Osteoarthritis, inflammation and obesity

aUniversity Pierre and Marie Curie, Paris VI, Sorbonne Universités, Paris bDepartment of Rheumatology, AP-HP Saint-Antoine hospital, Paris, France.
Current opinion in rheumatology (Impact Factor: 5.07). 10/2012; 25(1). DOI: 10.1097/BOR.0b013e32835a9414
Source: PubMed

ABSTRACT PURPOSE OF REVIEW: Obesity is one of the main risk factors of the incidence and prevalence of knee osteoarthritis. Recent epidemiological data showing an increased risk of hand osteoarthritis in obese patients opened the door to a role of systemic inflammatory mediators, adipokines, released by adipose tissue. RECENT FINDINGS: Recent experimental studies confirm the critical roles of adipokines in the pathophysiologic features of osteoarthritis, with an emphasis on a new member, chemerin. Animal models of diet-induced obesity show that overload cannot completely explain the aggravation of spontaneous or posttraumatic knee osteoarthritis. We now have data suggesting that some adipokines may be surrogate biomarkers for severity of osteoarthritis. SUMMARY: Preclinical studies targeting adipokines are now expected to provide new hope for patients with osteoarthritis, especially those with metabolic syndrome.

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    ABSTRACT: Osteoarthritis is a common and debilitating joint disease that affects up to 30 million Americans, leading to significant disability, reduction in quality of life, and costing the United States tens of billions of dollars annually. Classically, osteoarthritis has been characterized as a degenerative, wear-and-tear disease, but recent research has identified it as an immunopathological disease on a spectrum between healthy condition and rheumatoid arthritis. A systematic literature review demonstrates that the disease pathogenesis is driven by an early innate immune response which progressively catalyzes degenerative changes that ultimately lead to an altered joint microenvironment. It is feasible to detect this infiltration of cells in the early, and presumably asymptomatic, phase of the disease through noninvasive imaging techniques. This screening can serve to aid clinicians in potentially identifying high-risk patients, hopefully leading to early effective management, vast improvements in quality of life, and significant reductions in disability, morbidity, and cost related to osteoarthritis. Although the diagnosis and treatment of osteoarthritis routinely utilize both invasive and non-invasive strategies, imaging techniques specific to inflammatory cells are not commonly employed for these purposes. This review discusses this paradigm and aims to shift the focus of future osteoarthritis-related research towards early diagnosis of the disease process.
    Journal of Immunology Research 01/2015; 2015:1-13. DOI:10.1155/2015/192415 · 2.93 Impact Factor
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    ABSTRACT: Aim of the work To assess the carotid artery intima–media thickness (IMT) as an index of subclinical atherosclerosis in patients with primary osteoarthritis (OA) and its correlation to severity and insulin resistance (IR). Patients and methods This study included 40 primary OA patients (28 with predominant knee OA and 12 with hip OA) and 15 age and sex matched controls. They were subjected to full medical history, thorough clinical examination and radiological assessment by plain X-rays of knee and hip joints scored according to the Kellgren–Lawrence grading. In patients and control, the IR was calculated by the homeostasis model assessment (HOMA) and carotid IMT measured by ultrasonography. Results There was significant increased carotid IMT in OA patients (0.82 ± 0.12 mm) compared to controls (0.61 ± 0.02 mm) (p < 0.001) with cut-off value of 0.65 mm. There was significant higher HOMA in OA patients (2.55 ± 0.8) compared to controls (1.79 ± 0.44) (p < 0.001). OA patients with IMT > 0.65 mm (n = 34) had longer duration (9 ± 2.56y), higher Kellgren–Lawrence score (2.89 ± 0.45) and higher HOMA (3.8 ± 0.53) compared to those patients with IMT < 0.65 mm (n = 6) (3.41 ± 2.09 y, 2.01 ± 0.26 and 2.23 ± 0.32 respectively). Multi-regression analysis showed that disease duration, Kellgren–Lawrence Grading and HOMA are the best sensitive discriminators for patients having carotid intima >0.65 mm. (F ratio 36.54, p < 0.001). Conclusion Osteoarthritis patients have higher risk of subclinical atherosclerosis independent of traditional risk factors. The severity of OA may contribute to the progression of atherosclerotic disease. Measurement of insulin resistance in OA patients can identify those with higher risk of subclinical atherosclerosis and may help in their follow up and early intervention.
    04/2014; 36(2). DOI:10.1016/j.ejr.2013.12.001
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    ABSTRACT: Calorie restriction is a common strategy for weight loss in obese individuals. However, little is known about the impact of moderate hypocaloric diets on obesity-related laboratory parameters in a short-term period. Aim of this study was to evaluate the variation of laboratory biomarkers in obese individuals following a Mediterranean, hypocaloric (1400-1600 Kcal/die) diet. 23 obese, pharmacologically untreated patients were enrolled and subjected to the determination of anthropometric variables and blood collection at baseline, 1 and 4 months after diet initiation. After 4 months of calorie restriction, we observed a significant decrease in body weight and BMI (both P < 0.0001), insulin (P = 0.037), HOMA-IR (P = 0.026), leptin (P = 0.008), and LDH (P = 0.023) and an increase in EGF (P = 0.013). All these parameters, except LDH, varied significantly already at 1 month after diet initiation. Also, lower levels of insulin (P = 0.025), leptin (P = 0.023), and EGF (P = 0.035) were associated with a greater (>5%) weight loss. Collectively, our data support a precocious improvement of insulin and leptin sensitivity after a modest calorie restriction and weight reduction. Moreover, EGF and LDH may represent novel markers of obesity, which deserve further investigations.
    Mediators of Inflammation 03/2014; 2014:750860. DOI:10.1155/2014/750860 · 2.42 Impact Factor