ABSTRACT
BACKGROUND: The peptide hormone relaxin, found in pregnant and non-pregnant females, has been shown to have collagenolytic effects on ligamentous tissue. Relaxin receptors have recently been identified on the human female anterior cruciate ligament (ACL). Relaxin may affect the load bearing properties of the female ACL and contribute to non-contact ACL injuries. HYPOTHESIS: The administration of recombinant relaxin+/-estrogen will lead to a significant decrease in ACL integrity in the guinea pig model. STUDY DESIGN: Controlled laboratory study. METHODS: Adult female guinea pigs were divided into three experimental groups. Group 1 (n=4) was administered only 20 microg/h of recombinant porcine relaxin for 3 weeks. Group 2 (n=4) was administered 20 microg/h of recombinant porcine relaxin and 5 microg/h of estradiol for 3 weeks. Group 3 (n=4) served as both a normal control before surgical transection of the ACL and a positive ACL tear control after transection. All hormones were administered using separate implanted osmotic pumps. ACL laxity was tested by implanting radio-opaque markers in the femur and tibia of each leg. After applying a standard anterior force (22 N), the distance between markers was measured radiographically at day 0 and day 21. The animals were then sacrificed and the ACL's were analyzed for load-to-failure using a material testing machine. RESULTS: Load-to-failure testing indicated that animals treated with relaxin only had significantly weaker ACL's (micro=40.4 N, p=0.001) compared to controls (micro=64.1 N). The relaxin+estrogen group (micro=32.7 N) was also significantly weaker than controls (p=0.007). There were no statistical differences between relaxin and relaxin+estrogen groups. Both relaxin only and relaxin+estrogen groups showed an increase in anterior translation of the tibia after 3 weeks of infusion, but it did not achieve statistical significance. CONCLUSIONS: Relaxin significantly alters the mechanical properties of the ACL in an animal model. CLINICAL RELEVANCE: The effects of relaxin, possibly in conjunction with estrogen, may contribute to a comprehensive etiology for human female non-contact ACL injuries.
