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Jayden Wilson
Jayden Wilson

Oral Biofilms And Plaque Control

Humans have co-evolved with micro-organisms and have a symbiotic or mutualistic relationship with their resident microbiome. As at other body surfaces, the mouth has a diverse microbiota that grows on oral surfaces as structurally and functionally organised biofilms. The oral microbiota is natural and provides important benefits to the host, including immunological priming, down-regulation of excessive pro-inflammatory responses, regulation of gastrointestinal and cardiovascular systems, and colonisation by exogenous microbes. On occasions, this symbiotic relationship breaks down, and previously minor components of the microbiota outcompete beneficial bacteria, thereby increasing the risk of disease. Antimicrobial agents have been formulated into many oral care products to augment mechanical plaque control. A delicate balance is needed, however, to control the oral microbiota at levels compatible with health, without killing beneficial bacteria and losing the key benefits delivered by these resident microbes. These antimicrobial agents may achieve this by virtue of their recommended twice daily topical use, which results in pharmacokinetic profiles indicating that they are retained in the mouth for relatively long periods at sublethal levels. At these concentrations they are still able to inhibit bacterial traits implicated in disease (e.g. sugar transport/acid production; protease activity) and retard growth without eliminating beneficial species. In silico modelling studies have been performed which support the concept that either reducing the frequency of acid challenge and/or the terminal pH, or by merely slowing bacterial growth, results in maintaining a community of beneficial bacteria under conditions that might otherwise lead to disease (control without killing).

Oral biofilms and plaque control

Dental plaque is a biofilm that forms naturally on the surfaces of exposed teeth and other areas of the oral cavity. It is the primary etiological factor for the most frequently occurring oral diseases, such as dental caries and periodontal diseases. Specific, nonspecific, and ecologic plaque hypothesis explains the causation of dental and associated diseases. Adequate control of biofilm accumulation on teeth has been the cornerstone of prevention of periodontitis and dental caries. Mechanical plaque control is the mainstay for prevention of oral diseases, but it requires patient cooperation and motivation; therefore, chemical plaque control agents act as useful adjuvants for achieving the desired results. Hence, it is imperative for the clinicians to update their knowledge in chemical antiplaque agents and other developments for the effective management of plaque biofilm-associated diseases. This article explores the critical analysis of various chemical plaque control strategies and the current trends in the control and prevention of dental plaque biofilm.

The aim of this article is to review the properties of compounds available for the control of dental plaque biofilms, and describe their mode of action. The mouth is colonised by a diverse but characteristic collection of micro-organisms, which confer benefit to host. Numerous antiplaque (e.g. surfactants, essential oils) and antimicrobial agents (e.g. bisbiguanides, metal ions, phenols, quaternary ammonium compounds, etc.) have been successfully formulated into toothpastes and mouthrinses to control plaque biofilms. At high concentrations, these agents can remove biofilm and/or kill disease-associated bacteria, while even at sub-lethal levels they can inhibit the expression of pathogenic traits. Successful antimicrobial agents are able to meet the apparently contradictory requirements of maintaining the oral biofilm at levels compatible with oral health but without disrupting the natural and beneficial properties of the resident oral microflora.

In vitro plaque removal studies require biofilm models that resemble in vivo dental plaque. Here, we compare contact and non-contact removal of single and dual-species biofilms as well as of biofilms grown from human whole saliva in vitro using different biofilm models. Bacteria were adhered to a salivary pellicle for 2 h or grown after adhesion for 16 h, after which, their removal was evaluated. In a contact mode, no differences were observed between the manual, rotating, or sonic brushing; and removal was on average 39%, 84%, and 95% for Streptococcus mutans, Streptococcus oralis, and Actinomyces naeslundii, respectively, and 90% and 54% for the dual- and multi-species biofilms, respectively. However, in a non-contact mode, rotating and sonic brushes still removed considerable numbers of bacteria (24-40%), while the manual brush as a control (5-11%) did not. Single A. naeslundii and dual-species (A. naeslundii and S. oralis) biofilms were more difficult to remove after 16 h growth than after 2 h adhesion (on average, 62% and 93% for 16- and 2-h-old biofilms, respectively), while in contrast, biofilms grown from whole saliva were easier to remove (97% after 16 h and 54% after 2 h of growth). Considering the strong adhesion of dual-species biofilms and their easier more reproducible growth compared with biofilms grown from whole saliva, dual-species biofilms of A. naeslundii and S. oralis are suggested to be preferred for use in mechanical plaque removal studies in vitro.

Dental plaque is a structurally- and functionally-organized biofilm. Plaque forms in an ordered way and has a diverse microbial composition that, in health, remains relatively stable over time (microbial homeostasis). The predominant species from diseased sites are different from those found in healthy sites, although the putative pathogens can often be detected in low numbers at normal sites. In dental caries, there is a shift toward community dominance by acidogenic and acid-tolerating species such as mutans streptococci and lactobacilli, although other species with relevant traits may be involved. Strategies to control caries could include inhibition of biofilm development (e.g. prevention of attachment of cariogenic bacteria, manipulation of cell signaling mechanisms, delivery of effective antimicrobials, etc.), or enhancement of the host defenses. Additionally, these more conventional approaches could be augmented by interference with the factors that enable the cariogenic bacteria to escape from the normal homeostatic mechanisms that restrict their growth in plaque and out compete the organisms associated with health. Evidence suggests that regular conditions of low pH in plaque select for mutans streptococci and lactobacilli. Therefore, the suppression of sugar catabolism and acid production by the use of metabolic inhibitors and non-fermentable artificial sweeteners in snacks, or the stimulation of saliva flow, could assist in the maintenance of homeostasis in plaque. Arguments will be presented that an appreciation of ecological principles will enable a more holistic approach to be taken in caries control.

Dental plaque is the community of microorganisms found on a tooth surface as a biofilm, embedded in a matrix of polymers of host and bacterial origin [1, 2]. Of clinical relevance is the fact that biofilms are less susceptible to antimicrobial agents, while microbial communities can display enhanced pathogenicity (pathogenic synergism) [3]. The structure of the plaque biofilm might restrict the penetration of antimicrobial agents, while bacteria growing on a surface grow slowly and display a novel phenotype, one consequence of which is a reduced sensitivity to inhibitors [4]. Plaque is natural and contributes (like the resident microflora of all other sites in the body) to the normal development of the physiology and defenses of the host [5].

Once formed, the overall composition of the climax community of plaque is diverse, with many species being detected at individual sites. Molecular ecology approaches, in which 16S rRNA genes are amplified from plaque samples, have identified >600 bacterial and Archae taxa, of which approximately 50% are currently unculturable [9]. Once plaque forms, its species composition at a site is characterized by a degree of stability or balance among the component species, in spite of regular minor environmental stresses, e.g., from dietary components, oral hygiene, host defenses, diurnal changes in saliva flow, etc. This stability (termed microbial homeostasis) is not due to any biological indifference among the resident organisms, but is due to a balance imposed by numerous microbial interactions, including examples of both synergism and antagonism [10]. These include conventional biochemical interactions such as those necessary to catabolize complex host glycoproteins and to develop food chains, but in addition, more subtle cell-cell signalling can occur. This signalling can lead to coordinated gene expression within the microbial community, and these signalling strategies are currently being viewed as potential targets for novel therapeutics [11, 12].

In addition, identification of factors that regulate the natural homeostasis present in plaque during health but, when perturbed, drive the enrichment of putative oral pathogens could open up novel ways to control plaque composition. Manipulation of these ecological influences could help maintain the beneficial microbial composition and normal metabolic activity of plaque biofilms, and augment more conventional approaches to control caries. These concepts will be explored throughout the remainder of this paper.

The origin and role of oral pathogens has been the subject of much debate. Indeed, the resolution to this debate is pivotal to the development of effective plaque control strategies. Early studies using conventional culture techniques often failed to recover the putative pathogens from healthy sites or, when pathogens were present, they comprised only a small proportion of the microflora. However, the recent application of more sensitive molecular techniques has led to the frequent detection of low levels of several pathogens (implicated in caries and periodontal diseases) at a wide range of sites [23]. Bacterial typing schemes have shown that identical strains of putative cariogenic bacteria can be found in the plaque of mother (or other close caregiver) and infants [24], implying that transmission of such bacteria can occur. In either situation (i.e. natural low levels of "pathogens" or low levels of exogenously-acquired "pathogens"), these species would have to outcompete the already established residents of the microflora in order to achieve an appropriate degree of numerical dominance to cause disease. As argued above, in order for this to happen, the normal homeostatic mechanisms would need to be disrupted, and this is only likely to occur if there is a major disturbance to the local habitat (Figure 1). This suggests that plaque-mediated diseases result from imbalances in the resident microflora resulting from an enrichment within the microbial community of the pathogens due to the imposition of strong selective pressures. If so, interference with these driving forces could prevent pathogen selection and reduce disease incidence. 041b061a72


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