PURPOSE: Tendinopathy is one of the most common musculoskeletal issues in jumping sports. In sports like basketball and volleyball, tendinopathy rates reach greater than 45%. Interventions to prevent or treat tendinopathies would improve an athlete’s quality of life and team performance. The goal of any intervention to treat tendinopathy is to increase the content of directionally oriented collagen, decrease pain, and increase the tensile strength of the tendon. This study is designed to determine the molecular changes that promote tendon repair.
METHODS: Patellar tendon injury was induced in male Wistar Rats with a 2mm biopsy punch. Rats then recovered with normal cage activity for 15 days to allow a mature scar to form. Following scar formation, groups received either an isometric load (4 x 30 second contraction, 2 min rest) or an equivalent time under tension using dynamic loads (360 contractions lasting 333ms each). The injured region of the tendon was collected 18 hrs after loading and immediately frozen. RNA was isolated from the tendon for RT-qPCR determination of genes involved in tendon (collagen I, III, lysyl oxidase, and scleraxis) and fibrocartilage (collagen II, aggrecan, tenascin C, and Sox9) formation.
RESULTS: Tendon scar formation was confirmed by visual inspection. The injured region showed increased vascularity and greater volume. Our preliminary findings suggest that RNA within the tendon increases from 154.4±20.5µg at baseline to 497.9±128.1µg two weeks after injury. Acute isometric exercise of the scarred tendon decreased RNA in the injured region slightly to 341.1±16.8µg. At the time of submission the gene expression studies are being completed.
CONCLUSIONS: This pilot study confirms that following injury there is an increase in cell mass (greater RNA) in the scar. Further work on the expression of tendon and cartilaginous genes within the scar will help with the development of a loading program to repair patellar tendinopathy.