Osteoarthritis, inflammation an 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
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 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.
Available from: sciencedirect.com
- "Obesity , presents a major challenge to health across the life course around the world, has affected over one-third of the world's population today and emerged as a major public health concern (Visscher and Seidell, 2001; Yang and Colditz, 2015; Sengupta et al., 2015; Medehouenou et al., 2015). As a multifactorial disease with genetic, behavioral, socioeconomic , and environmental origins, obesity along with overweight, raises the risk of morbidity and mortality from cardiovascular disease, diabetes mellitus, cancer, osteoarthritis, and sleep apnea (Speliotes et al., 2010; Prospective Studies, C, et al., 2009; Gallagher and LeRoith, 2015; Berenbaum et al., 2013). "
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ABSTRACT: Objective: PBEF1 and its polymorphisms may be important in the physiopathology of obesity. We hypothesized that polymorphisms in PBEF1 gene may modify body mass index (BMI). Methods: Thus, we systematically screened 4 tagging polymorphisms (rs4730153, rs2058540, rs3801267 and rs16872158) in PBEF1 gene and evaluated the association between the genetic variants and BMI in a population-based study including 442 subjects in northern China. Results: We found that the SNP rs3801267 was significantly associated with decreased BMI (P=0.026 in additive model), while the other 2 SNPs (rs4730153 and rs16872158) showed a borderline significant association with decreased BMI (P=0.068 and 0.060 in additive models). Combined analysis of these 3 SNPs showed a significant allele-dosage association between the number of variant alleles and decreased BMI (Ptrend=0.007). Conclusions: These findings indicate that genetic variants in PBEF1 gene may modify individual BMI in the Chinese population.
Available from: Xinlin Yang
- "Subchondral bone releases cytokines while the fat pads release adipokines such as leptin, resistin, adiponectin, visfatin, and chemerin . 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)   , nitric oxide synthase (NOS) , Toll-like receptor (TLR) , and other cytokine production  . Additionally, joint-associated fat pads are innervated by Cfiber neurons which release substance P, thereby increasing pain sensitivity, proinflammatory cytokine production, and vascular permeability  . "
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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.
Available from: Tarik S Onur
- "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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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.
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.
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.
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.
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