The effect of metal ions released from different dental implant-abutment couples on osteoblast function and secretion of bone resorbing mediators

J Dent. 2017 Nov:66:91-101. doi: 10.1016/j.jdent.2017.08.002. Epub 2017 Aug 4.

Abstract

Objectives: The etiology of the reduced marginal bone loss observed around platform-switched implant-abutment connections is not clear but could be related to the release of variable amounts of corrosion products. The present study evaluated the effect of different concentrations of metal ions released from different implant abutment couples on osteoblastic cell viability, apoptosis and expression of genes related to bone resorption.

Methods: Osteoblastic cells were exposed to five conditions of culture media prepared containing metal ions (titanium, aluminum, vanadium, cobalt, chromium and molybdenum) in different concentrations representing the amounts released from platform-matched and platform-switched implant-abutment couples as a result of an earlier accelerated corrosion experiment. Cell viability was evaluated over 21days using the Alamar Blue assay. Induction of apoptosis was measured after 24h of exposure using flow cytometry. Expression of interleukin-6, interleukin-8, cyclooxygenase-2, caspase-8, osteoprotegerin and receptor activator of nuclear factor kappa-B ligand (RANKL) by osteoblastic cells were analysed after exposure for 1, 3 and 21days using real-time quantitative polymerase chain reaction assay RESULTS: Metal ions in concentrations representing the platform-matched groups led to a reduction in cell viability (P<0.01) up to 7days of exposure. Stimulated cells showed higher rates of early apoptosis (P<0.01) compared to non-treated cells. Metal ions up-regulated the expression of interleukin-6, interleukin-8, cyclooxygenase-2 and RANKL in a dose dependent manner after 1day of exposure (P<0.05). The up-regulation was more pronounced in the groups containing the corrosion products of platform-matched implant-abutment couples.

Conclusion: Osteoblastic cell viability, apoptosis, and regulation of bone resorbing mediators were significantly altered in the presence of metal ions. The change in cytokine levels expressed was directly proportional to the metal ion concentration.

Clinical significance: The observed biological responses to decreased amounts of metal ions released from platform-switched implant-abutment couples compared to platform-matched couples may partly explain the positive radiographic findings in respect to crestal bone level when utilising the "platform-switching" concept, which highlights the possible role of corrosion products in the mediation of crestal bone loss around dental implants.

Keywords: Corrosion; Dental implants; Ion release; Peri-implant bone loss; Platform-switching; Titanium.

MeSH terms

  • Aluminum / adverse effects
  • Aluminum / chemistry
  • Alveolar Bone Loss / etiology*
  • Apoptosis / drug effects
  • Caspase 8 / metabolism
  • Cell Culture Techniques
  • Cell Survival / drug effects
  • Chromium / adverse effects
  • Chromium / chemistry
  • Cobalt / adverse effects
  • Cobalt / chemistry
  • Corrosion
  • Cyclooxygenase 2 / metabolism
  • Dental Abutments*
  • Dental Alloys / adverse effects*
  • Dental Alloys / chemistry
  • Dental Implant-Abutment Design
  • Dental Implantation, Endosseous
  • Dental Implants*
  • Gene Expression / drug effects
  • Humans
  • Interleukin-6 / metabolism
  • Interleukin-8 / metabolism
  • Ions / adverse effects*
  • Metals / adverse effects*
  • Molybdenum / adverse effects
  • Molybdenum / chemistry
  • Osteoblasts / drug effects*
  • Osteoblasts / metabolism*
  • Osteoprotegerin / metabolism
  • RANK Ligand / metabolism
  • Time Factors
  • Titanium / adverse effects
  • Titanium / chemistry
  • Vanadium / adverse effects
  • Vanadium / chemistry

Substances

  • Dental Alloys
  • Dental Implants
  • Interleukin-6
  • Interleukin-8
  • Ions
  • Metals
  • Osteoprotegerin
  • RANK Ligand
  • TNFSF11 protein, human
  • Vanadium
  • Chromium
  • Cobalt
  • Molybdenum
  • Aluminum
  • Titanium
  • Cyclooxygenase 2
  • PTGS2 protein, human
  • Caspase 8