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The role of foreign body response in peri‐implantitis: What is the evidence?

Historically, there has been broad consensus that osseointegration represents a homeostasis between a titanium dental implant and the surrounding bone, and that the crestal bone loss characteristic of peri‐implantitis is a plaque‐induced inflammatory process. However, this notion has been challenged...

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Detalles Bibliográficos
Autores principales: Ivanovski, Sašo, Bartold, Peter Mark, Huang, Yu‐Sheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9804527/
https://www.ncbi.nlm.nih.gov/pubmed/35916872
http://dx.doi.org/10.1111/prd.12456
Descripción
Sumario:Historically, there has been broad consensus that osseointegration represents a homeostasis between a titanium dental implant and the surrounding bone, and that the crestal bone loss characteristic of peri‐implantitis is a plaque‐induced inflammatory process. However, this notion has been challenged over the past decade by proponents of a theory that considers osseointegration an inflammatory process characterized by a foreign body reaction and peri‐implant bone loss as an exacerbation of this inflammatory response. A key difference in these two schools of thought is the perception of the relative importance of dental plaque in the pathogenesis of crestal bone loss around implants, with obvious implications for treatment. This review investigates the evidence for a persistent foreign body reaction at osseointegrated dental implants and its possible role in crestal bone loss characteristic of peri‐implantitis. Further, the role of implant‐related material release within the surrounding tissue, particularly titanium particles and corrosion by‐products, in the establishment and progression in peri‐implantitis is explored. While it is acknowledged that these issues require further investigation, the available evidence suggests that osseointegration is a state of homeostasis between the titanium implant and surrounding tissues, with little evidence that a persistent foreign body reaction is responsible for peri‐implant bone loss after osseointegration is established. Further, there is a lack of evidence for a unidirectional causative role of corrosion by‐products and titanium particles as possible non–plaque related factors in the etiology of peri‐implantitis.