Wettability, Corrosion Resistance, and Osteoblast Response to Reduced Graphene Oxide on CoCr Functionalized with Hyaluronic Acid

Abstract

The durability of metal–metal prostheses depends on achieving a higher degree of lubrication. The beneficial effect of hyaluronic acid (HA) on the friction and wear of both natural and artificial joints has been reported. For this purpose, graphene oxide layers have been electrochemically reduced on CoCr surfaces (CoCrErGO) and subsequently functionalized with HA (CoCrErGOHA). These layers have been evaluated from the point of view of wettability and corrosion resistance in a physiological medium containing HA. The wettability was analyzed by contact angle measurements in phosphate buffer saline-hyaluronic acid (PBS-HA) solution. The corrosion behavior of functionalized CoCr surfaces was studied with electrochemical measurements. Biocompatibility, cytotoxicity, and expression of proteins related to wound healing and repair were studied in osteoblast-like MC3T3-E1 cell cultures. All of the reported results suggest that HA-functionalized CoCr surfaces, through ErGO layers in HA-containing media, exhibit higher hydrophilicity and better corrosion resistance. Related to this increase in wettability was the increase in the expressions of vimentin and ICAM-1, which favored the growth and adhesion of osteoblasts. Therefore, it is a promising material for consideration in trauma applications, with improved properties in terms of wettability for promoting the adhesion and growth of osteoblasts, which is desirable in implanted materials used for bone repair.

TBX3 regulates the transcription of VEGFA to promote osteoblasts proliferation and microvascular regeneration

“…The Wnt/ β -catenin signalling pathway plays an essential role in transforming preosteoblasts into osteoblasts inducing the expression of the osteoblast marker osterix ( Mora-Raimundo et al, 2019 ; Zhou et al, 2021 ). Under pathological conditions, osteoblasts undergo mechanical stress, and the expression of Dickkopf-related protein 1 (DKK1) and sclerostin are reduced, resulting in increased wnt/ β -catenin signaling and osteoblast activation, thereby promoting bone repair ( Li et al, 2022b ; Chico et al, 2022 ). IL-1R1/MyD88 signalling pathway is involved in the negative regulation of bone repair ( Martino et al, 2016 ).…”