Understanding the Role of Titanium Particles and Corrosion in Peri-implantitis
Peri-implantitis, from its recognition as an emerging concern in implant care, has been encased in confusion and controversy. Questions remain as to the treatment approaches, prevalence, incidence, and etiology. This thematic review of the literature suggests the etiology of peri-implantitis is founded on two main concepts. One concept is focused on the microbial challenge to the host-implant interface. This is a well-established etiologic model of a microbially induced inflammatory response consistent with periodontitis. The other etiologic concept looks at the role of titanium surface alterations and the release of titanium particles into the tissues as initiators of an inflammatory response. This latter model is consistent with orthopedic osteolysis. A review of our more recent literature begins to merge these two pathogenic concepts.
A systematic review by Delgado-Ruiz and Romanos (2018) describes several possible sources for titanium particles to enter the tissues as well as a role for corrosion to contribute to the development of an inflammatory response over the lifetime of the implant. Mombelli et al (2018) offer a critical review of the role of titanium particles and biocorrosion in the development of the inflammatory lesion. Their analysis suggests that while there is clear evidence that titanium particles are associated with an inflammatory response, it is postulated that the titanium particles may be a consequence of the inflammation rather than the cause of the inflammation. That is, this inflammatory environment may contribute to the biocorrosion of the implant surface.
In contrast, Noronha et al (2018) evaluated recent literature regarding the potential for titanium particles to stimulate an inflammatory response. Their findings are consistent with the titanium particles contributing to an inflammatory response, and suggest an important role for macrophages and neutrophil phagocytosis of the particles in this inflammatory response. Further, this report suggests that there may be an important relationship between the length of time of exposure to the titanium particles and the degree of inflammatory response. This time-dependence is consistent with our epidemiologic data showing an increasing prevalence of peri-implantitis over 5 or more years following placement.
Eger et al (2018) discuss their work using an animal model to show that titanium particles induce an inflammatory response, including resultant bone loss. This study also went a step further by using blockers to specific inflammatory cytokines. These inflammatory blockers were able to inhibit inflammation and bone loss in the presence of the titanium particles, therefore identifying a specific role for inflammatory cytokines in the development of titanium particle–induced peri-implantitis. Similarly, Wang et al (2019) used a different animal model to show that titanium particles can create inflammation and bone loss. This study took a different approach to inhibit the inflammatory response by blocking macrophage activity, but similar to Eger et al (2018), they found that the inflammation-induced bone loss could be inhibited. Most interestingly, this study also found that the titanium particles were able to induce inflammatory bone loss in the absence of bacterial infection.
Lastly, Daubert et al (2018) presented a unifying model that suggests titanium particles may play a role in triggering inflammation by modifying the peri-implant microbiome and that there is an interaction between the microbiome and titanium particles and corrosion. This very interesting study found that the submarginal microbial profile was more closely associated with the presence of titanium particles than with the presence or absence of peri-implantitis. This study suggests that the microbial environment and the titanium-induced inflammatory responses contribute through a codependent phenomenon to an increased susceptibility for peri-implantitis with our patients. Taken together, it appears that peri-implantitis is a complex, multifactorial condition developing through pathologic mechanisms triggered by both microbial and material interactions with the host. Going forward, our successful management and prevention of peri-implantitis will likely become increasingly guided by understanding the relationships of each of these relevant factors.
Thomas W. Oates, DMD, PhD
University of Maryland
Baltimore, Maryland, USA
Thematic Abstract Review Section Editor
Clark M. Stanford, DDS, PhD
The University of Illinois at Chicago, Chicago, Illinois, USA
Abstracts referenced:
This article was originally published in the May/June 2019 edition (Vol 34, issue 3) of The International Journal of Oral & Maxillofacial Implants.
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