A more robust view of the diversity of prokaryotes has come from sequencing rRNAs amplified directly from environmental samples. This approach has now been used to examine microbial communities in the human body, revealing populations rich in undescribed species whose impact on humans remains to be determined. (+info)
Characteristic distribution pattern of Helicobacter pylori in dental plaque and saliva detected with nested PCR.
(18/947)
The precise mode of transmission and the natural reservoir for Helicobacter pylori are unknown. PCR assays have proved to be highly sensitive and specific and are regarded as the method of choice for detecting H. pylori DNA in the oral cavity. The aim of this study was to investigate the prevalence and distribution of H. pylori in the oral cavity. Forty-two patients undergoing gastroscopy were investigated for the presence of H. pylori in dental plaque and saliva by nested PCR, and in the stomach by the 13C-urea breath test. Samples tested comprised dental plaque from molars, premolars and incisors and saliva. Two sets of primers homologous to the 860-bp fragment of H. pylori DNA, which have been shown previously to be highly sensitive and specific, were used for nested PCR. Eleven patients (26.2%) were infected with H. pylori in the stomach. H. pylori DNA was identified in dental plaque samples from 41 patients (97%) and in 23 saliva samples (55%). The prevalence in dental plaque from molars, premolars and incisors was 82%, 64% and 59%, with an odds ratio of 3.18, 1.24 and 1 (reference), respectively. In conclusion, H. pylori was present in the oral cavity of 97% of tested patients, with a characteristic distribution that was independent of the infection status of the stomach. Thus H. pylori may belong to the normal oral microflora. (+info)
The antimicrobial treatment of periodontal disease: changing the treatment paradigm.
(19/947)
Over the last 100 years, methods of surgical periodontal treatment have enjoyed a history of success in improving oral health. The paradigm of care is based on the "non-specific plaque hypothesis"--that is, the overgrowth of bacterial plaques cause periodontal disease, and the suppression of this overgrowth reduces disease risk. The central feature of this approach to care is the removal of inflamed gingival tissue around the teeth to reduce periodontal pocket depth, thereby facilitating plaque removal by the dentist and by the patient at home. Over the last 30 years, with the recognition that periodontal disease(s) is caused by specific bacteria and that specific antimicrobial agents can reduce or eliminate the infection, a second paradigm has developed. This new paradigm, the "specific plaque hypothesis", focuses on reducing the specific bacteria that cause periodontal attachment loss. The contrast between the two paradigms can be succinctly stated as follows: The antimicrobial therapy reduces the cause, while the surgical therapy reduces the result of the periodontal infection. The specific plaque hypothesis has two important implications. First, with the increasing attention to evidence-based models for prevention, treatment, outcome assessment, and reimbursement of care, increasing attention and financial effort will be channeled into effective preventive and treatment methods. Second, the recent observations that periodontal infections increase the risk of specific systemic health problems, such as cardiovascular disease, argue for the prevention and elimination of these periodontal infections. This review highlights some of the evidence for the specific plaque hypothesis, and the questions that should be addressed if antimicrobial agents are to be used responsively and effectively. (+info)
Molecular and genetic analyses of Actinomyces spp.
(20/947)
Members of the genus Actinomyces are predominant primary colonizers of the oral cavity and play an important role in initiating plaque development. These bacteria have evolved unique mechanisms that favor colonization and persistence in this micro-environment. The expression of cell-surface fimbriae is correlated with the ability of these bacteria to adhere to specific receptors on the tooth and mucosal surfaces, and to interact with other plaque bacteria. The elaboration of sialidase is thought to enhance fimbriae-mediated adherence by unmasking the fimbrial receptors on mammalian cells. The presence of certain cell-associated or extracellular enzymes, including those involved in sucrose or urea metabolism, may provide the means for these bacteria to thrive under conditions when other growth nutrients are not available. Moreover, these enzyme activities may influence the distribution of other plaque bacteria and promote selection for Actinomyces spp. in certain ecological niches. The recent development of a genetic transfer system for Actinomyces spp. has allowed for studies the results of which demonstrate the existence of multiple genes involved in fimbriae synthesis and function, and facilitated the construction of allelic replacement mutants at each gene locus. Analyses of these mutants have revealed a direct correlation between the synthesis of assembled fimbriae and the observed adherence properties. Further genetic analysis of the various enzyme activities detected from strains of Actinomyces should allow for an assessment of the role of these components in microbial ecology, and their contribution to the overall success of Actinomyces spp. as a primary colonizer and a key player in oral health and disease. (+info)
Denture plaque and adherence of Candida albicans to denture-base materials in vivo and in vitro.
(21/947)
The aim of this paper is to review our understanding of the mechanisms and clinical significance of adhesion of C. albicans to denture-base materials in relation to denture plaque and denture-related stomatitis. Earlier reports in the literature of a 65% prevalence level of denture-related stomatitis seem to be exaggerated. More recent studies indicate that denture-related stomatitis is considerably less common, particularly in normal healthy subjects. The etiology of the condition is discussed in this review, and although much of the literature supports the view that the condition is strongly associated with C. albicans, this is not always so. In some subjects, the cause appears to be related to a non-specific plaque. This review also considers the role of denture plaque in the pathogenesis of denture-related stomatitis, the sequential development of denture plaque, and its colonization by Candida organisms. Designing controlled in vivo studies is difficult, and as a consequence, many investigators have had to resort to in vitro studies. The majority of these studies have attempted to investigate the hydrophobicity of C. albicans, relating the surface free-energy of denture-base materials, particularly acrylic resin, to that of the organism. Surprisingly little work has been directed at surface roughness and how it affects retention of organisms. Further, no attention has been paid to the properties and character of the surface, other than average surface roughness, as it affects adhesion. A comparison of results from in vitro studies on the effect on adhesion of pre-coating the surfaces of denture-base materials with saliva has produced equivocal conclusions. This is largely due to little standardization of experimental protocols between studies, particularly in the collection and handling of the saliva used. In conclusion, the review strongly supports the suggestion that adherence of C. albicans to denture-base materials in vitro is related to the hydrophobicity of the organism. The clinical significance of the observation and the mechanisms for the development and maturation of denture plaque are yet to be understood. There is a clear need for further investigation of other factors that may moderate the adhesion of organisms and subsequent colonization of denture-base materials. (+info)
Characterization of recombinant, ureolytic Streptococcus mutans demonstrates an inverse relationship between dental plaque ureolytic capacity and cariogenicity.
(22/947)
Dental caries results from prolonged plaque acidification that leads to the establishment of a cariogenic microflora and demineralization of the tooth. Urease enzymes of oral bacteria hydrolyze urea to ammonia, which can neutralize plaque acids. To begin to examine the relationship between plaque ureolytic activity and the incidence of dental caries, recombinant, ureolytic strains of Streptococcus mutans were constructed. Specifically, the ureABCEFGD operon from Streptococcus salivarius 57.I was integrated into the S. mutans chromosome in such a way that the operon was transcribed from a weak, cognate promoter in S. mutans ACUS4 or a stronger promoter in S. mutans ACUS6. Both strains expressed NiCl(2)-dependent urease activity, but the maximal urease levels in ACUS6 were threefold higher than those in ACUS4. In vitro pH drop experiments demonstrated that the ability of the recombinant S. mutans strains to moderate a decrease in pH during the simultaneous metabolism of glucose and urea increased proportionately with the level of urease activity expressed. Specific-pathogen-free rats that were infected with ACUS6 and fed a cariogenic diet with drinking water containing 25 mM urea and 50 microM NiCl(2) had relatively high levels of oral urease activity, as well as dramatic decreases in the prevalence of smooth-surface caries and the severity of sulcal caries, relative to controls. Urease activity appears to influence plaque biochemistry and metabolism in a manner that reduces cariogenicity, suggesting that recombinant, ureolytic bacteria may be useful to promote dental health. (+info)
Serum immunoglobulin G (IgG) and IgG subclass responses to the RgpA-Kgp proteinase-adhesin complex of Porphyromonas gingivalis in adult periodontitis.
(23/947)
Serum immunoglobulin G (IgG), IgM, and IgG subclass responses to the RgpA-Kgp proteinase-adhesin complex of Porphyromonas gingivalis were examined by enzyme-linked immunosorbent assay using adult periodontitis patients and age- and sex-matched controls. Twenty-five sera from subjects with adult periodontitis (diseased group) and 25 sera from healthy subjects (control group) were used for the study. Sera and subgingival plaque samples from 10 sites were collected from each patient at the time of clinical examination. The level of P. gingivalis in the plaque samples was determined using a DNA probe. Highly significant positive associations between the percentage of sites positive for P. gingivalis and measures of disease severity (mean pocket depth, mean attachment loss, and percentage of sites that bled on probing) were found. The diseased group had significantly higher specific IgG responses to the RgpA-Kgp complex than did the control group, and the responses were significantly associated with mean probing depths and percentage of sites positive for P. gingivalis. Analysis of the IgG subclass responses to the RgpA-Kgp complex revealed that the subclass distribution for both the diseased and control groups was IgG4 > IgG2 > IgG3 = IgG1. The IgG2 response to the complex was positively correlated with mean probing depth, whereas the IgG4 response was negatively correlated with this measure of disease severity. Immunoblot analysis of the RgpA-Kgp complex showed that sera from healthy subjects and those with low levels of disease, with high IgG4 and low IgG2 responses, reacted with the RgpA27, Kgp39, and RgpA44 adhesins; however, sera from diseased subjects with low IgG4 and high IgG2 responses reacted only with the RgpA44 and/or Kgp44 adhesins. Epitope mapping of the RgpA27 adhesin localized a major epitope recognized by IgG4 antibodies in sera from subjects with high IgG4 and low IgG2 responses to the RgpA-Kgp complex which was not recognized by sera from diseased subjects with low IgG4 and high IgG2 responses. (+info)
Distribution and molecular characterization of Porphyromonas gingivalis carrying a new type of fimA gene.
(24/947)
Fimbriae of Porphyromonas gingivalis are filamentous appendages on the cell surface and are thought to be one of the virulence factors. The fimA gene encoding the subunit protein of fimbriae, fimbrillin (FimA), was classified into four typeable variants (types I to IV). We previously examined the distribution of P. gingivalis in terms of fimA genotypes in periodontitis patients using a fimA type-specific PCR assay. However, some patients harbored P. gingivalis with untypeable fimA. In this study, we have cloned a new type (type V) of fimA from dental plaque samples. P. gingivalis with type V fimA was isolated from dental plaque of a periodontitis patient, and the isolate was named HNA-99. The deduced amino acid sequences were compared with those of type I P. gingivalis ATCC 33277, type II strain HW24D1, type III strain 6/26, and type IV strain HG564, and the homologies were found to be 45, 44, 43, and 55%, respectively. Southern blot analysis showed that the clinical isolate HNA-99 possessed P. gingivalis-specific genes sod and kgp. However, in terms of serological specificities, type V FimA showed a difference from other types of FimA. In addition, type V P. gingivalis bacteria were detected in 16.4% (12 of 73) of the P. gingivalis-positive patients with periodontitis by PCR assay using specific primers. Thus, a new type of fimA gene is now established, and the fimA genotyping could be useful in determining the disease-associated genotypes of P. gingivalis involved in the development of adult periodontitis. (+info)