Department of Orthopaedic Surgery, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
Department of Nursing, Faculty of Health Science, Tohoku Fukushi University, 1-8-1 Kunimi, Aoba-ku, Sendai, 981-8522, Japan.
BMC Musculoskelet Disord. 2020 Nov 19;21(1):761. doi: 10.1186/s12891-020-03795-0.
Joint hemorrhage is caused by trauma, ligament reconstruction surgery, and bleeding disorders such as hemophilia. Recurrence of hemorrhage in the joint space induces hemosiderotic synovitis and oxidative stress, resulting in both articular cartilage degeneration and arthropathy. Joint immobilization is a common treatment option for articular fractures accompanied by joint hemorrhage. Although joint hemorrhage has negative effects on the articular cartilage, there is no consensus on whether a reduction in joint hemorrhage would effectively prevent articular cartilage degeneration. The purpose of this study was to investigate the effect of joint hemorrhage combined with joint immobilization on articular cartilage degeneration in a rat immobilized knee model.
The knee joints of adult male rats were immobilized at the flexion using an internal fixator from 3 days to 8 weeks. The rats were randomly divided into the following groups: immobilized blood injection (Im-B) and immobilized-normal saline injection (Im-NS) groups. The cartilage was evaluated in two areas (contact and non-contact areas). The cartilage was used to assess chondrocyte count, Modified Mankin score, and cartilage thickness. The total RNA was extracted from the cartilage in both areas, and the expression of metalloproteinase (MMP)-8, MMP-13, interleukin (IL)-1β, and tumor necrosis factor (TNF)-α was measured by quantitative real-time polymerase chain reaction.
The number of chondrocytes in the Im-B group significantly decreased in both areas, compared with that in the Im-NS group. Modified Mankin score from 4 to 8 weeks of the Im-B group was significantly higher than that of the Im-NS group only in the contact area. The expression of MMP-8 and MMP-13 from 2 to 4 weeks and TNF-α from 2 to 8 weeks significantly increased in the Im-B group compared with those in the Im-NS group, but there was no significant difference in IL-1β expression.
The results showed that joint hemorrhage exacerbated immobilization-induced articular cartilage degeneration. Drainage of a joint hemorrhage or avoidance of loading may help prevent cartilage degeneration during joint immobilization with a hemorrhage.
关节出血是由创伤、韧带重建手术和血友病等出血性疾病引起的。关节腔内的出血复发会引起含铁血黄素沉着性滑膜炎和氧化应激,导致关节软骨退变和关节炎。关节固定是伴有关节出血的关节骨折的常见治疗选择。尽管关节出血对关节软骨有负面影响,但对于减少关节出血是否能有效预防关节软骨退变尚无共识。本研究旨在探讨关节出血联合关节固定对大鼠固定膝关节模型关节软骨退变的影响。
成年雄性大鼠膝关节采用内置固定器从 3 天至 8 周固定在屈曲位。将大鼠随机分为以下两组:固定血注射(Im-B)和固定生理盐水注射(Im-NS)组。评估两个区域(接触区和非接触区)的软骨。软骨用于评估软骨细胞计数、改良 Mankin 评分和软骨厚度。从两个区域的软骨中提取总 RNA,通过定量实时聚合酶链反应测量金属蛋白酶(MMP)-8、MMP-13、白细胞介素(IL)-1β和肿瘤坏死因子(TNF)-α的表达。
Im-B 组在两个区域的软骨细胞数量均明显减少,与 Im-NS 组相比。Im-B 组从第 4 周到第 8 周的改良 Mankin 评分仅在接触区明显高于 Im-NS 组。Im-B 组从第 2 周到第 4 周的 MMP-8 和 MMP-13 以及从第 2 周到第 8 周的 TNF-α表达均明显高于 Im-NS 组,但 IL-1β 表达无显著差异。
结果表明关节出血加重了固定引起的关节软骨退变。关节出血引流或避免负重可能有助于防止关节固定伴出血时软骨退变。