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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Upper body obesity, related to visceral fat accumulation, is known to increase the risk of various adult diseases, especially type 2 diabetes and cardiovascular disease. This study was conducted to clarify the relationship between upper body obesity and periodontitis. We studied 643 apparently healthy, dentulous Japanese adults who attended programs at Fukuoka Health Promotion Center. Waist-hip ratio, body-mass index (BMI), and body fat were significant risk indicators for periodontitis after adjustment for known risk factors (p < 0.002). Subjects were divided into four BMI (or body fat) categories. In only the subjects with high waist-hip ratio, higher categories of BMI (or body fat) significantly increased the adjusted risk of periodontitis, compared with subjects with low waist-hip ratios and the lowest category of BMI (or body fat). The reported relationship between cardiovascular disease and periodontitis should be reconsidered, since abdominal adiposity or visceral fat can be related to both diseases.
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PMID:Relationship between upper body obesity and periodontitis. 1159 23

Obesity has a prevalence of approximately 10% among Dutch adults. It is a chronic, incurable disease with a high mortality and co-morbidity. The co-morbidity can be reduced significantly by a sustained moderate weight loss (5-15%). The main cause of obesity is an imbalance between energy intake and energy expenditure. The primary treatment combines dietary education, behaviour modification and increased physical activity, followed by pharmacotherapy or surgery when necessary. Obesity is related to several aspects of oral health, such as caries, periodontitis and xerostomia. In addition, obesity may have implications for dental treatment.
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PMID:[Obesity and oral health]. 1630 Mar 30

Type 2 diabetes mellitus and obesity are the most common nutritional disorders in developed and developing countries. Increased prevalence of periodontal disease is a well-known complication of type 2 diabetes mellitus (DM). As obesity is generally the first step toward type 2 diabetes mellitus, it is possible to find exacerbated periodontal disease in obese patients, also. The purpose of this cross-sectional study was to investigate the periodontal status and aspartate aminotransferase and lactate dehydrogenase enzyme activities in gingival crevicular fluid (GCF) of type 2 diabetic and/or obese chronic periodontitis patients. A total of 39 chronic periodontitis patients participated in the study. The study population was divided into four groups according to body mass index and type 2 DM status: 1) type 2 DM obese patients, n = 8; 2) type 2 DM patients, n = 12; 3) obese patients, n = 8; 4) systemically healthy control group, n = 11. Enzyme activities in gingival crevicular fluid and periodontal status were evaluated. No significant differences in age, gingival index, plaque index, aspartate aminotransferase and lactate dehydrogenase enzyme activities were observed, but probing depths were significantly higher in the DM groups than in the control group. Obesity did not seem to be a significant factor in any parameters evaluated. The present study showed increased probing depth values for the diabetic groups but failed to show any significant relation between obesity and enzyme activity or periodontal status. However, the slightly increased probing depth values in the obese groups might be a clue to an impaired immune response and predisposition to periodontitis in that patient group.
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PMID:Periodontal status and cytoplasmic enzyme activities in gingival crevicular fluid of type 2 diabetic and/or obese patients with chronic periodontitis. 1645 82

Previous epidemiologic studies have suggested that periodontal disease is closely related to obesity and glucose tolerance. As the level of adiponectin, an adipocyte-derived cytokine, in plasma had been reported to decrease in obese and type 2 diabetes patients, we explored the role of adiponectin in the etiology of periodontitis using the D clone of RAW264, a clone that exhibits highly efficient osteoclast formation, to determine whether adiponectin acts as a regulatory molecule in osteoclast formation stimulated by lipopolysaccharide of periodontopathic bacteria. We observed that adiponectin acted as a potent inhibitor of osteoclast formation stimulated by Toll-like receptor 4 (TLR4) ligand and receptor activator of NF-kappaB ligand (RANKL). Because NF-kappaB is an important transcription factor in osteoclast formation, we examined the effect of adiponectin on its transcriptional activity. A luciferase assay showed that adiponectin was able to inhibit the TLR4-mediated NF-kappaB activity in RAW264 cells. In addition, we observed that the cytokine was actually able to inhibit TLR4-mediated expression of the gene for inducible nitric oxide synthase and production of nitric oxide in the cells. These observations strongly suggest that adiponectin may function as a negative regulator of lipopolysaccharide/RANKL-mediated osteoclast formation in periodontal disease.
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PMID:Adiponectin inhibits osteoclast formation stimulated by lipopolysaccharide from Actinobacillus actinomycetemcomitans. 1709 90

Recent studies have suggested that several systemic conditions--such as obesity, hypertension, hyperlipidemia, and diabetes--are related to periodontitis. The objective of this study was to examine the relationship between periodontitis and 5 components of metabolic syndrome--abdominal obesity, triglyceride level, high-density lipoprotein cholesterol level, blood pressure, and fasting blood sugar level--in 584 Japanese women. In multivariate analyses, persons exhibiting more components of metabolic syndrome had significantly higher odds ratios for a greater pocket depth and clinical attachment loss than did those with no components; the odds ratios for a greater pocket depth and clinical attachment loss of the persons exhibiting 4 or 5 components were 6.6 (95% confidence interval = 2.6-16.4) and 4.2 (95% confidence interval = 1.2-14.8), respectively. These results indicate that metabolic syndrome increases risk of periodontitis, and suggest that people exhibiting several components of metabolic syndrome should be encouraged to undergo a periodontal examination.
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PMID:Relationship of metabolic syndrome to periodontal disease in Japanese women: the Hisayama Study. 1731 61

The prevalence of obesity has increased substantially over the past decades in most industrialized countries. Obesity is a systemic disease that predisposes to a variety of co-morbidities and complications that affect overall health. Cross-sectional studies suggest that obesity is also associated with oral diseases, particularly periodontal disease, and prospective studies suggest that periodontitis may be related to cardiovascular disease. The possible causal relationship between obesity and periodontitis and potential underlying biological mechanisms remain to be established; however, the adipose tissue actively secretes a variety of cytokines and hormones that are involved in inflammatory processes, pointing toward similar pathways involved in the pathophysiology of obesity, periodontitis, and related inflammatory diseases. We provide an overview of the definition and assessment of obesity and of related chronic diseases and complications that may be important in the periodontist's office. Studies that have examined the association between obesity and periodontitis are reviewed, and adipose-tissue-derived hormones and cytokines that are involved in inflammatory processes and their relationship to periodontitis are discussed. Our aim is to raise the periodontist's awareness when treating obese individuals.
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PMID:Obesity, inflammation, and periodontal disease. 1745 58

Obesity (Body Mass Index > or = 30 kg/m2) has a high prevalence of 15-30% among European and American populations. It is an incurable chronic disease with a considerable mortality and co-morbidity. The co-morbidity can be reduced substantially by a moderate weight loss of 5-15%. The main cause of obesity is an imbalance between energy intake and energy expenditure. Therefore, the treatment starts with an energy restricted diet, a reduction of sedentary lifestyle, increased physical activity, and behavioural therapy to change eating habits. When necessary, this treatment can be followed by pharmacotherapy or surgery. Obesity is related to several aspects of oral health, such as caries, periodontitis and xerostomia. In addition, obesity may have implications for the dental treatment plan.
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PMID:Oral aspects of obesity. 1784 83

Obesity has been suggested to be associated with an increased susceptibility to bacterial infection. However, few studies have examined the effect of obesity on the immune response to bacterial infections. In the present study, we investigated the effect of obesity on innate immune responses to Porphyromonas gingivalis infection, an infection strongly associated with periodontitis. Mice with diet-induced obesity (DIO) and lean control C57BL/6 mice were infected orally or systemically with P. gingivalis, and periodontal pathology and systemic immune responses were examined postinfection. After oral infection with P. gingivalis, mice with DIO had a significantly higher level of alveolar bone loss than the lean controls. Oral microbial sampling disclosed higher levels of P. gingivalis in mice with DIO vs. lean mice during and after infection. Furthermore, animals with DIO exposed to oral infection or systemic inoculation of live P. gingivalis developed a blunted inflammatory response with reduced expression of TNF-alpha, IL-6, and serum amyloid A (SAA) at all time points compared with lean mice. Finally, peritoneal macrophages harvested from mice with DIO and exposed to P. gingivalis exhibited reduced levels of proinflammatory cytokines compared with lean mice and when exposed to P. gingivalis LPS treatment had a significantly reduced recruitment of NF-kappaB to both TNF-alpha and IL-10 promoters 30 min after exposure. These data indicate that obesity interferes with the ability of the immune system to appropriately respond to P. gingivalis infection and suggest that this immune dysregulation participates in the increased alveolar bone loss after bacterial infection observed in mice with DIO.
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PMID:Diet-induced obesity in mice causes changes in immune responses and bone loss manifested by bacterial challenge. 1807 29

The interrelation between diabetes mellitus and inflammatory periodontal disease has been intensively studied for more than 50 years, a real bidirectional influence existing between patient's glycemic level disorder and periodontal territories alteration. Several studies developed in this direction emerged to the evidences that reveal a general increase of prevalence, extent and severity of gingivitis and periodontitis. Inflammation plays an important role in this interrelation, orchestrating both the periodontal disease and diabetes mellitus pathogeny and complications. Conversely, periodontal disease--infectious disease characterized by a significant inflammatory component--can seriously impair metabolic control of some diabetic patient. Moreover, treatment of periodontal disease and reduction of oral signs of inflammation may have a beneficial result on the diabetic condition (1). Less clear are the mechanisms governing this interrelation (even the literature is abundant in this direction), and, very probably, periodontal diseases serve as initiators of insulin resistance (in a way similar to obesity), thereby aggravating glycemic control. Further research is so imposed in order to clarify this aspect of the relationship between diabetes and periodontal disease.
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PMID:[Relationship diabetes mellitus-periodontal disease: etiology and risk factors]. 1829 11

Resistin and adiponectin, recently discovered adipokines, are secreted from adipose tissue, with postulated opposing functions in insulin resistance and inflammation. More recently, an abundance of resistin was detected in macrophages, which suggests its important role in inflammation. The aim of this study was to clarify circulating serum adipokine levels in women with periodontitis. Thirty-four women with moderate to severe periodontitis and 42 control individuals with healthy gingiva (50- to 59-year-old women) were selected. The serum level of adipokines was analyzed between groups, along with the obesity index, smoking status, and age. Having periodontitis was significantly associated with an increased level of resistin, both in bivariate (OR, 3.0; 95% CI, 1.2-7.6) and multivariate (adjusted OR, 3.1; 95% CI, 1.1-8.6) analyses. The association of periodontitis with a decreased level of adiponectin did not reach statistical significance. It was concluded that an increased serum resistin level in middle-aged Japanese women with periodontitis may affect systemic health.
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PMID:Serum levels of resistin and adiponectin in women with periodontitis: the Hisayama study. 1836 11


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