We have previously shown that one of the minimal active regions of statherin, a human salivary protein, for binding to Fusobacterium nucleatum is a YQPVPE amino acid sequence. In this study, we identified the FomA protein of F. nucleatum, which is responsible for binding to the statherin-derived YQPVPE peptide. Overlay analysis showed that a 40-kDa protein of the F. nucleatum cell envelope (40-kDa CE) specifically bound to the YQPVPE peptide. The equilibrium association constant between the affinity-purified 40-kDa CE and the YQPVPE peptide was 4.30 x 10(6). Further, the purity and amino acid sequence analyses of the purified 40-kDa CE revealed approximately 98.7% (wt/wt) purity and a high degree of homology with FomA, a major porin protein of F. nucleatum. Thus, a FomA-deficient mutant failed to bind to the YQPVPE peptide. In addition, increased levels of a FomA-specific mucosal IgA antibody (Ab) and plasma IgG and IgA Abs were seen only in mice immunized nasally with cholera toxin (CT) and the purified 40-kDa FomA protein. Interestingly, saliva from mice that received FomA plus CT as a mucosal adjuvant nasally prevented in vitro binding of F. nucleatum to statherin-coated polyvinyl chloride plates. Taken together, these results suggest that induction of specific immunity to the 40-kDa FomA protein of F. nucleatum, which specifically binds to the statherin-derived peptide, may be an effective tool for preventing the formation of F. nucleatum biofilms in the oral cavity.
The aim of this work was to obtain further information about the origin of fluoride profiles in cementum. Fluoride was administered to rats at varying doses (0, 50,100 ppm F in drinking water) and for different durations (4,13 and 25 weeks). Fluoride distribution across the full thickness of molar cementum in rats was measured by means of an abrasive micro-sampling technique. The average fluoride concentrations in cementum increased significantly with increasing dose and duration of fluoride administration. The relative reduction of the average fluoride concentrations after cessation of fluoride administration was 94.2-36.5% at 50 ppm F and 62.2–49.2% at 100 ppm F in the outer layers (1–60 μm) and 91.5–24.1% at 50 ppm F and 74.1–7.6% at 100 ppm F in the middle (61–120 μm) layers of the cementum, respectively. The reduction rates were more closely related to the time intervals following cessation rather than fluoride concentrations in drinking water or specificity within the cementum. Two factors which may influence this are new cementum formation after withdrawal of fluoride and some fluoride release from cementum surfaces when the fluoride supply stopped. It was concluded that the cessation of fluoride administration reduced the fluoride concentration on the outer layers of cementum differing from bone where reduction occurs across the entire thickness.
This study was undertaken to examine the influence of occlusion on the fluoride distribution in cementum following an experiment in which the occlusion in rats was locally altered by extracting the upper left molar. These and control rats with normal occlusion were given water containing 0 or 100 ppm fluoride for 12 weeks. The fluoride distributions in cementum from both first lower molars of the same animal were compared. The fluoride concentrations had increased throughout the tissue as a result of increased fluoride administration, irrespective of any changes in occlusion. They were, as usual, generally highest at or near the cementum surface and decrease towards the interior of the tissue. Where there had been a change in occlusion, the thickness of cementum was less than that of the contralateral tooth, but, despite this, the fluoride profiles in contralateral teeth were similar in both experimental and control rats. In the experimental rats, on the other hand, the total fluoride tended to be lower, and the mean fluoride tended to be higher in left molars without antagonists. These findings were never seen in the control rats. It was concluded that the alteration in occlusion influenced the fluoride distribution in the cementum through its effect on the rate of cementum formation.
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