Abstract
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 tendinosis1. 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: …
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: The Journal of bone and joint surgery. American volume
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.