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

It is well known that diabetes mellitus aggravates both the severity and progression of periodontal disease. We sought to further explore biologic mechanisms of this relationship using naturally occurring gingivitis rats (ODUS/Odu) rendered diabetic by 65 mg/kg intravenous injection of streptozotocin (STZ). Insulin was administered daily to one group of the rats beginning 4 weeks after STZ injection (STZ-insulin group). Others received no insulin (STZ group). A third group that received no STZ was kept as controls. Eight weeks after STZ injection, sterilized liquid paraffin was injected peritoneally into all three groups, and peritoneal macrophages were collected 4 days later. Macrophage chemotaxis was measured by the membrane filter method using a 48-well microchemotaxis chamber with zymosan activated serum used as a chemotactic stimulant. Blood glucose levels, body weight, plaque indices, pocket depths, serum triglyceride and hemoglobin A1C levels were also determined. We found that blood glucose levels, body weight and triglycerides recovered to normal values in the STZ-insulin group. Further, control of blood glucose resulted in diminished plaque indices, and pocket depths returned to values seen in the controls. Chemotaxis and phagocytosis of peritoneal macrophages improved slightly in the STZ-insulin group, but did not return to levels seen in the pretreatment state. Although insulin resulted in some improvement in leukocyte function damaged by induced diabetes mellitus, recovery was incomplete.
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PMID:Effect of insulin on naturally occurring gingivitis rats with diabetes. 1086 70

The study was performed on 31 diabetic patients of both sexes, divided in 2 groups: group I--17 patients with insulin-dependent diabetes (IDDM) and group II--14 patients with noninsulin-dependent diabetes (NIDDM) and compared with a control group of 16 non-diabetic subjects. Mixed saliva was sampled without stimulation during 2 periods of the day: 07:30-08:00 before breakfast and 17:30-18:00 before dinner. We determined: salivary flow rate, pH with Merck indicator and, after homogenization, the thiocianat with the FeCl3 method and LDH activity (the Norbert method adapted in our laboratory for saliva). Our study showed the same diurnal changes in flow rate and salivary pH in both diabetic and control groups: minimal values in the morning and maximal ones in the afternoon. In non-smoking diabetic patients the salivary thiocianat had maximal values in the morning and minimal ones in the afternoon; similar behaviour, but less obvious was observed in smoking diabetic patients and in the control group regardless of the smoking habit. LDH activity showed unsignificant diurnal variations in the diabetic patients. In the control group we found a significant decrease of LDH activity in the afternoon. The discussion is about the implication of these salivary parameters in the pathology of oral cavity: gingivitis, periodontitis and caries in diabetic patients.
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PMID:Diurnal behaviour of some salivary parameters in patients with diabetes mellitus (flow rate, pH, thiocianat, LDH activity)--note II. 1100 Aug 69

Regular home care by the patient in addition to professional removal of subgingival plaque is generally very effective in controlling most inflammatory periodontal diseases. When disease does recur, despite frequent recall, it can usually be attributed to lack of sufficient supragingival and subgingival plaque control or to other risk factors that influence host response, such as diabetes or smoking. Causative factors contributing to recurrent disease include deep inaccessible pockets, overhangs, poor crown margins and plaque-retentive calculus. In most cases, simply performing a thorough periodontal debridement under local anesthesia will stop disease progression and result in improvement in the clinical signs and symptoms of active disease. If however, clinical signs of disease activity persist following thorough mechanical therapy, such as increased pocket depths, loss of attachment and bleeding on probing, other pharmacotherapeutic therapies should be considered. Augmenting scaling and root planing or maintenance visits with adjunctive chemotherapeutic agents for controlling plaque and gingivitis could be as simple as placing the patient on an antimicrobial mouthrinse and/or toothpaste with agents such as fluorides, chlorhexidine or triclosan, to name a few. Since supragingival plaque reappears within hours or days after its removal, it is important that patients have access to effective alternative chemotherapeutic products that could help them achieve adequate supragingival plaque control. Recent studies, for example, have documented the positive effect of triclosan toothpaste on the long-term maintenance of both gingivitis and periodontitis patients. Daily irrigation with a powered irrigation device, with or without an antimicrobial agent, is also useful for decreasing the inflammation associated with gingivitis and periodontitis. Clinically significant changes in probing depths and attachment levels are not usually expected with irrigation alone. Recent reports, however, would indicate that, when daily irrigation with water was added to a regular oral hygiene home regimen, a significant reduction in probing depth, bleeding on probing and Gingival Index was observed. A significant reduction in cytokine levels (interleukin-1beta and prostaglandin E2, which are associated with destructive changes in inflamed tissues and bone resorption also occurs. If patient-applied antimicrobial therapy is insufficient in preventing, arresting, or reversing the disease progression, then professionally applied antimicrobial agents should be considered including sustained local drug delivery products. Other, more broadly based pharmacotherapeutic agents may be indicated for multiple failing sites. Such agents would include systemic antibiotics or host modulating drugs used in conjunction with periodontal debridement. More aggressive types of juvenile periodontitis or severe rapidly advancing adult periodontitis usually require a combination of surgical intervention in conjunction with systemic antibiotics and generally are not controlled with nonsurgical anti-infective therapy alone. It should be noted, however, that, to date, no home care products or devices currently available can completely control or eliminate the pathogenic plaques associated with periodontal diseases for extended periods of time. Daily home care and frequent recall are still paramount for long-term success. Nonsurgical therapy remains the cornerstone of periodontal treatment. Attention to detail, patient compliance and proper selection of adjunctive antimicrobial agents for sustained plaque control are important elements in achieving successful long-term results. Frequent re-evaluation and careful monitoring allows the practitioner the opportunity to intervene early in the disease state, to reverse or arrest the progression of periodontal disease with meticulous nonsurgical anti-infective therapy.
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PMID:Nonsurgical periodontal therapy. 1115 83

Periodontitis is a chronic bacterial infection of the supporting structures of the teeth. The host response to infection is an important factor in determining the extent and severity of periodontal disease. Systemic factors modify periodontitis principally through their effects on the normal immune and inflammatory mechanisms. Several conditions may give rise to an increased prevalence, incidence or severity of gingivitis and periodontitis. The effects of a significant number of systemic diseases upon periodontitis are unclear and often it is difficult to causally link such diseases to periodontitis. In many cases the literature is insufficient to make definite statements on links between certain systemic factors and periodontitis and for several conditions only case reports exist whereas in other areas an extensive literature is present. A reduction in number or function of polymorphonuclear leukocytes (PMNs) can result in an increased rate and severity of periodontal destruction. Medications such as phenytoin, nifedipine, and cyclosporin predispose to gingival overgrowth in response to plaque and changes in hormone levels may increase severity of plaque-induced gingival inflammation. Immuno-suppressive drug therapy and any disease resulting in suppression of the normal inflammatory and immune mechanisms (such as HIV infection) may predispose the individual to periodontal destruction. There is convincing evidence that smoking has a detrimental effect on periodontal health. The histiocytoses diseases may present as necrotizing ulcerative periodontitis and numerous genetic polymorphisms relevant to inflammatory and immune processes are being evaluated as modifying factors in periodontal disease. Periodontitis severity and prevalence are increased in diabetics and worse in poorly controlled diabetics. Periodontitis may exacerbate diabetes by decreasing glycaemic control. This indicates a degree of synergism between the two diseases. The relative risk of cardiovascular disease is doubled in subjects with periodontal disease. Periodontal and cardiovascular disease share many common risk and socio-economic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying aetiology of both diseases is complex as are the potential mechanisms whereby the diseases may be causally linked. It is thought that the chronic inflammatory and microbial burden in periodontal disease may predispose to cardiovascular disease in ways proposed for other infections such as with Chlamydia pneumoniae. To move from the current association status of both diseases to causality requires much additional evidence. Determining the role a systemic disease plays in the pathogenesis of periodontal disease is very difficult as several obstacles affect the design of the necessary studies. Control groups need to be carefully matched in respect of age, gender, oral hygiene and socio-economic status. Many studies, particularly before the aetiological importance of dental plaque was recognised, failed to include such controls. Longitudinal studies spanning several years are preferable in individuals both with and without systemic disease, due to the time period in which periodontitis will develop.
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PMID:Periodontal manifestations of systemic disease. 1135 36

In the 1960s and 1970s, data became available indicating that most of the adult population had periodontal disease and that effective bacterial removal prevented and treated periodontitis. This information led to a systematic approach to the management of periodontal disease and influenced teaching of periodontics in dental schools. We now know that most adults have only gingivitis and very mild localized periodontitis. A small percentage, albeit representing substantial numbers, of adults have generalized severe periodontitis. We also recognize that a few currently known and measurable risk factors, including diabetes, smoking, and genetics, can identify the patients who are at risk for the severe generalized cases that require extensive therapy and intensive prevention, as well as patients at risk for a less-predictable response to treatment. This review will discuss the evidence that supports the change in our knowledge and understanding of periodontal disease. The question now becomes at what point, and how, do we integrate this new knowledge into the dental curriculum?
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PMID:Patients are not equally susceptible to periodontitis: does this change dental practice and the dental curriculum? 1151 50

Alstrom syndrome is a rare disorder characterized by early obesity, loss of central vision, diabetes mellitus, hearing loss and short stature. Previous studies, have reported no information regarding oral findings. This article describes oral findings in two cases of Alstrom syndrome. In both cases, gingivitis was present and also light yellow-brown discolored enamel bands were observed on the anterior teeth. This staining may have resulted from discoloration of the preexisting slight band-like enamel hypoplasia. The gingiva was examined histologically by light and transmission electron microscopy. Irregular thickness of the basal lamina and delamination of the myelin sheath were detected by transmission electron microscopy. There is no information about pathological odontogenesis in Alstrom syndrome in previous reports. Oral present findings may contribute further information about the clinical manifestations of Alstrom syndrome.
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PMID:Alstrom syndrome: a case report. 1173 44

Periodontal disease is a complication of patients with type 1 diabetes mellitus (T1DM), although the mechanisms responsible for this relationship remain unclear. The aim of this study was to examine oral manifestations and the prevalence of periodontal pathogens from subgingival plaque samples and serum IgG antibody levels against them in young Japanese type 1 diabetic subjects. One hundred and seventeen Japanese T1DM subjects (53 male, 64 female, mean age +/- SD, 16 +/- 6.5 years) participated in this study. Thirty-nine periodontally healthy, age-matched nondiabetics served as controls. T1DM subjects were clinically assigned into three groups: 12 periodontitis, 32 gingivitis and 73 periodontally healthy. Microbiological tests for four periodontal pathogens, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia and Capnocytophaga ochracea were performed using 16S ribosomal RNA-based polymerase chain reaction methods. Serum IgG antibody levels against 12 periodontal bacteria including the four species assessed by polymerase chain reaction were measured by enzyme-linked immunosorbent assay. In the T1DM subjects, the Periodontitis group had a significantly longer mean duration of diabetes and a higher percentages of subjects harbouring P. gingivalis and P. intermedia than the Periodontally Healthy group. Serum IgG antibody levels against P. gingivalis were significantly elevated in the Periodontitis group compared with Gingivitis and Periodontally Healthy groups. These results indicate that Japanese T1DM subjects are a high-risk group for periodontal disease and both P. gingivalis infection and duration of T1DM are risk factors for the progression of periodontitis in patients with T1DM.
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PMID:Subgingival microflora and antibody responses against periodontal bacteria of young Japanese patients with type 1 diabetes mellitus. 1266 49

The ultrastructure of Langerhans cells has not been fully investigated in diabetes-associated gingival tissues. The present study was carried out to investigate the ultrastructure of gingival Langerhans cells in alloxan-induced diabetic rats. Gingival biopsies were obtained from 22 diabetic and 18 control rats. Langerhans cells were observed by transmission electron microscopy (TEM) in the basal layers of healthy oral epithelium. On rare occasions, Langerhans cells were found in the suprabasal layers of the oral epithelium. Langerhans cells in the oral epithelium of diabetic rats were seen in the basal and suprabasal layers. Usually, Langerhans cells had clear cytoplasm and convoluted or indented nuclei and few or no specific granules. The clear cytoplasm contained mitochondria, lysosomes and a small number of rough-surfaced endoplasmic reticulum regions, but it lacked tonofilament. Occasionally, centrioles were also observed in the cytoplasm. The membrane of Langerhans cells had no junctional complexes such as desmosomes. In diabetic rats, Langerhans cell precursors were developed into specific granule-bearing cells. Both Langerhans cells and their granules were more frequent in the gingiva of diabetic rats than in the control group. These data suggest that Langerhans cells play an important role in explaining the pathogenesis and development of diabetic gingivitis.
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PMID:Ultrastructural determination of gingival Langerhans cells in alloxan-induced diabetic rats. 1537 33

The location of plaque-associated gingivitis at the gingival portion of the tooth plays an essential role in its genesis. However, at times local and other host response modifying factors also have an influence. The pathogeny of periodontitis is more complex. The microorganisms that comprise subgingival plaque are capable of acting directly on periodontal tissues or of modifying the host response, whereas the participation of the plaque per se (normal, decreased, or increased) is as decisive as the action of the bacteria themselves in the emergence of the disease. Different types of periodontitis are associated with specific microorganisms. The most periodontopathogenic are A. actinomycetemcomitans, P. gingivalis, and T. forsythensis. Periodontitis as a whole, represent the source of complications such as root caries, endoperiodontal processes and periodontal abscesses. They are associated with various illnesses such as atherosclerosis, diabetes, and respiratory infections, amongst others, as well as pathological oral halitosis. The different modalities of PCR are particularly important in the microbiological diagnosis of periodontitis, although on the negative side of things, it must be pointed out that in vitro sensitivity studies cannot be performed using this technique. First line antibiotic treatment of periodontitis includes amoxicillin/ clavulanic acid, metronidazole (associated or not with amoxicillin) and clindamycin.
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PMID:Periodontal diseases: microbiological considerations. 1558 Jan 39

Many clinical trials conducted during the last decade have clarified controversial issues and resulted in changed periodontal paradigms. These modified concepts have therapeutic implications. Some salient altered periodontal concepts include the following: The mere presence of pathogens will not initiate periodontal diseases. Most subgingival bacteria reside in biofilms. Periodontal diseases are infections. Periodontal pathogens can be transferred between family members. The host response can be protective and destructive. Gingivitis does not usually proceed to periodontitis. Risk factors in conjunction with bacteria and the host response can affect the severity of disease, patterns of destruction, and the response to therapy. Many medical conditions (eg, diabetes, smoking, and HIV infection) may predispose patients to periodontitis. Associations between periodontitis and a number of systemic ailments (eg, diabetes, adverse pregnancy outcomes, and cardiovascular disease) have been detected and are being investigated to determine if there is a cause-and-effect relationship. Diagnostic and therapeutic implications of these altered paradigms are addressed throughout the article.
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PMID:Changing periodontal concepts: treatment considerations. 1594 13


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