Pan Feng, Tian Jing, Cicuttini Flavia, Jones Graeme
Menzies Institute for Medical Research, University of Tasmania, Private Bag 23, Hobart, TAS, 7000, Australia.
Department of Epidemiology and Preventive Medicine, Monash University Medical School, Commercial Road, Melbourne, VIC, 3181, Australia.
Pain Ther. 2022 Mar;11(1):107-119. doi: 10.1007/s40122-021-00341-1. Epub 2021 Nov 27.
Inflammation has been suggested to be involved in the pathogenesis of osteoarthritis and pain. We sought to explore the associations between inflammatory serum markers and magnetic resonance imaging-defined long-term structural change and pain trajectory.
A total of 169 randomly selected participants (mean age 63 years; 47% female) from a prospective cohort study were included in this study. Circulating levels of interleukin 6 (IL-6), tumour necrosis factor alpha (TNF-α) and high-sensitivity C-reactive protein (CRP) were measured at baseline. A knee MRI scan was performed to measure cartilage volume (CV) and bone marrow lesions (BMLs) at baseline and at 10.7 years. Knee pain at four visits was measured by the WOMAC pain questionnaire, and pain trajectories were identified using group-based trajectory modelling. Linear, log-binomial and multi-nominal logistic regression were used for the analyses.
IL-6 was associated with lateral but not medial tibial CV loss (β = - 0.25% per annum, per standard deviation [SD] log pg/ml; P < 0.05) in the multivariate analysis. IL-6 was also associated with a 'Moderate pain' trajectory (relative risk ratio 1.93 per SD log pg/ml; 95% confidence interval 1.02-3.65) relative to the 'Minimal pain' trajectory group. There was no significant association of TNF-α and CRP with CV loss and pain trajectory groups with the exception of a beneficial relationship between CRP and medial tibial CV loss (β = 0.20% per annum, per SD log mg/l). No association between inflammatory markers and change in BML size was observed.
IL-6 was independently associated with compartment-specific CV loss and worse pain trajectory, but the other markers studied were not, suggesting that components of inflammation are implicated in the pathogenesis of cartilage loss and developing a worse pain course.
炎症被认为与骨关节炎和疼痛的发病机制有关。我们试图探讨炎症血清标志物与磁共振成像定义的长期结构变化及疼痛轨迹之间的关联。
本研究纳入了一项前瞻性队列研究中随机选取的169名参与者（平均年龄63岁；47%为女性）。在基线时测量白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）和高敏C反应蛋白（CRP）的循环水平。在基线时和10.7年时进行膝关节磁共振成像扫描，以测量软骨体积（CV）和骨髓损伤（BMLs）。通过WOMAC疼痛问卷测量四次访视时的膝关节疼痛，并使用基于组的轨迹模型确定疼痛轨迹。采用线性、对数二项式和多项逻辑回归进行分析。
在多变量分析中，IL-6与外侧而非内侧胫骨CV丢失相关（每年-0.25%，每标准差[SD]对数皮克/毫升；P<0.05）。相对于“最小疼痛”轨迹组，IL-6还与“中度疼痛”轨迹相关（每SD对数皮克/毫升的相对风险比为1.93；95%置信区间为1.02-3.65）。除了CRP与内侧胫骨CV丢失之间存在有益关系（每年β = 0.20%，每SD对数毫克/升）外，TNF-α和CRP与CV丢失及疼痛轨迹组之间无显著关联。未观察到炎症标志物与BML大小变化之间的关联。
IL-6与特定部位的CV丢失和更差的疼痛轨迹独立相关，但研究的其他标志物并非如此，这表明炎症成分与软骨丢失的发病机制以及疼痛病程恶化有关。
