Why be down in the mouth? Three decades of research in oral microbiology

Abstract

This paper describes some of the work done in the author's laboratory over the past 35 years. The research covers the following areas: the physiology of oral streptococci and their interactions; the physiology of some Gram-negative anaerobes and their interactions in relation to periodontal diseases; preventing the major dental diseases; and the future of oral microbiology.Key words: Oral microbiology, dental plaque, dental caries, periodontal diseases.Abbreviations and acronyms: HSP = heat shock proteins; MS = mutans streptococci.(Accepted for publication 23 December 2004.) we devised a bacteriocin typing ("fingerprinting") scheme for various MS strains -especially those isolated from the plaque of individual members of family groups. We were subsequently able to demonstrate that most children harboured MS transmitted by their mother and were thus among the first to show that caries is an infectious transmissible disease.3 In a series of experiments with colleagues at the University of Nijmegen, The Netherlands, it was shown that bacteriocin activity in MS appears to confer on the organisms an ecological advantage in developing dental plaque. Briefly, a specific pathogen-free plaque ecosystem was established in the mouths of rats. In the early stage of plaque development, invading MS quickly became dominant. However, with time, as the ecosystem stabilized into a so-called "climax community", it became much more resistant to the invasion and establishment of MS. Nevertheless, bacteriocin-producing (bac + ) strains generally established at a higher level than bac -strains.4 This theme will be re-visited a little later in relation to the concept of "replacement therapy" as a cariespreventive measure.The next phase of our studies stemmed from two now widely-accepted concepts. Firstly, that oral infectious diseases are often polymicrobial in nature and result from disturbances in the microbial ecology of the mouth; and secondly, that understanding this ecology -both in terms of the metabolic capabilities of the resident bacteria as well as their interactions -is crucial in the prevention and treatment of such diseases.In studying the metabolic activities of oral streptococci and their subsequent interactions with one another, we elected to use continuous culture rather than the traditional batch culture technique. The latter is unnatural in the sense that it is a closed system in which a bacterium is cultured in a nutrient-replete environment where it can grow at rates approaching its maximum until lack of nutrient(s), biological space and the build-up of toxic metabolic end-products eventually cause growth to cease; the death-rate then begins to exceed the growth-rate and viable cell numbers decline. When growing in vivo (e.g. the mouth), the limitation INTRODUCTIONFrom the beginning of the last century it has been accepted that bacteria play a pivotal role in the aetiology of dental caries. However, this was not proven until the early 1960s and oral microbiology, as a discipline, did not gain momentum u...

Effect of Mode of Delivery on Early Oral Colonization and Childhood Dental Caries: A Systematic Review

“…Successful colonization by mutans streptococci depends on the number of other commensal bacteria already present in the oral cavity because they need to compete for nutrients [7, 10]. Therefore, as the density of other pioneer oral microbiota increases, the chance of successful colonization by mutans streptococci will decrease.…”

“…Therefore, as the density of other pioneer oral microbiota increases, the chance of successful colonization by mutans streptococci will decrease. Furthermore, a number of common plaque microorganisms such as Streptococcus sanguinis and Streptococcus gordonii are able to catabolize the amino acid arginine to ammonia favoring a pH rise [8, 10, 11] which could counteract the harmful effect of low pH on the tooth surface. Therefore, bacterial colonization in a child’s mouth is the most important event underlying the pathogenesis of ECC.…”