Development mechanisms and risk factors
The development of the pathology is based on dysbiosis—a disruption of delicate homeostasis in the oral biofilms. Various environmental factors provoke this microbial imbalance. First and foremost, these include dietary errors and the use of antibiotics, which suppress the normal microflora.
In addition, systemic hormonal changes and hyposalivation (reduced salivation) play an important role. Hyposalivation may result from taking certain medications or from radiation exposure to the maxillofacial area.
Non-inflammatory lesions: Caries
Caries is a classic example of a non-odontogenic infection affecting exclusively the hard tissues of the tooth. It serves as the triggering mechanism for the entire subsequent cascade of purulent-inflammatory diseases.
The leading causative agents here are various species of streptococci, in particular Streptococcus mutans, S. sanguis, S. oralis, S. gordoni, and S. mitis biovar 1. Their microbial association also includes bacteria of the genus Veillonella, actinomycetes, and lactobacilli.
Inflammatory infections of the tooth and periodontium
These infections are classified by the depth of pathogen penetration and the nature of the involved tissues. Their distinguishing feature is their polymicrobial nature. The composition of the microflora is extremely dynamic: it changes depending on the stage of the disease, the patient's immune status, age, and ongoing drug therapy.
- Pulpitis (damage to the soft tissues of the tooth). In the serous form of inflammation, streptococci, lactobacilli, and bacteroides predominate in the lesion. If the pathological process progresses to a purulent form, hemolytic streptococcus and Staphylococcus aureus come to the forefront.
- Periodontitis (inflammation of the periodontal ligament). In adult patients, gram-negative rods dominate. Among them are obligate anaerobes (Porphyromonas gingivalis, Tannerella forsythus, Prevotella melaninogenica), facultative anaerobes (Aggregatibacter actinomycetemcomitans), and spirochetes (Treponema denticola). In adolescents, the microbiological picture is different: Aggregatibacter actinomycetemcomitans and bacteria of the genus Capnocytophaga are more frequently isolated.
Purulent-inflammatory processes of the jaws and soft tissues
- Periostitis and osteomyelitis. When the periosteum and bone tissue are affected, Staphylococcus aureus becomes the dominant species in 30–50% of cases. Streptococci and anaerobic flora, including Peptococcus niger, Peptostreptococcus spp., and Bacteroides spp., are also active. If osteomyelitis is of traumatic origin, enterobacteria and Pseudomonas aeruginosa join the standard spectrum.
- Abscesses and phlegmon. Anaerobes (bacteroides, peptostreptococci) overwhelmingly predominate in soft tissue infections of the face and neck. Microbial associations involving Fusobacterium nucleatum and actinomycetes are common. In children, the flora differs: staphylococci and streptococci prevail, while in buccal cellulitis, Haemophilus influenzae type B (Haemophilus influenzae) and Streptococcus pneumoniae predominate.
Spread of infection and generalization
If the infection spreads beyond the primary focus (tooth or jaw), severe complications develop in adjacent areas or the systemic circulation.
- Maxillary sinusitis. Characterized by a mixed etiology, where anaerobes (Bacteroides spp., Peptostreptococcus spp.) are combined with typical respiratory pathogens (Haemophilus influenzae, S. pneumoniae). S. pyogenes or S. intermedius are detected less frequently.
- Lymphadenitis and adenophlegmon. Up to 80% of cases are caused by group A β-hemolytic streptococci and S. aureus. The anaerobic component is represented by specific species such as Propionibacterium acnes.
- Generalization. When pathogens enter the bloodstream, systemic lesions develop: sepsis, infective endocarditis (with valve involvement), mediastinitis, meningitis, and brain abscess. The causative agents are anaerobes, streptococci, and staphylococci (including S. epidermidis).
Non-odontogenic and specific infections
Inflammations of a different genesis, not directly related to dental pathology, develop in the maxillofacial region:
- Stomatitis. Can have a fungal etiology (Candida albicans), viral (herpes viruses), or bacterial (corynebacteria, hemophilic bacteria, actinomycetes). A feature of deep stomatitis is the predominance of anaerobic flora.
- Parotitis. Damage to the major salivary glands is most often caused by viral agents (mumps virus, influenza and parainfluenza viruses, Coxsackie virus), but a bacterial nature involving oral residents, Eikenella corrodens, and S. aureus is also possible.
- Specific infections. Classic bacterial infections (tuberculosis, syphilis, diphtheria, gonococcal infection) and viral lesions (HIV infection, foot-and-mouth disease, vesicular stomatitis) can occur in the oral cavity.
Briefly: answers to topical questions
Which microorganisms are part of the normal (resident) microflora of the oral cavity?
The normal (resident) microflora of the oral cavity includes a variety of bacteria, fungi, and protozoa, among which anaerobes dominate.
- Streptococci (Streptococcus salivarius, S. sanguis, S. mutans, S. milleri, S. mitis) make up about 50% of all residents.
- Obligate anaerobes (Veillonella, peptostreptococci, lactobacilli, bacteroides, prevotellae, porphyromonas, fusobacteria) predominate in specific areas (sublingual region, crypts).
- Other bacteria include bifidobacteria, eubacteria, actinomycetes, hemophilic bacilli, leptotrichia, neisseriae, staphylococci, peptococci, and spirochetes.
- Fungi (Candida) are representatives of the fungal flora.
- Protozoa (Entamoeba gingivalis, Trichomonas tenax).
What pathogenicity factors ensure the cariogenicity of Streptococcus mutans?
The cariogenicity of Streptococcus mutans in the cited sources is associated with its participation in the carious process, dental plaque, and acid production.
- Leading causative agent of caries — Streptococcus mutans is listed among the leading causative agents of caries.
- Acid production — streptococci break down carbohydrates with the formation of organic acids, predominantly lactic acid; acids leach minerals from the hard tissues of the tooth.
- Participation in dental plaque — the main link in the pathogenesis of caries is associated with the formation of dental plaque and subsequent biofilm formation; stages include adhesion of microorganisms to the pellicle, matrix formation, and active microbial reproduction.
What are the stages of microbial biofilm (dental plaque) formation in the oral cavity?
The formation of a microbial biofilm (dental plaque) goes through several successive stages.
- Initial stage — formation of the pellicle (soft dental plaque) on the tooth surface.
- Adhesion and early colonization — attachment of primary colonizers (aerobes and facultative anaerobes) to the pellicle, production of extracellular polysaccharides, and matrix formation.
- Active reproduction and microbial succession — rapid increase in biomass and creation of oxygen-free conditions by primary colonizers.
- Late colonization (coaggregation) — attachment of secondary colonizers (strict anaerobes and spirochetes) to the formed base with the accumulation of their metabolic products.
Class and exam questions
What is the difference between the microflora of periodontitis in adults and adolescents?
In adults, gram-negative rods (obligate anaerobes Porphyromonas gingivalis, spirochetes) predominate in the lesion, whereas in adolescents, Aggregatibacter actinomycetemcomitans and bacteria of the genus Capnocytophaga are more frequently detected.
Which bacteria dominate in facial abscesses and phlegmons?
The microflora in purulent soft tissue infections is primarily composed of anaerobes, namely Bacteroides and Peptostreptococcus. They frequently form associations with Fusobacterium nucleatum and Actinomyces.
How does the flora change during the transition from serous to purulent pulpitis?
In the serous form of pulp inflammation, streptococci, lactobacilli, and Bacteroides predominate. With the development of the purulent form, hemolytic streptococcus and Staphylococcus aureus (S. aureus) become dominant.
What else to study on this topic
- Pathogenesis of microbial biofilm formation and mechanisms of oral dysbiosis development.
- Features of traumatic osteomyelitis: why *Pseudomonas aeruginosa* becomes involved.
- Viral lesions of the oral mucosa: herpetic infections, foot-and-mouth disease, HIV manifestations.
- Clinical manifestations and microbiological diagnosis of maxillofacial actinomycosis.
- The role of Candida species in the development of deep stomatitis and hematogenous osteomyelitis.
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