Abstract

Implants trigger an inflammatory response, which is important for osseointegration. Here we studied neutrophil extracellular trap (NET) release of human neutrophils in response to sandblasted large-grit acid etched (SLA) implants using fluorescent, confocal laser scanning and scanning electron microscopy. Our studies demonstrate that human neutrophils rapidly adhered to SLA surfaces, which triggered histone citrullination and NET release. Further studies showed that albumin or acetylsalicylic acid had no significant effects on the inflammatory response to SLA surfaces. In contrast to bioinert materials, which do not osseointegrate, the bioactivity of SLA surfaces is coupled with the ability to release NETs. Further investigations are necessary for clarifying the role of NETosis for osseointegration.

Highlights

  • Endosteal implants are sterile foreign bodies surgically inserted into bone with an associated inflammatory host’s response [1,2,3]

  • Examination of blood cell attachment to the surfaces of the sandblasted large-grit acid etched (SLA) titanium plates under the fluorescence microscope revealed that after 4 hours of incubation, several types of nucleated cells had attached to the titanium surfaces of the plates of all three pre-treatment schedules (Fig. 1A, S1 Fig., Table 1)

  • We demonstrate that human neutrophils rapidly adhered to SLA surfaces and release extracellular DNA structures with characteristics of neutrophil extracellular trap’ (NET)

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Summary

Introduction

Endosteal implants are sterile foreign bodies surgically inserted into bone with an associated inflammatory host’s response [1,2,3]. In the initial stage of osseointegration, spaces around titanium implants are filled with blood coagulum infiltrated with leukocytes [2,3] Polymorphonuclear neutrophils, (PMNs) are rapidly recruited to sites of inflammation and have been shown to attach within minutes to artificial implant surfaces [4,5,6], triggering the production of reactive oxygen species (ROS) [7,8,9]. Besides these findings, the fate and functionalities of human PMNs in response to implants remained poorly understood. PMNs expel their own DNA, a process termed ‘neutrophil extracellular trap’ (NET) formation or ‘NETosis’, since the major

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