A new study appearing in February’s issue of the Journal of Bone and Joint Surgery has found that calcific tendinitis of the shoulder involves a significant increase in blood vessel and pain receptor growth among patients with this condition.
“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, ” said George A.C. Murrell, M.D., an Australian orthopedic surgeon and lead author of the study, in the February 3, 2016 news release. “This might explain the chronic inflammation and severe pain that patients with calcific tendinitis often experience.”
According to the news release, “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.”
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.
“To our knowledge, few works have investigated the presence and/or role of immune cells and their molecular messengers in calcific tendinitis, ” said Dr. Murrell. “The results could lead to new ways to manage the pain associated with this condition.”
Dr. Murrell told OTW, “I had conversations with my sonographer and lead author Lisa Hackett about the pain in calcific tendonitis. She thought there would be lots of nerves in the tissue. I said, ‘Well let’s test that hypothesis.’”
“I was surprised how great the changes were. There was nearly a 10- fold increase in nerve markers, blood vessels, mast cells and inflammatory cytokines compared with control tendon.”
“We have an explanation as to why calcific tendonitis can be so painful. When calcific material appears in tendon, our data supports the hypothesis that mast cells invade and try to get rid of the material. Inflammatory cytokines are released and small nerves and blood vessels grow into the area. I think it is these small nerves that cause the severe pain, especially on tendon activation.”
