Statement of problem Peri-implant biofilm formation is a key etiologic factor in peri-implant disease. Although probiotic supplementation has been proposed as an adjunct strategy to modulate oral biofilms, its effect on early biofilm development on implant-related titanium implant surfaces remains unclear. Purpose The purpose of this study was to evaluate whether exposure to Lactobacillus reuteri influenced early biofilm formation, architecture, and antimicrobial susceptibility on machined and airborne-particle abraded, large-grit, acid-etched (SLA) titanium implant surfaces. Material and methods A 2-part study was conducted. In vitro polymicrobial biofilms were formed on machined and SLA titanium implant surface disks for 2 or 24 hours under control (untreated), placebo (oil vehicle), or probiotic conditions. Viable counts, metabolic activity, and biofilm biomass were assessed. In situ, 4-day biofilms were developed intraorally using a randomized, double-blind, crossover palatal appliance model under identical treatments. Microbial counts, metabolic activity, biofilm architecture, and susceptibility to 0.12% chlorhexidine were evaluated. Data were analyzed using 2-way ANOVA and Tukey HSD tests (α=.05). Results In vitro, probiotic exposure increased early viable counts and metabolic activity ( P <.05), particularly on machined surfaces. After 24 hours, probiotic-treated groups showed higher viable counts than the control and placebo groups, while biofilm biomass was surface-dependent ( P <.05). In the intraoral model, L. reuteri exposure did not increase lactobacilli, anaerobes, or Candida albicans counts. Untreated SLA surfaces exhibited higher streptococcal and total viable counts, whereas placebo- and probiotic-treated SLA surfaces demonstrated reduced levels comparable to machined titanium. Probiotic-treated biofilms displayed a less compact architecture. Chlorhexidine susceptibility was unchanged. Conclusions Lactobacillus reuteri modulated early peri-implant biofilm organization, increasing microbial activity and viable counts in vitro, without increasing pathogenic burden or altering chlorhexidine susceptibility in situ, with effects more evident on SLA surfaces.
Takeda et al. (Mon,) studied this question.