Controlling plaque by disruptingthe process of plaque formation WILLIAMG . WADE& MARTINA . SLAYNE Periodontology 2000, Val. 15 5조 1번 고상훈
Charge and surface free energy• low surface charge and, therefore, high hydrophobicity favored bacterial adherence.• Therefore, an agent that could increase bacterial and/or surface charge could, in theory, reduce bacterial adherence.• It has been demonstrated that this surface free energy influences dental plaque growth on various substrata in vivo, with high surface free energy promoting bacterial accumulation• The influence of the oral environment on surface free energy values in vivo is unclear. Studies to date have not provided conclusive data as to the effects of saliva and the salivary pellicle layer on surface free energy. In an in vitro study, pellicle increased enamel surface free energy within 5 minutes
Hydrophobicity• An important force implicated in bacterial adherence to tissue surfaces is that of hydrophobicity.• An entity with a given degree of hydrophobicity will attract similarly hydrophobic structures.• Highly hydrophobic species of oral bacteria, including Actinomyces viscosus, Actinomyces naeslundii, Streptococcus sanguis, Streptococcus mitis and Porphyromonas gingivalis, have been shown to adhere to experimental salivary pellicles in significantly higher numbers than less hydrophobic or hydrophilic species, such as Preuotella intermedia, Prevotella melan inogenica, Streptococcus mu tans and Streptococcus salivarius.• Hydrophobic bond-disrupting agents such as the Li+ cation and the thiocyanate anion reduce the adherence of s. sanguis to saliva-coated hydroxyapatite by 81% and 94% respectively (561, and a hydrophobic bond diluent, sulfolane (thiophene, tetrahydro- 1, dioxide), has been shown to inhibit the adhesion of s. sanguis to saliva-coated hydroxyapatite by >50% (78)
Specific interactions and adhesins• Bacterial cell surface structures known as adhesins are thought to interact with specific receptor sites on tooth surfaces.• These specific adhesins therefore provide opportunities for plaque control strategies either by using analogues to block receptor sites or by raising antibodies for the same purpose• For example the adherence of S. mutans to adherence-promoting proteincoated hydroxyapatite could be blocked by a range of compounds all containing a primary amino- group such as galactosamine, mannosamine and spermine. Colonization by S. mutans in vivo could be prevented by local passive immunization with a monoclonal antibody directed against streptococcal antigen I/II , thought to be an adhesin (35).
Aggregation and coaggregation• Later in plaque maturation, the lectin-like interaction of P. gingivulis and Fusobacterium nucleutum may be of relevance.• A number of mechanisms have been elucidated for interbacterial aggregation.• These include protein-carbohydrate interactions such as the 38-kDa surface protein of S. sanguis with adhesin properties capable of mediating coaggregation with A. nueslundii (42). Such interactions have been demonstrated using lactose to block the binding of proteins with carbohydrate receptor groups (44). Additionally, S. sunguis possesses a surface polysaccharide receptor for a lectin-like protein adhesin of Cupnocytophugu ochruceu (4). This was demonstrated using the purified polysaccharide to block coaggregation and by observing the absence of the polysaccharide on a coaggregation-defective strain. Protein-protein interactions are also possible, such as between P.gingivulis and S. sunguis, as demonstrated by the inhibition of coaggregation using saliva and protease treatments
Conclusion• This knowledge has enabled the design of agents for the disruption of the plaque formation process.• There have been a number of reports of agents effective in vitro. In vivo, the results with antihydrophobic agents have been less successful, and information regarding the efficacy of agents directed against specific adherence mechanisms is awaited with interest.• The oral microflora, however, is remarkably complex, and because of this, in spite of intensive recent study, remains poorly understood.• For the time being, at least, it would appear likely that any one approach to plaque control could well be circumvented by alternative plaque formation mechanisms available to the oral flora.