General characteristics of microflora
Streptococci consistently dominate the oral cavity—they are found in absolutely all bacteriological samples and make up approximately half of the total local microorganisms. Notably, their count in saliva is twice as high as that in dental plaque or gingival crevicular fluid.
The basis of this flora is formed by the viridans group of streptococci, which includes species such as Streptococcus salivarius, S. sanguis, S. mutans, S. milleri, and S. mitis. Most of them are opportunistic or non-pathogenic bacteria. Their main metabolic feature is the ability to ferment carbohydrates with the release of organic acids (primarily lactic acid), which directly affects the acid-base balance in the mouth.
Classification and clinical significance
Based on the type of hemolysis and degree of virulence, oral streptococci are generally divided into three main groups: microaerophilic $\alpha$-hemolytic (the viridans group), $\gamma$-non-hemolytic, and anaerobic peptostreptococci.
From a clinical perspective, the following species are of greatest interest:
- S. milleri: stands out from typical viridans streptococci by the fact that 40% to 90% of its strains exhibit $\beta$-hemolysis. This is a highly virulent pathogen frequently associated with purulent-inflammatory conditions.
- S. intermedius: a representative of the $\alpha$-hemolytic group with pronounced periodontopathogenic properties.
- S. sanguis: a species that requires special attention from dental surgeons. During tooth extractions or curettage, it can enter the bloodstream, causing transient bacteremia and creating a risk of infective endocarditis.
Ecological niches: who lives where?
The distribution of bacteria in the mouth strictly depends on their ability to adhere (attach) to various types of tissue. Each species has its preferred localization:
- Tooth enamel (dental plaque): S. mutans and S. sanguis reign here, as they have maximum affinity for hard tissues.
- Dorsum of the tongue: the main habitat of S. salivarius. This microorganism is easily washed away by the saliva flow, which is why it forms the baseline microflora of oral fluid.
- Mucosal epithelium: this niche is occupied by S. mitis, S. milleri, and S. sanguis, which have high adhesive properties toward epithelial cells.
Colonization dynamics and competition
The process of oral cavity colonization by bacteria has a clear chronology. S. salivarius is a permanent resident capable of synthesizing dextrin—an insoluble biopolymer—from glucose, which helps form dental plaque.
The situation changes dramatically with the onset of tooth eruption, when hard surfaces for adhesion appear. The so-called "infection window" arises:
- Colonization by S. sanguis typically occurs at the 9th month of life.
- At the 26th month (late colonization), S. mutans joins, being the main culprit of dental caries.
Interestingly, a natural antagonism exists between S. sanguis and S. mutans. If S. sanguis manages to colonize the teeth at early stages, it significantly slows down the subsequent colonization by the cariogenic S. mutans. Thus, initial adhesion largely predetermines the future composition of dental plaque and the risk of caries development in a child.
Briefly: answers to topical questions
What virulence factors are characteristic of Streptococcus mutans?
The main virulence factors of Streptococcus mutans are its ability to adhere to hard tissues and active acid production.
- Adhesion (Streptococcus mutans) — synthesis of extracellular polysaccharides (glucans, dextrans) from sucrose, ensuring attachment to teeth and dental plaque formation.
- Acid production (Streptococcus mutans) — fermentation of dietary sugars with the formation of organic acids (primarily lactic acid), which leach minerals from the enamel.
Which specific bacterial species belong to the group of anaerobic oral peptostreptococci?
Among the provided materials, only one clinically significant representative of anaerobic peptostreptococci inhabiting the oral cavity is specifically mentioned.
- Anaerobic peptostreptococcus (Peptostreptococcus anaerobius) — an opportunistic microorganism that is part of the normal microflora. When entering sterile niches or during immunosuppression, it causes purulent processes in association with other microbes, with the pus having an unpleasant putrid odor.
Other specific species of this genus are not named in the text; only related anaerobic cocci are mentioned (e.g., Finegoldia magna).
What biochemical mechanisms and enzymes ensure the cariogenicity of streptococci?
The cariogenicity of streptococci is ensured by biochemical mechanisms of polysaccharide synthesis and carbohydrate fermentation; however, specific enzyme names are not mentioned in the sources.
- Polysaccharide synthesis (Streptococcus spp.) — formation of extracellular biopolymers (glucans and dextrans) from sucrose, ensuring bacterial fixation and the formation of microbial dental plaque.
- Fermentation (Streptococcus spp.) — breakdown of dietary carbohydrates with the release of organic acids (primarily lactic acid).
- Demineralization (Streptococcus spp.) — drop in the local pH level in plaque to critical values (4.5–5.0), leading to the leaching of minerals and destruction of the organic tooth matrix.
To remember localization: S. salivarius — Dorsum of the tongue (and Saliva), S. mutans — Mighty enamel (hard tissues).
Class and exam questions
Why does S. salivarius predominate in saliva rather than on teeth?
The primary habitat of this species is the dorsum of the tongue. From there, bacteria are easily washed away by the natural saliva flow, forming the basis of the oral fluid microflora.
Which streptococcal species protects against caries development in infants?
Early colonization of the oral cavity by S. sanguis inhibits the multiplication of cariogenic S. mutans due to natural interspecies competition.
What is the clinical feature of S. milleri among viridans streptococci?
Unlike most viridans streptococci, up to 90% of S. milleri strains exhibit beta-hemolysis. They possess high virulence and frequently cause purulent-inflammatory processes.
Why is S. sanguis dangerous during tooth extraction?
During invasive dental procedures, S. sanguis can enter the bloodstream, cause bacteremia, and provoke the development of infective endocarditis.
What else to study on this topic
- Mechanism of dextrin biosynthesis from glucose and dental plaque matrix formation
- Pathogenesis of infective endocarditis in transient bacteremia
- Periodontopathogenic factors of Streptococcus intermedius
- Biochemical basis of antagonism between S. mutans and S. sanguis
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