Calcific tendinitis within the rotator cuff tendon is a common shoulder disorder that should be differentiated from dystrophic calcification as the pathogenesis and natural history of both is totally different. Calcific tendinitis usually occurs in the fifth and sixth decades of life among sedentary workers. It is classified into formative and resorptive phases. The chronic formative phase results from transient hypoxia that is commonly associated with repeated microtrauma causing calcium deposition into the matrix vesicles within the chondrocytes forming bone foci that later coalesce. This phase may extend from 1 to 6 years, and is usually asymptomatic. The resorptive phase extends from 3 wk up to 6 mo with vascularization at the periphery of the calcium deposits causing macrophage and mononuclear giant cell infiltration, together with fibroblast formation leading to an aggressive inflammatory reaction with inflammatory cell accumulation, excessive edema and rise of the intra-tendineous pressure. This results in a severely painful shoulder. Radiological investigations confirm the diagnosis and suggest the phase of the condition and are used to follow its progression. Although routine conventional X-ray allows detection of the deposits, magnetic resonance imaging studies allow better evaluation of any coexisting pathology. Various methods of treatment have been suggested. The appropriate method should be individualized for each patient. Conservative treatment includes pain killers and physiotherapy, or “minimally invasive” techniques as needling or puncture and aspiration. It is almost always successful since the natural history of the condition ends with resorption of the deposits and complete relief of pain. Due to the intolerable pain of the acute and severely painful resorptive stage, the patient often demands any sort of operative intervention. In such case arthroscopic removal is the best option as complete removal of the deposits is unnecessary.

Calcium deposits within the rotator cuff tendon is a common shoulder disorder[1]. Calcium deposits may be in the form of calcific tendinitis or dystrophic calcification.

Calcific tendinitis is calcification within a viable and well vascularized rotator cuff. It occurs within the midsubstance of the cuff, 1 to 2 cm proximal to its insertion. Classically, the condition will end by spontaneous resolution and it is uncommon to see other signs of degenerative changes[2].

Dystrophic calcification is calcification within a non-viable and poorly vascularized rotator cuff. It occurs at the insertion site or at the edges of a cuff tear. Classically, the condition worsens by time and it is common to see other signs of degenerative changes[2].

Calcific tendinitis usually occurs during the fifth and sixth decades of life. It occurs within the supraspinatus tendon in almost 50% of cases. It is more common in females (60%). It occurs more commonly with sedentary workers than with heavy labor workers (45% are house wives)[3-5].

Controversy exists over the exact cause of calcific tendinitis. Burkhead[6] and Gohlke[7] proposed that it is a degenerative process that involves necrotic changes of tendon fibers that progress into dystrophic calcification.

Mclaughlin[8] believed that it proceeded from focal hyalinization of the fibers that become fibrillated and detached from the tendon, thus wounding up into rice-like bodies that later undergo calcification.

On the other hand, Uhthoff[9] pointed out that this may be true regarding dystrophic calcification. But regarding calcific tendinitis they believed that this explanation was most unlikely. They argued that calcific tendinitis occurred in viable and well vascularized tissues and thus could not be a degenerative process, instead they suggested that it was a reparative process progressing through a predictable disease cycle[9-12].

The calcium deposits may have a chalk-like consistency or a fluid consistency or a mixed one[13].

Many classifications have been suggested to describe calcific tendinitis. Some classified it according to the severity of the symptoms into acute, subacute and chronic[14]. Others classified it according to the radiological form into two categories. The first with localized, discrete, dense and homogenous deposits with spontaneous healing tendency and the second with diffuse, fluffy and heterogeneous deposits characterized by delayed and slow healing[15]. The French society of arthroscopy divided the condition into four types: Type A (20%) with homogenous deposits with well defined edges; Type B (45%) with heterogeneous fragmented deposits with well defined edges; Type C (30%) with heterogeneous deposits with ill defined edges and Type D which is not calcific tendinitis but degenerative dystrophic calcifications at the rotator cuff insertion[16].

Uhthoff et al[12] were the ones who described the complete cycle of the calcium deposits and explained the development of its natural history. They divided the condition into formative and resorptive phases. Lying within the two phases most authors motioned the presence of three stages; pre-calcification (silent), calcification (impingement) and post-calcification (acute)[17-20].

The chronic formative phase results from transient hypoxia that is commonly associated with repeated microtrauma and sometimes with a significant single trauma. This results in increased proteoglycan levels that induce tenocyte metaplasia into chondrocytes. This is followed by calcium deposits, mainly into the matrix vesicles within the chondrocytes. These deposits develop into bone foci that later coalesce.

During the acute resorptive phase the periphery of the calcium deposits shows vascularization with macrophage and mononuclear giant cell infiltration together with fibroblast formation. This produces an aggressive inflammatory reaction with inflammatory cell accumulation, excessive edema and rise of the intra-tendineous pressure. This leads to severe pain which is attributed by some to secondary impingement resulting from the increased tendon size, or due to rupture of the deposits into the subacromial space or into the bursa.

During the post-calcification stage the fibroblasts lay down collagen (mainly type II) that fills the gap. This will maturate into collagen type I within 12 to 16 mo[9,11,12].

The clinical presentation is highly variable and depends on the phase the patient is passing through. During the chronic formative phase that may extend anywhere from 1 to 6 years, the patient may be completely asymptomatic. In some cases the condition will only be discovered accidentally. Some patients may present with symptoms that mimic mild impingement. However during the acute resorptive phase, the patient usually presents with severe symptoms that may extend from 3 wk up to 6 mo. In general, the more severe the symptoms are, the shorter the duration of the condition is. The patient presents with tremendous pain all over the shoulder with tenderness over the supraspinatus insertion. Pain commonly extends to the root of the neck with difficulty during overhead activity associated with muscle spasm. It is very difficult to perform any of the special tests due to the unbearable pain.

Radiological investigations confirm the diagnosis and may even make the diagnosis in asymptomatic cases. It also suggests the phase of the condition and is used to follow its progression.

They include conventional X-ray in true anteroposterior, lateral and outlet views. Deposits within the subscapularis may be detected by anteroposterior view in external rotation. In internal rotation, the deposits within the infraspinatus and teres minor may be detected. “Skullcap appearance” indicate rupture of the deposits within the bursa[21].

Ultrasonographic examination was reported to be more sensitive in detecting the calcium deposits within the cuff[22].

Computed tomography allowed better localization of the deposits[21]. Although routine conventional X-ray allowed detection of the deposits, magnetic resonance imaging (MRI) studies allow better evaluation of any coexisting pathology. The deposits present with a low intensity signal in the T1 weighted images. In the T2 weighted images there may be perifocal low intensity signal denoting surrounding edema[23].

The thinned out cuff lateral to the deposits may be falsely interpreted as a cuff tear. MRI arthrography was more beneficial to avoid such false conclusions[23].

Various methods of treatment have been suggested. The appropriate method should be individualized for each patient depending on proper understanding of the pathophysiology and natural history of the condition, as well as proper clinical and radiological assessment of the patient, and finally accurate determination of the stage at which the patient presents.

The treatment may be “conservative” including pain killers and physiotherapy, or “minimally invasive” as needling and puncture and aspiration, or ”operative” whether arthroscopic or open.

Due to the intolerable pain of the acute and severely painful resorptive stage, the patient often demands any sort of intervention despite explaining to him that the condition is probably resolving.

Since the natural history of the condition ends with resorption of the deposits and complete relief of pain, usually conservative measures are successful in most of cases, reaching 80% in some studies and even 99% in others[12,24].

During the acute stage the aim is to relief of pain. The efficacy of non-steroidal drugs may be doubtful with frequent need to narcotic medications.