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      Microbial Ecology of Dental Plaque and its Significance in Health and Disease

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      Advances in Dental Research
      SAGE Publications

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          Abstract

          Dental plaque forms naturally on teeth and is of benefit to the host by helping to prevent colonization by exogenous species. The bacterial composition of plaque remains relatively stable despite regular exposure to minor environmental perturbations. This stability (microbial homeostasis) is due in part to a dynamic balance of both synergistic and antagonistic microbial interactions. However, homeostasis can break down, leading to shifts in the balance of the microflora, thereby predisposing sites to disease. For example, the frequent exposure of plaque to low pH leads to inhibition of acid-sensitive species and the selection of organisms with an aciduric physiology, such as mutans streptococci and lactobacilli. Similarly, plaque accumulation around the gingival margin leads to an inflammatory host response and an increased flow of gingival crevicular fluid. The subgingival microflora shifts from being mainly Gram-positive to being comprised of increased levels of obligately anaerobic, asaccharolytic Gram-negative organisms. It is proposed that disease can be prevented or treated not only by targeting the putative pathogens but also by interfering with the processes that drive the breakdown in homeostasis. Thus, the rate of acid production following sugar intake could be reduced by fluoride, alternative sweeteners, and low concentrations of antimicrobial agents, while oxygenating or redox agents could raise the Eh of periodontal pockets and prevent the growth and metabolism of obligately anaerobic species. These views have been incorporated into a modified hypothesis (the "ecological plaque hypothesis") to explain the relationship between the plaque microflora and the host in health and disease, and to identify new strategies for disease prevention.

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          Most cited references53

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          Colonization resistance of the digestive tract in conventional and antibiotic-treated mice.

          The effect of oral administration of antibiotics on the intestinal flora of conventional mice and their resistance to colonization by orally introduced Escherichia coli, Klebsiella pneumoniae and Pseudomonas aeruginosa was studied. Colonization resistance (CR) was expressed as the log of the oral bacterial dose followed by a persistent take in 50% of the contaminated animals. The intestinal flora was virtually eliminated by the antibiotics and this elimination was accompanied by a precipitous fall of CR. CR gradually returned to normal values during the period of repopulation of the intestinal tract by the organisms surviving the treatment. Antibiotic treatment resulted in the disappearance of Enterobacteriaceae, enterococci, staphylococci and yeasts and, under appropriate housing conditions, the animals remained free of these organisms indefinitely. Germ-free mice contaminated with the intestinal flora of an antibiotic-treated animal and their offspring housed in a germ-free isolator showed high values of CR. Their intestinal flora consisted of anaerobic bacteria only. Apparently, these anaerobes are responsible for CR in these and in conventional mice.
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            Role of Streptococcus mutans in human dental decay.

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              Bacterial adhesion to oral tissues: a model for infectious diseases.

              The majority of bacteria which colonize humans display sharp host and tissue tropisms; consequently, relatively little is known about how they initiate colonization on mucosal surfaces. The mouth has a variety of features which have enabled it to serve as a useful model for the discovery of basic principles of host-parasite interactions occurring in mucosal environments. Early studies demonstrated that indigenous bacteria attach to surfaces of the mouth in a highly selective manner; attachment was often observed to correlate with colonization. These studies led to the recognition that bacterial attachment is an essential step for colonization in environments which contain surfaces exposed to a fluid flow. Bacterial adhesion has subsequently grown into a major area of infectious disease research. Many bacteria have been found to possess proteinaceous components, called "adhesins", on their surfaces which bind in a stereochemically specific manner to complementary molecules, or "receptors", on the tissue surface. Adhesins are often lectins which bind to saccharide receptors, but some adhesins are thought to bind to proteinaceous receptors. Studies of components of human saliva, which adsorb to hydroxyapatite (HA) surfaces similar to those of teeth, and promote the attachment of prominent plaque bacteria, have revealed that the acidic proline-rich proteins (PRPs) promote the attachment of several important bacteria. These include strains of Actinomyces viscosus, Bacteroides gingivalis, some strains of Streptococcus mutans, and others. The salivary PRP's are a unique family of molecules. However, segments of PRPs are structurally related to collagen. This may be significant, since B. gingivalis and certain cariogenic streptococci bind to collagenous substrata, and such interactions may facilitate their invasion into gingival tissues, or into dentin or cementum, respectively. Another unexpected observation was that although A. viscosus and other bacteria bind avidly to PRPs adsorbed onto apatitic surfaces, they do not interact with PRPs in solution. PRP molecules evidently undergo a conformational change when they adsorb to HA, and adhesins of A. viscosus recognize cryptic segments which are only exposed in adsorbed molecules. This provides the bacteria with a mechanism for efficiently attaching to teeth while suspended in saliva. It also offers a molecular explanation for their sharp tropisms for human teeth. It has proven convenient to refer to such hidden receptors for bacterial adhesins as "cryptitopes" (from cryptic, meaning hidden, and topo, meaning place).(ABSTRACT TRUNCATED AT 400 WORDS)
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                Author and article information

                Journal
                Advances in Dental Research
                Adv Dent Res.
                SAGE Publications
                0895-9374
                1544-0737
                July 1994
                December 01 2016
                July 1994
                : 8
                : 2
                : 263-271
                Affiliations
                [1 ]Pathology Division PHLS Centre for Applied Microbiology and Research Porton Down Salisbury SP4 OJG England
                Article
                10.1177/08959374940080022001
                7865085
                06c26167-cb9c-43f1-9a78-1f58b31449c9
                © 1994

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