Periostin Contributes to Fibrocartilage Layer Growth of the Patella Tendon Tibial Insertion in Mice

Abstract

Background and Objectives: The influence of periostin on the growth of the patella tendon (PT) tibial insertion is unknown. The research described here aimed to reveal the contribution of periostin to the growth of fibrocartilage layers of the PT tibial insertion using periostin knockout mice. Materials and Methods: In both the wild-type (WD; C57BL/6N, periostin +/+; n = 54) and periostin knockout (KO; periostin −/−; n = 54) groups, six mice were euthanized on day 1 and at 1, 2, 3, 4, 6, 8, 10, and 12 weeks of age. Chondrocyte proliferation and apoptosis, number of chondrocytes, safranin O-stained glycosaminoglycan (GAG) area, staining area of type II collagen, and length of the tidemark were investigated. Results: Chondrocyte proliferation and apoptosis in KO were lower than those in WD on day 1 and at 1, 4, and 8 weeks and on day 1 and at 4, 6, and 12 weeks, respectively. Although the number of chondrocytes in both groups gradually decreased, it was lower in KO than in WD on day 1 and at 8 and 12 weeks. In the extracellular matrix, the GAG-stained area in KO was smaller than that in WD on day 1 and at 1, 4, 8, 10, and 12 weeks. The staining area of type II collagen in KO was smaller than that in WD at 8 weeks. The length of the tidemark in KO was shorter than that in WD at 4 and 6 weeks. Conclusion: Loss of periostin led to decreased chondrocyte proliferation, chondrocyte apoptosis, and the number of chondrocytes in the growth process of the PT tibial insertion. Moreover, periostin decreased and delayed GAG and type II collagen production and delayed tidemark formation in the growth process of the PT tibial insertion. Periostin can, therefore, contribute to the growth of fibrocartilage layers in the PT tibial insertion. Periostin deficiency may result in incomplete growth of the PT tibial insertion.