Koyama Tomohisa, Uchida Kentaro, Fukushima Kensuke, Ohashi Yoshihisa, Uchiyama Katsufumi, Inoue Gen, Takahira Naonobu, Takaso Masashi
Department of Orthopedic Surgery, Kitasato University School of Medicine, 1-15-1 Minami-ku, Kitasato, Sagamihara City, Kanagawa, 252-0374, Japan.
Department of Rehabilitation, Kitasato University School of Allied Health Sciences, 1-15-1 Minami-ku, Kitasato, Sagamihara City, Kanagawa, 252-0374, Japan.
BMC Musculoskelet Disord. 2021 Jan 6;22(1):33. doi: 10.1186/s12891-020-03888-w.
Labral tear can be the initiating factor in the onset of hip osteoarthritis (HOA). However, the physiopathology of labral tear is not fully understood. Our aim was to compare synovial tissue inflammatory cytokine levels between patients with labral tear and late-stage HOA.
Synovial tissue from sites showing the greatest inflammation was harvested from 106 hips from 100 subjects during hip surgery. RNA was extracted, and levels of TNFA, IL1B, IL6 and COX2 mRNA were compared among all patients using real-time PCR. Additionally, we examined whether femoroacetabular impingement (FAI) was associated with elevated levels of inflammatory cytokines in patients with labral tear. To analyze the effects of TNF-α on inflammatory mediators in hip synovial tissue, synovial fibroblasts were extracted from hip synovial tissue of patients with labral tear and late-stage HOA (n = 5 each). Mononuclear cells were extracted from synovial tissue, cultured for 7 days, and stimulated with control or 10 ng/mL human recombinant TNF-α for 1 day. mRNA was extracted from stimulated cells and IL1B, IL6, and COX2 levels were determined using real-time PCR.
TNFA, IL1B, and COX2 expression in synovial tissue were significantly higher in patients with labral tear than late-stage HOA (TNFA, p < 0.001; IL1B, p < 0.001; COX2, p = 0.001). There were no differences in expression between patients with labral tear with and without FAI (TNFA, p = 0.546; IL1B, p = 0.559; IL6, p = 0.599; COX2, p = 0.124). Compared to vehicle control, TNF-α stimulation significantly elevated IL1B, IL6, and COX2 expression in synovial fibroblasts collected from patients with labral tear and late-stage HOA (IL1B, p = 0.043 and p = 0.043; IL6, p = 0.043 and 0.043; COX2, p = 0.043 and p = 0.080, respectively).
TNFA, IL1B, and COX2 expression were elevated in the synovial tissue of patients with labral tear. Further investigations are needed to reveal the relationship between inflammatory cytokine levels and various aspects of labral tear pathology, including pain and the onset and progression of OA.
盂唇撕裂可能是髋关节骨关节炎(HOA)发病的起始因素。然而,盂唇撕裂的生理病理学尚未完全明确。我们的目的是比较盂唇撕裂患者与晚期HOA患者滑膜组织中炎性细胞因子水平。
在髋关节手术期间,从100名受试者的106个髋关节中采集炎症最严重部位的滑膜组织。提取RNA,使用实时聚合酶链反应比较所有患者中肿瘤坏死因子α(TNFA)、白细胞介素1β(IL1B)、白细胞介素6(IL6)和环氧化酶2(COX2)信使核糖核酸的水平。此外,我们研究了股骨髋臼撞击症(FAI)是否与盂唇撕裂患者炎性细胞因子水平升高有关。为了分析肿瘤坏死因子-α(TNF-α)对髋关节滑膜组织中炎性介质的影响,从盂唇撕裂患者和晚期HOA患者的髋关节滑膜组织中提取滑膜成纤维细胞(各n = 5)。从滑膜组织中提取单核细胞,培养7天,并用对照物或10纳克/毫升人重组TNF-α刺激1天。从受刺激的细胞中提取信使核糖核酸,使用实时聚合酶链反应测定IL1B、IL6和COX2水平。
盂唇撕裂患者滑膜组织中TNFA、IL1B和COX2的表达显著高于晚期HOA患者(TNFA,p < 0.001;IL1B,p < 0.001;COX2,p = 0.001)。有FAI和无FAI的盂唇撕裂患者之间的表达无差异(TNFA,p = 0.546;IL1B,p = 0.559;IL6,p = 0.599;COX2,p = 0.124)。与载体对照相比,TNF-α刺激显著提高了从盂唇撕裂患者和晚期HOA患者收集的滑膜成纤维细胞中IL1B、IL6和COX2的表达(IL1B,p = 0.043和p = 0.043;IL6,p = 0.043和0.043;COX2,p分别为0.043和p = 0.080)。
盂唇撕裂患者滑膜组织中TNFA、IL1B和COX2表达升高。需要进一步研究以揭示炎性细胞因子水平与盂唇撕裂病理各方面之间的关系,包括疼痛以及骨关节炎的发病和进展。