Quadriceps inhibition may not be a predecessor of posttraumatic osteoarthritis associated with ACL injury.

Dear Editor-in-Chief: The article entitled ‘‘A Neuromuscular Mechanism of Posttraumatic Osteoarthritis Associated with ACL Injury’’ presents an interesting theory that links quadriceps inhibition to early onset of posttraumatic osteoarthritis (1). The authors have to be commended for their effort in presenting a clear and logical hypothesis that was adequately substantiated by the existing literature. However, there are some potential limitations that I believe are important for the readers to consider when interpreting the information in this article. The authors’ view on the relationship between quadriceps weakness and idiopathic tibiofemoral osteoarthritis is strongly founded. However, their argument of arthrogenic muscle inhibition (AMI) as an explanation for the persistent quadriceps weakness after anterior cruciate ligament (ACL) injury and reconstruction is not well substantiated. Their premise is primarily based on either a single prospective study that demonstrated AMI 2 yr after ACL reconstruction or extrapolation of the results from people with acute ACL injury. The authors’ contention that the failure to directly target AMI would result in ineffective quadriceps strength recovery also is contrary to the available evidence, which suggests that baseline quadriceps activation does not predict changes in quadriceps strength after an exercise intervention and that a simple, clinically practicable exercise regimen could induce substantial gains in quadriceps strength and activation in people with knee osteoarthritis (2,3). While it is definite that AMI is common in patients with acute knee trauma, evidence supporting the presence of chronic activation deficits is limited and conflicting. The findings of Snyder-Mackler et al. (4) suggest that complete activation is a norm in subjects with chronic ACL tear, as well as in those who are at 3 months after ACL reconstruction, although they demonstrate substantial quadriceps weakness. Their findings are further supported by a recent study (5) that showed most people with ACL reconstruction can achieve full activation at 3 months after surgery. Voluntary activation data from people who are at several years after ACL reconstruction also indicate no evidence of chronic activation deficits (6,7). Additional evidence indicates that chronic quadriceps weakness after ACL reconstruction is minimal (G10%) (6,8), and it is related to peripheral physiological changes in the quadriceps muscle but not to voluntary activation deficits (6). Taken together, these results suggest that quadriceps inhibition may not be the underlying mechanism for the persistent quadriceps weakness in people with ACL pathology and therefore may not be a predecessor of posttraumatic osteoarthritis associated with ACL injury and/or surgery. It is important to note that the existing data on quadriceps activation in people with ACL injury or surgery are from a joint angle that is considered to be safe for testing people with ACL pathology (60-Y90of flexion) (4Y7). Applicability of the study results to other knee angles, especially those that are more frequently used in activities of daily living (i.e., near end range of motion), is not clear. Future research on quadriceps inhibition after ACL injury and reconstruction should consider evaluating strength and activation at a more physiologically functional knee angle.