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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The interpretation of epidemiological data of periodontal disease is difficult, due to inconsistencies in the methodology used. It is not possible, therefore, to accurately assess if the prevalence of the periodontal diseases shows a world-wide decline. As long as the disease is assessed through accumulated clinical attachment loss, retention of the natural dentition in older ages entails increased prevalence in these cohorts. Contemporary epidemiological studies should ideally employ full-mouth examination of the periodontal tissues. Partial recording estimates are generally biased, especially when the prevalence of the disease is low. 2. Early-onset periodontitis is infrequent in all populations. Adult periodontitis is rather prevalent; however, advanced disease affects limited subfractions of the population (probably less than 10 to 15%). Although prevalence figures vary with race and geographic region, in most cases, the progression pattern of the disease seems compatible with the retention of a functional dentition throughout life. 3. Of a plethora of behavioral and environmental risk markers identified by multi-variate analysis, smoking and presence of certain subgingival microorganisms have been proven to be true risk factors. The same holds true for diabetes mellitus, a systemic condition that confers a risk for periodontal disease which is independent of the effect of other significant factors. 4. In certain cases, periodontal infections appear to have a systemic impact on the host. Most recent data indicate that periodontal disease may confer risk for coronary heart disease and pre-term low birth weight.
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PMID:Periodontal diseases: epidemiology. 911 56

Serum IgG responses to the cell envelope proteins (CEPs) from Capnocytophaga sputigena, Capnocytophaga ochracea, and Capnocytophaga gingivalis were examined in periodontally healthy and periodontitis subjects, both with and without type 1 diabetes (n = 60). Serum IgG responses to CEPs were determined by immunoblotting with biotin-goat anti-human IgG and an alkaline phosphatase-streptavidin system. Reactivity was analyzed by transmission densitometry, digitization, and computer manipulation. The patients with diabetes showed significantly (p < 0.01) fewer responses to 14 CEPs (from 81 to 10 kDa) from C. sputigena, 5 CEPs (from 90 to 17 kDa) from C. gingivalis, and the 27-kDa CEP from C. ochracea than in the non-diabetic group. The periodontitis patients showed significantly (p < 0.01) fewer responses to the 25- and 11-kDa CEPs from C. sputigena, the 125- and 17-kDa CEPs from C. gingivalis, and the 42-kDa CEP from C. ochracea than in the periodontally healthy group. HLA-DR4, HLA-DR53, and HLA-DQw3 were associated with periodontitis, while only HLA-DR4 was associated with diabetes (p < 0.02). Significant (p < 0.01) correlations were found between HLA-DR2 and IgG reactivity patterns associated with non-diabetics, and between HLA-DR4 and IgG reactivity patterns associated with diabetic and periodontitis subjects. These results indicate that both type 1 diabetics and periodontitis subjects have a depressed IgG antibody profile to Capnocytophaga, which may account for an increased susceptibility to periodontitis infection. Periodontitis in type 1 diabetes may be related more to the HLA-D type and altered immune function than to the diabetes itself.
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PMID:HLA-D types and serum IgG responses to Capnocytophaga in diabetes and periodontitis. 939 Apr 75

This study examined cellular and vascular changes in gingival connective tissue samples by stereologic point-counting procedures and interactive digital analyzing systems in long-term insulin-dependent diabetes mellitus patients. Gingival connective tissue capillaries representing a clinically healthy sulcus with no evidence of periodontal disease at the site of biopsy were studied in 29 patients with diabetes. Based upon their long-term medical records, 19 were identified as having poorly controlled (PIDD) and 10 as controlled insulin-dependent diabetes mellitus (CIDD). Ten nondiabetic, age- and gender-matched individuals served as controls. Thirty-nine biopsies were processed for light microscopy, and the blood vessel area was analyzed using an interactive digital analyzing system; 9 gingival biopsies, 5 diabetic and 4 controls, were processed for morphometric electron microscopic analysis. For each individual, site-specific recordings were made for the plaque index, bleeding index, probing depth, loss of attachment, and radiographic loss of interproximal alveolar bone. No evident signs of periodontitis occurred at the biopsy sites. For each PIDD patient, respective volumetric and numeric densities of cellular components including fibroblasts, neutrophilic granulocytes, monocyte/macrophages, mast cells, lymphocytes, blast cells, and plasma cells were recorded in the inflamed connective tissue (ICT). Non-cellular components such as collagen fibers and blood vessels were also recorded. PIDD patients had elevated plasma cell levels relative to controls and they appeared also to have a decreased collagen fiber density. In addition, fibroblasts occupied less volume in the ICT of PIDD patients than in controls. PIDD patients had the largest mean area of cross-section of the blood vessels, but this difference was not statistically significant (P > or = 0.211; t-test). No specific characteristics of ICT or vascular changes were detectable in adult well-controlled long-term diabetics under similar plaque conditions. Swollen and proliferated endothelial cells were frequently found in PIDD patients and the mean distance from the lumen to the outer border of basement membrane was greater in the PIDD than in the controls (P < 0.001; t-test). Overall, our findings that cellular, vascular, and connective tissue changes indicative of increased catabolism rather than anabolism detected in gingiva are especially associated with poorly controlled long-term insulin-dependent diabetes.
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PMID:Morphometric analysis of cellular and vascular changes in gingival connective tissue in long-term insulin-dependent diabetes. 944 1

Assessment of risk for periodontitis is still in its infancy. Nevertheless, a sufficient amount of dependable information exists to begin using risk assessment in the day to day practice of dentistry. The purpose of this paper is to summarise existing information about risks for periodontitis in a manner that is useful to practitioners. Risks for moderate to severe periodontitis that have been identified include cigarette smoking, advancing age, diabetes mellitus and certain other systemic conditions. These include, osteoporosis and HIV infection and conditions such as irradiation and immunosuppressive drugs that interfere with normal host defences, specific pathogenic bacteria in the subgingival flora, microbial deposits and poor oral hygiene status, bleeding on probing, previous disease experience and severity, and inheritance. Some risks such as pathogenic bacteria in the subgingival flora are strongly linked to causation of the disease while others such as bleeding on probing may indicate enhanced risk for future disease but are not known to be involved in causation and still others such as advancing age may be background factors that enhance susceptibility. While some risks such as cigarette smoking can be modified to lower the level of risk, others such as ageing are immutable and cannot be modified but need to be considered in overall risk assessment. A goal of periodontal diagnosis, treatment planning and therapy is to lower risk for future periodontal deterioration to the maximal extent. One approach to achieving this goal is described.
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PMID:Risk assessment for periodontal diseases. 944 91

A reasonable interpretation of the present evidence indicates that diabetes, when a complication of periodontitis, acts as a modifying and aggravating factor in the severity of periodontal infection. Diabetics with periodontitis who were young and poorly controlled, those who were long-duration diabetics, especially those over 30 years old, demonstrated more attachment loss, bone loss, and deeper probing pocket depths than their nondiabetic controls. It seems that the earlier the onset of diabetes and the longer the duration, especially without consistent control, the more susceptible the individual will be to periodontal disease. Consequently, once a diabetic contracts periodontal disease, it is usually more destructive. Although plaque scores of diabetics may be comparable to or even less than those of nondiabetics, diabetics often exhibit higher gingival index scores. The elevation of this particular clinical parameter is indicative of the microangiopathy associated with diabetes. Diabetic microangiopathy contributes to compromised delivery of nutrients to surrounding tissues and poor elimination of metabolic waste products. The complications associated with diabetes such as macroangiopathy, microangiopathy (i.e., retinopathy), ketoacidosis, and hyperglycemia result in impaired wound healing, immunosuppression, and susceptibility to bacterial infection. Individuals ages 30 to 40 suffering from diabetic retinopathy had significantly more gingival inflammation than controls or diabetics without complications. Collagen metabolism is defective in diabetics and is one component underlying delayed wound healing. Animal studies have been instrumental in elucidating the details of delayed wound healing. Hyperglycemia was associated with increased collagenase and protease activity in the gingiva of rats. Vascular wound healing in rats, particularly new re-endothelialization across vascular anastomoses, was significantly impaired. Diabetic abnormalities in immune response include impaired neutrophil chemotaxis, phagocytosis, and adhesion. Decreased neutrophilic chemotactic response seems to be attributable to protein factors in diabetic serum that competitively bind neutrophil receptors, thereby preventing complement-mediated phagocytosis. Because diabetics are not able to eliminate circulating immune complexes (CIC) effectively, serum CIC levels are elevated. There are microbiological differences in the characteristic flora of NIDDM patients and IDDM patients with periodontitis. These differences are not associated with diabetic impaired immune response. Ultimately, bacterial plaque is the primary etiology of periodontal diseases. Evidently, the host's response to bacterial plaque and ability to heal following surgery is altered by diabetic disease. Therefore, a thorough history regarding onset of diabetes, duration, and diabetic control would prove useful in the clinical management of diabetics presenting for treatment of periodontal disease.
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PMID:Periodontal disease, diabetes, and immune response: a review of current concepts. 947 64

Periodontitis is a chronic inflammatory disease characterized by a progression that is very much dependent on host response. The gingiva can be considered to be in a constant state of wounding (pathologic wounding by bacterial plaque) and a constant state of maintenance/repair. In this context, any metabolic disturbance in the host which compromises tissue repair/wound healing will exacerbate the progression of periodontitis. Diabetes presents an interesting example because two major complications of diabetes are delayed wound healing and periodontitis. Our previous studies indicate that delayed wound healing and periodontitis may be manifestations of a general systemic deficit in diabetes involving alteration of macrophage cytokine gene expression. The present study was designed to determine whether: 1) diabetes-induced metabolic alterations affect gingival cytokine levels; and 2) diabetes-induced metabolic alterations modify the gingival cytokine profile in periodontitis. Sprague-Dawley rats (N=12/group) were injected with streptozotocin (65 mg/kg) into the tail vein to induce diabetes (defined by blood glucose levels > 250 mg/dl) or received the injection vehicle or no treatment as controls. Periodontitis was induced in additional groups of diabetic and control rats by gavage with Porphyromonas gingivalis A7436. After 90 days, serum glucose was analyzed to document diabetes; alveolar bone level was measured to document severity of periodontitis; gingiva was harvested circumferentially from the first and second molars; and cytokines in gingival homogenates were assayed by ELISA using commercial kits. Cytokine levels were expressed as mean+/-SEM pg/microg protein. Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1beta), transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha). Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. Diabetes superimposed on periodontitis prevented these increases. Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1beta.
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PMID:Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model. 952 9

Recent epidemiologic surveys and studies have provided important information on the prevalence, extent, and severity of periodontal diseases in the United States. Over 50% of adults had gingivitis on an average of 3 to 4 teeth. Subgingival calculus was present in 67% of the population. Adult periodontitis, measured by the presence of periodontal pockets > or = 4 mm, was found in about 30% of the population on an average of 3 to 4 teeth. Severe pockets > or = 6 mm were found in less than 5% of the population. Attachment loss > or = 3 mm was found in 40% of the population. Gingival recession accounted for a significant amount of attachment loss. The prevalence of early-onset periodontitis ranged from less than 1% in 14- to 17-year-olds to 3.6% in young adults aged 18 to 34. Extensive and severe periodontitis was much more prevalent in minorities, people with less than a high school education, and those who had seen a dentist infrequently and had subgingival calculus. Smoking and diabetes have been identified as risk factors, especially diabetics with poor metabolic control, a long duration of the disease, and extensive subgingival calculus. Under managed care, there has been an expansion of soft tissue management programs in the offices of general dentists and referral guidelines which limit referral of patients with moderate periodontitis. Quality-assurance mechanisms will be essential for the diagnosis and treatment of persons with periodontitis.
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PMID:Periodontal diseases in the United States population. 952 27

The association between diabetes mellitus and periodontal disease has long been discussed, with conflicting conclusions. On the one hand, numerous reports indicate a high prevalence of periodontal disease in diabetics compared to healthy controls, while others fail to show such a relationship. Clarification of this dilemma has been occurring as the diagnostic criteria for periodontal disease destruction improve and the number and size of the populations surveyed grow. This review is based on a selective review of the literature from the present decade. To date, based mainly on an extensive study of the Pima Indians who have an extremely high incidence of non-insulin-dependent diabetes mellitus (NIDDM), it seems to be clear that patients with NIDDM have a higher prevalence and severity of periodontal disease destruction than non-diabetics in the same population. However, it must be borne in mind that these data are for a special population. Studies on patients with insulin-dependent diabetes mellitus (IDDM) indicate results similar to those found in studies on NIDDM. There is an increase in prevalence and severity of periodontitis compared to controls. For both IDDM and NIDDM, there does not appear to be any correlation between the prevalence or the severity of periodontal disease and the duration of diabetes. Well-controlled diabetic patients as measured by blood glycated hemoglobin levels have less severe periodontal disease than poorly controlled diabetics. The principles of treatment of periodontitis in diabetics are the same as those for non-diabetic patients and are consistent with our approach to all high-risk patients who have already developed periodontal disease. The major efforts should be directed at the prevention of periodontitis in patients at risk of developing diabetes. Another important clinical question relates to the influence of periodontal disease on the control of the diabetic state. Here again the literature is unclear; however, a recent development suggests that effective control of periodontal infection in patients with diabetes reduces the level of advanced glycosylation end products in the serum. If future studies can confirm this effect, then periodontal infection control must be considered an integral part of diabetic control.
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PMID:Epidemiological and clinical aspects of periodontal diseases in diabetics. 972 85

Based on our clinical observations that patients with insulin-dependent diabetes mellitus (IDDM) are subject to periodontal disease, we developed the hypothesis that hyper- or hypoglycemia might contribute to the pathogenesis of diabetic periodontitis. In this article, experimental facts that substantiate this hypothesis are presented on the basis of our studies and then discussed. Hyperglycemia progressively glycates body proteins, forming advanced glycation end products (AGE), which stimulate phagocytes to release inflammatory cytokines such as TNF-alpha and IL-6. In this context, to understand the effects of hyperglycemic episodes on periodontal health, 24 adolescent IDDM patients were examined for their periodontal status, and 3 of them were found to have periodontitis. Laboratory analyses on these 3 patients revealed that 2 had elevated serum TNF-alpha levels. These results may partly support the current hypothesis of a mechanism of diabetic complications in which abnormal cytokine levels induced by AGE could exacerbate inflammatory responses. In IDDM patients, the diabetes is often accompanied not only by hyperglycemic episodes but also by iatrogenic hypoglycemia. Periodontal ligament cells (PDL) cultured under hyperglycemic conditions were impaired in such biological functions as adhesion and motility, while cells cultured under hypoglycemic conditions (10 mg/dL) gradually dissociated from their anchor and underwent cell death. These phenomena correlated well with the expression profile of fibronectin receptor. Interestingly, these changes due to the different glucose levels were observed more intensively in PDL than in other fibroblastic cells, suggesting that the biological functions of PDL are easily led to impairment by variation or rapid fluctuation of glucose levels. These observations suggest that hyperglycemia could indirectly exacerbate inflammatory tissue destruction through the body's scavenger system against AGE, and that both hyper- and hypoglycemia might directly impair the biological functions of periodontal connective tissues through cell-matrix interactions.
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PMID:Periodontal disease as a complication of diabetes mellitus. 972 87

Diabetes mellitus is a systemic disease that affects more than 12 million people in the United States and represents a risk factor for periodontitis with odds ratios of 2.1 to 3.0. New data support the concept that in diabetes-associated periodontitis, the altered host inflammatory response plays a critical role. We have recently examined the gingival crevicular fluid (GCF) mediator level, monocytic secretion, and clinical presentation of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 non-diabetic patients with various degrees of periodontal health and disease. First, we found that there was an unexpected high level of GCF mediators among the IDDM subjects, even in the gingivitis and mild periodontitis patients. Furthermore, the GCF and monocytic mediator responses were obviously bimodal in distribution with respect to periodontal status. Gingivitis patients and mild periodontitis patients represented one low response group, and the moderate and severe periodontitis subjects the high response group. Accordingly, these 4 periodontal subgroups were pooled to form 2 main groups for analyses--group A (AAP Types I-II) and group B (AAP Types III-IV). Diabetics had significantly higher GCF levels of both PGE2 and IL-1 beta when compared to non-diabetic controls with similar periodontal status. Within the diabetic group, the GCF levels of these inflammatory mediators were almost 2-fold higher in group B subjects when compared to diabetics from group A. Among diabetics, GCF TNF-alpha levels were only marginally detectable and no significant difference was found between group A and group B patients. Insulin-dependent diabetic patients with gingivitis or mild periodontitis (group A) and moderate to severe periodontitis (group B) have abnormal monocytic inflammatory secretion in response to LPS challenge from Porphyromonas gingivalis (P. gingivalis) as compared to non-diabetic periodontal patients. Data suggest that the diabetic state results in a significantly upregulated monocytic secretion of PGE2 (4.2-fold), IL-1 beta (4.4-fold), and TNF-alpha (4.6-fold) when compared to non-diabetic controls. Within diabetics, LPS dose-response curves demonstrated that monocytes from group B patients secreted approximately 3 times more PGE2 and 6.2 times more TNF-alpha than those from group A; however, there was no significant difference in monocytic IL-1 beta secretion between the 2 diabetic groups. This upregulated monocytic trait is thought to exist independently of the presence of severe periodontal disease since, in non-diabetic patients with adult periodontitis, Gram-negative bacterial infections alone are not sufficient to elicit a systemic hyperresponsive monocytic trait. Between group A and group B diabetics, there was no significant difference in metabolic control as expressed by mean level of glycosylated hemoglobin (HbA1c). In conclusion, our data suggest that diabetic patients have exaggerated inflammatory responses when compared to non-diabetic controls. Furthermore, within diabetics, individuals with moderate to severe periodontitis (group B) have significantly elevated monocytic secretion of PGE2 and TNF-alpha upon LPS challenge and significantly higher GCF levels of PGE2 and IL-1 beta when compared to patients with gingivitis or mild periodontal disease (group A). Thus, we suggest that insulin-dependent diabetes mellitus is a significant risk factor for more severe periodontal disease because, as compared to non-diabetics, diabetic subjects react with an abnormally high degree of inflammation to an equivalent bacterial burden.
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PMID:PGE2, IL-1 beta, and TNF-alpha responses in diabetics as modifiers of periodontal disease expression. 972 89


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