Obesity fuels the upsurge in rheumatoid arthritis.
Department of Health Sciences Research, Mayo Clinic, Mayo Clinic College of Medicine, Rochester, Minnesota, USA
Arthritis care & research
OBJECTIVE: To determine whether the "obesity epidemic" could explain the recent rise in the incidence of RA. BACKGROUND: Obesity is an under-recognized risk factor for RA. In recent years both the prevalence of obesity and the incidence of RA have been rising. METHODS: An inception cohort of Olmsted County, Minnesota residents who fulfilled 1987 American College of Rheumatology criteria for RA in 1980-2007 was compared to population-based controls (matched on age, sex and calendar year). Heights, weights and smoking status were collected from medical records. Obesity was defined as body mass index (BMI) = 30 kg/m2. Conditional logistic regression was used to assess the influence of obesity on developing RA. Population attributable risk was used to estimate the incidence of RA in the absence of obesity. RESULTS: The study included 813 patients with RA and 813 controls. Both groups had extensive medical history available prior to incidence/index date (mean 32.2 years), and approximately 30% of each group were obese at incidence/index date. The history of obesity was a significant risk factor for developing RA (OR:1.24; 95 % CI: 1.01, 1.53 adjusted for smoking status). In 1985-2007 the incidence of RA rose by an increment of 9.2 per 100,000 among women. Obesity accounted for 4.8 per 100,000 (or 52%) of this increase. CONCLUSION: Obesity is associated with a modest risk for developing RA. Given the rapidly increasing prevalence of obesity, this has had a significant impact on RA incidence and accounts for much of the recent increase in incidence of RA. © 2012 by the American College of Rheumatology.
Available from: Mark A Reynolds
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ABSTRACT: Inflammatory periodontal diseases exhibit an association with multiple systemic conditions. Currently, there is a lack of consensus among experts on the nature of these associations and confusion among health care providers and the public on how to interpret this rapidly growing body of science. This article overviews the current evidence linking periodontal diseases to diabetes, cardiovascular disease, osteoporosis, preterm low birth weight babies, respiratory diseases, and rheumatoid arthritis.
Evidence was taken from systematic reviews, clinical trials, and mechanistic studies retrieved in searches of the PubMed electronic database. The available data provide the basis for applied practical clinical recommendations.
Evidence is summarized and critically reviewed from systematic reviews, primary clinical trials, and mechanistic studies
Surrogate markers for chronic periodontitis, such as tooth loss, show relatively consistent but weak associations with multiple systemic conditions. Despite biological plausibility, shorter-term interventional trials have generally not supported unambiguous cause-and-effect relationships. Nevertheless, the effective treatment of periodontal infections is important to achieve oral health goals, as well as to reduce the systemic risks of chronic local inflammation and bacteremias. Inflammatory periodontal diseases exhibit an association with multiple systemic conditions. With pregnancy as a possible exception, the local and systemic effects of periodontal infections and inflammation are usually exerted for many years, typically among those who are middle-aged or older. It follows that numerous epidemiological associations linking chronic periodontitis to age-associated and biologically complex conditions such as diabetes, cardiovascular disease, osteoporosis, respiratory diseases, rheumatoid arthritis, certain cancers, erectile dysfunction, kidney disease and dementia, have been reported. In the coming years, it seems likely that additional associations will be reported, despite adjustments for known genetic, behavioral and environmental confounders. Determining cause-and-effect mechanisms is more complicated, especially in circumstances where systemic effects may be subtle. Currently, however, there is a lack of consensus among experts on the nature of these associations and confusion among health care providers and the public on how to interpret this rapidly growing body of science. This article overviews the current evidence linking periodontal diseases to diabetes, cardiovascular disease, osteoporosis, preterm/low birth weight babies, respiratory diseases, and rheumatoid arthritis.
The journal of evidence-based dental practice 09/2012; 12(3 Suppl):20-8. DOI:10.1016/S1532-3382(12)70006-4
Available from: Jorge A Roman-Blas
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ABSTRACT: To study whether hypercholesterolemia increases articular damage in a rabbit model of chronic arthritis.
Hypercholesterolemia was induced in eighteen rabbits by administrating a high-fat diet (HFD). Fifteen rabbits were fed normal chow as controls. Chronic arthritis (AIA) was induced in half of the HFD and control rabbits, previously immunized, by intra-articular injections of ovalbumin. After sacrifice, lipid and systemic inflammation markers were analyzed in blood serum. Synovium was analyzed by Krenn score, multinucleated cell counting, immunohistochemistry of RAM11 and CD31, and TNF-alpha and MCP-1 gene expression. Active bone resorption was assessed by protein expression of RANKL, OPG and quantification of cathepsin K, contact surface and invasive area of pannus into bone.
Rabbits receiving HFD showed higher total serum cholesterol, HDL, triglycerides and CRP levels than rabbits fed normal diet. Synovitis score was increased in HFD, and particularly in AIA and AIA+HFD groups. AIA+HFD synovium was characterized by a massive infiltration of RAM11+ cells, higher presence of multinucleated foam cells and bigger vascularization than AIA. Cathepsin K+ osteoclasts and contact surface of bone resorbing pannus were also increased in rabbits with AIA+HFD compared with AIA alone. Synovial TNF-alpha and MCP-1 gene expression was increased in AIA and HFD rabbits compared with healthy animals. RANKL protein expression in AIA and AIA+HFD groups was higher compared with either HFD or normal groups.
This experimental model demonstrates that hypercholesterolemia increments joint tissue damage in chronic arthritis, being foam macrophages key players in this process.
Arthritis research & therapy 08/2013; 15(4):R81. DOI:10.1186/ar4261 · 3.75 Impact Factor
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The objective of this study was to evaluate the incidence of diabetes among patients with PsA and RA in the general population.
We conducted a cohort study using an electronic medical records database representative of the UK general population (1986-2010). We estimated hazard ratios (HRs) for incident diabetes in PsA, psoriasis and RA cohorts compared with age- and sex-matched comparison cohorts without the corresponding conditions, adjusting for BMI, smoking, alcohol use, co-morbidities and glucocorticoids at baseline.
Cohorts included 4196 persons with PsA, 59 281 with psoriasis and 11 158 with RA, with mean follow-up times of 5.9, 5.8 and 5.5 years, respectively. Incidence rates for diabetes were 7.3, 6.4 and 6.3 cases per 1000 person-years among individuals with PsA, psoriasis and RA, respectively. Age- and sex-matched HRs for diabetes were 1.72 (95% CI 1.46, 2.02) in PsA, 1.39 (95% CI 1.32, 1.45) in psoriasis and 1.12 (95% CI 1.01, 1.25) in RA. After adjustment for BMI, smoking and alcohol, the HRs were attenuated substantially (1.43, 1.24 and 1.00, respectively). With further adjustment for baseline glucocorticoid use and co-morbidities, the HRs were 1.33 (1.09, 1.61) in PsA, 1.21 (1.15, 1.27) in psoriasis and 0.94 (0.84, 1.06) in RA.
This general population study suggests an increased incidence of diabetes in PsA and RA, which is substantially explained by obesity and lifestyle factors. These findings support the importance of managing such factors in PsA and RA patients.
Rheumatology (Oxford, England) 10/2013; 53(2). DOI:10.1093/rheumatology/ket343 · 4.48 Impact Factor
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