Pathogenesis of fibrosis in patella-patellar tendon junction induced by jumping load in a rabbit model.

The mechanism of fibrosis at the patella-patellar tendon junction (PPTJ) was investigated using a rabbit overuse jumping model. Thirty-two female New Zealand White rabbits were randomly divided into control and jumping groups, and each group was further divided into four groups at 2, 4, 6, and 8 wk. The rabbit in the jumping group jumped 150 times/day, 5 days/wk. The PPTJ was removed at the corresponding time point and subjected to hematoxylin and eosin, safranin O, and immunohistochemical staining. Significant differences were observed in histological changes and fibrosis-related factors between the jumping and control groups ( < 0.01). Comparison within the jumping group indicated that the changes in the fibrocartilage zone thickness and proteoglycan area were pronounced at ; the expressions of transforming growth factor β (TGF-β1), Smad3, CTGF, α-SMA, COL-I, and COL-III peaked at ( < 0.05). The jumping load can lead to morphological and fibrotic changes in the patella-patellar tendon junction, with peak changes occurring at . The fibrosis in the patella-patellar tendon junction may be associated with increased secretion of TGF-β1 and Smad3 due to jump loading, which upregulates CTGF expression and thus promotes the synthesis of α-SMA, COL-I, and COL-III. The temporal pattern of fibrosis in the patella-patellar tendon junction (PPTJ) was determined by observing changes in histology and fibrosis-related factors at different time points in an overused jumping rabbit model. The results revealed that ) the peak fibrotic changes in the PPTJ occurred at of jump training; ) fibrosis in PPTJ may be associated with the changes in TGF-β1/Smad3. This study contributes to the development of targeted early interventions.