Association of Knee Osteoarthritis with the Accumulation of Metabolic Risk Factors Such as Overweight, Hypertension, Dyslipidemia, and Impaired Glucose Tolerance in Japanese Men and Women: The ROAD Study
ABSTRACT To clarify the association of knee osteoarthritis (KOA) with overweight (OW), hypertension (HTN), dyslipidemia (DL), and impaired glucose tolerance (IGT), which are components of metabolic syndrome (MS), in a Japanese population.
We enrolled 1690 participants (596 men, 1094 women) from the large-scale cohort study Research on Osteoarthritis Against Disability (ROAD), begun in 2005 to clarify epidemiologic features of OA in Japan. KOA was evaluated by the Kellgren-Lawrence grade, minimum joint space width (MJSW), minimum joint space area (JSA), and osteophyte area (OPA). OW, HTN, DL, and IGT were assessed using standard criteria.
The prevalence of KOA in the total population in the age groups ≤ 39, 40-49, 50-59, 60-69, 70-79, and ≥ 80 years was 2.2%, 10.7%, 28.2%, 50.8%, 69.0%, and 80.5%, respectively. Logistic regression analyses after adjustment for age, sex, regional difference, smoking habit, alcohol consumption, physical activities, regular exercise, and history of knee injuries revealed that the OR of KOA significantly increased according to the number of MS components present (1 component: OR 1.21, 95% CI 0.88-1.68, p = 0.237; 2 components: OR 1.89, 95% CI 1.33-2.70, p < 0.001; 3 or more components: OR 2.72, 95% CI 1.77-4.18; p < 0.001). The number of MS components was inversely related to medial MSJW (ß = -0.148, R(2) = 0.21, p < 0.001), medial JSA (women only; ß = -0.096, R(2) = 0.18, p = 0.001), and positively related to OPA (ß = 0.12, R(2) = 0.11, p < 0.001).
The accumulation of MS components is significantly related to presence of KOA. MS prevention may be useful to reduce cardiovascular disease and KOA risk.
- SourceAvailable from: Sultana Monira Hussain
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- "We found the accumulation of components of MetS to be associated with the incidence of severe knee OA as assessed by knee replacement, independent of BMI. The ROAD study, which examined radiological knee OA, reported similar findings, but they were not adjusted for obesity  . Our results suggest that, although the relationship between some of the individual components of MetS and knee OA might be weak, the cumulative MetS components increase the risk of severe knee OA. "
ABSTRACT: To examine whether components of metabolic syndrome (MetS), either singly or additively, were associated with the incidence of severe knee and hip OA, and whether these associations were independent of obesity assessed by body mass index (BMI). Twenty thousand, four hundred and thirty participants who had blood lipids, anthropometric and blood pressure measurements during 2003-2007 were selected from the Melbourne Collaborative Cohort Study. MetS was defined as central obesity assessed by waist circumference and any two of raised triglyceride level, reduced HDL cholesterol level, hypertension or impaired fasting glycaemia. The incidence of total knee and hip replacement was determined by linking cohort records to the Australian Orthopaedic Association National Joint Replacement Registry. Six hundred and sixty participants had knee OA and 562 had hip OA. After adjustment for age, gender, country of birth, education, physical activity and BMI, central obesity [hazard ratio (HR) 1.59, 95% confidence interval (CI) 1.25-2.01] and hypertension (1.24, 1.05-1.48) were associated with increased risk of knee OA. The accumulation of MetS components was associated with knee OA risk, independent of BMI: one component, 2.12 (1.15-3.91); two components, 2.92 (1.60-5.33) and three or more components, 3.09 (1.68-5.69). No statistically significant associations were observed for hip OA. Cumulative number of MetS components and central obesity and hypertension were associated with increased risk of severe knee OA, independent of BMI. No associations were observed with severe hip OA. These findings suggest that the pathogenesis of knee and hip OA differ and that targeting the management of MetS may reduce the risk of knee OA.Seminars in arthritis and rheumatism 09/2013; 43(4). DOI:10.1016/j.semarthrit.2013.07.013 · 3.63 Impact Factor
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ABSTRACT: Osteoarthritis (OA) a common disease of aged population and one of the leading causes of disability. Incidence of knee OA is rising by increasing average age of general population. Age, weight, trauma to joint due to repetiting movements in particular squatting and kneeling are common risk factors of knee OA. Several factors including cytokines, leptin, and mechanical forces are pathogenic factors of knee OA. In patients with knee pain attribution of pain to knee OA should be considered with caution. Since a proportion of knee OA are asymptomatic and in a number of patients identification of knee OA is not possible due to low sensitivity of radiographic examination. In this review data presented in regard to prevalence, pathogenesis, risk factors.03/2011; 2(2):205-212.
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ABSTRACT: Chondrocyte aging is associated with cartilage degeneration and senescence impairs the regenerative potential of mesenchymal stem cells (MSCs). Estrogen exerts profound effects on human physiology including articular cartilage and MSCs. The present study should analyze the effects of pre- and postmenopausal estrogen concentrations on chondrogenic cells. Physiologic premenopausal concentrations of 17β-estradiol (E(2)) significantly decelerated telomere attrition in MSCs and chondrocytes while postmenopausal E(2) concentration had no significant effects. The estrogen agonist-antagonist tamoxifen did not affect telomere biology, but inhibited the E(2) -stimulated reduction in telomere shortening. E(2) and tamoxifen did not influence cell proliferation, cell morphology, and β-galactosidase staining in chondrogenic cells. E(2) treatment did not affect the telomere-associated proteins TRF1 and TRF2. E(2) had no regulatory effects on the expression rates of the cell cycle regulator p21 and the DNA repair proteins SIRT1 and XRCC5. In spite of reducing telomere shortening in aging MSCs and chondrocytes, estrogen is not able to prevent somatic cells from replicative exhaustion and from finally entering senescence. The fade of telomere shortening under pre- to postmenopausal estrogen concentrations suggests, at least in part, a senescence-dependent cause for the onset of osteoarthritis in women after menopause.Journal of Orthopaedic Research 10/2011; 29(10):1563-71. DOI:10.1002/jor.21424 · 2.97 Impact Factor