Calcific tendinitis is an interesting clinical condition in the shoulder, as it can be clinically silent and can be found incidentally in an asymptomatic patient, or it can also present with severe and acute pain. The underlying pathophysiology is not well understood. In addition, due to our lack of understanding of what initiates formation of the calcific deposit in the tendon, we also do not know what factors trigger the pain that can acutely develop in patients with a calcific deposit.

The study by Hackett et al. demonstrates that there is an accumulation of inflammatory cells, neovascularization, and nerve fiber ingrowth in and around calcific deposits in symptomatic patients. This is consistent with the clinical presentation in patients with calcific tendinitis, as they can present with acute pain. The immunohistochemistry findings are consistent with the basic pathophysiology of inflammation, as it is known that inflammation is associated with neovascularization. Furthermore, neoinnervation is associated with new capillary formation. Similar findings of new capillary formation and expression of nociceptive mediators have been reported in analyses of angiofibroblastic hyperplasia lesions seen in rotator cuff tendinosis. The presence of nociceptive chemicals and mediators in the rotator cuff, as found by Hackett et al., is consistent with the severe pain in these patients.

A distinct limitation in this study is the inability to study biopsy specimens in asymptomatic patients with calcific deposits. This leads to consideration of one of the primary outstanding questions related to calcific tendinitis: what initiates the onset of acute pain in a patient who has a chronic calcific deposit? A patient may have a quiescent, asymptomatic lesion that then becomes acutely painful. It is not known what factors trigger this process. The current understanding is that the calcific deposit begins to undergo a cell-mediated process of active resorption. The influx of inflammatory cells and new capillaries reported in the current study is consistent with such a mechanism. It is believed that osteoclasts eventually invade the lesion and activate resorption of the calcium. Patients who present with acute pain are presumably in this active resorption phase, and it is fascinating to see that a radiograph made several weeks later can often show complete resorption of the calcific deposit. Of course, as a clinician, it is hard to do nothing when the patient presents with very severe pain, and thus subacromial injection is often performed. The patient has improvement, and we as clinicians assume that the injection was helpful. The reality is that this improvement in pain may just be the natural history of the condition, and the patient may well have improved spontaneously as the calcific deposit underwent resorption, even if no treatment was rendered. This is indeed a fascinating condition.