The job to be done with biofilm and titanium implants

© Frontiers of Oral and Maxillofacial Medicine. All rights reserved. Front Oral Maxillofac Med 2021;3:21 | http://dx.doi.org/10.21037/fomm-21-54 Once, Clayton Christensen was asked about the prospect of starting a new dental implant company when there were already hundreds of implant companies around the world. “If you proceed,” he advised, “you have to ask one question: What is the job to be done?” Interestingly, the job to be done remains one that the dental profession has wrestled with from the beginning: to inhibit or arrest the development of microbial biofilms on titanium surfaces of an intraoral implant. The peculiarity of the oral cavity is that endogenous b a c t e r i a a n d f u n g u s — c o m m e n s a l , p a t h o g e n i c , opportunistic—all evolved a highly stable self-regulating, and often symbiotic, environment for the dentate niche, termed biofilm that supplements their planktonic growth strategy. A biofilm is a community of aggregated microbial cells organized as micro-communities, colonizing solid oral surfaces in contact with liquids and air. And this unique biofilm strategy is several orders of magnitude more resistant to natural sheer forces from deglutition, mastication and salivary flow that otherwise readily clear nonadherent pathogens from the mouth. The biofilm matrix comprises an aqueous network of mixed nucleic acids, polysaccharides, proteins and lipids, all of microbial origin. The interacting extracellular polymeric substances (EPS) are non-covalently associated into a robust matrix to embed and protect aggregated bacterial and fungal cells within the biofilm. Microbe-microbe, microbe-EPS, microbe-liquid/air, and microbe-substrate interactions all determine formation, properties and behaviors of biofilm. Polymicrobial biofilms are most common, representing complex dynamic communities of diverse, spatially aggregated organisms. One characteristic feature of biofilm is its physical barrier functions that provide microbial protection, particularly in the deeper layers. Biofilm protections are diverse, spanning microbial physical resistance to phagocyte engulfment and biofilm extraction, and reduced exposure to antimicrobials by limited biofilm permeation. Additionally, microbial density within EPS highly favors plasmid exchange, facilitating the transfer of resistance genes and virulence factors. Other genetic programming and regulation also occurs within biofilms, allowing populations of pathogens to undergo senescence to avoid susceptibility to metabolically targeted antimicrobials. Sleeper or persister cells re-awaken post-exposure to exert virulence. Furthermore, should the biofilm become mechanically or pharmacologically disrupted, they readily and rapidly reform in the oral cavity within several hours. Biofilm, therefore, is highly refractory to elimination from the oral niche. Importantly, commensal and probiotic endogenous oral biofilms are an essential component of oral health and therefore should not be disturbed. Opportunistic, pathogenic oral biofilms are a source of oral disease and niche compromise. Despite highly disparate contributions to oral health and demise, all biofilms are structurally and biologically integral to the oral environment. Effective mitigation and selective neutralization of pathogenic oral biofilms while preserving and promoting commensal host-beneficial oral biofilms is therefore the job to be done. Restoring and maintaining a probiotic balance in promoting healthy biofilms as a defense against pathogenic biofilms is an essential goal. Natural teeth re-implanted into alveolar bone and invested with supportive soft tissue attachment are, to a degree, self-cleansing, and when teeth and jaw structures are aligned, promote a type of stand still equilibrium with biofilm. But this scenario can become imbalanced Editorial