Researchers suggest in a recent study that the damaged tissue from calcific tendinitis may foster the growth of cells, blood vessels, and pain receptors.

“We found a 3-to-8-fold increase in the number of small blood vessels, nerves and inflammatory cytokines (proteins that direct cell growth) in patients with calcific tendinitis in one of four rotator cuff tendons, as compared to patients with a torn yet normal tendon,” says George A.C. Murrell, MD, an Australian orthopaedic surgeon and lead author of the study, published recently in the Journal of Bone and Joint Surgery.

“This might explain the chronic inflammation and severe pain that patients with calcific tendinitis often experience,” he adds.

In the study, 30 patients received an ultrasound during arthroscopic surgery to identify and remove samples of calcium within the shoulder tendon. Each patient had calcific tendinitis, but no prior surgeries or fractures in the affected shoulder, and no history of rheumatoid arthritis or osteoarthritis. They were compared to similar patients with tears in normal rotator cuff muscles, without calcification or rheumatoid arthritis, and patients with healthy rotator cuff muscles, explains a media release from the American Academy of Orthopaedic Surgeons.

Overall, the results showed significantly elevated blood vessel growth (neovascularization) and nerve growth (neoinnervation) in the calcific tendinitis lesions. In addition, the calcific tendinitis group had more frequent pain during sleep and more extreme pain in general. The findings are similar to, but much more pronounced than, those found in studies looking at patients with frozen shoulder and other tendon disorders and diseases, the release continues.

“To our knowledge, few works have investigated the presence and/or role of immune cells and their molecular messengers in calcific tendinitis,” Murrell states in the release. “The results could lead to new ways to manage the pain associated with this condition.”

[Source(s): American Academy of Orthopaedic Surgeons, EurekAlert]