Calcific tendinitis in the shoulder can be a perplexing problem for orthopaedists and patients. While it’s a painless, asymptomatic condition in some people, for others it’s extremely painful and impairs range of motion and shoulder function.
In the February 3, 2016 edition of The Journal of Bone & Joint Surgery, a prospective cohort observational study by Hackett et al. helps explain why that might be. After immunohistochemically evaluating biopsied tendon samples from three groups of patients (ten with painful calcific tendinitis, ten undergoing rot
ator cuff repair, and ten “controls” undergoing a surgical stabilization procedure), the authors found a twofold to eightfold increase of nerve markers, neovascularization, macrophages, M2 macrophages, and mast cells in the calcific tendinitis group compared with the two other groups. The authors conclude that these findings “are consistent with the hypothesis that, in calcific tendinitis, the calcific material is inducing a vigorous inflammatory response within the tendon with formation of new blood vessels and nerves.”
In an insightful commentary on the study, Scott Rodeo cites the study’s main limitation—that biopsy specimens from patients with asymptomatic calcific tendinitis were not studied. That leads the commentator to ask what triggers the transition from asymptomatic lesion to an acutely painful one—and to review some of the current explanatory theories. One posits that osteoclasts drawn to the lesion activate resorption of the calcium. Active resorption causes pain, the theory goes, and that’s when patients frequently receive subacromial steroid injections. Dr. Rodeo suggests that subsequent pain relief may arise more from the natural completion of the resorption process than from the treatment.
Dr. Rodeo further discusses the possibility that active cell-mediated calcium resorption might be a response to microscopic tendon injury in the area of the calcific deposit. He also summarizes interesting stem cell-based theories on what might initiate the deposition of calcium crystals in the first place.
