Calcific tendonitis of the rotator cuff: From formation to resorption

Abstract

Calcific tendonitis of the rotator cuff is due to apatite deposits in the shoulder tendons. Patients affected by calcific tendonitis have chronic shoulder pain and disability. Although the disease is frequent, about 10 to 42% of painful shoulders, mechanisms leading to this pathological mineralization are still largely unknown. Research reported in the 1990s suggested that the formation of calcific deposits is linked to cells looking like chondrocytes identified around calcium deposits within a fibrocartilage area. They were considered to be derived from tenocytes but more recently, tendon stem cells, able to differentiate into chondrocytes, were isolated. The pro-mineralizing properties of these chondrocytes-like cells, especially the role of alkaline phosphatase, are not currently clarified. The calcium deposits contain poorly crystalline carbonated apatite associated with protein. Among these proteins, only osteopontin has been consistently identified as a potential regulating factor. During the disease, spontaneous resorption can occur with migration of apatite crystals into the subacromial bursa causing severe pain and restriction of movement. In in vivo and in vitro experiments, apatite crystals were able to induce an influx of leucocytes and a release of IL-1β and IL-18 through the activation of the NLRP3 inflammasome. However, mechanisms leading to spontaneous resolution of this inflammation and disappearance of the calcification still need to be elucidated.