Division of Rheumatology, Geneva University Hospital and Faculty of Medicine, University of Geneva, HUG Av. de Beau-Séjour 26, 1206, Geneva, Switzerland.
The University of Western Australia, School of Human Sciences, Perth, WA, Australia.
Sci Rep. 2024 Nov 22;14(1):29021. doi: 10.1038/s41598-024-80345-x.
Prior meta-analyses have suggested a protective link between smoking and knee osteoarthritis (KOA), but they relied on aggregate data, potentially obscuring the true relationship. To address this limitation, we conducted an Individual Participant Data (IPD) meta-analysis using data from three large cohorts: the Osteoarthritis Initiative (OAI), the Multicenter Osteoarthritis Study (MOST), and the Cohort Hip and Cohort Knee (CHECK) study. Participants from 16 centers in the USA and Netherlands were categorized as current, former, or never smokers. We assessed six outcomes, three related to structural changes over 4-5 years of follow-up, and three related to changes in KOA symptoms over 2-2.5 years, 5 years, and 7-8 years of follow-up. First, the incidence of radiographic KOA was evaluated in 10,072 knees, defined as having a Kellgren-Lawrence grade ≥ 2 ('radiographic KOA') at follow-up but not at baseline. Second, the progression of radiographic KOA was evaluated in 5274 knees, defined as an increase in Kellgren-Lawrence grade between baseline and follow-up in knees that had radiographic KOA at baseline. Third, the incidence of symptomatic KOA was evaluated in 12,910 knees, defined as having radiographic KOA in addition to symptoms at follow-up but not at baseline. Fourth, fifth, and sixth, we investigated changes between baseline and all follow-ups in scores for the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) subscales of pain, disability, and stiffness (in 2640 knees). There were no differences between smoking groups in any of these six outcomes. Our study, leveraging data from three large cohorts and the advantages of IPD, finds no evidence that smoking offers any protection against KOA, refuting the notion that smoking may benefit joint health.
先前的荟萃分析表明，吸烟与膝关节骨关节炎（KOA）之间存在保护关联，但这些分析依赖于汇总数据，可能掩盖了真实的关系。为了解决这一局限性，我们使用来自三个大型队列的数据（骨关节炎倡议（OAI）、多中心骨关节炎研究（MOST）和队列髋部和队列膝关节（CHECK）研究）进行了个体参与者数据（IPD）荟萃分析。来自美国和荷兰 16 个中心的参与者被分为当前吸烟者、以前吸烟者或从不吸烟者。我们评估了六个结局，其中三个与随访 4-5 年内的结构变化有关，三个与随访 2-2.5 年、5 年和 7-8 年内 KOA 症状的变化有关。首先，在 10072 个膝关节中评估了放射学 KOA 的发生率，定义为在随访时但不在基线时具有 Kellgren-Lawrence 分级≥2（“放射学 KOA”）。其次，在 5274 个膝关节中评估了放射学 KOA 的进展，定义为基线时有放射学 KOA 的膝关节中 Kellgren-Lawrence 分级在基线和随访之间的增加。第三，在 12910 个膝关节中评估了症状性 KOA 的发生率，定义为在随访时除了基线时的症状外还具有放射学 KOA。第四、第五和第六，我们研究了基线和所有随访时 Western Ontario 和 McMaster 大学骨关节炎指数（WOMAC）疼痛、残疾和僵硬子量表评分的变化（在 2640 个膝关节中）。在这六个结局中，吸烟组之间没有差异。我们的研究利用来自三个大型队列的数据和 IPD 的优势，没有发现吸烟对 KOA 有任何保护作用的证据，驳斥了吸烟可能有益于关节健康的观点。
