Extension loss following ACL reconstruction: A narrative review of mechanisms and phase-specific management

Extension loss is a prevalent and clinically debilitating complication following anterior cruciate ligament reconstruction (ACLR). Joint immobilization is widely recognized as a primary etiology of range of motion (ROM) restriction across various musculoskeletal pathologies. Even following ACLR, diminished joint excursion during activity likely contributes to the development of extension loss, and postoperative joint immobilization exacerbates extension loss by facilitating intra-articular adhesion formation. Although early mobilization strategies, such as continuous passive motion, have traditionally been the cornerstone of postoperative rehabilitation aimed at counteracting the deleterious effects of immobilization, this approach often fails to fully prevent or resolve extension loss. Translational research indicates that post-ACLR extension loss progresses through distinct biological stages. During the acute postoperative period, termed the active arthrofibrosis phase, intra-articular hemorrhage and subsequent inflammation trigger fibrotic responses, resulting in adhesion formation and joint capsule thickening. In the later residual arthrofibrosis phase, persistent fibrosis may lead to persistent extension loss despite resolution of inflammation. Crucially, the efficacy of therapeutic interventions is highly phase-dependent. Aggressive exercise during the active arthrofibrosis phase may paradoxically exacerbate inflammation and fibrosis, whereas mechanical loading during the residual arthrofibrosis phase may facilitate ROM recovery. In addition, adjunctive pharmacological and physical modalities targeting inflammation may mitigate subsequent fibrotic progression. This narrative review synthesizes clinical and basic research evidence to elucidate the pathophysiological mechanisms underlying extension loss after ACLR and proposes a phase-dependent framework for its management. A paradigm shift toward biologically informed, timing-specific interventions is essential to minimize the risk of persistent extension loss.