Immune responses in the peri-implant soft tissue barrier are independently worthy of mention because they are distinctly different to these around teeth. One of the most major advancements in our understanding of bone remodeling and inflammatory peri-implantitis around dental implants comes from the findings that titanium material breakdown can cause immune activation in the peri-implant tissues. It was recently shown that while titanium implants are extremely resistant to corrosion in atmospheric conditions, if these surfaces are abraded such as during dental hygiene procedures with metal instruments, the environment in the peri-implant crevice with the pH fluctuations, bacterial reducing activity and tribocorrosion all contribute to the release of titanium particles (Figure 17a). These titanium particles are in the submicron and micron range and activate macrophages and multiple other phagocytic and non-phagocytic cells to elicit pro-inflammatory responses. Thus by acting as an environmental threat these particles alter the local microenvironment both with direct effects, such as IL-1β and RANKL upregulation as well as indirect effects through the change of the local conditions that affect microbiome composition (Figure 17b). As a result immune surveillance in the peri-implant soft tissue barrier is modified by the presence of titanium and results in a different clinical response, which is consistent with the much more rampant tissue destruction in peri-implantitis as compared to periodontitis as well as the resistance to antibiotic and scaling treatments. This new data have paved the way for immunomodulatory treatments for peri-implantitis that may be impactful in its management.