F Pan1, L Blizzard2, J Tian3, F Cicuttini4, T Winzenberg5, C Ding6, G Jones7. 1. Menzies Institute for Medical Research, University of Tasmania, Private Bag 23, Hobart, Tasmania 7000, Australia. Electronic address: Feng.Pan@utas.edu.au. 2. Menzies Institute for Medical Research, University of Tasmania, Private Bag 23, Hobart, Tasmania 7000, Australia. Electronic address: Leigh.Blizzard@utas.edu.au. 3. Menzies Institute for Medical Research, University of Tasmania, Private Bag 23, Hobart, Tasmania 7000, Australia. Electronic address: J.Tian@utas.edu.au. 4. Department of Epidemiology and Preventive Medicine, Monash University Medical School, Commercial Road, Melbourne 3181, Australia. Electronic address: Flavia.Cicuttini@monash.edu. 5. Menzies Institute for Medical Research, University of Tasmania, Private Bag 23, Hobart, Tasmania 7000, Australia. Electronic address: Tania.Winzenberg@utas.edu.au. 6. Menzies Institute for Medical Research, University of Tasmania, Private Bag 23, Hobart, Tasmania 7000, Australia. Electronic address: ChangHai.Ding@utas.edu.au. 7. Menzies Institute for Medical Research, University of Tasmania, Private Bag 23, Hobart, Tasmania 7000, Australia. Electronic address: Graeme.Jones@utas.edu.au.
Abstract
OBJECTIVE: Although being overweight or obese is an important risk factor for the development of knee osteoarthritis (OA), the interplay between weight and genetic factors remains unclear. This study aimed to examine the associations between weight and knee cartilage volume/defects over 10 years in offspring having at least one parent with a total knee replacement (TKR) for primary knee OA and in controls without a knee OA family history. METHOD: 367 participants (183 offspring and 184 controls) aged from 26 to 61 years were recruited at baseline, and followed at 2 and 10 years later. T1-weighted magnetic resonance imaging (MRI) of the right knee was used to measure cartilage volume/defects at each time-point. Mixed-effects models were used with adjustment for potential confounders. RESULTS: Study participants were middle-age adults (mean age 45 years, mean weight 77.5 kg at baseline). In multivariable analysis, increasing body weight was deleteriously associated with medial tibiofemoral cartilage volume (β = -0.28 ml, per 1 SD increase, 95% CI -0.49 to -0.07) and presence of medial tibiofemoral cartilage defects (RR = 1.27, per 1 SD increase, 95% CI 1.07 to 1.51) in offspring over 10 years. Similar associations were observed for lateral tibiofemoral cartilage volume (β = -0.19 ml, P = 0.059), and defects (RR = 1.24, P = 0.049). However, there were no statistically significant associations between weight and cartilage volume or defects in controls. CONCLUSION: The adverse effects of increasing weight are stronger in the offspring of people with knee replacement for knee OA suggesting genetics-environment interaction with regard to overweight/obesity in the pathogenesis of knee OA particularly in the early stages.
OBJECTIVE: Although being overweight or obese is an important risk factor for the development of knee osteoarthritis (OA), the interplay between weight and genetic factors remains unclear. This study aimed to examine the associations between weight and knee cartilage volume/defects over 10 years in offspring having at least one parent with a total knee replacement (TKR) for primary knee OA and in controls without a knee OA family history. METHOD: 367 participants (183 offspring and 184 controls) aged from 26 to 61 years were recruited at baseline, and followed at 2 and 10 years later. T1-weighted magnetic resonance imaging (MRI) of the right knee was used to measure cartilage volume/defects at each time-point. Mixed-effects models were used with adjustment for potential confounders. RESULTS: Study participants were middle-age adults (mean age 45 years, mean weight 77.5 kg at baseline). In multivariable analysis, increasing body weight was deleteriously associated with medial tibiofemoral cartilage volume (β = -0.28 ml, per 1 SD increase, 95% CI -0.49 to -0.07) and presence of medial tibiofemoral cartilage defects (RR = 1.27, per 1 SD increase, 95% CI 1.07 to 1.51) in offspring over 10 years. Similar associations were observed for lateral tibiofemoral cartilage volume (β = -0.19 ml, P = 0.059), and defects (RR = 1.24, P = 0.049). However, there were no statistically significant associations between weight and cartilage volume or defects in controls. CONCLUSION: The adverse effects of increasing weight are stronger in the offspring of people with knee replacement for knee OA suggesting genetics-environment interaction with regard to overweight/obesity in the pathogenesis of knee OA particularly in the early stages.