ACL重建术后伸直受限：机制与分期处理的叙述性综述
简介
ACL重建术后伸膝受限是常见且影响功能的并发症。关节制动是导致关节活动度丧失的主要因素，术后制动会促进关节内粘连形成，加剧伸膝受限。尽管早期活动（如持续被动活动）是传统康复核心，但常无法完全预防或解决该问题。基础研究表明，术后伸膝受限经历两个生物学阶段：急性期（活动性关节纤维化期）以关节内出血和炎症触发纤维化、粘连及关节囊增厚为特征；后期（残留关节纤维化期）…
英文摘要
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.