On Peri-Implant Bone Loss Theories: Trying To Piece Together the Jigsaw

Abstract

This review aims to explore the plausibility of new theories on the etiopathogenesis of marginal bone loss (MBL) and peri-implantitis (PI) and to discuss possible underlying pathogenic mechanisms. The former concept of osteointegration of dental implants can now be conceptualized as a foreign body response histologically characterized by a bony demarcation in combination with chronic inflammation. Different risk factors can provoke additional inflammation and, therefore, pro-inflammatory cytokine release in soft tissues and bone, leading to an overpass of the threshold of peri-implant bone defensive and regenerative capacity. Progressive bone loss observed in MBL and PI is ultimately due to a localized imbalance in the receptor activator of nuclear factor kappaB ligand (RANKL)/Receptor activator of nuclear factor κ B (RANK)/osteoprotegerin (OPG) pathway in favor of increased catabolic activity. The genetic background and the severity and duration of the risk factors could explain differences between individuals in the threshold needed to reach an imbalanced scenario. MBL and PI pathogenesis could be better explained by the "inflammation-immunological balance" theory rather than a solely "infectious disease" conception. The link between the effect of biofilm and other risk factors leading to an imbalanced foreign body response lies in osteoclast differentiation and activation pathways (over)stimulation.

Emerging factors affecting peri‐implant bone metabolism

“…Inadequate positioning of implants may increase by 48.2 times the risk for developing peri-implantitis mainly due to limited amounts of buccal hard tissues and keratinized mucosa and impairment of oral hygiene. 24,248 Some surgical factors like bone quality/density, implant insertion torque/ bone compression, and early bone remodeling have been previously described in a review by the same authors 249 and were out of the scope of this text.…”

“…24 Some authors proposed that the objective of the treatment should not only be the control of bacterial plaque but also to avoid or minimize a pro-inflammatory microenvironment surrounding the implant. 24 A paradigm shift should be made to avoid osteoclast differentiation and activation caused by the local or systemic release of proinflammatory cytokines and other molecules. [25][26][27][28] This overexpression of inflammatory mediators is generated not only with the colonization and activity of pathogenic bacteria 28,29 but also due to other factors such as the presence of Ti particles, corrosion, wear, abutment micromovement, occlusal overload, and the presence of cement remnants.…”

“…[25][26][27][28] This overexpression of inflammatory mediators is generated not only with the colonization and activity of pathogenic bacteria 28,29 but also due to other factors such as the presence of Ti particles, corrosion, wear, abutment micromovement, occlusal overload, and the presence of cement remnants. 24 It is important to point out that only 28.8% of peri-implantitis cases were considered purely plaque-induced peri-implantitis, while 40.8% and 30.4% were considered surgically and prosthetically triggered cases. 30 Indeed, in some cases, several risk factors may act synergistically and make it difficult to find the initial triggering factor.…”

“…Nevertheless, many other contributing factors that affect bone metabolism have not yet been fully explored. As marginal bone loss and peri‐implantitis can be considered conditions with a complex and multifactorial pathogenesis, the synergistic action of several of these factors (implant‐, surgical‐, prosthetic‐, microbiological‐, and host‐related) may be necessary to exceed the individualized threshold of each patient for the pathology to appear 24 . Some authors proposed that the objective of the treatment should not only be the control of bacterial plaque but also to avoid or minimize a pro‐inflammatory microenvironment surrounding the implant 24 .…”

“…As marginal bone loss and peri‐implantitis can be considered conditions with a complex and multifactorial pathogenesis, the synergistic action of several of these factors (implant‐, surgical‐, prosthetic‐, microbiological‐, and host‐related) may be necessary to exceed the individualized threshold of each patient for the pathology to appear 24 . Some authors proposed that the objective of the treatment should not only be the control of bacterial plaque but also to avoid or minimize a pro‐inflammatory microenvironment surrounding the implant 24 . A paradigm shift should be made to avoid osteoclast differentiation and activation caused by the local or systemic release of proinflammatory cytokines and other molecules 25‐28 .…”