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The contribution of age and obesity to the number of painful joint sites in individuals reporting osteoarthritis: A population-based study

TitleThe contribution of age and obesity to the number of painful joint sites in individuals reporting osteoarthritis: A population-based study
Year of Publication2020
AuthorsBadley, E. M., Wilfong J. M., Yip C., Millstone D. B., and Perruccio A. V.
JournalRheumatology
VolumeePub ahead of Print
Pages1 - 8
Keywordsage, bmi, generalized osteoarthritis, goa, joints, mjoa, obesity, osteoarthritis, sex
Abstract

Objective To investigate the association of OA risk factors with number of painful joint sites in a representative population sample. Methods Analysis of the 2009 Survey on Living with Chronic Diseases in Canada - Arthritis Component (n = 1614) for respondents reporting symptomatic OA. Variables: painful joints sites (hands, wrists, elbows, shoulders, hips, knees, ankles, feet, back, neck), joint symptom duration, sociodemographic characteristics, smoking, comorbidities and BMI. Zero-truncated negative binomial regressions were used to investigate the association between number of painful joint sites and the variables. Generalizability of findings was assessed by a similar analysis in a clinical hip/knee OA sample. Results The sample comprised 73% women and 56% were aged 2 sites, and 45% at =>4 sites. Age, BMI, education and smoking were not associated with the number of joint sites. Significant associations were found with being female [rate ratio (RR) = 1.23, 95% CI 1.09, 1.39], having more comorbidities (RR = 1.11, 95% CI 1.07, 1.15) and longer symptom duration (RR = 1.16, 95% CI 1.09, 1.24), although the increase in joint sites with duration was small. Similar regression results were found with the clinical OA sample. Conclusion The lack of an association of age and BMI (obesity) with number of painful joint sites in OA raises questions about the role of these risk factors and our understanding of OA as a multi-joint disease. Filling this knowledge gap is critical to making progress with defining OA phenotypes and identifying potential aetiological mechanisms.

URLhttps://academic.oup.com/rheumatology/article/doi/10.1093/rheumatology/keaa138/5822564
DOI10.1093/rheumatology/keaa138
Document URLhttps://academic.oup.com/rheumatology/article-pdf/doi/10.1093/rheumatology/keaa138/33103474/keaa138.pdf