A rat model of arthrofibrosis developed after anterior cruciate ligament reconstruction without rigid joint immobilization

Purpose: Complications including arthrofibrosis have been reported after anterior cruciate ligament reconstruction (ACLR) even under accelerated rehabilitation. To overcome this, we developed an animal model of ACLR-induced arthrofibrosis without immobilization. Materials and Methods: Thirteen male Wistar rats were divided into ACL transection (ACLT) and ACLR groups. Surgery was performed in the right knees and untreated left knees were used as controls. After surgery, rats could move freely without joint immobilization. Results: One week after surgery, flexion contracture represented by passive ROM reduction was 49 +/- 5 degrees and 21 +/- 6 degrees in ACLR and ACLT groups, respectively. Thereafter, flexion contractures were gradually reduced to 21 +/- 8 degrees and 12 +/- 6 degrees after 12 weeks, respectively. Fibrosis, which is characterized by significant upregulation of fibrosis-related genes, thickening, and adhesion in the posterior joint capsule, was observed in the ACLR group after 12 weeks of surgery. Nociceptive behavior and joint swelling were more apparent in the ACLR group than in the ACLT group, especially after 1 week of surgery. Discussions: We developed a rat model of ACLR-induced joint contracture due to arthrofibrosis without rigid immobilization. Joint contracture was also observed in the ACLT group, but to a considerably milder degree than in the ACLR group. Thus, signs of inflammation as a result of reconstruction surgery, rather than ACL transection, play an important role in the formation of joint contracture after ACLR. Our animal model is suited to examine the mechanisms and efficacy of therapeutic strategies for arthrofibrosis following ACLR treated without rigid joint immobilization.

Automated summary

An animal model of ACLR-induced arthrofibrosis without immobilization was successfully developed in rats, demonstrating a significant increase in joint contracture and fibrosis-related gene expression in the ACLR group compared to the ACLT group. This model is ideal for studying the mechanisms and effectiveness of therapeutic strategies for arthrofibrosis following ACLR.