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: 4.89). 10/2012; 25(1). DOI: 10.1097/BOR.0b013e32835a9414
Source: PubMed


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.

Preclinical studies targeting adipokines are now expected to provide new hope for patients with osteoarthritis, especially those with metabolic syndrome.

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    • "Subchondral bone releases cytokines while the fat pads release adipokines such as leptin, resistin, adiponectin, visfatin, and chemerin [7]. Although the role of adipokines in OA remains to be conclusively elucidated, many studies have implied that they may act as chemokines and increase matrix-degrading enzymes matrix metalloproteinase (MMP) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) [7] [8] [9], nitric oxide synthase (NOS) [10], Toll-like receptor (TLR) [7], and other cytokine production [7] [11]. Additionally, joint-associated fat pads are innervated by Cfiber neurons which release substance P, thereby increasing pain sensitivity, proinflammatory cytokine production, and vascular permeability [12] [13]. "
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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 06/2015; 2015:1-13. DOI:10.1155/2015/192415 · 2.93 Impact Factor
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    • "Factors such as diet, increased body mass and obesity have been studied in both clinical and basic scientific research, as they relate to osteoarthritis onset and progression.3,7,8,9-15 Additionally, the literature also investigated the role that increased adipose tissue plays in increased inflammatory response in the joint tissues.7,16,17 "
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    ABSTRACT: Objectives: Our objective in this article is to test the hypothesis that type 2 diabetes mellitus (T2DM) is a factor in the onset and progression of osteoarthritis, and to characterise the quality of the articular cartilage in an appropriate rat model. Methods: T2DM rats were obtained from the UC Davis group and compared with control Lewis rats. The diabetic rats were sacrificed at ages from six to 12 months, while control rats were sacrificed at six months only. Osteoarthritis severity was determined via histology in four knee quadrants using the OARSI scoring guide. Immunohistochemical staining was also performed as a secondary form of osteoarthritic analysis. Results: T2DM rats had higher mean osteoarthritis scores than the control rats in each of the four areas that were analysed. However, only the results at the medial and lateral femur and medial tibia were significant. Cysts were also found in T2DM rats at the junction of the articular cartilage and subchondral bone. Immunohistochemical analysis does not show an increase in collagen II between control and T2DM rats. Mass comparisons also showed a significant relationship between mass and osteoarthritis score. Conclusions: T2DM was found to cause global degeneration in the UCD rat knee joints, suggesting that diabetes itself is a factor in the onset and progression of osteoarthritis. The immunohistochemistry stains showed little to no change in collagen II degeneration between T2DM and control rats. Overall, it seems that the animal model used is pertinent to future studies of T2DM in the development and progression of osteoarthritis. Cite this article: Bone Joint Res 2014;3:203-11.
    06/2014; 3(6):203-11. DOI:10.1302/2046-3758.36.2000244
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    • "Known risk factors for OA are age, female gender, and obesity [2]. Recently, it has been pointed out that OA is not a mere degenerative joint disease but a complex pathology that, besides the cartilage, involves the synovial membrane and the subchondral bone with a significant local inflammatory reaction [3]. Furthermore , OA is also associated with an increase in comorbid risk factors including cardiovascular disease (CVD) and hypertension [4] [5] [6]. "
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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.
    Egyptian Rheumatologist 04/2014; 36(2). DOI:10.1016/j.ejr.2013.12.001
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