Bone Cells Dynamics during Peri-Implantitis: a Theoretical Analysis

Abstract

ObjectivesThe present manuscript aims a detailed characterization of the bone cells dynamics during physiological bone remodelling and, subsequently, to address the cellular and molecular mechanisms that play a fundamental role in the immune-inflammatory-induced uncoupled bone remodelling observed in peri-implantitis.ResultsAn intimate relationship between the immune system and bone is acknowledged to be determinant for bone tissue remodelling and integrity. Due to the close interaction of immune and bone cells, the two systems share a number of surface receptors, cytokines, signalling pathways and transcription factors that are involved in mutual regulatory mechanisms. This physiological equilibrium is disturbed in pathological conditions, as verified in peri-implantitis establishment and development. Activation of the innate and adaptive immune response, challenged by the local bacterial infection, induces the synthesis of high levels of a variety of pro- and anti-inflammatory cytokines that disturb the normal functioning of the bone cells, by uncoupling bone resorption and formation, ending up with a net alveolar bone loss and subsequent implant failure. Most data points to an immune-inflammatory induced osteoclast differentiation and function, as the major underlying mechanism to the uncoupled bone resorption to bone formation. Further, the disturbed functioning of osteoblasts, reflected by the possible expression of a fibro-osteoblastic phenotype, may also play a role.ConclusionsAlveolar bone loss is a hallmark of peri-implantitis. A great deal of data is still needed on the cellular and humoral crosstalk in the context of an integrated view of the osteoimmunologic interplay occurring in the peri-implantitis environment subjacent to the bone loss outcome.

Titanium particles: An emerging risk factor for peri-implant bone loss

“…Biofilm accumulation is considered to be a key causal factor in peri-implantitis. The association between peri-implant disease and its microbial aetiology is a consequence of the lipopolysaccharide (LPS) component of bacterial cell walls, which activates neutrophils, macrophages, T cells and B cells and sets up, through a cascade of cytokine release and osteoclast differentiation, tissue reactions in the soft tissue and bone ( Fernandes and Gomes, 2016 , Taira et al, 2010 ). Some cytokines have been over-expressed in peri-implant crevicular fluid in diseased implant sites ( Erhan and Tolga, 2016 ).…”

MicroRNA sequence analysis identifies microRNAs associated with peri-implantitis in dogs

“…Additionally, this local immune-inflammatory process is associated with disrupted bone remodeling. Osteoclastogenesis induction appears to be a major determinant of the uncoupling of bone resorption and bone formation, resulting in loss of the supporting alveolar bone and, subsequently, implant failure [ 10 ].…”

MiR-128 promotes osteogenic differentiation of bone marrow mesenchymal stem cells in rat by targeting DKK2

“…Notably, most of the available data point to immune-inflammatory induced osteoclast differentiation and function, as the major underlying mechanism to peri-implantitis. Further, the disturbed function of bone cells and unbalanced state of bone remodeling processes may also play a role [6]. BMSCs, as the name implies, originate from bone marrow and have a great potential for regenerative therapy due to their multipotential differentiation capacity.…”

“…Clinically, guided bone regeneration (GBR) techniques are recommended to fill bone defects and re-establish the bone-to-implant contact caused by peri-implantitis [3]. Nevertheless, the evidence is limited with regard to the success and reliability of this treatment method from a long-term survival point of view [4], which is partly due to the disrupted behavior of the local osteoblast cells in an immune-inflammatory microenvironment [5,6]. Therefore, a deep exploration of the underlying molecular mechanisms of peri-implantitis is imperative in order to optimize bone regenerative therapy.…”