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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The periodontal health of smokers and non-smokers with non-insulin-dependent diabetes mellitus (NIDDM) and non-smokers with periodontitis who were not suffering from a systemic disease was assessed. The investigation was carried out on 60 adult subjects. Levels of blood glucose, glycosylated haemoglobin and immunoglobulins G, A and M were determined, together with the plaque index, gingival index, probing pocket depths and clinical attachment level. Periodontitis was more severe in smokers and non-smokers with NIDDM than non-smokers without NIDDM, and the periodontal condition (clinical attachment level, probing pocket depth and gingival bleeding) was better in non-smokers with NIDDM than smokers with NIDDM. The results suggest that diabetes and smoking are high-risk factors for periodontal disease.
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PMID:The influence of smoking and non-insulin-dependent diabetes mellitus on periodontal disease. 1202 18

Periodontal disease is the result of a complex interplay of bacterial infection and host responses, and is often modified by various systemic diseases such as diabetes mellitus. Such diseases are capable of affecting the periodontium and/or the treatment of periodontal disease. However, recent research has changed our concept of how periodontal disease should be treated. Here we present several concerns directed towards the periodontal therapy of patients with diabetes mellitus based on our studies. When treating periodontitis patients who have diabetes mellitus it is important to consider the type of diabetes. Patients with non-insulin dependent diabetes mellitus can be further classified according to the degree of insulin resistance, since recent epidemiological studies have suggested that successful anti-microbial therapy might result in improved insulin resistance in highly insulin resistant patients. Because the major contributing factor for insulin resistance is currently considered to be the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha), and because periodontal surgery may cause transient bacteremia which may up-regulate the serum TNF-alpha level, which in turn suppresses insulin action, patients should be strictly treated non-surgically and their serum TNF-alpha levels should be periodically monitored. On the other hand, diabetic patients positive for serum anti-glutamate decarboxylase auto-antibody should be examined for the source of this antibody, since 1) gingival and periodontal ligament fibroblasts were found to express glutamate decarboxylase, and 2) some otherwise healthy periodontitis patients develop anti-glutamate decarboxylase antibody. Thus, chronic periodontitis may influence the level of this antibody which is widely used as a predictive marker for slowly progressive insulin dependent diabetes mellitus. Not only is periodontal disease thereby affected by systemic diseases, but carefully managed periodontal therapy may also have a positive effect on the general health of patients with systemic diseases.
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PMID:Negative effects of chronic inflammatory periodontal disease on diabetes mellitus. 1266 61

Infections of the tissue surrounding the teeth (periodontitis) are usually caused by anaerobic gram-negative microorganisms. This infection causes destruction of the supporting alveolar bone and can lead to tooth loss. Removal of these microorganisms can slow or arrest the progression of periodontitis. Diabetes patients are at greater risk of developing periodontitis, may not respond as well to periodontal therapy as nondiabetic patients, and may require more aggressive treatment to manage periodontitis. Microorganisms that cause periodontitis and the host response to these may increase insulin resistance in diabetic patients. Treatment of periodontitis could improve glycemic control. A model is presented in which periodontal pathogens may cause increases in proinflammatory cytokines that mediate increases in insulin resistance, resulting in an increase in blood glucose. Following periodontal therapy, this process may be reversed.
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PMID:Periodontal disease and diabetes mellitus. 1476 80

Studies indicate that a dual pathway between diabetes mellitus and periodontal disease exists. Elimination of periodontal infection by using systemic antibiotics in conjunction with scaling and root planing (SRP) improved metabolic control in diabetic patients, as defined by reduction in glycated haemoglobin or reduction in insulin requirements (Grossi and Genco, 1998). The aim of this randomised pilot clinical trial was to determine if type 1 diabetes patients with periodontitis will experience a reduction in HbA1c levels when treated with locally delivered minocycline microspheres (Arestin) as an adjunct to scaling and root planing. Twenty adult patients with poorly controlled diabetes (HbA1c 7.5%) and adult periodontitis, as determined by the presence of four teeth with 5 mm periodontal pockets, two of which had 6-9 mm pockets and bleeding on probing, were included in the study. All patients received full mouth SRP at baseline. Arestin was administered to all pockets > or => or = 5 mm at baseline and again at 12 weeks in the test group. Probing depth (PD), clinical attachment level (CAL), plaque index (PI), gingival index (GI), and HbA1c were evaluated at baseline and at weeks 6, 12, 18 and 24. The results demonstrated that local administration of Arestin as an adjunct to scaling and root planing is significantly more effective in reducing probing depths and providing a gain in clinical attachment levels than scaling and root planing alone in type 1 diabetic patients. Hb1Ac was reduced in all patients; however the difference between the test and control groups was not significant.
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PMID:Periodontal treatment by Arestin and its effects on glycemic control in type 1 diabetes patients. 1553 85

Comprehensive stomatologic examination of 45 patients with chronic generalized parodontitis (CGP) was combined with parallel determination of immunoreactive insulin (IRI) in blood. In 30 patients CGP developed on the background of metabolic syndrome (MS). Clinical and X-ray examination of periodontal tissues disclosed that CGP in patients with MS was characterized by active and aggressive course. A correlation between CGP severity degree and level of IRI in blood was established.
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PMID:[Inflammatory diseases of the parodontium in patiens with metabolic syndrome]. 1560 67

An elevated level of C-reactive protein (CRP) predicts the future development of coronary heart disease. Periodontitis appears to up-regulate CRP. CRP is produced by hepatocytes in response to interleukin-6 (IL-6). A major source of IL-6 in obese subjects is adipocytes. We hypothesized that lipopolysaccharide (LPS) from periodontal pathogens stimulated adipocytes to produce IL-6, and that the production was suppressed by the drugs targeted against insulin resistance, thiazolidinedione (pioglitazone), since this agent potentially showed an anti-inflammatory effect. Mouse 3T3-L1 adipocytes were stimulated with E. coli, P. gingivalis, and F. nucleatum LPS. The IL-6 concentration in culture supernatants was measured. All LPS stimulated adipocytes to produce IL-6. Although pioglitazone changed adipocyte appearance from large to small, and completely suppressed P. gingivalis and F. nucleatum LPS-induced IL-6 production, E. coli LPS-induced IL-6 production was not efficiently blocked. Thus, pioglitazone completely blocked periodontal-bacteria-derived LPS-induced IL-6 production in adipocytes, a major inducer of CRP.
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PMID:Thiazolidinedione (pioglitazone) blocks P. gingivalis- and F. nucleatum, but not E. coli, lipopolysaccharide (LPS)-induced interleukin-6 (IL-6) production in adipocytes. 1572 63

The problem of treatment of periodontitis remains one of the hot topics in practical stomatology. It has been established that modern adaptogenic infection is rather aggressive to whole organism of a human being. All these demands accurate approach while choosing of a conservative method of treatment for such forms as acute and chronic periodontitis. There were 27 children under observation with diabetes mellitus of type 1 (I group). Mean age was 10.5+/-0.75 years. 15 were girls and 13 boys. All patients from the I group were examined for the pathologies of oral cavity. In 100% dryness in a mouth and in 67% bleeding from the gum had been revealed. The mild form of chronic catarrhal gingivitis was revealed in 12 patients, moderate in 5, chronic hypertrophic gingivitis in 8 respectively. Studying of pH of saliva and lactate dehydrogenase (LDH) activity in children with periodontitis developed on the background of recently diagnosed type 1 diabetes mellitus has shown, that pH of saliva was equal to 5.3+/-0.18. In control group (healthy children) pH of saliva was 6.8+/-0.06. In the conclusion it should be emphasized, that we have tried to explain some aspects of multiple character of development of periodontitis at recently discovered insulin-depended diabetes mellitus. Character of changes of some properties of saliva pH and of enzyme activity of LDG promotes to carrying out medical and preventive actions, influencing the main blocks of pathogenesis of this pathological process. Besides, we consider possibility of inclusion the studied parameters of mixed saliva in the algorithm of investigation of periodontitis in children with recently diagnosed type 1 diabetes mellitus.
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PMID:[Diagnostic value of definition of lactate dehydrogenase in mixed saliva in children with periodontitis at diabetes mellitus, type I]. 1651 Sep 13

Dendritic cells (DC) are innate immune effectors and are critically involved in regulating T cell immunity. Osteoclasts (OC) are bone-resorbing cells derived from the monocyte/macrophage lineage in response to receptor activator of NF-kappaB ligand (RANKL). DC and T cells form aggregates in the inflammatory infiltrates at active disease sites in human and in experimental rheumatoid arthritis and periodontitis. We investigated whether DC interactions with T cells in the bone environment can support the development of functional OC. In the present study, we demonstrate that upon proper activation by microbial or protein Ags (namely Actinobacillus actinomycetemcomitans, bovine insulin, and outer membrane protein-1) and during immune interactions with CD4+ T cells in vitro, murine BM-derived and splenic CD11c+ DC (CD11b- F4/80- Ly-6C- CD31-) develop into TRAP+ CT-R+ cathepsin-k+ functional OC in a RANKL/RANK-dependent manner. Rescue and blocking experiments using CD11c+ DC derived from Csf-1(-/-) op/op mice show that M-CSF is required "before" developing such osteoclastogenic potential upstream of RANKL/RANK signaling, suggesting that immature CD11c+ DC can indeed act like OC precursors. In addition, these CD11c+ DC-derived OC are capable of inducing bone loss after adoptive transfer in vivo. These data suggest a direct contribution of DC during immune interactions with CD4+ T cells to inflammation-induced osteoclastogenesis. Therefore, our findings not only provide further evidence for DC plasticity, but also extend the current paradigm of osteoimmunology.
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PMID:Immune interactions with CD4+ T cells promote the development of functional osteoclasts from murine CD11c+ dendritic cells. 1692 Sep 72

This paper focused on the relationship between periodontitis and Type 2 diabetes mellitus (T2DM). There is an abundance of evidence that diabetes mellitus play important etiological roles in periodontal diseases. In addition, periodontal diseases have powerful and multiple influences on the occurrence and severity of systemic conditions and diseases, such as diabetes mellitus, cardiovascular disease, respiratory disease and pregnancy complications. The relationship of periodontitis and diabetes has been supported by sufficient evidences in the past twenty years: (1) diabetes is an independent risk factor of chronic periodontitis; (2) metabolic control will improve the prognosis of chronic periodontitis; (3) the treatment of chronic periodontitis will improve the metabolic level. Our recent investigation on periodontal status in the families of type 2 diabetes mellitus further confirmed the relationship. It was showed that the periodontal index such as probing depth (PD), attachment loss (AL) and numbers of tooth loss in diabetes family members were significantly higher than non-diabetes family members, while no difference of periodontal parameters was found between well control family members and non diabetes family members. In the development of type 2 diabetes (T2DM) and its complications, the advanced glycation end products (AGEs) and its receptors were to be recognized as important factors. The distributions of AGEs and the receptor for AGEs (RAGE) are highly consistent in various tissues. One study in our laboratory demonstrated that RAGE was strongly expressed in gingival tissues gathered from T2DM patients with periodontitis compared with systemically healthy chronic periodontitis patients, the expression of RAGE was positively correlated with the expression of TNF-alpha, indicating that AGE-RAGE pathway was involved in the development of periodontitis in T2DM patients. It is known that inflammation could induce the prediabetic status characterized by insulin resistance and dyslipidemia. However, it is still unclear whether periodontitis is a risk factor of type 2 diabetes mellitus or not. In a current study, the effect of periodontitis on serum levels of lipid and glucose of aggressive periodontitis (AgP) patients was implied, as the average serum levels of triglycerides and glucose of a large number of AgP patients were both significantly higher than healthy control group, and serum level of total cholesterol in AgP group was positively associated with the percentage of severe attachment loss sites. It seems that periodontitis may alter serum lipid and glucose levels. Furthermore, the effect of periodontitis on diabetes in an animal study has also demonstrated that experimental moderate periodontitis as well as castration could induce insulin resistance and beta cell impairment in rats, and that combination of the two factors would aggravate the degree of insulin resistance (IR). In conclusion, interrelationship between periodontitis and diabetes has been further approved recently.
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PMID:[Association between periodontitis and diabetes mellitus]. 1730 19

Periodontitis is a chronic, dental-plaque induced inflammatory disease of the tooth-supporting tissues, resulting in a gradual loss of connective tissue attachment and alveolar bone. The interrelationship between diabetes mellitus and periodontitis has been studied for many years. At,present, there is strong evidence to suggest that the incidence and severity of periodontitis is influenced by the presence or absence of diabetes mellitus as well as by the degree of diabetes control by patients. Elevated blood glucose levels in poorly controlled diabetics result in an increase of protein glycosylation leading to amplified formation of so-called Advanced Glycation End products (AGE). AGEs are glucose products that have the ability to attract and stimulate inflammatory cells to produce inflammatory cytokines, elevating the risk of periodontal attachment and/or alveolar bone loss. Gram-negative periodontal infection significantly decreases glucose tolerance and can lead, like other types of inflammation, to an increase in the severity of diabetes. Thus, diabetes and periodontal disease form a system in which periodontitis is aggravated and metabolic control of blood glucose levels becomes more difficult. This in turn leads to mutual aggravation that results in a self-enforcing catabolic process, a vicious circle of inflammation, tissue destruction and insulin resistance.
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PMID:[The relationship of periodontitis and diabetes mellitus]. 1804 71


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