Complications of calcific tendinitis of the shoulder: a concise review

Calcifying tendinitis (CT) of the shoulder is a frequently occurring painful disorder characterized by the presence of calcified deposits in the tendons of the rotator cuff (RC) mainly affecting the supraspinatus tendon but occasionally is seen in the infraspinatus and subscapularis [1‐5].

The prevalence has been reported to be 2.7 percent in asymptomatic individuals, more common in females between the 4th and 6th decades of life and in sedentary workers [6, 7]. Two speculative hypotheses have been introduced to explain the etiology of CT [8]. The first one was proposed by Codman as an initial degeneration within the tendon fibers which is followed by calcification [9]. Moseley expanded on this further by defining a ‘‘critical zone’’ in the tendon-bone insertion area [10].The second one was proposed by Uhthoff who considered CT as a reactive calcification within a healthy tendon [11]. CT is a disabling clinical condition that in the acute phase induces severe pain and limitation of shoulder function. Although most cases of CT elapse almost asymptomatically, it is not uncommon that some of them present in an emergency or with frequent outpatient office visits due to the ineffectiveness of the various conservative treatment modalities. CT heals either spontaneously or by conservative methods such as nonsteroidal anti-inflammatory drugs (NSAIDs), physiotherapy, subacromial injections, bursal lavage and extracorporeal shock-wave therapy (ESWT) (Fig. 1a–c) [3, 12‐21]. In cases resistant to non operative measures, surgical removal of the calcium deposits is recommended [11, 22‐25].

To our knowledge no review articles have been elaborated on the complications of CT. Hence, in this paper a literature review has been done on the various complications or sequelae of the CT of the shoulder preceded by a brief overview on its histopathology, classification and diagnostic imaging.

The evolution of CT essentially passes through 3 distinct stages: pre-calcific, calcifying and post-calcific [26]. In the pre-calcific stage, numerous factors stimulate a metaplastic change of the tenocytes into chondrocytes. This is followed by the calcific stage which is subdivided into three phases—formation, resting and resorption—characterized by deposition of amorphous calcium phosphate followed by vascularisation and finally by resorption which coincides with significant clinical pain. The post calcific stage is demonstrated by the collagenisation of the lesion by fibroblasts [26]. Intra-operatively, the gross specimens of CT can be either in the form of a sandy tough mass or a toothpaste-like fluid or an amorphous mass composed of many small round or ovoid bodies [27]. The material of these deposits has been identified to be calcium carbonate apatite [28]. This carbonate apatite has been further classified as an A and B-type apatite [29]. Chiou et al. [30] studied the chemical components in CT and found that both types of the carbonate apatite varied in quantities during the formative, resting and resorption phases. Histochemical studies have demonstrated the presence of extracellular matrix vesicles near calcified deposition of the RC [26, 31, 32] and the authors have tried to correlate this finding in the pathogenesis of CT. Normally, the vesicles are inhibited from mineralization but in the presence of any pathology, the inhibitory stimulus may be lost leading to vesicles getting mineralized.

Radiographically, these deposits have been classified by different authors as described in Table 1.

Maier M et al. [36] assessed the intra- and interobserver reliability of the various classification systems using plain radiographs and CT scans and concluded that all the scores showed insufficient reliability and reproducibility. Although marginal improvement could be seen using CT scans it still remained statistically insignificant to be recommended as a routine investigation.

The first imaging modalities to identify CT were X-ray and ultrasound, as calcium deposits are readily identifiable on both. Radiograms should be performed in anterior-posterior (AP)—neutral, internal rotation and external rotation—axillary and outlet view. On radiographs calcific deposits appear homogeneous, amorphous densities without trabeculation, which allows a differentiation from heterotopic ossification or accessory ossicles [37]. Most of calcifications are ovoid, and the margins may be smooth or ill-defined. Ultrasound (US) is advantageous in the diagnosis of CT as it helps to detect other associated conditions as well such as rotator cuff tears and long head of the biceps (LHB) pathologies [38]; moreover, it also characterizes deposit consistency, their tendon location, and can be helpful to assist injections and bursal lavage [39]. According to the morphology of the calcium deposit, US has been used to classify the different type of CT due to its ability to discriminate between well defined calcifications with strong shadowing, and those with faint or absent shadowing. Chiou et al. [40] classifies calcific depositions into four shapes: an arc shape (echogenic arc with clear shadowing), a fragmented or punctate shape (at least two separate echogenic spots or plaques, with or without shadowing), a nodular shape (echogenic nodule without shadowing), and a cystic shape (a bold echogenic wall with an anechoic area, weak internal echoes or layering content). Conditions associated with non arc-shape calcifications include hypervascularity, widening of subacromial-subdeltoid bursa and the large size of calcifications. High resolution US in combination with color Doppler can differentiate between formative or resorptive status. In the resorptive phase, the deposits are nearly liquid and can be successfully aspirated. US has been also used with success in overhead athletes to identify CT showing a prevalence greater than that reported in the general population and that the presence of calcific tendinopathy correlates positively with age [41]. CT scan and MRI should be reserved for doubtful cases [42]. Computed tomography has an excellent resolution to detect calcium deposit as high density foci of solid stippled or amorphous character, but the cost and the exposure to radiation limit its use. MRI should not be used as a first line imaging modality, because deposits appear as vague regions of low signal on T1 and T2, and can be missed. Some enhancement around the deposit can be seen after contrast, and surrounding areas of hyperintensity on T2, due to peripheral edema or subacromial-subdeltoid bursal fluid are possible. MRI is advisable when the deposit is so large as to produce a strong shadow on US thus confusing it with RCTs.

The ideal treatment for the CT of the shoulder is not well established and for some aspects still controversial. The clinical course may be complicated by several conditions that should be diagnosed and treated when we manage a patient with CT of the RC. Whereas pain and stiffness are generally recognized and treated, the risk of RC tears ìs not well considered and the related surgical approach is a concern. Greater tuberosity osteolysis is less known and often not identified on radiograms or ultrasound, therefore, we would suggest to investigate with MRI in those patients with persistent chronic pain and doubtful standard X-ray. Finally, ossifying tendinitis is very rare and only recently reported as complication of CT that should be considered and investigated with X-ray in subjects with CT already treated with conservative or operative measures. We do believe that this review gives a quick summary of the potential complications of the CT, inviting all professionals (orthopaedic surgeons, physiatrists, radiologists and physiotherapists) who deal with this disease to consider not only the regular course of the CT but also the complications that must be identified and treated as well as possible.