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

This study is aimed at the evaluation of a 1% clindamycin hydrochloride containing gel on the microbial flora of periodontal pockets deeper than 5 mm. In order to achieve that purpose, 20 patients with pocketing in the premolar-molar regions were selected. Active and placebo gel were inserted once during the first 2 weeks of this experimental study. Microbial samplings were performed 1, 2, 4 and 12 weeks after the experiment started. The samples were submitted to microscopic examination and also to culture. Changes in the microbial content of the periodontal pockets treated by subgingival scaling and clindamycin 1% gel were significant, compared with those obtained with subgingival scaling and placebo gel, particularly with respect to anaerobic black-pigmented bacteria and the motile gram-negative flora. However, after 3 months, most of the treated cases were recolonized by the same initial species, though never at pre-clindamycin levels. In the light of this study, it will be concluded that the use of a small amount of clindamycin hydrochloride inserted into a periodontal pocket, once a week for 2 weeks as a complement to periodontal subgingival scaling, is beneficial in the treatment of adult periodontitis, by eliminating more effectively the microbial pocket colonization.
Infection
PMID:The effect of clindamycin gel insert in periodontal pockets, as observed on smears and cultures. 822 29

Oral health care has been an integral part of the care of patients with HIV infection and AIDS since the disease was first identified in the early eighties. The spectrum of HIV-associated opportunistic diseases occurring in the oral cavity propelled dental health care providers to the forefront of patient care. Infection control issues soon became important in oral health care for patients infected with HIV, and for the first decade these two issues overshadowed the concerns about appropriate management of the dental needs of HIV-infected patients. Several concerns need to be considered in the management of dental care for patients infected with HIV. These include decreased salivary flow and increased sugar intake, prevention and management of routine inflammatory gingival and periodontal disease as well as the atypical forms of gingival and periodontal disease associated with HIV infection (linear gingival erythema [LGE], necrotizing ulcerative gingivitis [NUG] and necrotizing ulcerative periodontitis [NUP]). Finally, although reports of complications secondary to dental treatment of HIV-infected individuals are rare, it is important to consider those factors related to the medical status of HIV-infected patients which may interfere with oral health care. These include potential bleeding problems related to thrombocytopenia and disease or medication related liver abnormalities, increased risk of local infection particularly in patients with severe neutropenia and adverse effects of multiple medications taken by HIV patients. Prevention and management of dental and periodontal disease in HIV-infected individuals is important to self esteem, quality of life and maintenance of adequate nutritional intake. Oral health care continues to be an important component of overall health care for HIV-infected patients.
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PMID:Dental lesions: diagnosis and treatment. 945 96

The established risk factors for ischemic stroke do not sufficiently explain all clinical and epidemiological features of the disease, such as the winter peak of stroke incidence, the decline of stroke during this century and the time point of cerebral ischemia. A role of infectious disease as stroke risk factor may partly explain above features. Several case-control studies with both hospital and population control groups showed that acute infection within the preceding week and mainly respiratory infection of both viral and bacterial origin increase the risk of cerebral ischemia independent from other risk factors (odds ratio 2.9-14.5). Infection as a risk factor appears to be most important in young age groups. Infection may cause a procoagulant state and thus, trigger thrombosis and cerebral ischemia. There is increasing evidence for chronic infection as stroke risk factor. A case-control study indicated chronic and recurrent bronchitis to increase stroke risk. Two case-control and one cohort study showed that chronic dental infection, mainly parodontitis, is a risk factor for stroke. There are conflicting results on chronic infection with cytomegalovirus and insufficient evidence for a role of Helicobacter pylorii infection in pathogenesis of stroke. Seroepidemiological studies and analyses of carotid plaques indicate a role of Chlamydia pneumoniae in ischemic stroke. However, causality can not yet be inferred from present results. Acute and chronic infectious diseases are treatable and partly preventable conditions. Their recognition as stroke risk factors could therefore be important for stroke prevention.
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PMID:[Infection, atherosclerosis and acute ischemic cerebrovascular disease]. 1069 60

This case history describes the course of disease in a 17-year-old boy with Ehlers-Danlos syndrome type III and early-onset periodontitis. Flow cytometric tests showed a reduced cell count in the specific immune system. Immunoglobulin concentrations in saliva and serum were within normal limits. Infection with T-lymphotropic viruses was excluded. The phagocytic capacity of the peripheral blood polymorphonuclear leukocytes was unimpaired. The anaerobic infection present in the early-onset periodontitis was treated with systemic antibiotic therapy and closed curettage. Following 14 days of this treatment, signs of acute inflammation subsided, and 18 months after therapy ended, a slight gain in clinical attachment was found, and bone growth was visible via radiology. However, a continuing lack of adequate oral hygiene represents a risk to the success of therapy in the long term.
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PMID:Early-onset periodontitis in a patient with Ehlers-Danlos syndrome type III. 1076 79

Atherosclerosis is a complex pathologic process initialed by the formation of cholesterol-rich plaque. Macrophages play a central role in the development of atherosclerosis, specifically in the initial accumulation of cholesterol in the arterial wall. It has been suggested that infection and chronic inflammatory conditions such as periodontitis may influence the atherosclerosis process. Porphyromonas gingivalis, one of the major pathogens involved in periodontitis, has been detected in human atheromas, suggesting that P. gingivalis infection may be associated with atherosclerosis. However, a causal relationship between this pathogen and the disease process has not yet been established. The purpose of the present investigation was to determine whether P. gingivalis could induce macrophages to form foam cells using the murine macrophage cell line (J774) as a model system. For inocula smaller than one bacterium per ten cells, P. gingivalis 381, as well as its lipopolysaccharide (LPS), induced foam cell formation of macrophages when cultured in the presence of human low-density lipoprotein (LDL). Infection of macrophages with increasing doses of P. gingivalis resulted in higher levels of foam cell formation. More than 70% of the cultured macrophages form cholesterol ester droplet-rich cells in the presence of 100 mug/ml of LDL when the inocula was more than 10 bacteria per cell. Low concentrations of P. gingivalis outer membrane vesicles also induced foam cell formation in the presence of LDL. In addition, it was demonstrated that P. gingivalis LPS alone was able to induce macrophage foam cell formation. P. gingivalis and its vesicles not only promoted LDL binding to macrophages but also induced macrophages to modify native LDL, which plays an important role in foam cell formation and the pathogenesis of atherosclerosis. Therefore, P. gingivalis cells or its vesicles released from periodontal lesions into the circulation may deliver virulence factor(s) such as LPS to the arterial wall to initiate or promote foam cell formation in macrophages and contribute to atheroma development.
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PMID:Porphyromonas gingivalis induces murine macrophage foam cell formation. 1458 Mar 89

Infections of the tissue surrounding the teeth (periodontitis) are usually caused by anaerobic gram-negative microorganisms. This infection causes destruction of the supporting alveolar bone and can lead to tooth loss. Removal of these microorganisms can slow or arrest the progression of periodontitis. Diabetes patients are at greater risk of developing periodontitis, may not respond as well to periodontal therapy as nondiabetic patients, and may require more aggressive treatment to manage periodontitis. Microorganisms that cause periodontitis and the host response to these may increase insulin resistance in diabetic patients. Treatment of periodontitis could improve glycemic control. A model is presented in which periodontal pathogens may cause increases in proinflammatory cytokines that mediate increases in insulin resistance, resulting in an increase in blood glucose. Following periodontal therapy, this process may be reversed.
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PMID:Periodontal disease and diabetes mellitus. 1476 80

Neutrophils are initially the predominant cells involved in the host defence of bacterial infections, including periodontal disease. Aggressive periodontitis is associated with Actinobacillus actinomycetemcomitans, a Gram-negative capnophilic microorganism. Infections caused by A. actinomycetemcomitans are not resolved by the host immune response despite the accumulation of neutrophils at the site of inflammation. To better understand the role of natural host defence mechanisms in A. actinomycetemcomitans infections, the interaction of phenotypically diverse strains of this pathogen with human neutrophils was assessed directly using techniques such as genetic labelling with the gene for green fluorescent protein, fluorescence-activated cell sorting and fluorescence imaging. The study included clinical isolates of A. actinomycetemcomitans represented by self-aggregating, biofilm-associated and isogenic planktonic variants. Data obtained showed that complement-mediated phagocytosis of A. actinomycetemcomitans was generally inefficient regardless of strain-specific serotype or leukotoxin production. Furthermore, the majority of ingested bacteria remained viable after exposure to neutrophils for 1 h. Interestingly, uptake of antibody-opsonized bacteria resulted in the rapid cell death of neutrophils. This was in contrast to ingestion of complement-opsonized bacteria, which did not affect neutrophil viability. The methods used in this study provided reliable and reproducible results with respect to adherence, phagocytosis and killing of A. actinomycetemcomitans when encountering human neutrophils.
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PMID:Resistance of fluorescent-labelled Actinobacillus actinomycetemcomitans strains to phagocytosis and killing by human neutrophils. 1636 67

Accumulating evidence indicates that herpesviruses may be putative pathogens in various types of periodontal diseases. The present study was performed to examine infections with different genotypes of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) in subgingival samples from a Chinese population and to analyze the correlation with periodontal status. A nested PCR assay was used to identify the presence of HCMV, EBV type 1 (EBV-1), and EBV-2; and the amplicons were further analyzed by restriction fragment length polymorphism analysis. HCMV was detected in 79.0% of 143 chronic periodontitis (CP) patients, 78.5% of 65 gingivitis patients, and 76.3% of 76 periodontally healthy individuals, while EBV was found in 63.6%, 32.3%, and 30.3% of the three groups of subjects, respectively. The HCMV-positive PCR products from all the samples were identified as corresponding to gB genotype I (gB-I) or gB-II. HCMV gB-II (62.9%), EBV-1 (43.4%), and EBV-2 (18.2%) were associated with CP at higher frequencies (P < 0.05), whereas HCMV gB-I was more often observed in gingivitis patients (40.0%) and healthy individuals (40.8%) (P < 0.05). Furthermore, a higher rate of coinfection with HCMV and EBV was shown in CP patients (52.4%), especially dual infections with HCMV gB-II and EBV-1 (30.8%) or HCMV gB-II and EBV-2 (12.6%), compared with the rates of single infections with HCMV or EBV (P < 0.05). Infection with HCMV gB-II, EBV-1, or EBV-2 was correlated with higher rates of bleeding on probing (P < 0.05). In patients infected with HCMV gB-II or both HCMV and EBV, including HCMV gB-II and EBV-1, a deeper probing depth or more serious attachment loss was found (P < 0.05). These findings clearly indicate that HCMV gB-II is the dominant genotype detected in subgingival samples in CP. HCMV gB-II infection and HCMV gB-II coinfection with EBV-1 are closely associated with periodontal tissue inflammation and destruction.
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PMID:Correlation between infections with different genotypes of human cytomegalovirus and Epstein-Barr virus in subgingival samples and periodontal status of patients. 1780 55

Infection, survival, and proliferation of pathogenic bacteria in humans depend on their capacity to impair host responses and acquire nutrients in a hostile environment. Among such nutrients is heme, a co-factor for oxygen storage, electron transport, photosynthesis, and redox biochemistry, which is indispensable for life. Porphyromonas gingivalis is the major human bacterial pathogen responsible for severe periodontitis. It recruits heme through HmuY, which sequesters heme from host carriers and delivers it to its cognate outer-membrane transporter, the TonB-dependent receptor HmuR. Here we report that heme binding does not significantly affect the secondary structure of HmuY. The crystal structure of heme-bound HmuY reveals a new all-beta fold mimicking a right hand. The thumb and fingers pinch heme iron through two apical histidine residues, giving rise to highly symmetric octahedral iron co-ordination. The tetrameric quaternary arrangement of the protein found in the crystal structure is consistent with experiments in solution. It shows that thumbs and fingertips, and, by extension, the bound heme groups, are shielded from competing heme-binding proteins from the host. This may also facilitate heme transport to HmuR for internalization. HmuY, both in its apo- and in its heme-bound forms, is resistant to proteolytic digestion by trypsin and the major secreted proteases of P. gingivalis, gingipains K and R. It is also stable against thermal and chemical denaturation. In conclusion, these studies reveal novel molecular properties of HmuY that are consistent with its role as a putative virulence factor during bacterial infection.
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PMID:Unique structure and stability of HmuY, a novel heme-binding protein of Porphyromonas gingivalis. 1942 22

Preterm birth (PTB) is a leading cause of infant mortality and morbidity in the US and across the globe. Infection and associated inflammation are important initiators for PTB pathways; an estimated 40% of PTBs are attributed to amniochorionic-decidual or systemic inflammation. Historically, intrauterine infections have been implicated in PTB; recent evidence suggests that infections remote from the fetal site may also be causative. There is strong epidemiological evidence that bacterial vaginosis and periodontitis--two syndromes characterized by perturbations in the normal vaginal and oral bacterial microflora, respectively--are linked to infection-associated PTB. Oral and vaginal environments are similar in their bacterial microbiology; identical bacterial species have been independently isolated in periodontitis and bacterial vaginosis. Periodontitis and bacterial vaginosis also share many behavioral and sociodemographic risk factors suggesting a possible common pathophysiology. Genetic polymorphisms in host inflammatory responses to infection are shared between bacterial vaginosis, periodontitis and PTB, suggesting common mechanisms through which host genotype modify the effect of abnormal bacterial colonization on preterm birth. We review the state of knowledge regarding the risk of PTB attributable to perturbations in bacterial flora in oral and vaginal sites and the role of host genetics in modifying the risk of infection-related PTB. We posit that bacterial species that are common in perturbed vaginal and oral sites are associated with PTB through their interaction with the host immune system.
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PMID:Vaginal and oral microbes, host genotype and preterm birth. 1994 83


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