatically but the treatment of subacute and chronic cases is less clear. There are no prospective randomized studies comparing different treatments, and these should be a priority of future clinical research. The pathological processes involved in the evolution of calcifying tendinitis continue to be unravelled but the initiating stimulus for the fibrocartilagenous metaplasia and the stimulus for calcium resorption remain elusive.