This document discusses various mechanisms by which dental plaque forms, including bacterial adherence influenced by surface charge and free energy, hydrophobic interactions, specific adhesins, and aggregation. It notes that while knowledge of these mechanisms has enabled agents to disrupt plaque formation, results of anti-hydrophobic agents in vivo have been less successful. The oral microbiome is complex and not fully understood, so circumventing any single plaque control approach may be possible through alternative mechanisms.

1. Controlling plaque by disrupting
the process of plaque formation
WILLIAMG . WADE& MARTINA . SLAYNE
Periodontology 2000, Val. 15
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2. 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

3. 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)

4. 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).

5. 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

6. 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.