Diabetes-induced Osteoarthritis
Diabetes-induced Osteoarthritis
Several epidemiological and experimental data support the hypothesis that diabetes could be an independent risk factor for osteoarthritis (OA), at least in some patients, leading to the concept of a diabetes-induced OA phenotype. If confirmed, this new paradigm will have a dramatic impact on prevention of OA initiation and progression.
Osteoarthritis (OA) is the leading cause of musculoskeletal handicap in the world. Ageing and obesity are the two main risk factors for OA. Since prevalence of these conditions are going to exponentially expand, an epidemic of the disease in the next decade is expected, leading to a dramatic increase in the number of total joint replacements and so entails significant costs to society. In order to attenuate the individual and societal consequences, and because no disease-modifying drugs have proven their efficacy yet, any preventive policies should have a dramatic impact on the quality of life and on countries economy. A better delineation of the different risk factors of the disease should lead to a better personalisation of the preventive messages delivered by doctors and stakeholders. To date, the main OA phenotypes described in the literature are ageing, post-traumatic, hormonal, genetic and metabolic OA.
Metabolic OA has been recently individualised based on recent data showing an increased incidence of OA in patients who are overweight/obese even in non-weight bearing joints. In that case, mechanical overload being not able to explain this increased incidence, a new paradigm based on the role of systemic mediators called adipokines and defined as cytokines produced by fat adipose tissue, has been proposed. Moreover, recent epidemiological studies have strengthened this hypothesis by showing an increased incidence of OA in patients with metabolic syndrome (MetS). MetS, also known as syndrome X, is defined as a condition mixing several independent risk factors for cardiovascular (CV) events, including insulin resistance (identified by type 2 diabetes, impaired fasting glucose or impaired glucose tolerance) plus any two of the following: hypertension, elevated plasma triglycerides, decreased high-density lipoprotein cholesterol, obesity, proteinuria. Indeed, estimation of the prevalence of diabetes reaches over 10% of the population in industrialised countries, coexisting with obesity in specific geographic patterns because of a convergence of prevailing social norms, community and environmental factors, socioeconomic status and genetic risk factors among ethnically similar groups. The demonstration of an association between MetS and OA is challenging because obesity, a component of the MetS, is also a strong risk factor for knee OA. However, a large body of evidence indicates that OA is part of a generalised metabolic disorder in which various interrelated metabolic factors contribute to the OA process. A recent logistic regression analysis assessing the association between MetS and population-weighted variables in a representative sample of the general US population showed appealing results. Interestingly, MetS was prevalent in 59% of the OA population and in 23% of the population without OA. Each of the five CV risk factors that comprise MetS was more prevalent in the OA population. This association remained strong when obesity was controlled for. It is noteworthy that in this work, prevalence of diabetes was 30% in the OA population versus 13% in the control population. The role of diabetes independently of obesity as a risk factor for OA remains unclear.
Abstract and Introduction
Abstract
Several epidemiological and experimental data support the hypothesis that diabetes could be an independent risk factor for osteoarthritis (OA), at least in some patients, leading to the concept of a diabetes-induced OA phenotype. If confirmed, this new paradigm will have a dramatic impact on prevention of OA initiation and progression.
Introduction
Osteoarthritis (OA) is the leading cause of musculoskeletal handicap in the world. Ageing and obesity are the two main risk factors for OA. Since prevalence of these conditions are going to exponentially expand, an epidemic of the disease in the next decade is expected, leading to a dramatic increase in the number of total joint replacements and so entails significant costs to society. In order to attenuate the individual and societal consequences, and because no disease-modifying drugs have proven their efficacy yet, any preventive policies should have a dramatic impact on the quality of life and on countries economy. A better delineation of the different risk factors of the disease should lead to a better personalisation of the preventive messages delivered by doctors and stakeholders. To date, the main OA phenotypes described in the literature are ageing, post-traumatic, hormonal, genetic and metabolic OA.
Metabolic OA has been recently individualised based on recent data showing an increased incidence of OA in patients who are overweight/obese even in non-weight bearing joints. In that case, mechanical overload being not able to explain this increased incidence, a new paradigm based on the role of systemic mediators called adipokines and defined as cytokines produced by fat adipose tissue, has been proposed. Moreover, recent epidemiological studies have strengthened this hypothesis by showing an increased incidence of OA in patients with metabolic syndrome (MetS). MetS, also known as syndrome X, is defined as a condition mixing several independent risk factors for cardiovascular (CV) events, including insulin resistance (identified by type 2 diabetes, impaired fasting glucose or impaired glucose tolerance) plus any two of the following: hypertension, elevated plasma triglycerides, decreased high-density lipoprotein cholesterol, obesity, proteinuria. Indeed, estimation of the prevalence of diabetes reaches over 10% of the population in industrialised countries, coexisting with obesity in specific geographic patterns because of a convergence of prevailing social norms, community and environmental factors, socioeconomic status and genetic risk factors among ethnically similar groups. The demonstration of an association between MetS and OA is challenging because obesity, a component of the MetS, is also a strong risk factor for knee OA. However, a large body of evidence indicates that OA is part of a generalised metabolic disorder in which various interrelated metabolic factors contribute to the OA process. A recent logistic regression analysis assessing the association between MetS and population-weighted variables in a representative sample of the general US population showed appealing results. Interestingly, MetS was prevalent in 59% of the OA population and in 23% of the population without OA. Each of the five CV risk factors that comprise MetS was more prevalent in the OA population. This association remained strong when obesity was controlled for. It is noteworthy that in this work, prevalence of diabetes was 30% in the OA population versus 13% in the control population. The role of diabetes independently of obesity as a risk factor for OA remains unclear.
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