Calcific tendonitis is the name given to a shoulder condition in which there is a slow accumulation of calcium, usually in the body of the supraspinatus tendon. As the calcification builds up over time, it becomes chalk-like. There may not be symptoms, since there are no vascular or cellular reactions taking place in this stage. This disease goes through a chronic period before it ever reaches an acute stage. Some of the symptoms in this chronic stage may be localized tenderness at the anterior portion of the shoulder near the anterior acromion, pain while sleeping on the side of the pain, and a painful arc between 70 and 110 degrees of abduction. Patients may feel a catching upon shoulder elevation and an impingement between the calcium deposit and the coracoacromial ligament.1 Sometimes, a painful arc may be the only finding.
If spontaneous resorption of the calcium occurs, the condition progresses to the acute stage, and the calcium will be removed by macrophages and giant cells. During this phase, there is extremely acute pain, and the calcific deposit develops a thick, white, toothpaste-like consistency.1 There is vascular proliferation and an increase in cells, which raises the intratendinous pressure, causing pain as the tendon impinges on the surrounding bursa. Interestingly, during the chronic stage, the presence of calcium is usually painless, and as it dissipates, the pain increases. Excruciating pain may last from one to 14 days, but the condition is self-limited. If the deposit ruptures spontaneously, the patient will experience immediate relief. However, if the excruciating, acute pain persists, the patient may have to be referred for needling or aspiration.
With all the studies, the etiology of this condition is still not clear. In a recent study,2 the condition was classified as either idiopathic type 1 or a secondary endocrine-related type II. The condition occurs at a mean age of 47 years in men and 51 years in women, with a female predisposition. Type II, which may occur during pregnancy or hypothyroidism, improves rapidly (chronic phase) when the endocrine system is treated.
Thyroxine is important for both collagen synthesis and matrix metabolism. Hypothyroidism causes an accumulation of glycosaminogycans in the extracellular matrix, predisposing to calcification in the tendon.2 For chronic, unremitting tendinopathy, we should always check the thyroid. Disorders of estrogen metabolism may be linked with calcific tendonitis. According to Harvie P, et al.,2 "Patients with associated endocrine disease have symptoms develop at a younger age, have a significantly more protracted natural history, and more frequently undergo surgical treatment than patients with no associated endocrine disease."
It is important in the chronic stage to differentially distinguish calcific tendonitis from dystrophic calcification. Radiologically, the calcium in tendonitis is inside the body of the tendon and not in contact with the bone while in dystrophic calcification. The calcification is small and stippled and lies just over the greater tuberosity at the tendon insertion into the bone.1 Dystrophic calcification is associated with degenerative conditions such as acromioclavicular and glenohumeral arthritis and chronic rotator-cuff tears. There is deterioration in which there is calcification of necrotic tissue.3
Treatment in the acute stage may require an arm sling, ice and various modalities. Techniques such as ART, Graston Technique and friction massage are contraindicated. The calcium deposit will be tender under direct pressure. In the chronic stage, the above techniques may be useful if there is not severe tenderness over the area.
References
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