Dental plaque develops as a complex biofilm on the tooth surface and is a direct precursor of periodontal diseases, one of the most common bacterial infections in developed countries. The general principles that cause the transformation of a commensal plaque biofilm into a potentially pathogenic entity include binding to the tooth surface by early colonizers such as oral streptococci, which then provide an attachment substrate for the subsequent colonization and biofilm formation by periodontal pathogens such as Porphyromonas gingivalis. Co-adhesion between S. gordonii and P. gingivalis is thus considered to be an important factor that facilitates the persistence of P. gingivalis in the oral cavity. Investigations in our laboratory have revealed that this adherence interaction is multimodal, involving several interacting adhesin and receptor molecules. Adhesins identified to date include the P. gingivalis major and minor fimbriae, the latter recognizing the SspB protein on the S. gordonii cell surface. Binding of SspB is dependent upon a structural binding domain conferred by amino acid residues asparagine at position 1182, and valine at position 1185. This minor fimbriae-SspB interaction provides the impetus for the formation of a P. gingivalis biofilm. The objectives of this application are: to define the structural requirements of the S. gordonii SspB receptor; to define the functionality of the P. gingivalis minor fimbrial adhesin; to identify the S. gordonii cognate receptor(s) for the P. gingivalis major fimbrial protein; and to determine differential expression of P. gin gingivalis genes induced by adhesin-receptor interactions.
These Aims will thus provide a more detailed molecular picture of the components responsible for P. gingivalis-S. gordonii co-adhesion and their mechanisms of action. Furthermore, we will begin to appreciate the pathways and circuitry by which co-adhesion leads to biofilm development. The information provided by these studies will enhance our understanding of how pathogenic and commensal plaque bacteria interact on a cellular and molecular level during the process of colonization and biofilm development. Such insights will provide a knowledge base that will facilitate the development of novel methods to control periodontal disease based on inhibition of colonization mechanisms or interference with the regulatory mechanisms that control the expression of adhesins or the accumulation of biofilms.
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