Impact on the Progression, Morphology, and Cellular Integrity of Biofilm Formation on the Surfaces of Implants; Current Knowledge and Future Perspectives.

The capacity of to adhere to diverse oral substrates constitutes a pivotal preliminary phase in the formation of a pathogenic fungal biofilm. Yeast cells demonstrate a considerable ability to bind to host tissues, encompassing dental structures and mucosal surfaces, in addition to synthetic, non-biological materials such as dental appliances. Biomaterials utilized for the restoration of oral functionality are prone to biofilm formation, which can detrimentally affect oral health. Oral microorganisms can adhere to both hydrophobic and hydrophilic surfaces; however, in vivo investigations indicate that hydrophobic surfaces tend to accumulate minimal biofilm due to differential shear forces. Rough surfaces are observed to retain more biofilm compared to their smooth counterparts. The presence of biofilms on composite materials and glass-ionomer cement types results in surface degradation, consequently fostering additional biofilm development. While the leaching of residual monomers from composites has been shown to influence biofilm proliferation in vitro, the effect in vivo appears to be less consequential, likely attributable to the dilution and continual renewal of saliva. Furthermore, research has produced inconsistent findings regarding the influence of fluoride release from glass-ionomer cement types. A comparative analysis is conducted between biomaterial-associated infections in implants and devices situated in other anatomical regions and the formation of oral biofilms. The discourse critically evaluates alterations to biomaterials aimed at diminishing biofilm formation on implants and devices, taking into account their prospective applications within dentistry. The conclusion reached is that for dental applications, antimicrobial coatings that exterminate fungi upon contact are deemed more efficacious than those that gradually release antimicrobial agents.