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

Fructosamine assay, which is used in diagnosing and monitoring diabetic patients, is compared with the hemoglobin and plasma glucose assays in children and adolescent insulin-dependent diabetes mellitus patients. We demonstrated that the gingival index scores were correlated with fructosamine values in insulin-dependent diabetes mellitus patients but not in non-diabetic controls. We also found that there was no correlation between gingivitis scores and fasting plasma glucose and HbA1c values. Periodontitis was found to be rare in diabetic children and adolescents.
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PMID:Serum fructosamine correlates with gingival index in children with insulin-dependent diabetes mellitus (IDDM). 798 22

The role of smoking as a risk factor for periodontitis was assessed separately in diabetic and nondiabetic study groups. Subject listings stratified for age (19 to 40 years) and sex were obtained for subjects with insulin-dependent diabetes mellitus (IDDM) and nondiabetic subjects. For both the IDDM group (n = 132) and the nondiabetic group (n = 95), age and sex stratified samples were constructed by random selection of subjects from each subject listing. Patients were recruited by phone, examined, and their medical and dental histories obtained. Among nondiabetic subjects, the prevalence of periodontitis was markedly higher among current smokers compared with never smokers (P < or = 0.005) in both the 19 to 30 year-old (46% vs. 12%) and 31 to 40 year-old groups (88% vs. 33%). The subject mean percent of sites with gingival pocket depth > or = 4 mm was higher among current smokers than never smokers (P = 0.001) in the 19 to 30 (8.2% vs. 3.4%) and 31 to 40 (14.3% vs. 4.3%) age groups. The effects of smoking among IDDM subjects were similar to that observed in the nondiabetic population. There were no differences between current and never smokers in the proportion of sites positive for plaque. Attributable risk percents from prevalence data suggest that among nondiabetic subjects, a large proportion, perhaps as much as 51% of the periodontitis in the 19 to 30 year old group and 32% of the periodontitis in the 31 to 40 year old group, is associated with smoking.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for cigarette smoking as a major risk factor for periodontitis. 842 85

Tetracyclines have recently been shown to inhibit the activity of some but not all mammalian matrix metalloproteinases believed to mediate periodontal destruction. However, the specificity of this effect, which could have significant therapeutic implications for different periodontal diseases, has not been examined in detail. Doxycycline and 4-de-dimethylaminotetracycline (CMT-1) have been tested in vitro for their ability to inhibit human neutrophil and fibroblast interstitial collagenases and collagenase in human gingival crevicular fluid (GCF). The GCF samples were obtained from systemically healthy and insulin-dependent diabetic adult periodontitis patients and from localized juvenile periodontitis (LJP) patients. The concentrations of these 2 tetracyclines required to inhibit 50% of the collagenase activity (IC50) were found to be 15 to 30 microM for human neutrophil collagenase and for collagenase in GCF of systemically healthy and diabetic adult periodontitis patients. These concentrations approximate the tetracycline levels observed in vivo during treatment with these drugs. In contrast, human fibroblast collagenase and GCF collagenase from LJP patients were both relatively resistant to tetracycline inhibition; the IC50 for doxycycline and CMT-1 for these 2 sources of collagenase were 280 and 500 microM, respectively. Based on these and other findings, we propose the following: 1) that systemic levels of tetracycline may inhibit connective tissue breakdown by inhibiting neutrophil collagenase; 2) that tetracyclines do not inhibit fibroblast-type collagenase, which may help explain their lack of effect on normal connective tissue remodeling; 3) that tetracycline inhibition of collagenases may serve to identify the cellular origin of the enzyme; and 4) that tetracyclines can also prevent the oxidative activation of latent human procollagenases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tetracycline inhibition and the cellular source of collagenase in gingival crevicular fluid in different periodontal diseases. A review article. 843 57

The aim of this study was to define a population of diabetics exhibiting an increased risk of developing severe periodontitis by comparing the medical status of 2 groups of diabetics, 1 with no/minor periodontal disease and 1 with severe periodontal disease. The case-control study consisted of 2 parts, a baseline study and a follow-up study. 39 case-control pairs were selected. They were adult, long-duration, insulin-dependent diabetics matched according to sex, age and diabetes duration. One individual in each pair (the CASE) exhibited severe periodontal disease while the other (the CONTROL) exhibited gingivitis or only minor alveolar bone loss. The median age of the cases was 58 years (range 36 to 70 years) and of the controls 59 years (range 37 to 69 years). The median disease duration in cases and controls was 24 years and 25 years, respectively. The median follow-up time was 6 years. The medical variables analysed were weight, insulin dose, systolic and diastolic blood pressure, vibratory threshold, triglycerides, total-cholesterol, HDL-cholesterol, creatinine, HbA1, proteinuria, ECG, retinopathy, stroke, transient ischemic attacks (TIA), angina, myocardial infarct, heart failure, hypertension, intermittent claudication, foot ulcer, death, cause of death, and smoking habit. Biochemical analyses and clinical variables used as a routine in the monitoring of diabetics failed to differentiate between diabetics with severe and minor periodontal disease. In the follow-up study, significantly higher prevalences of proteinuria and cardiovascular complications such as stroke, TIA, angina, myocardial infarct and intermittent claudication were found in the case group. An association between renal disease, cardiovascular complications and severe periodontitis seems to exist. This indicates that a closer cooperation between the diabetologist and the dentist is necessary in monitoring the diabetic patient.
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PMID:Medical status and complications in relation to periodontal disease experience in insulin-dependent diabetics. 870 78

Although it is accepted that the primary cause of periodontitis is bacterial infection of long duration, there are a number of risk factors which may increase the probability of recurrence of periodontal disease during supportive periodontal care. The risk may in such cases be caused by other factors than poor oral hygiene measures per se. Cross-sectional and longitudinal studies show conflicting results concerning age as a risk factor for periodontal disease. The effect of smoking on the periodontal tissues has been discussed for decades and only lately has it been possible to demonstrate that smokers definitely have more periodontal problems than non-smokers. Another important risk factor for periodontitis relates to the insulin dependent and non-insulin dependent forms of diabetes mellitus. Poorly-controlled long-duration diabetics have more periodontitis and tooth loss than well-controlled or non-diabetics. Finally, the issue of compliance deserves attention. The medical literature has suggested that patients with chronic illnesses tend to comply poorly, especially if the disease is not perceived to be particularly threatening, if the therapy is time-consuming, or if the symptoms are non-disturbing. Suggestions for improved compliance are called for.
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PMID:Risk assessment of recurrence of disease during supportive periodontal care. Epidemiological considerations. 870 83

In this study, salivary peroxidase activity was measured in a group of 10 patients with insulin-dependent (type I) diabetes mellitus (IDDM) who had a tendency towards periodontitis. In healthy subjects (N : 10), mean salivary peroxidase activity was 0.0025 +/- 0.001 IU/ml, while in this group of type I diabetic patients it was 0.051 +/- 0.015 IU/ml, a significantly higher level (p < 0.001). Approximal plaque index (API), modified sulcus bleeding index (mod SBI) and pocket depths were assessed clinically. The values for mod SBI and API were 60% and 68% respectively for the diabetic patients while for the control group mod SBI was measured 0.0% and the value for API was 10.67% (p < 0.001). The administration of this simple and practical test may provide an early marker of a tendency towards periodontitis in IDDM patients.
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PMID:Salivary peroxidase activity in whole saliva of patients with insulin-dependent (type-1) diabetes mellitus. 889 41

This study tested the hypothesis that severe periodontitis in persons with non-insulin-dependent diabetes mellitus (NIDDM) increases the risk of poor glycemic control. Data from the longitudinal study of residents of the Gila River Indian Community were analyzed for dentate subjects aged 18 to 67, comprising all those: 1) diagnosed at baseline with NIDDM (at least 200 mg/dL plasma glucose after a 2-hour oral glucose tolerance test); 2) with baseline glycosylated hemoglobin (HbA1) less than 9%; and 3) who remained dentate during the 2-year follow-up period. Medical and dental examinations were conducted at 2-year intervals. Severe periodontitis was specified two ways for separate analyses: 1) as baseline periodontal attachment loss of 6 mm or more on at least one index tooth; and 2) baseline radiographic bone loss of 50% or more on at least one tooth. Clinical data for loss of periodontal attachment were available for 80 subjects who had at least one follow-up examination, 9 of whom had two follow-up examinations at 2-year intervals after baseline. Radiographic bone loss data were available for 88 subjects who had at least one follow-up examination, 17 of whom had two follow-up examinations. Poor glycemic control was specified as the presence of HbA, of 9% or more at follow-up. To increase the sample size, observations from baseline to second examination and from second to third examinations were combined. To control for non-independence of observations, generalized estimating equations (GEE) were used for regression modeling. Severe periodontitis at baseline was associated with increased risk of poor glycemic control at follow-up. Other statistically significant covariates in the GEE models were: 1) baseline age; 2) level of glycemic control at baseline; 3) having more severe NIDDM at baseline; 4) duration of NIDDM; and 5) smoking at baseline. These results support considering severe periodontitis as a risk factor for poor glycemic control and suggest that physicians treating patients with NIDDM should be alert to the signs of severe periodontitis in managing NIDDM.
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PMID:Severe periodontitis and risk for poor glycemic control in patients with non-insulin-dependent diabetes mellitus. 891 Aug 27

The aim of the present study was to identify whether monocytic TNF alpha secretion patterns could serve as a potential phenotypic discriminator for periodontal disease susceptibility within insulin-dependent diabetes mellitus (IDDM) patients. In 32 IDDM individuals the lipopolysaccharide (LPS) stimulated monocytic TNF alpha secretion dose-response characteristics were analyzed and related to two different periodontal status categories. Diabetics were divided into group A (gingivitis or mild periodontal disease) and group B (moderate to severe periodontal disease). In addition, 17 non-diabetic individuals with various degrees of periodontal disease served as control patients. Diabetics as a group had a significantly higher monocytic TNF alpha production in response to increasing Porphyromonas gingivalis A 7436 lipopolysaccharide concentrations (0, 0.003, 0.03, 0.3 and 3.0 micrograms/ml) as compared to non-diabetic patients with gingivitis or adult periodontitis (p < 0.05). A significant difference in the dose response was also noted in the level of TNF alpha secreted as a function of P. gingivalis LPS concentrations between group A and B diabetics, as determined by two-way repeated measurements ANOVA (p < 0.05). Furthermore, there was no significant difference in the mean HbA1C between the two diabetic groups, and the TNF alpha level was not significantly associated with the HbA1C level within diabetic patients. These data suggest that the diabetic state results in an upregulated monocytic TNF alpha secretion phenotype (4.6-fold increase) which, in the presence of Gram-negative bacterial challenge, is associated with a more severe periodontal disease expression. In addition, approximately 40% (10 of 24) IDDM periodontitis patients in group B demonstrated a 62-fold elevation in TNF alpha secretion relative to non-diabetic gingivitis or periodontitis patients and a 13.5-fold increase relative to IDDM group A (gingivitis or mild periodontitis) patients.
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PMID:Monocytic TNF alpha secretion patterns in IDDM patients with periodontal diseases. 904 92

The gingival crevicular fluid (GCF) and monocytic secretion of prostaglandin E2 (PGE2) and interleukin 1 beta (IL-1 beta) were measured in a group of 39 insulin-dependent diabetes mellitus (IDDM) patients and 64 systemically healthy individuals. Diabetics were divided into Group A (gingivitis or mild periodontal disease) and Group B (moderate or severe periodontal disease). Diabetics had significantly higher GCF levels of both PGE2 and IL-1 beta as compared to non-diabetic controls who were matched with regard to periodontal disease severity (P < 0.00001 and P = 0.0005, respectively). Within the diabetic population, the GCF levels of these inflammatory mediators were almost 2-fold higher in Group B as compared to Group A (P = 0.01, P = 0.006, respectively for GCF-PGE2 and IL-1 beta). Furthermore, diabetics as a group had a significantly higher monocytic PGE2 and IL-1 beta production in response to various concentrations of both Escherichia coli and Prophyromonas gingivalis lipopolysaccharide (LPS) as compared to non-diabetic patients with adult periodontitis (P = 0.0001). LPS dose-response curves demonstrated that monocytes from Group B diabetics produced approximately 3 times more PGE2 than Group A monocytes; however, there was no significant difference in monocytic IL-1 beta secretion within the IDDM patients. The levels of GCF or monocytic mediators did not correlate with age, race, or glycosylated hemoglobin (HbA1C) levels. Our data suggest that the high GCF and monocytic secretion of PGE2 and IL-1 beta in IDDM patients may be a consequence of a systemic response trait and that the presence of Gram-negative infections such as periodontal diseases may interact synergistically to yield high local levels of these mediators and a more severe periodontal condition.
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PMID:Inflammatory mediator response as a potential risk marker for periodontal diseases in insulin-dependent diabetes mellitus patients. 905 29

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


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