These findings support known mechanisms of chronic inflammation and fibrosis identified in other musculoskeletal diseases where abnormal S100A9, IL-33 and HMGB1 expression has been implicated in the initiation and propagation of various chronic inflammatory and autoimmune disorders.18 27–29 HMGB1 immunostaining was increased in post-treatment pain-free tendon tissues, suggesting HMGB1 may play a potential role in tissue healing. Here, HMGB1 is linked to musculoskeletal system disorder.