Department of Orthopedic Surgery, Ibaraki Prefectural University of Health Sciences, 4669-2 Ami Ami-machi, Inashiki-gun, Ibaraki, Ami 300-0394, Japan.
Department of Agriculture, Ibaraki University, 3-21-1 Chuo, Ibaraki, Ami 300-0393, Japan.
Medicina (Kaunas). 2022 Jul 19;58(7):957. doi: 10.3390/medicina58070957.
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. In both the wild-type (WD; C57BL/6N, periostin +/+; = 54) and periostin knockout (KO; periostin -/-; = 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. 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. 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.
骨膜蛋白对髌腱(PT)胫骨止点生长的影响尚不清楚。本研究旨在通过骨膜蛋白敲除小鼠揭示骨膜蛋白对 PT 胫骨止点纤维软骨层生长的贡献。在野生型(WD;C57BL/6N,骨膜蛋白+/+;n=54)和骨膜蛋白敲除(KO;骨膜蛋白-/-;n=54)两组中,分别于 1 天和 1、2、3、4、6、8、10 和 12 周龄时处死 6 只小鼠。研究了软骨细胞增殖和凋亡、软骨细胞数量、番红 O 染色糖胺聚糖(GAG)面积、Ⅱ型胶原染色面积和潮线长度。KO 中的软骨细胞增殖和凋亡低于 WD 组在 1 天和 1、4 和 8 周以及 1 天和 4、6 和 12 周。虽然两组的软骨细胞数量逐渐减少,但 KO 组在 1 天和 8 及 12 周时均低于 WD 组。在细胞外基质中,KO 中的 GAG 染色面积小于 WD 组在 1 天和 1、4、8、10 和 12 周。KO 中的Ⅱ型胶原染色面积小于 WD 组在 8 周。KO 中的潮线长度短于 WD 组在 4 和 6 周。骨膜蛋白缺失导致 PT 胫骨止点生长过程中软骨细胞增殖、软骨细胞凋亡和软骨细胞数量减少。此外,骨膜蛋白减少并延迟 GAG 和Ⅱ型胶原的产生,延迟 PT 胫骨止点生长过程中的潮线形成。因此,骨膜蛋白可以促进 PT 胫骨止点纤维软骨层的生长。骨膜蛋白缺乏可能导致 PT 胫骨止点生长不完全。