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

Abstract

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.

Keywords: foreign body reaction; macrophages; osseointegration; peri-implantitis; titanium particles.

FIGURE 1

Current understanding of the possible sequelae of dental implant placement into alveolar bone. During osseointegration, the initial inflammatory response is followed by timely resolution and pro‐reparative processes leading to osseointegration and bone formation at the implant interface. The inability to resolve the initial inflammatory response leads to a chronic inflammatory state and fibrous encapsulation of the implant, which is characteristic of a foreign body response that leads to early implant failure. FBR: foreign body response

FIGURE 2

Diagrammatic representation of the plaque‐associated pathogenic mechanism for crestal bone loss. In this mechanism, an inflammatory response to biological mediators released from plaque induces an inflammatory response from the host that results in the activation of osteoclasts responsible for crestal bone loss. Pg LPS: Porphyromonas gingivalis lipopolysaccharide; OPG: osteoprotegerin; RANK: receptor activator of nuclear factor‐κB; RANKL: receptor activator of nuclear factor‐κB ligand. Diagram adapted from ref. [51]

FIGURE 3

Diagrammatic representation of the “foreign body equilibrium” disturbance theory of peri‐implant bone loss. In this concept, the osseointegrated implant is considered “encapsulated in bone,” thus representing a chronic inflammatory state characterized by the presence of “foreign body giant cells” (FBGCs). In response to a variety of external stimuli, these foreign body giant cells are activated and are responsible for the peri‐implant bone loss. L: lymphocyte; Ost: osteocyte. (Diagram adapted from ref. [32])