Propolis, a resinous hive product secreted by Apis mellifera bees, has been shown to reduce the incidence of dental caries in rats. Several compounds, mainly polyphenolics, have been identified in propolis. Apigenin and tt-farnesol demonstrated biological activity against mutans streptococci. We determined here their effects, alone or in combination, on glucosyltransferase activity, biofilm viability, and development of caries in rats. Sprague-Dawley rats were infected with Streptococcus sobrinus 6715 and treated topically twice daily as follows: (1) tt-farnesol, (2) apigenin, (3) vehicle control, (4) fluoride, (5) apigenin +tt-farnesol, and (6) chlorhexidine. Apigenin (1.33 mM) inhibited the activity of glucosyltransferases in solution (90-95%) and on the surface of saliva-coated hydroxyapatite beads (35-58%); it was devoid of antibacterial activity. tt-Farnesol (1.33 mM) showed modest antibacterial activity against biofilms and its effects on glucosyltransferases were minimal. The incidence of smooth-surface caries was significantly reduced by apigenin +tt-farnesol (60%), fluoride (70%), and chlorhexidine (72%) treatments compared to control (P < 0.05).

Although the presence of coronal caries is declining in much of the Western Hemisphere, the prevalence of root surface caries is likely to increase as teeth are retained longer than heretofore. At the same time, an increasing number of the population suffer from dry mouth as a result of taking prescription drugs, with an apparent concomitant increased susceptibility to root surface caries. This study attempted to develop an animal model which would aid in the exploration of the effects of desalivation and the development of root surface caries. Animals were desalivated, infected with Actinomyces viscosus and Streptococcus mutans (sobrinus) 6715, and fed a cariogenic diet. Coronal caries developed rapidly in the animals; sufficient disease was present after two weeks to permit evaluation of potential therapeutic agents. Alveolar bone loss and root surface lesions developed in three to four weeks. S. mutans (sobrinus) and A. viscosus established readily in all animals; however, as the investigation progressed, populations of the latter declined, possibly because of the highly acidogenic environment. This model will facilitate investigation of the influence of hyposalivation and help in the exploration of agents to alleviate the adverse effects of salivary gland dysfunction.

T-cell deprived mice heavily infected with Schistosoma mansoni suffer from severe microvesicular damage to hepatocytes within seven weeks of infection. The damage can be prevented by administration of serum (CIS) obtained from mice chronically infected with S. mansoni or from mice immunized with intact or homogenized S. mansoni eggs. Reaction of serum samples from individual chronically infected mice in immunoelectrophoresis with S. mansoni egg homogenate has enabled the identification of at least 12 distinct immuno precipitation reactions. Precipitating antibody against one S. mansoni egg antigen, omega 1, has been detected in all mice with patent chronic infections, and anti-omega 1 antibody is the most concentrated of the precipitating anti-egg antibody species in pooled CIS. Pooled serum obtained from infected intact mice reacting predominantly against omega 1 was found partially to prevent the hepatotoxicity reaction on transfer to infected deprived mice. Serum samples from mice injected with egg homogenate fractionated either by preparative electrophoresis or by cation exchange chromatography, and containing antibodies reactive with antigen omega 1 in immunoprecipitation, were fully protective against liver cell damage induced by S. mansoni in deprived mice. Sera from mice immunized with other S. mansoni egg fractions, and which did not contain antibodies reactive with omega 1, were not hepatoprotective. Antigen omega 1 is compared and contrasted with other S. mansoni egg antigens that have been described.

Within seven weeks of infection with 200 Schistosoma mansoni cercariae, T-cell deprived mice have been shown to suffer from extensive microvesicular damage to hepatocytes, and an inability to excrete parasite eggs at the same rate as comparably infected, immunologically intact controls. Administration of serum (CIS) from chronically infected, immunologically intact donors prevented the development of microvesicular cell damage and partially restored egg excretion rates in infected deprived mice. Serum pools obtained from mice injected either with intact S. mansoni eggs or with a homogenate of eggs emulsified in Freund's complete adjuvant (FCA) were as effective as CIS in preventing hepatotoxicity and restoring the rate of egg excretion in infected deprived recipients. The degree of protection of liver tissue afforded by immune sera could be monitored either by histopathological examination of liver sections or by estimation of serum transaminase concentrations, the results from both assays being generally in agreement. Sera from donor mice injected with cercarial or worm antigens in FCA were relatively inactive either in protecting against S. mansoni-induced liver damage or in reconstituting egg excretion rates in infected deprived mice. Serum from donor mice infected with 25 cercariae became hepato-protective between 49 and 53 days after infection of the donors, and the degree of hepatoprotective activity and egg excretion reconstituting capacity in the serum of 25 cercariae-infected donors was shown to increase between 8 and 16 weeks after infection. Increasing the size of infection of the serum donors to 100 cercariae gave only a marginal increase of hepatoprotective activity at 7 weeks when compared with serum donors infected with 25 cercariae for 7 weeks. Liver parenchymal cells of very heavily infected, immunologically intact mice were found to show microvesicular damage similar to that in livers of infected deprived mice, and administration of CIS to these normal mice was histopathologically protective. However, the elevated serum transaminase concentrations obtaining in the infected normal mice were not reduced to any extent by CIS. The results obtained from serum-reconstituted deprived mice are discussed in terms of the contribution they may make to a better understanding of the host-parasite relationship in immunologically intact mice.

The evidence that dental caries is an infectious and transmitted disease in rodents is unequivocal. However, the factors controlling the transmission of micro-organisms from one animal to another have not been extensively explored. Results from previous studies in our laboratory showed that desalivated animals became infected by Streptococcus sobrinus in a shorter period of time than did intact animals. Furthermore, an additional study in our laboratory showed that animals with intact salivary function caged with desalivated animals harbored more S. sobrinus immediately following establishment of infection than did intact animals housed with other intact animals. Therefore, it seemed appropriate to determine the influence on caries development of caging a desalivated animal with an intact animal. In this study, intact Sprague-Dawley rats were caged with desalivated animals; additional groups of intact animals were housed with chlorhexidine-treated animals that were either intact or desalivated. Although chlorhexidine suppressed both caries development and the level of infection by S. sobrinus, nevertheless, intact animals caged with desalivated animals invariably developed more caries than did intact animals housed with other intact animals. Treating intact animals with chlorhexidine did not affect caries scores in untreated intact cagemates. Overall, the results suggest that a highly acidogenic flora with enhanced virulence (including S. sobrinus) is selected in the desalivated animals; this flora is apparently readily transmitted to intact cagemates, leading to enhanced levels of smooth-surface caries.