Dysbiosis of Oral Cavity

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Oral microbiota looks like explicitly complex, multi-component and multi-functioning assemble of microbial communities that is characterized by contemporaneous cross-linked interplays between aerobic, facultatively anaerobic and obligate anaerobic bacteria with their multiple species of gram-positive and gram-negative agents. Stable but fragile equilibrium established within oral microbiota through the years of long evolution maintains the healthy state of oral cavity.

The shift in this balance may deeply deregulate normal metabolism and function of oral ecosystem.

For instance, indiscriminate use of antimicrobial agents (antibiotics or antiseptics) especially with broad-spectrum of activity can easily provoke oral dysbiosis (or dysbacteriosis). It promotes the damage of oral mucosa resulting in drug-related stomatitis, glossitis or other ailments. These disorders are caused predominantly by Candida fungi, or sometimes by enterococci and various gram-negative rods.

The most common etiological agent of oral dysbiosis is yeast-like dimorphic fungal species Candida albicans. These fungi demonstrate enhanced adhesive capacity to epithelial cells. Carious excavations create efficient ecological niche for candidal colonization and successful propagation. Under long-term therapy with antibiotics of broad spectrum or following secondary immunodeficiencies candidal overgrowth results in candidiasis. Fungal hydrolytic enzymes (e.g., numerous proteases, neuraminidase and others) take active part in its pathogenesis.

The interaction between yeasts and oral mucosal membranes starts from fungal adhesion. Sucrose, maltose, glucose and other sugars contribute to tight microbial adherence.

Adhesive capacity of fungal cells alternates depending on microbial strain. It is responsible for virulence of certain candidal isolate. The most pathogenic С. albicans absorb upon human epithelium approximately 1.5 times faster than the members of other species. Antibacterial treatment promotes yeast adherence whereas complement activation through fungal mannans seriously dampens it.

When propagating, yeast-like fungi take part in dental enamel decay and caries progression. Similarly, they may cause mycotic stomatites and tonsillitis.

In most pathological cases the fungi of Candida genus are associated with other microorganisms of oral cavity (mixed infection). Their synergistic interplays ensue from fungal synthesis of numerous growth factors (namely, vitamins) that stimulate propagation of many bacterial species, e.g., lactobacilli or actinomycetes. By contrast, lactobacilli generate large amounts of lactic acid; and acidification of local environment suppresses candidal growth.

Thus, ordinary fungal colonization doesn’t expand into visible pathology. Nevertheless, in conditions mentioned above (extensive antibiotic treatment or local immunodeficiency) latent fungal infection transforms into clinical candidiasis (typical opportunistic infection). Predominant clinical forms of candidiasis are local oral lesions, but in severe cases they grow into devastating generalized mycosis with multiple organ failure.