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

Microbial factors involved in the genesis of periodontitis are related with supragingival (coronal) and subgingival plaque. The microorganisms in the supragingival plaque reach the gingival sulcus, and are influenced by ecological determinants in this zone which condition the establishment of adherent plaque. This plaque may subsequently form the substrate for particularly periodon to pathogenic bacteria, which may then form plaques adhered to the epithelium, or develop as floating (nonadhered) populations. After microbial colonization of the gingival sulcus, bacteria or substances they produce may reach the junctional epithelium and alveolar bone, leading to direct tissular destruction to an extent determined by the host's immune response. Damage may be local or generalized, depending on additional factors.
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PMID:Oral ecology and its pathogenic relation with the origin of primary periodontitis associated with plaque. 175 28

The oral cavity is populated by a prodigious microbial flora that exhibits a unique successional colonization of enamel and subgingival root surfaces. A wide range of oral sites provide different ecologic conditions and are, therefore, populated by different commensal microbial combinations. The sequence of microbial colonization, regardless of location within the oral cavity, commences with the acquisition of salivary and/or crevicular fluid-derived pellicle. As the process of successional colonization of the gingival crevice area proceeds uninterrupted, achieving critical mass between 10 and 21 days, gingivitis becomes evident at a clinical level. However, at a histologic level, gingivitis may be evident within 2-3 days of plaque accumulation. The inflammatory response sufficiently alters the ecological conditions so as to allow proliferation of supragingival plaque into subgingival areas. The subgingival plaque becomes progressively more Gram-negative and anaerobic in nature as the periodontal pocket deepens, leading ultimately to a chronic, progressive deterioration of the periodontium--adult periodontitis. Both gingivitis and adult periodontitis are characterized by the successive colonization of cocci, short and long rods, filamentous microbes with "corn cob" and "bristle brush" formations, flagellated microbes, and spirochetes. Localized juvenile periodontitis (LJP), in contrast to the adult form of periodontitis, features a comparatively sparse microbial flora. The subgingival microbial colonization characteristically features cocci, short rods, coccobacilli, and spirochetes.
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PMID:Microbial colonization in human periodontal disease: an illustrated tutorial on selected ultrastructural and ecologic considerations. 208 Apr 31

Research over the past decade has identified many of the microorganisms involved in the etiology of human periodontitis such as Actinobacillus actinomycetemcomitans. Efforts are now directed toward defining these species' role in the pathogenic process. Since microbial colonization of host tissues is a key first step in developing a bacterial infection, determining the source of the periodontal pathogens and their route of transmission is likely to be crucial in formulating preventive strategies. Recently, a technique from molecular biology, restriction endonuclease analysis, has been used to track bacterial infections. In the present study, this method was used to investigate the epidemiology of A. actinomycetemcomitans infection. One hundred twenty-four human subgingival plaque isolates of A. actinomycetemcomitans were examined including bacterial strains from the United States, Korea, and Norway as well as 15 strains from cynomolgus (Macaca fascicularis) and spider monkeys (Macaca iris) and 4 reference strains. The genomic DNA from each strain was purified, digested with each of 16 restriction endonucleases, and the DNA digests were resolved by electrophoresis. The resulting patterns of DNA fragments were compared and also correlated with the A. actinomycetemcomitans serotype determined using serotype-specific antisera in immunofluorescence. Human isolates of A. actinomycetemcomitans even from disparate geographic sources showed little diversity by restriction endonuclease analysis. Three major restriction patterns were found. Restriction pattern I was common to all 20 of the serotype a isolates, restriction pattern II was associated with 58% of the 73 serotype b isolates examined, while restriction pattern III was associated with the remaining serotype b strains and with all 15 of the serotype c strains.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular genetic analysis of Actinobacillus actinomycetemcomitans epidemiology. 215 41

There is overwhelming evidence that bacteria cause periodontitis and that they do so by extending apically along the surfaces of the tooth roots and creating pockets. A very complex mixture of microbial species, mostly although not exclusively gram-negative, anaerobic, and motile, is involved. Infection probably occurs in a progressive and sequential manner. The bacteria involved include various species of Bacteroides, Actinobacillus, Eikenella, Fusobacterium, Capnocytophaga, and Eubacterium. Local oral conditions such as tooth position play an aetiologic role by affecting plaque accumulation and retention. Host defence factors, particularly the phagocytic cells and the immune system, play a determinative role in the aetiology by monitoring, controlling, and regulating microbial colonization and infection. These diseases begin as an acute inflammation of the marginal gingiva, and they progress through orderly stages to the formation of a gingival pocket. Transition from gingivitis to periodontitis is not well-understood, but it probably involves colonization by additional microbial species or invasion of the periodontal tissue by species already present. Progression of periodontal destruction is episodic, possibly as a consequence of successful host defence. In most patients, periodontal destruction occurs more infrequently than previously suspected. In both treated and untreated patients, a small subgroup accounts for most of the disease activity. The most important problem we now face is to develop diagnostic methods to identify individuals in this subgroup and devise ways to prevent and control their diseases.
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PMID:Current understanding of the aetiology and progression of periodontal disease. 353 87

Associations between oral malodor, measures of periodontal disease, and trypsin-like activity of periodontal pathogens on tongue and teeth were examined in 127 subjects. Volatile sulphur compound (VSC) measurements were made with a portable sulphide monitor; oral malodor was also estimated by organoleptic methods. Measurements repeated one week apart indicated that steady-state VSC levels (r = 0.72; P = 0.0001) and peak VSC levels (r = 0.63; P = 0.0001) were reproducible but these r values were not significantly different (P > 0.1). There was a significant correlation between tongue odor and peak VSC levels (r = 0.40; P = 0.0001) and between tongue odor and whole mouth organoleptic measures (r = 0.55; P = 0.0001). To study the effect of reducing microbial colonization on oral malodor, chlorhexidine gluconate (0.2%) rinsing was prescribed for 7 days. Reductions of VSC levels were significant for both peak (37%) and steady-state (41%) data (P = 0.0001). Anaerobic periodontal pathogens on the tongue estimated by the proportions of positive BANA tests were reduced 19% (P = 0.001) and this was concomitant with a 40% (P = 0.0001) decrease in organoleptic measurement of the tongue dorsum. Mean pH measurements of the tongue dorsum showed large reductions from 6.9 initially to 6.3 post-treatment (P = 0.0001). Subjects were divided into periodontitis/no periodontitis based on periodontal inflammation and probing depth (> or = 5 mm). Of the 37 subjects with periodontitis, 23 had oral malodor whereas 52 out of 90 periodontally healthy subjects exhibited malodor. Chi square analysis comparing halitosis in subjects with and without periodontitis showed no statistically significant association (chi 2 = 0.208; P 0.65) between these two factors although the intensity of malodor as based on VSC concentration in periodontally healthy subjects was 19% less (mean = 111 ppb) than in subjects with periodontitis (mean = 136 ppb). The odds ratio was 1.2, indicating that oral malodor was not associated with periodontitis. These data indicate that a large proportion of individuals with oral malodor are periodontally healthy and that the mucosal surface of the tongue is a major site of oral malodor production.
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PMID:Relationship of oral malodor to periodontitis: evidence of independence in discrete subpopulations. 813 14

This study clinically evaluates the use of decalcified freeze-dried bone allograft (DFDBA) in conjunction with an expanded polytetrafluoroethylene (ePTFE) membrane specifically designed for the treatment of interproximal intraosseous defects. It also examines by SEM, plaque contaminated membranes retrieved from patients. 15 advanced periodontitis patients with two bilateral interproximal probing depths of > or = 6 mm participated. After hygiene phase, measurements were made to determined soft tissue recession, pocket depth, clinical attachment levels and amount of keratinized tissue. Defects from each pair were randomly treated with ePTFE plus DFDBA (experimental) or DFDBA alone (control). Measurements were made during the surgery to determine crestal resorption, defect resolution and defect fill. Membranes were removed at 4 to 6 weeks and analyzed by SEM. Each site was surgically reentered and measurements repeated at six months. Both groups showed clinical and statistically significant changes when compared to baseline (P < 0.01), but no difference between groups. The experimental group showed increased soft tissue recession vs control group, 0.9 versus 0.4 mm, and loss of keratinized tissue 1.6 versus 0.1 mm (P < 0.0001). Control sites showed a 58% bone fill while experimental sites had 70% bone fill. There were no clear patterns of microbial colonization or cell adherences in either side of the membrane. It was concluded that the presence of plaque on the membranes did not compromise the initial clinical healing during the first 4-6 weeks. Results suggest a beneficial effect with the use of either technique for the treatment of intraosseous defects.
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PMID:Healing in periodontal defects treated by decalcified freeze-dried bone allografts in combination with ePTFE membranes (I). Clinical and scanning electron microscope analysis. 835 29

The objective of this study was to evaluate the relationship between the presence of bacteria on the tooth-facing surface of ePTFE barriers and the clinical outcome of membrane supported reconstructive periodontal surgery. 20 systemically healthy subjects affected by chronic periodontitis were enrolled. One tooth site per patient, associated with an angular bony defect and a probing attachment loss of > 4 mm, was selected to be treated by means of a guided tissue regeneration procedure using an ePTFE barrier membrane. Antibiotics (Augmentin 1 g/day) for 2 weeks were prescribed. In addition to the use of chlorhexidine for post-surgical plaque control, all patients were recalled once a week for professional tooth cleaning. The barrier material was harvested for SEM analysis after 4-6 weeks. Professional tooth cleaning and reinforcement of sel-performed oral hygiene measures were given at 1 mouth intervals after membrane removal. For each treated site, the difference in probing attachment loss between baseline examination and a follow-up examination after 6 months of healing was calculated. The results of the SEM-analysis revealed that bacterial colonization was evident in the collar area of all the retrieved membranes. In the mid part of the membranes 30 out of 60 microscopic fields (50%) demonstrated microbial colonization, and in the most apical part 9 out of 60 fields (15%). Regression analysis indicated that gain in probing attachment level was positively correlated to initial attachement loss and negatively correlated to microbial colonization of the mid part of the membranes. It was concluded that bacterial colonization in the mid part of the ePTFE membrane reduced the potential gain in probing attachment following GTR-therapy with almost 50%.
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PMID:Bacterial colonization of barrier material and periodontal regeneration. 895 34

The objective of the study was to evaluate bacterial colonization of the tooth-facing surface of bioabsorbable membranes and to determine its effect on the clinical outcome of membrane supported reconstructive periodontal surgery. Twenty systemically healthy subjects affected by chronic adult periodontitis were enrolled in the study. One non-furcation tooth site per patient, associated with an angular bony defect and a probing attachment loss of > 5 mm, was selected to be treated by means of a guided tissue regeneration procedure using a polyglicolactic membrane. Antibiotics (amoxicillin/clavulanate potassium 1 g per day) for 2 weeks were prescribed, in addition to the use of chlorhexidine for post-surgical plaque control. All patients were recalled once a week for 5 weeks for professional tooth cleaning. At 5 weeks sites with clinically exposed membranes underwent a second surgery to harvest residual barrier material which was analyzed by scanning electronic microscopic (SEM) for bacterial colonization. Sites with no membrane exposure at 5 weeks were allowed to heal without any other surgical intervention. Professional tooth cleaning and reinforcement of self-performed oral hygiene measures were given at 1 month intervals for the duration of the study. For each treated site the difference in probing attachment loss between baseline examination and a follow-up examination made 6 months after the second surgery was calculated. Gain of probing attachment was statistically (P < 0.001) greater in sites with no membrane exposure when compared to sites with partially exposed barrier material (4.2 +/- 0.5 vs. 3.3 +/- 0.6). The results of SEM analysis revealed that bacterial colonization was evident in all the microscopic fields of the exposed areas of the membranes. In the mid-part of the membranes 16 out of 39 microscopic fields (41%) demonstrated microbial colonization, while no bacteria-positive field was observed in the most apical portion of the membranes. Regression analysis indicated that gain in probing attachment level was negatively correlated to microbial colonization of the mid-part of the membranes. It was suggested the midportion of the tooth-facing surface of polyglicolactic membrane is a critical area for the healing process since its bacterial colonization was detrimental to the outcome of the GTR surgery.
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PMID:Bacterial colonization of bioabsorbable barrier material and periodontal regeneration. 895 69

This study aimed to investigate and compare the lipid and polysaccharide content of the cemental surfaces of healthy and periodontally-involved teeth. Thirty periodontally-involved single-rooted teeth from fifteen patients with localized juvenile, adult and rapidly progressive periodontitis were included in the experimental group and 5 healthy teeth were assessed in the control group. Frozen serial sections were obtained and stained with hematoxylin-eosin for morphological assessment. Oil-Red-O and Alcian Blue-Periodic Acid Schiff stains were used to evaluate the presence of lipids, neutral and acidic polysaccharides using light microscopy. It was found that with hematoxylin-eosin staining in the experimental group, both the involved and uninvolved cementum surfaces of teeth, which belong to all periodontitis groups, showed generally irregular surfaces that contain some resorption areas. Alcian Blue-Periodic Acid Schiff positive staining was observed only superficially and at the areas associated with microbial dental plaque. However, Oil-Red-O staining was positive only superficially at 5 teeth that belonged to localized juvenile and rapidly progressive periodontitis groups. Apparent lipopolysaccharide staining into cementum was not seen in any of the diseased teeth. The results presented here suggest that endotoxin was only localized in superficial layers and associated with only microbial colonization.
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PMID:Histological assessment of root cementum at periodontally healthy and diseased human teeth. 1069 94

Periodontal disease is a significant cause of tooth loss among adults. It is initiated by pathogenic bacteria, which trigger an inflammatory response that is effective in preventing significant microbial colonization of the gingival tissues. In some individuals, the reaction to bacteria may lead to an excessive host response, resulting in periodontal tissue destruction. Recent developments suggest that interleukin (IL)-1 genetic polymorphisms may identify certain individuals who have a predisposed susceptibility to periodontal breakdown and that elevated levels of IL-1 are found in individuals with periodontal disease. However, there is no direct evidence that IL-1 per se is responsible for the critical events that occur in periodontitis. We investigated the role of IL-1 in periodontal disease in a Macaca fascicularis primate model, using human soluble IL-1 receptor type I as a specific inhibitor. The results indicate that inhibition of IL-1 alone significantly reduces inflammation, connective tissue attachment loss, and bone resorption that are induced by periodontal pathogens.
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PMID:Inflammation and tissue loss caused by periodontal pathogens is reduced by interleukin-1 antagonists. 1219 78


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