Ervin I. Weiss

Oral diseases represent a significant global health and economic burden, necessitating the development of effective diagnostic tools. This study investigates the volatile organic compound (VOC) profiles of bacteria associated with dental caries and periodontal disease to explore their potential as diagnostic biomarkers. Four microbial strains—Streptococcus mutans (700610), Streptococcus sanguis (NCO 2863), Porphyromonas gingivalis (ATCC 33277), and Fusobacterium nucleatum (PK1594)—were cultured (N = 24), alongside intraoral samples (N = 60), from individuals with common oral diseases. Headspace VOCs were analyzed using gas chromatography-mass spectrometry (GC-MS), and statistical analyses were conducted by applying non-parametric Wilcoxon and Kruskal–Wallis tests. VOC identification was performed using the NIST14 database. Strain-specific VOC signatures were identified, with P. gingivalis and F. nucleatum exhibiting distinct profiles from each other and from Streptococcus strains. Comparative analysis of disease cohorts revealed statistically significant differences at multiple retention times between caries, gingivitis, and periodontitis. These findings suggest that VOC profiling enables differentiation between bacterial strains and disease phenotypes, supporting their potential application as diagnostic biomarkers for oral diseases. This study establishes a foundational framework for VOC-based diagnostic methodologies in dental pathology.

Biofilm formation on prostheses and implanted devices can lead to serious complications and increased healthcare expenditures. Once formed, biofilm management is difficult and may involve a long course of antibiotics, additional surgery, and, occasionally, implant removal. This study evaluated the antibacterial properties of medical-grade silicone samples integrated with novel, non-leaching, antibacterial, quaternary ammonium silica (QASi) particles. Our collaborators (Nobio, Israel) prepared silicone sheets integrated with antibacterial QASi nanoparticles. Samples containing 0.5%, 0.75%, and 1%, QASi particles were evaluated for antibacterial properties against S. epidermidis, S. aureus, methicillin-resistant S. aureus (MRSA), E. faecalis, and P. aeruginosa using the direct contact test. The tested silicone samples integrated with QASi particles showed no bacterial growth, while growth was observed in control silicone samples without QASi. In addition, the agar diffusion test, used to evaluate the leaching of antibacterial components, exhibited no inhibition zone around the samples indicating that the QASi particles do not leach into surrounding milieu. The QASi nanoparticles exhibited very potent antibacterial surface properties, killing all viable bacteria placed on their surface. Incorporating QASi nanoparticle technology into medical products during production has the potential to create an antimicrobial surface that prevents microbial colonization and biofilm formation.

Diabetes and associated comorbidities are a global health threat on the rise. We conducted a six-month dietary intervention in pre-diabetic individuals (NCT03222791), to mitigate the hyperglycemia and enhance metabolic health. The current work explores early diabetes markers in the 200 individuals who completed the trial. We find 166 of 2,803 measured features, including oral and gut microbial species and pathways, serum metabolites and cytokines, show significant change in response to a personalized postprandial glucose-targeting diet or the standard of care Mediterranean diet. These changes include established markers of hyperglycemia as well as novel features that can now be investigated as potential therapeutic targets. Our results indicate the microbiome mediates the effect of diet on glycemic, metabolic and immune measurements, with gut microbiome compositional change explaining 12.25% of serum metabolites variance. Although the gut microbiome displays greater compositional changes compared to the oral microbiome, the oral microbiome demonstrates more changes at the genetic level, with trends dependent on environmental richness and species prevalence in the population. In conclusion, our study shows dietary interventions can affect the microbiome, cardiometabolic profile and immune response of the host, and that these factors are well associated with each other, and can be harnessed for new therapeutic modalities.

Ole T. Jensen, DDS, MS/Ervin Weiss, DMD/David W. Grainger, PhD: Clayton Christensen, the famous Harvard Business School professor and author of The Innovator?s Dilemma, was once asked about the prospect of starting a new dental implant company, given the hundreds of implant companies already found 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 prevent and arrest bacterial infection at the bone-implant interface without the use of pharmaceutical agents. The peculiarity of the oral cavity is that endogenous commensal, opportunistic bacteria have evolved a highly stable, self-regulating, and symbiotic environment for the dentate niche, termed ?biofilm.? Oral biofilm exhibits an extremely organized 3D architecture that facilitates protection, nutrient and waste transport, and mechanical resilience. This resilience is several orders of magnitude more resistant to natural forces from mastication, deglutition, and salivary flow than that of free-living planktonic bacteria. When biofilm becomes mechanically disrupted, it readily and rapidly reforms within hours. Biofilm is an aqueous network of mixed nucleic acids, polysaccharides, proteins, and lipids, virtually all microbial in origin. These interacting extracellular polymeric substances (EPS) are noncovalently associated into a robust matrix, which embeds and protects aggregated bacteria within. This physical barrier function provides microbial protection, particularly in the deeper layers, establishing physical resistance to phagocytosis and to permeation of antimicrobial agents. Microbial biofilm density within EPS favors chemical communication (quorum sensing) and plasmid exchange, facilitating transfer of resistance and virulence genes, enabling senescence, that is, ?sleeper? cells, that reawaken postexposure to antibiotics to exert latent virulence. When normal symbiotic oral biofilm becomes pathogenic, a dysbiotic chain of events occurs at the titanium-bone interface, resulting in peri-implant disease. Therefore, eliminating or mitigating pathogenic microorganisms at the bone-implant interface suggests a need for an intrinsic antimicrobial property at the implant and abutment surfaces to defend against dysbiosis. Natural teeth ?implanted? within the alveolar bone and supported by a connective tissue barrier as well as epithelial attachment, which inhibits bacterial invasion, are remarkably stable and self-cleansing. However, this natural state can quickly become imbalanced by a change in oral structural basis, which is found with a dental implant?supported fixed denture, and many other factors, such as a reduction in quantity or quality of saliva, a change in diet, immune compromise, or disturbance in vascular dynamics, etc. Preventing biofilm completely is impossible and counterproductive to ensuring the essential niche benefits of a healthy balanced microbiome; intermittent or prolonged use of antibiotics for such a mission is not the solution. The canonical stages of biofilm formation, including microbial attachment, proliferation, maturation, and dispersion, are the focus in addressing biofilm disruption. Of these, microbial surface attachment and proliferation are considered essential for preventing early biofilm development. Therefore, once titanium implants (and abutments) are developed with surfaces that inhibit plaque and biofilm, this can be essential for getting the job done of preventing and curtailing peri-implant disease. But is this possible? Novel dental materials, such as antimicrobial composite restoratives, were developed for the prevention of dental caries by using a surface-contact bactericidal strategy to reduce bacterial viability. This novel material prevents enamel demineralization from bacterial plaque that otherwise leads to recurrence of caries more than 50% of the time by 5 years. Within several years of placement, titanium dental implants exhibit an incidence of significant peri-implant disease of more than 10% within several years of placement and cannot so easily be removed and replaced like a failed dental restoration. Therefore, a reliable site-specific biofilm-prevention strategy for titanium like that used for dental restoratives could represent a solution to this unmet need. As host tolerance changes relative to general systemic health, including immunodeficiencies, individual and oral hygiene effectiveness, and local factors such as periodontitis of teeth adjacent to dental implants, there is increased susceptibility of the exposed implant surface. These physiologic changes can suddenly emerge to adversely influence the implant risk profile and new host biofilm dynamics, necessitating enhanced oral hygiene measures to keep dysbiotic biofilm from further compromising the dental device. Exposure of an implant surface to the oral environment is speculated to occur in up to 30% of implants by 10 years in function. Causation can be host-related but can also be related to practitioner error, such as poor surgical placement including inadequate bone grafting or unsatisfactory prosthetic management, such as the use of misfit components, poorly executed restorations, or restorations designed with compromised cleanability. Of course, if clinician mistakes are not made and patient compliance is circumspect, a steady state can be maintained. However, clinician work-product is not always ideal, and patients do not always comply with preventive hygiene measures. In any case, host biology may become more susceptible due to physiologic, pharmacologic, or ingestion-related insults, such as tobacco smoking, leading to unhealthy catabolic changes at the bone-implant interface. One replacement implant study showed a mean late time frame for implant loss of 11 years, implying exposure of the implant surface over time with attendant loss of...

Polak D, Wilensky A, Shapira L, Weiss EI, Houri‐Haddad Y. Vaccination of mice with Porphyromonas gingivalis or Fusobacterium nucleatum modulates the inflammatory response, but fails to prevent experimental periodontitis. J Clin Peridontol 2010; 37: 812–817. doi: 10.1111/j.1600‐051X.2010.001598.x. Aim: To assess the potential of using vaccination with Porphyromonas gingivalis or Fusobacterium nucleatum, in modulating local subcutaneous inflammatory response and alveolar bone loss following coinfection with both bacteria.Materials and Methods: Mice were immunized against either P. gingivalis or F. nucleatum. The cytokine response to mixed infection with P. gingivalis and F. nucleatum was evaluated using the subcutaneous chamber model. The alveolar bone loss induced by oral mixed infection was evaluated by micro‐CT using the experimental periodontitis model. Serum levels of specific antibodies were determined by ELISA.Results: Vaccination with either bacterium produced a specific humoral response before infection. Animals immunized against either bacteria following a mixed infection with P. gingivalis and F. nucleatum, showed decreased TNFα (but not IL‐1β) levels as compared with non‐immunized animals. However, the vaccination did not change the level of mixed infection‐induced alveolar bone loss when compared with non‐immunized animals. Six weeks following the oral mixed infection, specific antibody titres remained high. Furthermore, specific antibodies against the non‐immunized bacterium were present at high levels.Conclusions: While vaccination produced specific antibodies and suppressed the inflammatory response, it failed to prevent or reduce the progression of experimental periodontitis induced by mixed infection with P. gingivalis and F. nucleatum.