Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan.
Cell Tissue Res. 2011 Nov;346(2):263-71. doi: 10.1007/s00441-011-1259-6. Epub 2011 Oct 19.
Partial-thickness articular cartilage defects (PTCDs) do not heal spontaneously and are thought to be a predisposing factor for the development of osteoarthritis. Younger and smaller animals have a better healing capacity for many types of injuries including those to articular cartilage. Our aim was to examine the longitudinal histological changes of immature murine articular cartilage after the creation of small PTCDs and to compare them to PTCDs in mature cartilage. Single linear PTCDs were created in 3-week-old and 16-week-old rats in the direction of joint motion. At 6 and 12 weeks after PTCD creation, histological changes were examined in the defect sites and surrounding cartilage. Immature cartilage showed a higher repair capability than mature cartilage. Although repaired immature cartilage had fibrocartilage, it exhibited better quality than any PTCD model, except for a fetus model and comparable quality to full-thickness cartilage defects (FTCD) after bone marrow stimulation. Elucidation of the underlining mechanisms that immature cartilage possesses for repairing PTCDs is necessary in order to aid the prevention or develop treatment for osteoarthritis.
部分厚度关节软骨缺损 (PTCD) 不会自发愈合，被认为是骨关节炎发展的一个诱发因素。许多类型的损伤，包括关节软骨损伤，在年轻和较小的动物中具有更好的愈合能力。我们的目的是研究在创建小的 PTCD 后未成熟鼠关节软骨的纵向组织学变化，并将其与成熟软骨中的 PTCD 进行比较。在关节运动方向上，在 3 周龄和 16 周龄大鼠中创建单个线性 PTCD。在 PTCD 形成后 6 周和 12 周，检查缺陷部位和周围软骨的组织学变化。未成熟软骨表现出比成熟软骨更高的修复能力。尽管修复的未成熟软骨具有纤维软骨，但它的质量比任何 PTCD 模型都要好，除了胎儿模型和与骨髓刺激后的全层软骨缺损 (FTCD) 相当。为了帮助预防或开发治疗骨关节炎的方法，有必要阐明未成熟软骨在修复 PTCD 方面所具有的潜在机制。
