Abstract
BackgroundThe anterior cruciate ligament (ACL) is responsible for braking forward movement of the tibia relative to the femur and for tibial rotation. After ACL injury, this braking performance deteriorates, inducing abnormal joint movement. The purpose of this study was to clarify the effects of controlled abnormal joint movement on the molecular biological response in intra-articular tissues during the acute phase of ACL injury.MethodsEighty-four mature Wistar male rats were randomly assigned to a controlled abnormal movement (CAM) group, an ACL-transection (ACL-T) group, a sham-operated group, or an intact group. The ACL was completely transected at its midportion in the ACL-T and CAM groups, and a nylon suture was used to control abnormal tibial translation in the CAM group. The sham-operated group underwent skin and joint capsule incisions and tibial drilling without ACL transection. Animals were not restricted activity until sacrifice 1, 3, or 5 days after surgery for histological and gene expression assessments. Acute-phase inflammation requires an important balance between degenerative and biosynthetic processes and is controlled by the activities of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). Both types of gene were analyzed in this study.ResultsThe ACL-T and CAM groups exhibited cleavage of the ACL at all time points. However, for the CAM group, the gap in the ligament stump was extremely small, and fibroblast proliferation was observed around the stump. Relative to the ACL-T group, the CAM group demonstrated significantly lower expression of MMP-13 mRNA and a lower MMP-13/TIMP-1 ratio on days 1 and 5 in the ACL, the medial meniscus and the lateral meniscus. The expression of TIMP-1 mRNA was not significantly different between the ACL-T and CAM groups.ConclusionsThe study results suggested that controlling abnormal movement inhibited the inflammatory reaction in intra-articular tissues after ACL injury. This reaction was down-regulated in intra-articular tissues in the CAM group. Abnormal joint control caused prolonged inflammation and inhibited remodeling during the acute phase of ACL rupture.
Highlights
The anterior cruciate ligament (ACL) is responsible for braking forward movement of the tibia relative to the femur and for tibial rotation
There was no significant difference in tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA expression between the ACL-T group and the controlled abnormal movement (CAM) group (p = 0.384, Fig. 4d–f)
As with matrix metalloproteinase-13 (MMP-13) mRNA in the matrix metalloproteinases (MMPs)-13/tissue inhibitors of metalloproteinases (TIMPs)-1 ratio, a significant difference was observed in the ACL and medial meniscus between ACL-T and CAM groups (p < 0.01, Fig. 4g and h)
Summary
The anterior cruciate ligament (ACL) is responsible for braking forward movement of the tibia relative to the femur and for tibial rotation. After ACL injury, this braking performance deteriorates, inducing abnormal joint movement. The purpose of this study was to clarify the effects of controlled abnormal joint movement on the molecular biological response in intra-articular tissues during the acute phase of ACL injury. ACL deficiency can induce the degeneration of other intra-articular tissues (i.e., cartilage and meniscus), which is a risk factor for the development of osteoarthritis [8]. Previous studies have generally attributed injury-induced knee degeneration to the long-term biomechanical changes in the microenvironment of the knee joint and have primarily focused on the long-term molecular kinetics in injured ACLs [9, 10]. ACL is recognized as a ligament difficult to heal after injury
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