New Insights into Peri-Implant Disease: The Role of Metallosis
Recent advancements have shifted the understanding and management of peri-implant disease, highlighting the detrimental effects of certain debridement techniques and materials on implant surfaces. Central to these findings is the concept of metallosis, a pathogenic process triggered by oral biofilm and exacerbated by titanium particle release. Understanding these mechanisms is crucial for improving long-term treatment success and maintaining implant health.
There has been a recent and profound shift in the management of peri-implant disease. Many of the materials and techniques previously used to debride and regenerate intrabony defects have proven harmful to the implant surface.1 In large part, this is due to new thinking in one of the driving etiologies for peri-implant disease — metallosis. This phenomenon was adopted from histopathological findings in prosthetic joint complications and describes a pathogenic process that is initiated by the destructive sequela of the oral biofilm. A secondary inflammatory response results from the titanium particle and ion release of the dioxide layer around implants.
Implant insertion, corrosion, fretting, and a combination of these factors called tribocorrosion contribute to metallosis.1 Certain chemical agents can also damage wound-healing cells and stifle their regenerative potential.2 Therefore, learning to readily identify and treat peri-implant disease can improve long-term treatment success and health.
It is important to first understand the unique progression and presentation of peri-implant disease in the context of today’s literature. Peri-implant mucositis is an inflammatory mucosal lesion without supporting bone loss. Bleeding on probing is the hallmark sign, while suppuration, swelling and erythema may also appear as early as four months post-loading.3 If peri-implant mucositis is left untreated, it can progress to peri-implantitis given local, systemic and/or environmental risk factors.
Peri-implantitis has clinical and radiographic signs of bone loss that include bleeding on probing, probing depths more than 6 mm, and/or suppuration. These histologic lesions are twice the size of those seen in periodontitis. The pattern of bone loss is often rapid and nonlinear, with significantly increased proportions of pro-inflammatory cytokines, neutrophils, neuropeptides and macrophages.4
Furthermore, the peri-implant microbiome is unique. Titanium readily forms a thin dioxide layer when inserted into the alveolar bone, which contributes to its biocompatibility and passivation. The electrostatic forces and ionic bonding differ between tooth- and implant-bound biofilms because this titanium dioxide alters bacterial adhesion and colonization during biofilm maturation. The alteration is such that the resulting biofilm has proven resistant to beta-lactam antibiotics normally effective against periodontal niches as a monotherapy.5 Additionally, 16S rRNA gene sequencing of healthy and diseased periodontal and peri-implant sites found that a vast majority of individuals shared less than 8% of species between teeth and implants.6
Titanium dissolution can destabilize the peri-implant biofilm, making way for more virulent, opportunistic bacteria and dysbiosis.5 Implants cannot fully reform their dioxide layer once it is lost, as was previously thought, and because no metal or alloy is ever completely inert, particles are readily released into the surrounding tissues from function and inflammatory attacks. More specifically, particle release may result due to friction from implant installation, micro-movements from abutments, or wear from implant debridement.7 Therefore, treatment modalities must meet the new model of peri-implant infection to safeguard the integrity of the implant body and dioxide layer.
References
- Wilson TG Jr. Bone loss around implants — is it metallosis? J Periodontol. 2021;92:181–185.
- Berglundh T, Jepsen S, Stadlinger B, Terheyden H. Peri-implantitis and its prevention. Clin Oral Implants Res. 2019;30:150–155.
- Heitz-Mayfield LJ, Salvi GE. Peri-implant mucositis. J Clin Periodonto 2018;45:S237–S245.
- Schwarz F, Derks J, Monje A, Wang H-L. Peri-implantitis. J Clin Periodontol. 2018;45(Suppl 20):S246–S266.
- Kotsakis GA, Olmedo DG. Peri-implantitis is not periodontitis: Scientific discoveries shed light on microbiome-biomaterial interactions that may determine disease phenotype. Periodontol 2000. 2021;86:231–240.
- Dabdoub SM, Tsigarida AA, Kumar PS. Patient-specific analysis of periodontal and peri-implant microbiomes. J Dent Res. 2013;92(Suppl 12):168S–175S.
- Berbel LO, Banczek ED, Karoussis IK, Kotsakis GA, Costa I. Correction: Determinants of corrosion resistance of Ti-6Al-4V alloy dental implants in an in vitro model of peri-implant inflammation. PLoS One. 2019;14:e0217671.
This information originally appeared in Saltz A. Evolving management of peri-implant disease. Decisions in Dentistry. 2021;7(11)16-21.
