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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The total hemolytic complement activity (CH50) and its fractions C3 and C4 were determined in 50 patients with Type II or non-insulin dependent diabetes mellitus (NIDDM) and 50 nondiabetic patients with periodontitis. The values were compared with those of 50 age and sex matched controls. An elevation of CH50 was observed in both the diabetic and nondiabetic patients, compared to controls. The diabetic patients with periodontitis showed a significantly higher complement activity compared to nondiabetic patients with periodontitis. The C3 and C4 values were significantly elevated in both diabetic and nondiabetic patients when compared with the control group. The elevation being more pronounced in diabetic groups.
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PMID:Total hemolytic complement (CH50) and its fractions (C3 and C4) in the sera of diabetic patients with periodontitis. 210 97

Epidemiologic studies have suggested that the severity of periodontitis is greater in juvenile and adult onset diabetes. In juvenile diabetic patients, the periodontal disease seems to be initiated around puberty and progresses by age. Reviewing the medical literature indicates a similar age of onset for known systemic complications resulting from diabetes. Angiopathy, abnormal collagen metabolism, abnormal PMN function, and altered sulcular microbial flora have been found to be closely associated with the severity of periodontitis in diabetic patients. The association between abnormal neutrophil function and severity of periodontal disease in diabetic patients provides an opportunity for examining the role of neutrophil in periodontal disease. Future investigation in the function of sulcular PMN may shed light on the complex mechanism of periodontal disease.
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PMID:Periodontal disease in juvenile and adult diabetic patients: a review of the literature. 635 23

The close association between restorations with overhanging margins and chronic destructive periodontitis has been known for many years. However, the mechanisms by which overhanging restorations will interact in the pathogenesis of periodontal disease are still unknown. Generally it is accepted that overhanging restorations contribute to the promotion of the disease process by virtue of their capacity to retain bacterial plaque. The purpose of the present study was to determine if the placement of subgingival restorations with overhanging margins results in changes in the subgingival microflora. 9 dental students with clean teeth and clinically healthy gingivae (GI less than 0.1) gave their consent to participate in the study. 5 MOD cast gold onlays with 1 mm proximal overhanging margins were placed in mandibular molars for 19-27 weeks. They were replaced in a cross-over design by 5 similar onlays with clinically perfect margins which served as controls. Another 5 onlays were placed in reverse order in the remaining patients. Prior to and every 2-3 weeks after insertion, subgingival microbiological samples were obtained by inserting a fine sterile paper point for 30 sec into the gingival sulcus subjacent to the restoration. The predominant cultivable flora was determined using continuous anaerobic culturing techniques. Following the placement of restorations with overhanging margins, a subgingival flora was detected which closely resembled that of chronic periodontitis. Increased proportions of Gram-negative anaerobic bacteria, black-pigmented Bacteroides and an increased anaerobe: facultative ratio were noted. Following the placement of the restorations with clinically perfect margins, a microflora characteristic for gingival health or initial gingivitis was observed. Black-pigmented Bacteroides were detected in very low proportions (1.6-3.8%). These changes in the subgingival microflora were obvious irrespective of whether the restorations with the overhanging margins were placed in the first period of the experiment or following the cross-over. Clinically, increasing gingival indices were detected at the sites where overhanging margins were placed. Bleeding on gentle probing always preceded the peak level of black-pigmented Bacteroides. Loss of attachment was not detected in any site. Changes in the subgingival microflora after the placement of restorations with overhanging margins document a potential mechanism for the initiation of periodontal disease associated with iatrogenic factors.
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PMID:Clinical and microbiological effects of subgingival restorations with overhanging or clinically perfect margins. 658 Nov 73

The aim of the present study was to characterize the eventual presence and molecular forms of gelatinase/type IV collagenase activities in gingival crevicular fluid (GCF) and saliva in different forms of periodontitis; patients with clinically healthy periodontium served as controls. Enzyme activities were monitored electrophoretically by zymography using gelatin and type IV collagen as substrates and analyzed visually and/or densitometrically. Both saliva and GCF collected from adult periodontitis, localized juvenile periodontitis and type II diabetes mellitus periodontitis patients contained species moving identically with gelatinase isolated from human neutrophils or MMP-9 (mean 98 kD), and species with mobility similar to gelatinase in fibroblast cell culture supernatants or MMP-2 (mean 76 kD). Hitherto, undescribed high molecular weight forms (mean 128 kD), were found, possibly representing polymerized or complexed enzyme active/activated in situ in the gel matrix. Small molecular forms of gelatinases (mean 51 kD and 46 kD), unable to cleave type IV collagen, were also found, most likely representing in vivo proteolytically activated, truncated enzymes. Although multiple forms of gelatinases/type IV collagenases in saliva and GCF may take part in the tissue destruction in periodontitis, their profile judged according to molecular weights does not differentiate between different forms of periodontitis.
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PMID:Multiple forms of gelatinases/type IV collagenases in saliva and gingival crevicular fluid of periodontitis patients. 812 40

The study was conducted to estimate the concentration of immunoglobulins in the saliva of diabetic and nondiabetic patients with periodontitis. The salivary immunoglobulins G, A and M (IgG, IgA, IgM) were determined in 50 patients with type II or noninsulin dependent diabetes mellitus (NIDDM) and 50 non diabetic patients with periodontitis. The values were compared with that of 50 age and sex matched controls. IgG, IgA were found to be significantly increased in diabetic patients with periodontitis, compared to nondiabetic patients and controls. Though an increase in IgM was found in diabetic patients it was not significant. The altered immune response observed may be due to the response to a greater antigenic challenge which in turn may be responsible for the increased incidence of periodontitis in diabetic patients. Further studies in this field may help to establish this association.
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PMID:Immunoglobulins in the saliva of diabetic patients with periodontitis. 857 41

The present investigation was performed to study the frequency of recurrence of periodontitis in diabetic subjects, who, prior to the initiation of a 5-year period of monitoring, were treated for moderate to advanced periodontal disease. 20 patients with diabetes, type 1 (IDDM) or type 2 (NIDDM) and 20, sex and age matched, controls with similar amounts of periodontal tissue destruction, were selected for the study. Following a screening examination, all patients were subjected to non-surgical periodontal therapy (oral hygiene instruction, supra- and subgingival scaling). 3 months later, the baseline examination for the study was performed. This included assessments of several parameters such as: number of teeth, plaque, gingivitis, probing pocket depth and probing attachment level. 6 months after the baseline examination, all 40 subjects were recalled for a 2nd examination. Sites which at this 6-month examination exhibited bleeding on probing, and had probing depth > 5 mm, were scheduled for additional surgical therapy (modified Widman flap). Following this selective additional therapy, the main period of monitoring was initiated. During this period, a plaque control program was repeated every 3 months. Re-examinations regarding plaque, gingivitis, probing depth and probing attachment level were performed 12, 24 and 60 months after the baseline examination. The findings from the examinations disclosed that diabetics and non-diabetics alike, treated for moderately to advanced forms of adult periodontitis, during a subsequent 5-year period, were able to maintain healthy periodontal conditions. Thus, the frequency of sites which exhibited signs of recurrent disease was similar in the 2 study groups.
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PMID:The effect of periodontal therapy in diabetics. Results after 5 years. 884 44

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

The periodontal status of 25 patients with non-insulin dependent diabetes mellitus (NIDDM) (age range 58 to 76) was investigated and compared with 40 non-diabetic control subjects (age range 59 to 77). Surfaces with visible plaque and bleeding after probing, calculus, recessions, and pathological pockets were examined. The total attachment loss was calculated as a sum of recessions and pockets in millimeters. Mesial and distal bone loss was measured from panoramic radiographs and mean alveolar bone loss was calculated. Periodontal disease was considered advanced when mean alveolar bone loss was over 50%, or 2 or more teeth had pockets > or = 6 mm. Microbiological analysis comprised the detection of Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Bacteroides forsythus by a polymerase chain reaction (PCR) method. Patients with NIDDM had significantly more often advanced periodontitis than control subjects, 40.0% and 12.5%, respectively. Diabetic patients did not harbor more pathogens than the control subjects. The HbA1C level deteriorated in patients with advanced periodontitis, but not in other patients with NIDDM, when compared to the situation 2 to 3 years earlier. Advanced periodontitis seems to be associated with the impairment of the metabolic control in patients with NIDDM, and a regular periodontal surveillance is therefore necessary.
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PMID:Periodontal findings in elderly patients with non-insulin dependent diabetes mellitus. 977 23

One hundred and two dentate patients with type II diabetes mellitus and 98 non-diabetic subjects were examined for oral conditions and metabolic state. Self-reported health behaviour was analysed. From factor analysis four factors emerged: general health behaviour (GHB), perceived fatigue (PF), diet control (DC) and regular diet (RD). In diabetics PF, DC and RD were significantly higher than that in non-diabetics. Patients with diabetes were more likely to control their disease through a programme of decreased kilojoule intake leading to weight management. However, they tended to tire. The mean gingivitis index was significantly higher (p < 0.01) among diabetics (2.39) than among non-diabetics (1.99). The number of missing teeth was significantly higher (p < 0.01) for diabetics (6.7) when compared with non-diabetics (4.3). On the other hand, aetiological factors (plaque, calculus) and the level of dental health behaviour as expressed in the HU-DBI scores were similar. Probing pocket depth did not differ statistically between groups. The increasing number of missing teeth in diabetics may primarily result from severe periodontitis with tooth mobility or deep pockets. Findings in this study suggest that the difference in the severity of periodontitis between diabetics and non-diabetics was significant although aetiological factors and the level of dental health behaviour were similar.
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PMID:Comparison of health behaviour and oral/medical conditions in non-insulin-dependent (type II) diabetics and non-diabetics. 984 81


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