Hennerbichler A, Moutos F T, Hennerbichler D, Weinberg J B, Guilak F
Department of Surgery, Division of Orthopaedic Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Osteoarthritis Cartilage. 2007 Sep;15(9):1053-60. doi: 10.1016/j.joca.2007.03.003. Epub 2007 Apr 19.
Injury or removal of the knee meniscus leads to progressive joint degeneration, and current surgical therapies for meniscal tears seek to maximally preserve meniscal structure and function. However, the factors that influence intrinsic repair of the meniscus are not well understood. The goal of this study was to investigate the capacity of meniscus tissue to repair a simulated defect in vitro and to examine the effect of pro-inflammatory cytokines on this process.
Cylindrical explants were harvested from the outer one-third of medial porcine menisci. To simulate a full-thickness defect, a central core was removed and reinserted immediately into the defect. Explants were cultured for 2, 4, or 6 weeks in serum-containing media in the presence or absence of interleukin-1 (IL-1) or tumor necrosis factor alpha (TNF-alpha), and meniscal repair was investigated using mechanical testing and fluorescence confocal microscopy.
Meniscal lesions in untreated samples showed a significant capacity for intrinsic repair in vitro, with increasing cell accumulation and repair strength over time in culture. In the presence of IL-1 or TNF-alpha, no repair was observed despite the presence of abundant viable cells.
This study demonstrates that the meniscus exhibits an intrinsic repair response in vitro. However, the presence of pro-inflammatory cytokines completely inhibited repair. These findings suggest that increased levels of pro-inflammatory cytokines post-injury or under arthritic conditions may inhibit meniscal repair. Therefore, inhibition of these cytokines may provide a means of accelerating repair of damaged or injured menisci in vivo.
膝关节半月板损伤或切除会导致关节进行性退变，目前针对半月板撕裂的手术治疗旨在最大程度地保留半月板结构和功能。然而，影响半月板自身修复的因素尚未完全明确。本研究的目的是探讨半月板组织在体外修复模拟缺损的能力，并研究促炎细胞因子对这一过程的影响。
从猪内侧半月板外侧三分之一处获取圆柱形外植体。为模拟全层缺损，去除中央核心并立即重新植入缺损处。外植体在含血清培养基中培养2、4或6周，培养过程中存在或不存在白细胞介素-1（IL-1）或肿瘤坏死因子α（TNF-α），并通过力学测试和荧光共聚焦显微镜研究半月板修复情况。
未处理样本中的半月板损伤在体外显示出显著的自身修复能力，随着培养时间延长，细胞积聚增加，修复强度增强。在存在IL-1或TNF-α的情况下，尽管有大量活细胞，但未观察到修复。
本研究表明半月板在体外表现出自身修复反应。然而，促炎细胞因子的存在完全抑制了修复。这些发现提示，损伤后或关节炎状态下促炎细胞因子水平升高可能抑制半月板修复。因此，抑制这些细胞因子可能为加速体内受损半月板的修复提供一种方法。
