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. Thiry-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 weeks. The rabbits in the jumping group jumped 150 times per day, 5 days per week. 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 ( P<0.01). Comparison within the jumping group indicated that the changes in the fibrocartilage zone thickness and proteoglycan area were pronounced at week 6; the expressions of TGF-β1, Smad3, CTGF, α-SMA, COL-I, and COL-III peaked at week 6 ( P<0.05). The jumping load can lead to morphological and fibrotic changes in the patella-patellar tendon junction, with peak changes occurring at week 6. The fibrosis in the patella-patellar tendon junction may be associated with increased secretion of TGF-β1 and Smad3 due to jump loading, which up-regulates CTGF expression and thus promotes the synthesis of α-SMA, COL-I and COL-III.