Department of Surgery, Duke University Medical Center, Durham, NC, USA.
Osteoarthritis Cartilage. 2010 Jun;18(6):830-8. doi: 10.1016/j.joca.2010.02.009. Epub 2010 Feb 14.
Meniscal tears are a common knee injury and increased levels of interleukin-1 (IL-1) have been measured in injured and degenerated joints. Studies have shown that IL-1 decreases the shear strength, cell accumulation, and tissue formation in meniscal repair interfaces. While mechanical stress and IL-1 modulate meniscal biosynthesis and degradation, the effects of dynamic loading on meniscal repair are unknown. The purpose of this study was to determine the effects of mechanical compression on meniscal repair under normal and inflammatory conditions.
Explants were harvested from porcine medial menisci. To simulate a full-thickness defect, a central core was removed and reinserted. Explants were loaded for 4h/day at 1 Hz and 0%-26% strain for 14 days in the presence of 0 or 100 pg/mL of IL-1. Media were assessed for matrix metalloproteinase (MMP) activity, aggrecanase activity, sulfated glycosaminoglycan (S-GAG) release, and nitric oxide (NO) production. After 14 days, biomechanical testing and histological analyses were performed.
IL-1 increased MMP activity, S-GAG release, and NO production, while decreasing the shear strength and tissue repair in the interface. Dynamic loading antagonized IL-1-mediated inhibition of repair at all strain amplitudes. Neither IL-1 treatment nor strain altered aggrecanase activity. Additionally, strain alone did not alter meniscal healing, except at the highest strain magnitude (26%), a level that enhanced the strength of repair.
Dynamic loading blocked the catabolic effects of IL-1 on meniscal repair, suggesting that joint loading through physical therapy may be beneficial in promoting healing of meniscal lesions under inflammatory conditions.
半月板撕裂是一种常见的膝关节损伤，在受伤和退化的关节中，白细胞介素-1（IL-1）的水平升高。研究表明，IL-1 降低了半月板修复界面的剪切强度、细胞堆积和组织形成。虽然机械应力和 IL-1 调节半月板的生物合成和降解，但动态加载对半月板修复的影响尚不清楚。本研究旨在确定在正常和炎症条件下机械压缩对半月板修复的影响。
从猪的内侧半月板中采集标本。为了模拟全层缺损，取出并重新插入一个中央核心。标本在存在 0 或 100pg/ml IL-1 的情况下，每天以 1Hz 和 0%-26%的应变率加载 4 小时，共 14 天。评估培养基中基质金属蛋白酶（MMP）活性、聚集酶活性、硫酸糖胺聚糖（S-GAG）释放和一氧化氮（NO）产生。14 天后，进行生物力学测试和组织学分析。
IL-1 增加了 MMP 活性、S-GAG 释放和 NO 产生，同时降低了界面处的剪切强度和组织修复。动态加载拮抗了 IL-1 对修复的抑制作用，在所有应变幅度下均如此。IL-1 处理或应变均未改变聚集酶活性。此外，单独的应变除了在最高应变幅度（26%）下没有改变半月板愈合，在这个水平上增强了修复的强度。
动态加载阻断了 IL-1 对半月板修复的分解代谢作用，这表明通过物理治疗进行关节加载可能有助于在炎症条件下促进半月板损伤的愈合。
