Traditionally, lactobacilli have been considered the principal cause of caries, but recent findings have questioned this concept. Orland ( 1 ) succeeded in producing experimental caries by infecting gnotobiotic rats with a strain of streptococcus. More recently, Fitzgerald et a1 ( 2 ) confirmed these findings, and Fitzgerald and Keyes (3) established the cariogenicity of another strain of streptococcus in hamsters. These 2 strains of streptococci were shown to be host-specific with regard to cariogenicity: the hamster strain (designated HS1) produced caries only in the hamster and not in the rat, and the rat strain (designated FA1) produced caries in the rat and not in the hamster. Fitzgerald and Keyes also demonstrated that experimental dental caries in animals is an infectious and contagious pathological state which could be transmitted from mother to young. *Aided by research grant DE 01519, Nat. Inst. Dental Res., U.S.P.H.S. Studies of cultures from human caries have brought out evidence for the presence of streptococci similar to the HS1 and FA1 strains.Preliminary findings indicate that the human streptococci similar to the HS1 strain may be causally associated with human caries. Studies related to human streptococci similar to FA1 strains are being investigated.Materials and methods. Collection of specimens from human carious lesions. A sterile spoon excavator was used to remove carious material from the depths of lesions in both enamel and dentine from human teeth in situ.This material was inoculated in Todd-Hewitt broth, supplemented with 0.5% lactalbumin hydrolysate and incubated at 37°C for 18-24 hours.Production of antiserum. Rabbits were immunized with a vaccine prepared from heatkilled streptococcal cultures (60OC for 1 hr). The bacterial suspensions were washed twice in saline and adjusted to the density of the
Eight strains of streptococci were isolated from human carious lesions by the fluorescent-antibody (FA) technique. Seven of these strains produced experimental caries in hamsters or rats maintained on a high sucrose diet. The eighth strain was noncariogenic in animals but possessed some antigenic components in common with the cariogenic strains. On the basis of antigen-antibody reactions by microprecipitin and agar-gel diffusion patterns, the strains were divided into four groups; these groups differed with regard to their cariogenic activity in hamsters. Fluorescein-conjugated antisera, prepared against the human strains, showed some cross-reactions which interfered with the efficacy of the FA technique in differentiating between the related streptococcal groups. To eliminate these cross-reactions, a small amount of related-strain antisera was added to the fluorescein-conjugated antisera to the cariogenic strains. This technique is effective in blocking crossreactions and should be tried wherever cross-reactions are encountered in the FA technique.
Diet, extent of dental plaque, and oral hygiene scores for caries-free and caries-active students were significantly different. Results of this study suggest that these three parameters are contributing supplementary factors to the development of dental caries in the caries-active group. An experimental dietary questionnaire method used in this study may be used by dentists to identify children with a caries-conducive diet and to prescribe treatment accordingly.
The qualitative and quantitative chemical compositions of the cell walls of five strains of oral streptococci (four human and one rat) are presented. Presumptive evidence for glycerol teichoic acid in Streptococcus mutans group II cell walls is given.
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