Dental Materials for Oral Microbiota Dysbiosis: An Update

Abstract

The balance or dysbiosis of the microbial community is a major factor in maintaining human health or causing disease. The unique microenvironment of the oral cavity provides optimal conditions for colonization and proliferation of microbiota, regulated through complex biological signaling systems and interactions with the host. Once the oral microbiota is out of balance, microorganisms produce virulence factors and metabolites, which will cause dental caries, periodontal disease, etc. Microbial metabolism and host immune response change the local microenvironment in turn and further promote the excessive proliferation of dominant microbes in dysbiosis. As the product of interdisciplinary development of materials science, stomatology, and biomedical engineering, oral biomaterials are playing an increasingly important role in regulating the balance of the oral microbiome and treating oral diseases. In this perspective, we discuss the mechanisms underlying the pathogenesis of oral microbiota dysbiosis and introduce emerging materials focusing on oral microbiota dysbiosis in recent years, including inorganic materials, organic materials, and some biomolecules. In addition, the limitations of the current study and possible research trends are also summarized. It is hoped that this review can provide reference and enlightenment for subsequent research on effective treatment strategies for diseases related to oral microbiota dysbiosis.

Metals Biotribology and Oral Microbiota Biocorrosion Mechanisms

“…However, the microbiota of saliva is mainly supplied by the bio-membrane of the tongue (mainly Prevotella and Streptococcus spp.) [ 98 ]. Several studies report that the oral microbiota of people in less well-off conditions are characterized by a lower biodiversity with the presence of bacteria at higher concentrations such as Aggregatibacter Segnis , Achromobacter xylosoxidans , and Neisseria cluster II , with the risk of periodontal and systemic diseases [ 95 , 99 ].…”

“…The correction decreases as the molecular weight of the acid increases. The metabolites consist of various organic acids such as formic, succinic, citric, isocitric, aconitic, and 2- oxoglutaric , whereas enzymes associated with certain bacteria would preferentially attack the zinc and magnesium present in aluminum alloys [ 97 , 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 , 108 , 109 , 110 , 111 , 112 , 113 , 114 , 115 , 116 , 117 , 118 , 119 ]. Some bacteria can then reduce the sulphates or iron or produce.…”

Anticariogenic Activity of Celastrol and Its Enhancement of Streptococcal Antagonism in Multispecies Biofilm

“…The overgrowth of S. mutans contributes to the occurrence of caries by producing lactic acid [14,15], as well as water-insoluble glucan, the main component of exopolysaccharide (EPS), which facilitates bacterial adhesion [16][17][18]. In this context, managing the antagonism among the microecology of oral streptococci that boost commensals and keep pathogenic species in check could be an ideal approach to maintain the symbiosis of oral microecology for prospective anticaries therapy [19,20]. Due to the bacterial etiology of dental caries, the application of antibacterial agents has long been considered an effective strategy for anticaries therapy [21].…”

Root Canal Infection and Its Impact on the Oral Cavity Microenvironment in the Context of Immune System Disorders in Selected Diseases: A Narrative Review

“…In the case of the structure of teeth, their sensitive part, which is the pulp and the root canal system, is an intact place to which both pathogens and commensal bacteria in the oral cavity should not have access [ 6 , 7 ]. When the dentinal barriers are damaged by caries, fissures, or trauma, both opportunistic and pathogenic microorganisms gain access to the pulp chamber and root canal system to which they should never have access [ 8 , 9 , 10 ]. This situation could lead to harmful effects such as inflammation, pulp necrosis, and periodontitis [ 11 , 12 , 13 ].…”