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Anterior cruciate ligament (ACL) injuries are the most common ligament injury of the knee, accounting for between 100,000 and 200,000 injuries among athletes per year. ACL injuries occur via contact and non-contact mechanisms, with the former being more common in males and the later being more common in females. These injuries typically require surgical repair and have relatively high re-rupture rates, resulting in a significant psychological burden for these individuals and long rehabilitation times. Numerous studies have attempted to determine risk factors for ACL rupture, including hormonal, biomechanical, and sport- and gender-specific factors. However, the incidence of ACL injuries continues to rise. Therefore, we performed a systematic review analyzing both ACL injury video analysis studies and studies on athletes who were pre-screened with eventual ACL injury. We investigated biomechanical mechanisms contributing to ACL injury and considered male and female differences. Factors such as hip angle and strength, knee movement, trunk stability, and ankle motion were considered to give a comprehensive, joint by joint analysis of injury risk and possible roles of prevention. Our review demonstrated that poor core stability, landing with heel strike, weak hip abduction strength, and increased knee valgus may contribute to increased ACL injury risk in young athletes.

Tendinopathy is a common musculoskeletal injury whose treatment is limited by ineffective therapeutic interventions. Previously we have shown that tendons ineffectively repair early sub-rupture fatigue damage. In contrast, physiological exercise has been shown to promote remodeling of healthy tendons but its utility as a therapeutic to promote repair of fatigue damaged tendons remains unknown. Therefore, the objective of this study was to assess the utility of exercise initiated 1 and 14 days after onset of fatigue damage to promote structural repair in fatigue damaged tendons. We hypothesized that exercise initiated 14 days after fatigue loading would promote remodeling as indicated by a decrease in area of collagen matrix damage, increased procollagen I and decorin, while decreasing proteins indicative of tendinopathy. Rats engaged in 6-week exercise for 30 min/day or 60 min/day starting 1 or 14 days after fatigue loading. Initiating exercise 1-day after onset of fatigue injury led to exacerbation of matrix damage, particularly at the tendon insertion. Initiating exercise 14 days after onset of fatigue injury led to remodeling of damaged regions in the midsubstance and collagen synthesis at the insertion. Physiological exercise applied after the initial biological response to injury has dampened can potentially promote remodeling of damaged tendons.

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