Association of Metabolic Markers with self-reported osteoarthritis among middle-aged BMI-defined non-obese individuals: a cross-sectional study

Abstract

BackgroundOsteoarthritis (OA) is a chronic degenerative joint disease. While it is well-established that obesity affects OA through increased axial loading on the joint cartilage, the indirect effect of obesity through metabolic processes among the body mass index (BMI)-defined non-obese population, i.e., BMI < 30 kg/m2, is less known. Our goal was to evaluate the association of metabolic markers including body fat percentage (BF%), waist circumference, maximum weight gain during adulthood and serum creatinine with self-reported OA to establish if such measures offer additional information over BMI among the non-obese population between 40 and 65 years of age.MethodsCross-sectional data from two cycles of the Canadian Health Measures Survey (CHMS) in 2007–2009 and 2009–2011 were analyzed. Sex-specific logistic regression models were developed to evaluate the association of self-reported OA with metabolic markers. Models were separately adjusted for age, BMI categories and serum creatinine, and a stratified analysis across BM categories was performed. In a secondary analysis, we evaluated the association of self-reported OA, cardiovascular diseases and hypertension across BF% categories.ResultsOf 2462 individuals, 217 (8.8%) self-reported OA. After adjusting for age and BMI, those within BF%-defined overweight/obese category had 2.67 (95% CI: 1.32–3.51) and 2.11(95% CI: 1.38–3.21) times higher odds of reporting self-reported OA compared to those within BF%-defined athletic/acceptable category for females and males, respectively. BF% was also significantly associated with self-reported OA after adjusting for age and serum creatinine only among females (OR: 1.47, 95%CI: 1.12–1.84). Furthermore, among the BMI-defined overweight group, the age-adjusted odds of self-reported OA was significantly higher for overweight/obese BF% compared to athletic/acceptable BF% in both females and males. In a secondary analysis, we showed that the association of self-reported OA and hypertension/cardiovascular diseases is significantly higher among BF% overweight/obese (OR: 1.37, 95%CI: 1.19–3.09) compared to BF% athletic/acceptable (OR: 1.13, 95%CI: 0.87–2.82).ConclusionOur results provide corroborating evidence for a relationship between body fat and OA in a population-based study, while no significant independent correlates were found between other metabolic markers and OA prevalence. Future investigation on the longitudinal relationship between BF and OA among this sub-population may inform targeted prevention opportunities.Electronic supplementary materialThe online version of this article (10.1186/s40608-018-0201-9) contains supplementary material, which is available to authorized users.

Association between body composition and osteoarthritis: A systematic review and meta‐analysis

“…Then, full articles were extracted for further assessment after reviewing the titles and abstracts. Eventually, 19 studies (10 cross‐sectional, 5 case‐control and 4 cohort studies) were included in the present systematic review and meta‐analysis. The study screening process is shown in Figure , and the study characteristics and NOS score of the 19 included articles are shown in Table .…”

“…Three studies reported the OR of knee OA for each standard deviation or 5‐unit increase in fat mass percentage. Three studies reported the OR comparing the highest category to lowest category in fat mass percentage. The pooled results showed that fat mass percentage was positively associated with knee OA, with statistical significance (OR = 1.72, 95% CI: 1.26‐2.35 for per SD or five units; OR = 1.97, 95% CI: 1.27‐3.04 for the highest category to lowest category) (Figure ).…”

Association of Obesity With Prescription Opioids for Painful Conditions in Patients Seeking Primary Care in the US

“…28 The pathogenesis of osteoarthritis is related to obesity through excessive joint loading, altered biomechanics, inflammation related to adipose tissue, and potential hormonal dysregulation. 16,29,30 Thus, osteoarthritis may cause pain in weight-bearing and non-weight-bearing joints. 31,32 Obesity duration may also increase the risk of osteoarthritis.…”

Genome Engineering for Osteoarthritis: From Designer Cells to Disease-Modifying Drugs

“…At present, there are no disease-modifying OA drugs (DMOADs), and the primary therapies include exercise and nonsteroidal anti-inflammatory drugs until total joint replacement at the end-stage of the disease. Clinical risk factors for the development of OA include increasing age, female sex, obesity, repetitive joint overloading, previous joint injury, lower limb deformity, smoking history, and family history of OA [5][6][7][8][9][10][11][12][13][14][15][16][17][18]. This wide array of contributing factors for the initiation and progression of OA supports the notion that OA is not simply one disease, but rather a family of conditions that have similar endpoints that involve a multitude of pathways that lead to joint failure.…”

“…As the severity of symptomatic arthritic diseases and pain can fluctuate over time [39], development of specific therapeutic strategies that can sense and respond to varying degrees of endogenous inflammatory mediators in OA may mitigate unwanted adverse effects. In recent studies, CRISPR-Cas9 gene editing was used to develop an autoregulated anti-cytokine stem cell system in mouse induced pluripotent stem cells (iPSCs), which provides the opportunity to theoretically differentiate them into a variety of cell types [11,12]. These cells were designed to transcribe the soluble receptor for TNF-a (sTNFR1), interleukin-1 receptor antagonist (IL1Ra), or luciferase (control) in a feedback-controlled manner driven by the endogenous macrophage chemoattractant protein-1 (Ccl2) promoter (Fig.…”