Research lecturesIs osteoarthritis a metabolic disease?
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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