Dental caries is a multi-factorial disease in which the virulence of microbes in the plaque biofilm, salivary function and diet and nutrition play important roles. We hypothesize that salivary components of both mammalian and non-mammalian origin are associated with risk for the development of dental caries. It is speculated that no single salivary component is important than the others, rather each of these components interact in a concerted fashion and a cumulative effect is important in protecting against caries. We will develop sandwich enzyme-linked immunoassays (ELISA) to quantitate the levels of salivary mucins MG1 and MG2; acidic proline- rich proteins 1 and 3, basic proline-rich proteins PRB-1 and PRB-2; glycosylated proline-rich protein PRG; cystatins S and SN; statherin; histatins 1, 3 and 5; lysozyme; lactoferrin and peroxidase; microbial enzymes glucosyltransferase and glucosyltransferase from Streptococcus mutans; and food preservative benzoate in a large number of subjects. We have already accumulated more than 4000 samples of resting whole saliva. The data obtained will be analyzed for the intra-subject stability of the analyte levels; the cross-sectional association of the decay, missing, filled surfaces (DMFS) index of the subjects analyte levels; and the longitudinal association of the DMFS with salivary analyte levels. The comprehensive survey and the cluster analysis of multiple salivary components should generate a useful data set to test for the association of these components with the caries experience and to identify parameters that will indicate increased risk for dental caries. This study will also provide useful information to determine whether there is a clinical relationship between benzoate levels in saliva and caries experience.

Agency
National Institute of Health (NIH)
Institute
National Institute of Dental & Craniofacial Research (NIDCR)
Type
Research Program Projects (P01)
Project #
5P01DE011549-07
Application #
6564063
Study Section
Special Emphasis Panel (ZDE1)
Project Start
2002-01-01
Project End
2002-12-31
Budget Start
Budget End
Support Year
7
Fiscal Year
2002
Total Cost
$115,583
Indirect Cost
Name
University of Rochester
Department
Type
DUNS #
208469486
City
Rochester
State
NY
Country
United States
Zip Code
14627
Bowen, W H; Koo, H (2011) Biology of Streptococcus mutans-derived glucosyltransferases: role in extracellular matrix formation of cariogenic biofilms. Caries Res 45:69-86
Bowen, William H; Lawrence, Ruth A (2005) Comparison of the cariogenicity of cola, honey, cow milk, human milk, and sucrose. Pediatrics 116:921-6
Barboza-Silva, E; Castro, A C D; Marquis, R E (2005) Mechanisms of inhibition by fluoride of urease activities of cell suspensions and biofilms of Staphylococcus epidermidis, Streptococcus salivarius, Actinomyces naeslundii and of dental plaque. Oral Microbiol Immunol 20:323-32
Chatfield, Christa H; Koo, Hyun; Quivey Jr, Robert G (2005) The putative autolysin regulator LytR in Streptococcus mutans plays a role in cell division and is growth-phase regulated. Microbiology 151:625-31
Culp, D J; Quivey, R Q; Bowen, W H et al. (2005) A mouse caries model and evaluation of aqp5-/- knockout mice. Caries Res 39:448-54
Zhu, Qingyuan; Quivey, Robert G; Berger, Andrew J (2004) Measurement of bacterial concentration fractions in polymicrobial mixtures by Raman microspectroscopy. J Biomed Opt 9:1182-6
Fozo, Elizabeth M; Quivey Jr, Robert G (2004) The fabM gene product of Streptococcus mutans is responsible for the synthesis of monounsaturated fatty acids and is necessary for survival at low pH. J Bacteriol 186:4152-8
Fozo, Elizabeth M; Quivey Jr, Robert G (2004) Shifts in the membrane fatty acid profile of Streptococcus mutans enhance survival in acidic environments. Appl Environ Microbiol 70:929-36
Phan, T-N; Buckner, T; Sheng, J et al. (2004) Physiologic actions of zinc related to inhibition of acid and alkali production by oral streptococci in suspensions and biofilms. Oral Microbiol Immunol 19:31-8
Fozo, Elizabeth M; Kajfasz, Jessica K; Quivey Jr, Robert G (2004) Low pH-induced membrane fatty acid alterations in oral bacteria. FEMS Microbiol Lett 238:291-5

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