Peri-Implant Crestal Bone Loss: A Putative Mechanism

Abstract

Purpose. The immunological mechanisms of peri-implant crestal bone loss have, hitherto, not been elucidated. We hypothesized that bacterial products from the microgap cause upregulation of cytokines in otherwise healthy peri-implant cells, which results in osteoclast formation and, ultimately, in bone resorption. Materials and Methods. We used RT-PCR and ELISA to assay mediators of osteoclastogenesis in rat and human macrophages (r-and hMO); bone marrow derived stromal cells (r-and hBMCs); and human gingival fibroblasts (hGF)—with or without stimulation by LPS. TRAP positive multinucleate cells were assessed for their resorptive ability. Results. We show that IL-1α, IL-1β, and IL-6 were expressed by all examined cell types, and TNF-α was upregulated in hGF. Secretion of IL-1α and IL-1β proteins was stimulated in hMO by LPS, and IL-6 protein secretion was highly stimulated in hBMCs and hGF. Both LPS and RANKL stimulated macrophages to form osteoclast-like TRAP positive cells, which resorbed calcium phosphate substrates. Conclusion. Taken together, the results of our study support the hypothesis that bacterial endotoxins upregulate enhanced mediators of osteoclastogenesis in resident cells found in the healthy peri-implant compartment and that the local synergistic action of cytokines secreted by such cells results in the genesis of resorptively active osteoclasts.

Comparative Evaluation of Osseointegrated Dental Implants Based on Platform-Switching Concept: Influence of Diameter, Length, Thread Shape, and In-Bone Positioning Depth on Stress-Based Performance

“…Nevertheless, a proper osseointegration process may be counteracted by the activation of histological resorption mechanisms [9, 14–16] that can induce bone weakening or loss at the peri-implant region. Bone resorption mainly affects the bone region around the implant neck, producing a cratering morphology, and it may be activated by surgical trauma or bacterial infection, as well as by overloading states [4, 5, 14–22].…”

“…Bone resorption mainly affects the bone region around the implant neck, producing a cratering morphology, and it may be activated by surgical trauma or bacterial infection, as well as by overloading states [4, 5, 14–22]. Under functional or pathological (e.g., induced by bruxism) loads, overloading at the peri-implant bone may occur by a shortcoming in load transfer mechanisms, mainly due to bad occlusion, improper implant use, wrong prosthesis and/or implant design, and improper implant placement.…”

Basis of bone metabolism around dental implants during osseointegration and peri‐implant bone loss

“…When early implant marginal bone loss exposes the implant microtexture, contamination by bacterial and its byproducts is facilitated and thus, the infiltration of large proportions of CD68‐ and myeloperoxidase‐positive cells are capable of breaking down the peri‐implant structures . It has been suggested that the microgap in two‐piece implants might be associated with the up regulation of the inflammatory cell infiltrate leading to crestal bone loss . The abutment connection on the endosseous portion of the implant leaves a gap in a range of 10–50 μm .…”

“…A pumping effect of the fluid contained in the implant cavities might shift inwards to the peri‐implant compartment due to the cyclical loading of the implant/abutment interface and facilitate the colonization of the gap by putative pathogens. These organic fluids with bacteria products and endotoxins could upregulate the expression of proinflammatory cytokines in the peri‐implant tissues and stimulate the chemotaxis of active osteoclasts . Over the time, leakage associated to micromovements leads to steady inflammatory reaction, bone loss around the implant neck and later, in the presence of biofilm, to peri‐implantitis .…”

Effects of uncontrolled periodontitis on marginal bone alterations around implants: A case‐control study

“…Some authors assumed that the etiologic factor of peri‐implantitis was similar to that of periodontitis, and bone resorption around implant was mainly due to bacterial infection . The reason for this hypothesis was that a similar gram (–) anaerobic pathological micro‐flora formed around diseased teeth and affected implants …”