Gene/Protein Disease Symptom Drug Enzyme Compound
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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 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

Alterations in the connective tissue of the arterial wall have been suggested to play a role in the development of macrovascular disease in diabetes mellitus. The present study deals with changes in the content of GAG in aortic tunica media in human diabetes by separately analysing normal areas and areas with fibrous plaques. The thoracic aorta from 15 diabetic patients (7 with IDDM, 8 with NIDDM), and 30 sex- and age-matched non-diabetic subjects were collected at autopsy. Tunica intima was removed and GAG were isolated from the dried defatted and pulverized tunica media. GAG were quantified by uronic acid analysis and characterized by electrophoresis on cellulose acetate. Results showed that IDDM patients had a relative and absolute increase in hyaluronic acid in normal tunica media compared to non-diabetic subjects. There was a significant positive correlation between hyaluronic acid content of normal tunica media and duration of diabetes, but not between hyaluronic acid content and age. When tunica media from plaque areas was compared to normal areas the same pattern was evident in diabetic patients as in non-diabetic patients--significantly increased proportion of dermatan sulphate and reduced hyaluronic acid. The data agree with the notion that the arterial wall is subject to different pathological processes in diabetes, one of classical atherosclerosis with changes in GAG similar to non-diabetic subjects, and the other seen in areas without plaques with dissimilar alterations in GAG. These data therefore support the concept of the presence of a macrovascular disease in diabetes different from atherosclerosis.
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PMID:Glycosaminoglycans in the human aorta in diabetes mellitus: a study of tunica media from areas with and without atherosclerotic plaque. 817 43

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

Periodontal disease is a common infection-induced inflammatory disease among individuals suffering from diabetes mellitus. The purpose of this study was to assess the effects of treatment of periodontal disease on the level of metabolic control of diabetes. A total of 113 Native Americans (81 females and 32 males) suffering from periodontal disease and non-insulin dependent diabetes mellitus (NIDDM) were randomized into 5 treatment groups. Periodontal treatment included ultrasonic scaling and curettage combined with one of the following antimicrobial regimens: 1) topical water and systemic doxycycline, 100 mg for 2 weeks; 2) topical 0.12% chlorhexidine (CHX) and systemic doxycycline, 100 mg for 2 weeks; 3) topical povidone-iodine and systemic doxycycline, 100 mg for 2 weeks; 4) topical 0.12% CHX and placebo; and 5) topical water and placebo (control group). Assessments were performed prior to and at 3 and 6 months after treatment and included probing depth (PD), clinical attachment level (CAL), detection of Porphyromonas gingivalis in subgingival plaque and determination of serum glucose and glycated hemoglobin (HbA1c). After treatment all study groups showed clinical and microbial improvement. The doxycycline-treated groups showed the greatest reduction in probing depth and subgingival Porphyromonas gingivalis compared to the control group. In addition, all 3 groups receiving systemic doxycycline showed, at 3 months, significant reductions (P < or = 0.04) in mean HbA1c reaching nearly 10% from the pretreatment value. Effective treatment of periodontal infection and reduction of periodontal inflammation is associated with a reduction in level of glycated hemoglobin. Control of periodontal infections should thus be an important part of the overall management of diabetes mellitus patients.
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PMID:Treatment of periodontal disease in diabetics reduces glycated hemoglobin. 928 60

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 physiological meaning of platelets has been best documented for acute coronary syndromes where platelets act as "first responsive elements" triggering the final occlusive thrombus after plaque rupture has occurred. This situation is particularly relevant for patients with NIDDM-type diabetes regularly showing complicated plaque architecture. Predictive power for acute ischemic events e.g. following angioplasty has been proven, and this has dominated the attention exclusively towards the hemostatic function of platelets. Meanwhile, a variety of particularly important platelet features have been identified: a) promotion of liquid phase coagulation; b) regulation of the local vascular tone; c) active modulation of tissue modeling at lesion sites; d) adhesion molecule-mediated communication with a variety of corpuscular blood (and non-blood cells). With emerging recognition of the latter role, the pathophysiological scope of platelets exceeds the well-established role as microemboli, local atherosclerosis amplifiers and triggers of gross thrombosis. In diabetes mellitus of either type, increased populations of circulating platelets have been identified expressing activation dependent adhesion molecules such as activated alpha 2 beta 3 (GPIIbIIIa), lysosomal GP53, thrombospondin or, perhaps most importantly "P-selectin" (CD62 p). This suggests that these adhesion molecules among others can also mediate platelet-leukocyte interactions potentially resulting in inflammatory tissue damaging processes in addition to the immanent tendency towards (micro-)thrombosis. This review works out a more general view on the meaning of platelet activation beyond hemostaseology and updates the actual knowledge of platelet-leukocyte communication checkpoints with particular reference to the diabetic state outlining new pharmacological concepts for intervention.
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PMID:Platelet-leukocyte-cross-talk in diabetes mellitus. 949 1

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

The mechanisms underlying macrovascular complications in NIDDM are partially understood. In addition to increased prevalence and severity of systemic cardiovascular risk factors, local alterations of arterial wall and hemodynamics may play a role. Atherosclerotic lesions usually lie in regions of low wall shear stress. We therefore investigated the wall shear stress--that is, the frictional force acting tangentially to the endothelial surface--in the common carotid artery of diabetic and control subjects. Enrolled were 18 male NIDDM subjects and 18 age-matched control subjects. None of the participants were hypertensive, hyperlipidemic, or a cigarette smoker. Common carotid wall shear stress was calculated according to the following equation: blood viscosity x blood velocity/internal diameter. Blood viscosity was measured by use of a cone/plate viscometer. Blood velocity and internal diameter were measured by high-resolution echo-Doppler. Wall shear stress was significantly lower in NIDDM subjects than in control subjects (mean wall shear stress: 9.7 +/- 2.4 vs. 11.7 +/- 2.6 dynes/cm2, P < or = 0.005). Six diabetic participants had a plaque in one carotid tree and no lesions in the contralateral carotid. Among these subjects, mean wall shear stress was significantly lower in the side with lesion (8.1 +/- 1.6 vs. 10.5 +/- 2.4 dynes/cm2, P < or = 0.02). These findings suggest that diabetes is associated with a more atherosclerosis-prone carotid hemodynamic profile, which might represent an additional factor contributing to the increased prevalence and severity of carotid atherosclerosis in diabetic patients compared with general population.
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PMID:NIDDM is associated with lower wall shear stress of the common carotid artery. 989 42

To clarify the relationship between circulating thrombomodulin (TM) and endothelial cell damage in diabetes mellitus, plasma levels of TM were quantitated by an enzyme linked immunoabsorbant assay (ELISA) in 164 type 2 diabetes mellitus and 72 normal control subjects, and these levels were compared with those of von Willebrand factor antigen (vWf: Ag), thrombin antithrombin III complexes (TAT), plasmin-alpha2-plasmin inhibitor complexes (PIC), fibrinogen, D-dimer, urinary albumin excretion rate (AER), intima-media thickness (IMT) and plaque score of the common carotid artery assessed with high resolution B-mode ultrasonography. Plasma levels of TM, vWf: Ag, TAT, PIC, AER, IMT and plaque score were significantly increased in the diabetic patients compared to the normal control subjects. Plasma TM levels showed significant correlation with vWf: Ag (r=0.350, p<0.0001), TAT (r = 0.334, p < 0.0001), PIC (r = 0.450, p < 0.0001), AER (r = 0.334, p < 0.0001), IMT (r = 0.181, P<0.01), plaque score (r=0.385, p<0.0001). Among four groups of diabetic patients, divided based on their severity of diabetic retinopathy, there were no significant differences in age, sex, systolic and diastolic blood pressure levels, HbA,1c, or plasma lipid levels, although the plasma levels of TM, vWf: Ag, TAT, PIC, AER, IMT and the plaque score in the patients with proliferative retinopathy were significantly higher than those of the healthy controls and patients with simple retinopathy. Among the 43 normoalbuminuric patients without intima-media thickness or thickened plaque (AER<30 mg/g Creatinine, IMT<1.0 mm, plaque score = 0), plasma levels of TM, vWf: Ag, TAT, PIC were significantly higher in those patients with retinopathy than in those without retinopathy. Multivariate analysis showed TM, TAT and PIC levels to be independent predictors of diabetic retinopathy. In conclusion, circulating TM reflects endothelial cell damage in patients with diabetic retinopathy, and hypercoagulability might play an important role in endothelial cell damage.
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PMID:Circulating thrombomodulin and hematological alterations in type 2 diabetic patients with retinopathy. 1007 54


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