Elsevier

Joint Bone Spine

Volume 80, Issue 6, December 2013, Pages 568-573
Joint Bone Spine

Research lectures
Is osteoarthritis a metabolic disease?

https://doi.org/10.1016/j.jbspin.2013.09.007Get rights and content

Abstract

Obesity, together with aging and injury, is among the main risk factors for osteoarthritis. Obesity-related osteoarthritis can affect not only the weight-bearing joints, but also the hands, suggesting a role for circulating mediators released by the adipose tissue and known as adipokines. Thus, osteoarthritis may have a systemic metabolic component. Evidence from both epidemiological and biological studies support the concept of metabolic osteoarthritis, defined as a broad clinical phenotype that includes obesity-related osteoarthritis. Thus, osteoarthritis can be related to metabolic syndrome or to an accumulation of metabolic abnormalities. In addition, studies have demonstrated associations linking osteoarthritis to several components of the metabolic syndrome, such as hypertension and type 2 diabetes, independently from obesity or any of the other known risk factors for osteoarthritis. Both in vitro and in vitro findings indicate a deleterious effect of lipid and glucose abnormalities on cartilage homeostasis. Chronic low-grade inflammation is a feature shared by osteoarthritis and metabolic disorders and may contribute to the genesis of both. Thus, osteoarthritis is emerging as a disease that has a variety of phenotypes including a metabolic phenotype, in addition to the age-related and injury-related phenotypes.

Introduction

Osteoarthritis is the most common joint disease with nearly 6 millions affected individuals in France. The prevalence of symptomatic knee osteoarthritis has been estimated in France at 4.7% in men and 6.6% in women [1].

Osteoarthritis covers a broad range of presentations in terms of the joints involved (hips, knees, hands…), imperfect correlation between the structural damage and the clinical symptoms, considerable interindividual variability in pain severity and functional impairments, and complex pathophysiological mechanisms. The current view is that osteoarthritis is a group of diseases that can be differentiated based on the risk factors involved and the pathophysiological mechanisms underlying the joint damage (aging, obesity, genetic factors, or injury) (Table 1) [2].

Obesity-related osteoarthritis is a readily identifiable phenotype. Converging evidence from numerous studies indicates that obesity-related osteoarthritis is one aspect of a vaster phenotypic group known as metabolic osteoarthritis, which also includes osteoarthritis related to hypertension, type 2 diabetes, and dyslipidemia [2], [3], [4] (Fig. 1).

Section snippets

Osteoarthritis and obesity

Many epidemiological studies have established that lower-limb osteoarthritis is associated with obesity [5], [6], [7], [8]. Obese individuals are at increased risk for symptomatic or radiological knee osteoarthritis, particularly with bilateral involvement [5], [6]. Obesity is also associated with greater radiological progression of established knee osteoarthritis [6]. A weaker association with hip osteoarthritis has been reported [7], [8]. In a recent study, however, obesity was linked to

Pathophysiology of metabolic osteoarthritis

The association between osteoarthritis and metabolic syndrome can be approached from two different angles. If the metabolic disturbances are viewed as risk factors for osteoarthritis, then it makes sense to study the impact of each component of the syndrome (glucose, lipids, hypertension) on joint tissues and cells. The other approach sees chronic low-grade inflammation as the link between the two conditions via the induction of systemic complications including type 2 diabetes, dyslipidemias,

Therapeutic implications

Dietary therapy combined with physical exercise and bariatric surgery are effective treatments not only for obesity, but also for the associated metabolic disturbances and knee osteoarthritis [78], [79]. In contrast, there is no proof that interventions designed to control hypertension, diabetes, or dyslipidemia alleviate the symptoms of osteoarthritis. Furthermore, to date, statin therapy has not demonstrated relevant clinical efficacy on knee osteoarthritis [80].

In the current state of our

Conclusion

Obesity-related osteoarthritis can now be viewed as one aspect of the broader metabolic osteoarthritis phenotype. Robust epidemiological studies support a role for metabolic factors in osteoarthritis, and accumulating experimental data suggest that diabetes, dyslipidemia, and hypertension may independently promote joint damage, even in the absence of obesity. Interestingly, many of the same molecules seem involved in the pathophysiology of both osteoarthritis and metabolic disturbances, and the

Disclosure of interest

The authors declare that they have no conflicts of interest concerning this article.

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