Читать книгу Musculoskeletal Disorders - Sean Gallagher - Страница 36

Rotator cuff (RC) injuries are generally considered to be the result of a degenerative disorder of the RC tendons, which begins with acute tendinitis (inflammation) that leads to tendinosis (degeneration), ultimately leading to tendon tears (partial or full), as shown in Figure 2.6 (Neer, 1983). There is mounting evidence of some level of inflammation in all tendon injuries (Abraham, Shah, & Thomopoulos, 2017). Animal models of RC pathology in which the tissue are collected long before a surgical repair endpoint show clear evidence of inflammation in rotator cuff tendon proper, epitendon, or surrounding capsule (Abraham et al., 2017; Kietrys, Barr, & Barbe, 2011; Thomas et al., 2014). Yet, histological studies of the affected RC tendons tend to show a minimal amount of inflammatory cells at the time of surgery (Fukuda, Hamada, & Yamanaka, 1990), and serum biomarker studies of patients with long‐term RC injuries show increased levels of circulating markers of enzymes that contribute to tissue degradation (matrix metalloproteinases), angiogenesis (increased production of vascular endothelial growth factor, VEGF), and axonal sprouting that may be related to the enhanced pain associated with RC injuries (summarized in Gold et al., 2016). These inflammation and degeneration changes are typically intrinsic factors that can enhance RC injuries (Seitz, McClure, Finucane, Boardman, & Michener, 2011). Extrinsic factors can also enhance RC injuries and impingement of the RC tendons. Some injuries are also thought to be the result of a combination of extrinsic and intrinsic factors.