Shoulder tendon injuries including impingement, rotator cuff disease, and biceps tendon pathology are common clinical conditions and are a significant source of joint pain, instability, and dysfunction. These injuries may progress into partial tears then to complete tendon ruptures, which have limited healing capacity even when surgically repaired. These injuries are frequently seen in the presence of abnormal scapulothoracic joint kinematics (termed scapular dyskinesis). However, the cause and effect relationship between scapular dyskinesis and shoulder injury has not been directly defined. Additionally, while the incidence of shoulder injuries and recurrent failure of repairs is well-documented, the mechanisms behind them are not well-established, making optimal clinical management difficult. Therefore, the objectives of this study were to examine the effect of scapular dyskinesis on the initiation and progression of pathological changes in the rotator cuff and biceps tendon and to define the mechanical processes that lead to these changes. Unfortunately, clinical and cadaveric studies are unable to address the underlying causes of injury and cannot evaluate the injury process over time. Therefore, a rat model of scapular dyskinesis (created by denervating the trapezius and serratus anterior) was developed and used, both alone and in combination with overuse, to investigate the cause and effect relationships between changes in joint loading and alterations in tendon mechanical, histological, organizational, and biological properties. We hypothesized that scapular dyskinesis would result in altered joint loading conditions that would lead to degeneration of the rotator cuff and long head of the biceps. We found that scapular dyskinesis diminished joint function and passive joint mechanics and significantly reduced tendon properties. We also investigated the effect of overuse on tendon properties and found that overuse activity in the presence of scapular dyskinesis resulted in significantly more structural and biological adaptations than scapular dyskinesis alone. We also investigated the effect of scapular dyskinesis on supraspinatus tendon healing and found that scapular dyskinesis was detrimental to tendon properties. These results indicate that scapular dyskinesis is a causative mechanical mechanism of shoulder tendon injury. Identification of scapular dyskinesis as a mechanism of pathological changes will help inform and guide clinicians in developing optimal prevention and long-term rehabilitation strategies.