The aim of the present randomized controlled clinical trial was to investigate the adjunctive effect of systemic antibiotics and the local use of chlorhexidine for implant surface decontamination in the surgical treatment of peri-implantitis. One hundred patients with severe peri-implantitis were recruited. Surgical therapy was performed with or without adjunctive systemic antibiotics or the local use of chlorhexidine for implant surface decontamination. Treatment outcomes were evaluated at 1 y. A binary logistic regression analysis was used to identify factors influencing the probability of treatment success, that is, probing pocket depth ≤5 mm, absence of bleeding/suppuration on probing, and no additional bone loss. Treatment success was obtained in 45% of all implants but was higher in implants with a nonmodified surface (79%) than those with a modified surface (34%). The local use of chlorhexidine had no overall effect on treatment outcomes. While adjunctive systemic antibiotics had no impact on treatment success at implants with a nonmodified surface, a positive effect on treatment success was observed at implants with a modified surface. The likelihood for treatment success using adjunctive systemic antibiotics in patients with implants with a modified surface, however, was low. As the effect of adjunctive systemic antibiotics depended on implant surface characteristics, recommendations for their use in the surgical treatment of peri-implantitis should be based on careful assessments of the targeted implant (ClinicalTrials.gov NCT01857804).

Peri-implantitis is a biological complication of implants in function that poses a threat to their long-term survival. It may develop earlier around implants with rough surfaces and it may represent a true infection. Microbiological sampling methods should be improved and uniformed so as to fully unveil the microbiological profile of the disease.

Peri-implant health may not be easy to establish, especially in cases that develop disease early. Homogenous treatment protocols rather than empirical treatment attempts should be adopted.

Biofilms are complex microbial communities that grow on various surfaces in nature. The oral micobiota tend to form polymicrobial biofilms, particularly on the hard mineralized surfaces of teeth, which may impact on oral health and disease. They can cause inflammation of the adjacent tooth-supporting (periodontal) tissues, leading to destructive periodontal disease and tooth loss. The emergence of osseointegrated dental implants as a restorative treatment option for replacing missing teeth has also brought along new artificial surfaces within the oral cavity, on which oral bacteria can form biofilms. As in the case of natural teeth, biofilms on implant surfaces may also trigger infection and cause inflammatory destruction of the peri-implant tissue (i.e. peri-implantitis). While there are strong similarities in the composition of the mixed microbial flora between periodontal and peri-implant infections, there are also a few distinctive differences. The immunological events underlying the pathogenesis of peri-implant infections are qualitatively similar, yet more extensive, compared to periodontal infections, resulting in a faster progression of tissue destruction. This chapter summarizes the current knowledge on the microbiology and immunology of peri-implant infections, including findings from the peri-implant crevicular fluid, the inflammatory exudate of the peri-implant tissue. Moreover, it discusses the diagnosis and current approaches for the treatment of oral infections.

Osseointegrated dental implants are now a well-established treatment option in the armament of restorative dentistry. These technologically advanced devices are designed to functionally and esthetically replace missing teeth. Despite the revolutionary advances that implants have incurred, they have also provided the oral cavity with new artificial surfaces prone to the formation of oral biofilms, similarly to the hard tissue surfaces of natural teeth. Biofilm formation on the implant surface can trigger the inflammatory destruction of the peri-implant tissue, in what is known as peri-implantitis. The mixed microbial flora of peri-implant infections resembles that of periodontal infections, with some notable differences. These are likely to expand with the ever increasing application of metagenomics and metatrascriptomics in the analysis of oral ecology. This review presents the wealth of knowledge we have gained from microbiological methods used in the characterization of peri-implant microflora and sheds light over potential new benefits, as well as limitations, of the new sequencing technology in our understanding of peri-implant disease pathogenesis.

It is suggested that (i) the local use of chlorhexidine has minor influence on treatment outcome, (ii) resolution of peri-implantitis following surgical treatment without the adjunctive use of local and systemic antimicrobial agents is possible and (iii) the results are influenced by implant surface characteristics.

The predominant cultural subgingival flora in dogs shows great similarities with the subgingival bacteria from humans at the genus level, but distinct differences at the species level; however, a genetic relatedness could be disclosed for most strains investigated.

The aim of this study was to identify sites at risk for future progression, during 2 yr of maintenance, in patients with chronic periodontitis (CP), based on longitudinal clinical and microbiological monitoring. At baseline (2003), clinical and microbiological features were recorded in 50 patients with CP. Two microbial samples were obtained from each patient (one from a clinically healthy site and one from a periodontitis site) and these were analyzed using DNA-DNA hybridization involving 25 bacterial species. After non-surgical periodontal therapy, clinical and microbiological re-examinations were performed at the same or similar sites at 2 yr (2006) and 4 yr (2008) of maintenance. Plaque, bleeding on probing (BoP), and the number of sites with periodontitis (≥4 mm) and severe periodontitis (≥6 mm) all showed a significant decrease at 2 and 4 yr of maintenance after non-surgical intervention. Checkerboard analysis revealed that various bacteria with a high colonization score (≥3) corroborated the clinical findings of pathology at 2003, 2006, and 2008. Different clusters of bacteria, not just the 'red complex', were able to predict progression of chronic periodontitis during 2 yr of maintenance (2006-2008). Therefore, quantified bacterial markers (reflecting bacterial load) and the clinical markers BoP and periodontal probing depth show comparable prediction of future disease condition.