Conventional thinking says that tendinopathy—defined as chronic tendon degeneration—is due to tendon overload, leading to microscopic collagen fiber failure and a failed healing response. It also says that inflammation is not part of the pathologic process, because inflammatory cells are not seen in biopsies obtained at the time of surgery in patients with tendinosis.
Fig. 1 Histologic appearance of tendinosis tissue shows a characteristic pattern of fibroblasts and vascular, atypical, granulation-like tissue. Courtesy of Scott A. Rodeo, MD
According recent studies have demonstrated that stress deprivation leads to increases of collagenase (which breaks down collagen in tendons) expression and a loss of tendon cells.
Stem cells may also play a role in the development of tendinopathy. Tendon stem cells can differentiate into tenocytes, which lead to tendon repair, or into osteocytes or adipocytes.
The expression of inflammatory mediators may occur in the early stages of tissue injury. MMPs play an important role in tissue degradation and matrix remodeling and that inflammatory mediator expression can increase MMP activity.
Eccentric exercise may work via mechanical stimulation, leading to modulation of inflammatory mediators and a shift in the balance of MMPs and catabolic and anabolic gene expression.
- Recent studies have found that mechanical understimulation of tendon cells, rather than tendon overload, may cause tendinopathy and that abnormal differentiation of tendon stem cells may play a role in its development.
- Research also indicates important interactions occur among load, inflammatory mediator expression, and MMP expression at the microscopic level.
- Future studies involving the role of mechanical load may suggest ways to modulate the loading environment to stimulate tissue repair.
- MMP inhibitors may have the potential to prevent ongoing tendon degeneration.
May 2011 Issue