Abstract

Immediately after dental implant insertion, blood will be in direct contact and interact with the implant surface and activates inflammatory responses and complement cascades within seconds. The aim of the present study was to determine the ability of fluoride-modified titanium surfaces to activate complement cascades using the human buffy coat as model. The buffy coats were exposed to hydrofluoric acid-modified surfaces for a short time and its responses were compared to controls. Identification and quantification of complement cascade biomarkers were conducted using ELISA kits and multianalyte profiling using Luminex. A lower level of C3 at 30 min and increased levels of C4, MIP-4, CRP, and pigment epithelium-derived factor at 360 min were found on modified surfaces as compared to controls. We found no significant differences in the levels of C3a, C5a, C Factor H, α2M, ApoA1, ApoC3, ApoE, Prealbumin, α1AT, and SAP in modified surfaces in the buffy coats. We conclude that titanium surfaces treated with hydrofluoric acid modify the levels of specific biomarkers related to the complement cascade and angiogenesis and, thus, tissue growth, remodeling and repair, as this may play a role in the enhanced clinical performance of fluoride-modified Ti dental implants.

Highlights

  • More than 5 million dental implants are inserted yearly in the U.S alone, according to Grand ViewResearch

  • We have previously studied the effect of fluoride treatment on human primary osteoblasts and human gingival fibroblasts [14,15], without different cellular responses to fluoride and non-fluoride treated surface

  • A lower level of C3 was found after exposure to TiO2 surface (TiF) surfaces compared to non-modified surfaces at earliest time point, 30 min (p < 0.05)

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Summary

Introduction

More than 5 million dental implants are inserted yearly in the U.S alone, according to Grand ViewResearch. Fluoride treated surface dental implant (Osseospeed®, Dentsply, York, PA, USA). Fluoride-treated dental implants have shown clinically successful results with increased bone-to-implant contact and functional bone attachment [4,5,6,7,8]. It has been well reported that fluoride improve the peri-implant tissue responses [9,10,11,12,13]. Despite these satisfactory clinical results, the identification of molecular mechanisms behind the success is still unidentified. We have previously studied the effect of fluoride treatment on human primary osteoblasts and human gingival fibroblasts [14,15], without different cellular responses to fluoride and non-fluoride treated surface

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