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

Accelerated periodontal tissue destruction in patients with labile insulin-dependent diabetes mellitus (DM) and localized juvenile periodontitis (LJP) has been suggested to be related to functional abnormalities of neutrophils. We have recently found that collagenase in gingival crevicular fluid (GCF) of adult periodontitis patients is primarily derived from neutrophils and that neutrophil collagenase activity is more sensitive to inhibition by tetracyclines than collagenase produced by fibroblasts. This study is to characterize the cellular sources, activation and inhibition of collagenase in GCF of DM patients and to compare it with collagenase in LJP GCF. We found differences which may have therapeutic implications. Specific doxycycline inhibition tests revealed that GCF collagenase in DM is derived from neutrophils, whereas the enzyme in LJP originates primarily from fibroblasts. Oxidant, sodium hypochlorite, activated efficiently GCF collagenase of DM but not LJP patients. In contrast, plasmin activated LJP GCF collagenase but not that of DM patients. In GCF of DM patients 50-60% of collagenase existed in an active form, whereas in LJP GCF, the enzyme was almost completely in a latent form. The results suggest that collagenase in GCF of periodontitis patients with labile DM is primarily derived from neutrophils and that tetracycline therapy may be an effective adjunct in treatment aimed at controlling the periodontal breakdown in these patients. On the other hand, in LJP the anti-collagenase property of tetracyclines may be less important for control of periodontal tissue destruction because of the tetracycline-resistance of fibroblast collagenase.
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PMID:Cellular source and tetracycline-inhibition of gingival crevicular fluid collagenase of patients with labile diabetes mellitus. 131 30

A cross-sectional study was designed to evaluate the periodontal status of 85 12-18 year-old French adolescents with insulin-dependent diabetes (IDDM) and 38 healthy controls in the same age group. The clinical examination consisted of plaque control and gingival inflammation evaluation and probing attachment level. The interproximal marginal bone level was assessed with bitewing radiographs taken on the first molars and on areas presenting an attachment loss over 2 mm. Diabetic children had significantly more gingival inflammation than children without diabetes, in spite of similar plaque scores. No significant relation between gingival condition and age, Tanner's index, HbAlc level or disease duration could be demonstrated. None of the subjects had sites with attachment loss > or = 3 mm or radiographic signs of periodontitis.
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PMID:Periodontal status in insulin-dependent diabetic adolescents. 143 Feb 90

The objective of this study was to evaluate the polymorphonuclear leukocyte (PMN) function in a poorly controlled adult insulin-dependent diabetic patient (IDDM) with severe recurrent periodontitis, while describing the microbiological and clinical findings. Chemotaxis, superoxide production, and phagocytosis and killing of Porphyromonas (Bacteroides) gingivalis by the IDDM PMN were evaluated 1 week before treatment relative to a healthy, matched control. These analyses revealed a significant (P less than .05) depression in the number of IDDM PMNs migrating along an FMLP gradient (Boyden chamber assay). In addition, a significant (P less than .05) enhancement of IDDM PMN superoxide production in response to opsonized zymosan (cytochrome C reduction) was observed. Phagocytosis and killing (fluorochrome phagocytosis assay) by IDDM PMN of two P. gingivalis strains was also impaired significantly (P less than .05). The subgingival microflora contained significant levels of P. gingivalis, Actinobacillus actinomycetemcomitans, Eikenella corrodens, and Peptostreptococcus micros. Periodontal treatment consisted of extraction of hopeless teeth, scaling and root planing and 3 weeks of Augmentin therapy. The antibiotic therapy resulted in unrecoverable numbers of the putative pathogens and a reduction in both gingival inflammation and disease progression. The IDDM healing response to previous surgical treatment and extractions was poor, presumably due to a marked thrombocytopenia (91 x 10(3) platelets/mm3).
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PMID:Defective neutrophil function in an insulin-dependent diabetes mellitus patients. A case report. 165 89

The relationship between diabetes mellitus and oral health status was determined in Pima Indians from the Gila River Indian Community in Arizona. This tribe of native Americans has the world's highest reported incidence and prevalence of non-insulin-dependent (type 2) diabetes mellitus. The probing attachment level, alveolar bone loss, age, sex, Calculus Index, Plaque Index, Gingival Index, fluorosis, and DMFT as well as the diabetic status was assessed in 1,342 Pima Indians who were at least partially dentate. The prevalence and severity of destructive periodontal disease was determined by measuring probing attachment loss and radiographically apparent interproximal crestal alveolar bone loss, two independent but correlated indicators of periodontal destruction. Only diabetic status, age, and the presence of subgingival calculus were significantly associated with both increased prevalence and greater severity of destructive periodontal disease in this population. Diabetic status was significantly and strongly related to both the prevalence and severity of disease after adjusting for the effects of demographic variables and several indices of oral health including the Plaque Index. Subjects with type 2 diabetes have an increased risk of destructive periodontitis with an odds ratio of 2.81 (95% confidence interval 1.91 to 4.13) when attachment loss is used to measure the disease. The odds ratio for diabetic subjects was 3.43 (95% confidence interval 2.28 to 5.16) where bone loss was used to measure periodontal destruction. These findings demonstrate tht diabetes increases the risk of developing destructive periodontal disease about threefold. Furthermore, diabetes increases the risk of developing periodontal disease in a manner which cannot be explained on the basis of age, sex, and hygiene or other dental measures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Periodontal disease in non-insulin-dependent diabetes mellitus. 202 65

Seven juvenile periodontally diseased patients were evaluated for clinical, microbiologic and local or systemic host factors. Three patients showed the localized from of periodontitis clinically and radiographically and by deep periodontal pockets associated with the molars and incisors. Four were in the generalized froms, in which in most cases all teeth were affected. The results in both diseased froms on the predominant cultivable subgingival microflora, the composition of which was not different from that in adult periodontitis, consisted of significantly increased proportions of Gram-negative anaerobic rods, Bacteroides sp. and B. gingivalis, Haemophilus sp. and H. actinomycetemcomitans were detected in 1/3 of the localized and 2/4 of the generalized periodontitis. They were of no value in distinguishing activity that enhanced disease in the generalized from. Elevated serum IgG responses were noted with B. gingivalis. No markedly functional abnormalities of neutrophils from peripheral blood have been demonstrated, however it might function with systemic factors, like an insulin-dependent diabetes. Morphologic characteristics of the oral and periodontal tissue in localized periodontitis were that the pattern of destruction was confined to specific teeth groups characterized by extensive the bucco-lingual width ratio of the dental crown to alveolar bone width. These observations indicate that the generalized form of juvenile periodontitis lesions were associated not only with the presence of subgingival bacteria, but also with conditions such as local morphologic and systemic or constitutional factors, individual variation in relation to destructive and protective aspects of the defense mechanisms.
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PMID:[The clinical and etiological study on juvenile periodontal disease]. 213 90

Circulating immune complexes were estimated in the sera of 50 patients with Type II or non-insulin-dependent diabetes mellitus (NIDDM) and 50 nondiabetic patients with periodontitis. The values were compared with that of 50 age- and sex-matched controls. There was a significant rise in circulating immune complexes (CIC) in both the groups of patients compared to controls. The levels of CIC were significantly higher in diabetic patients with periodontitis compared to nondiabetics. The study shows that the circulating immune complexes may have a role in the pathogenesis of periodontal disease in diabetic patients.
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PMID:Circulating immune complexes in diabetic patients with periodontitis. 227 78

Cell-mediated and humoral immune responses were assessed in 50 patients with type II or non-insulin-dependent diabetes mellitus and 50 nondiabetic patients with periodontitis. The values were compared with those of 50 age and sex-matched control subjects. The cell-mediated immunity assessed by enumerating the total and high-affinity rosette-forming cells of the patient did not show any significant variation from that of the normal control subjects. The humoral immune response was assessed by estimating serum immunoglobulins G, A, M, D, and E by single radial immunodiffusion. Except IgD, all other immunoglobulins were found to be elevated significantly in both diabetic and nondiabetic subjects. The alteration in humoral immune response may be the cause or the effect of periodontitis. The defective host response reported in diabetic patients may be responsible for the increased incidence of periodontitis in diabetic patients as compared to nondiabetic patients.
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PMID:Cell-mediated and humoral immune response in diabetic patients with periodontitis. 237 Oct 49

The prevalence of periodontitis was studied in a population of 157 insulin dependent diabetes mellitus patients aged 8-78 years attending the outpatients diabetic clinic of a large general hospital in Cork, Ireland. Every third diabetic patient attending the clinic was selected for examination. The dental parameters measured were plaque index (PI), gingivitis index (GI), periodontal pocket depth (PD) and periodontal attachment loss (PAL). Diabetic control was measured by estimating percentage haemoglobin glycolysation (% Hb Alc) known duration of diabetes (KDD) and insulin dependence. It was found that none of the diabetic measurements showed any consistent pattern in relation to any of the periodontal measurements. The findings are in agreement with other studies which suggest that no significant correlation between diabetic parameters and periodontal disease can be demonstrated. When the diabetic patient suffered periodontitis it was due to factors (such as genetic predisposition) other than impaired glucose metabolism.
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PMID:Diabetes mellitus and periodontal disease in an Irish population. 253 53

Systemic diseases--like diabetes mellitus--are able to injure the local and common resistance of an organism. Therefore we must expect a more intensive and severer progress of gingivitis and periodontitis in diabetic patients in comparison with a non-diabetic control-group. On the Gondar College of Medical Sciences in Northwest-Ethiopia are investigated 77 Insulin-obliged diabetics and 312 persons for control by means of the plaque-Index, the Oral-Hygiene-Index simplified. The DMF/T-Index and the Gingivitis-respectively Periodontal-Disease-Index for evaluation of the oral health situation. The comparison shows that the diabetic group has a moderate higher Plaque-pictures of gingivitis or periodontitis. This confirms our opinion that the diabetes mellitus is a risk-factor for the development of periodontal diseases. Therefore patients with diabetes mellitus should perform a very intensive care for mouth-hygiene.
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PMID:[Report on experiences with a one-year action at the Gondar College of Medical Sciences in Ethiopia. 3. Influence of diabetes mellitus on the teeth supporting apparatus]. 263 34

Juvenile diabetics have been shown to have an increased susceptibility to gingivitis and periodontitis following puberty. However, little data are available on changes in the microbial flora that occur at the onset of puberty. This study was performed to determine if antibacterial antibody titers to selected periodontal disease-associated microorganisms might be helpful in revealing changes in plaque flora at the onset and conclusion of puberty. Sera was obtained from 35 subjects (ages 7 to 18 years) selected from a population of insulin-dependent diabetics. The subjects were given a thorough medical examination which included an assessment of sexual maturation and a dental examination which included the recording of onset and magnitude of bleeding according to the papillary bleeding score. Antibody titers to A. naeslundii (AN), B. intermedius (BI), B. gingivalis (BG), F. nucleatum (FN), A. actinomycetemcomitans (AA), C. ochracea (CO) and T. denticola (TD) were determined using the microELISA. Stratification of antibody titers by age groups (less than or equal to 12 years, 12 to 15 years, greater than 15 years) revealed that titers to AN increased significantly (P less than 0.025, ANOVA) and progressively (P less than 0.05, regression analysis) with increasing age. In contrast, the titers to FN were maximal in the under 12 year group and decreased with age (ANOVA, P less than 0.05; regression analysis, P less than 0.05). There were no significant variations in titers observed for the other microorganisms. Stratification by sexual maturity revealed a similar progressive decrease of the titer to FN (ANOVA, P less than 0.05; regression analysis, P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Humoral immune response to selected subgingival plaque microorganisms in insulin-dependent diabetic children. 272 33


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