The ability of oral Streptococcus strains to utilize oligosaccharide chains in mucin as a source of carbohydrate was studied in batch cultures. Pig gastric mucin, as a substitute of human salivary mucin, was added to chemically defined medium containing no other carbohydrates. Strains of S. mitior attained the highest cell density, while mutans streptococci: S. mutans, S. sobrinus, S. rattus, grew very little in the medium with mucin. S. mitis, S. sanguis, and S. milleri in decreasing order, showed intermediate growth. Mucin breakdown as measured by sugar analyses indicated that oligosaccharide chains were only partially degraded. Every strain produced one or more exoglycosidases potentially involved in hydrolysis of oligosaccharide. The enzyme activities occurred mainly associated with the cells, and very little activity was found in the culture fluids. The relationships between glycosidase activities and growth, or mucin degradation were not always clear.

This study describes the effects of varnishes containing 0, 25, 33 and 40% chlorhexidine diacetate on mutans streptococci in human approximal dental plaque. The chlorhexidine release from the varnishes was determined in vitro. Eleven subjects participated in the clinical experiment, each with at least five approximal areas harboring high levels of mutans streptococci. The approximal areas in each of the individuals were randomly assigned to five experimental groups, in each of which one of the varnishes was tested; 40% chlorhexidine varnish was tested in two experimental groups. The varnish treatment consisted of a single application of a small amount of varnish onto the selected approximal areas. From one of the sites receiving the 40% chlorhexidine varnish, all visible varnish was removed 15 min after application. The volunteers were asked to leave the varnish on the remaining treated sites and not to brush their teeth for 8 h. All chlorhexidine varnishes strongly suppressed mutans streptococci until 4 months after the varnish application. The extent of the suppression depended upon the concentration of chlorhexidine in the varnish, 40% chlorhexidine varnish giving the greatest suppression of mutans streptococci. No significant difference was found between the numbers of mutans streptococci from sites where the 40% varnish was removed after 15 min and sites where the 40% chlorhexidine varnish was left. The results suggested that 40% chlorhexidine varnish can be used successfully for the long-term suppression of mutans streptococci. A contact time of the varnish with the tooth surface of only 15 min is sufficient to achieve this long-term suppression.

The treatment of tooth surfaces with chlorhexidine varnish may lead to long-lasting suppression of mutans streptococci in dental plaque. Microbiological observations following varnish treatment suggest that this prolonged suppression might be caused by bacterial interference. To investigate whether physiologically related organisms, such as other Streptococcus species, compete with mutans streptococci in the ecosystem, we have analyzed streptococcal populations on the tooth surface before and after chlorhexidine varnish treatment. Occlusal surfaces with high numbers of mutans streptococci were selected in human volunteers and treated with chlorhexidine varnish. Analyses of sequentially collected plaque samples confirmed that S. oralis-group streptococci returned to baseline levels shortly after the chlorhexidine application, while Actinomyces naeslundii populations reached prestudy or even higher levels only several days after treatment. Mutans streptococci, however, were below the detection level in the 14-day samples, except in 1 individual. The pattern of recolonization by individual Streptococcus species after chlorhexidine application closely resembled that of cleaned enamel surfaces: S. oralis and S. sanguis were primary colonizers while S. gordonii became dominant at a later stage. It is concluded that after intensive chlorhexidine treatment, a normal oral microflora reestablished, characterized by low proportions of mutans streptococci.

Several subgingival microorganisms were tested for their ability to utilize human immunoglobulin G (IgG) as a substrate for growth. This was done using a protein-free chemically defined medium, supplemented with IgG. Stimulation of growth was observed for Capnocytophaga ochracea, Porphyromonas asaccharolytica, Porphyromonas endodontalis, Porphyromonas gingivalis, Prevotella intermedia, Prevotella oralis, Lactobacillus catenaforme and Streptococcus intermedius. Immunoelectrophoresis, sodium dodecyl sulfate-polyacrylamide gel electrophoresis and a protein assay demonstrated that P. intermedia and P. endodontalis completely degraded the protein chains of IgG. Partial breakdown of IgG was observed for P. asaccharolytica and C. ochracea, whereas P. oralis cleaved the IgG heavy chain, yielding Fc and Fab fragments. All these bacteria utilized IgG as a substrate for growth. Binding studies using an enzyme-linked immunosorbent assay, revealed complete loss of in vitro antigen-antibody binding capacity after incubation of specific IgG with P. endodontalis and partial loss of binding with P. intermedia, P. gingivalis, C. ochracea or Fusobacterium nucleatum. Degradation or inactivation of IgG by oral bacteria is thought to be important in the causation of polymicrobial infections.

This report is the first to describe the occurrence of sulfate‐reducing bacteria in the human mouth. Samples of subgingival dental plaque were examined for the presence of sulfate‐reducing bacteria. Using enrichment cultures, sulfate‐reducing bacteria were detected in 25 (58%) of 43 individuals, and in 39 (48%) of the 82 samples. Pure isolates of sulfate‐reducing bacteria, obtained from a limited number of enrichment cultures, belonged to the genera Desulfobacter and Desulfovibrio. These genera are also the predominant sulfate‐reducing bacteria in the human large intestine. The sulfate‐reducing bacteria use sulfate as terminal electron acceptor to oxidize low‐molecular‐weight organic compounds, mainly products of microbial fermentation such as acetate, lactate etc. The numbers of sulfate‐reducing bacteria in the mouth are assumed to be limited by sulfate. Potential sources of sulfate in the subgingival area include free sulfate in pocket fluid and glycosaminoglycans from periodontal tissues.