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An Improved Mechanical Testing Method to Assess Bone-implant Anchorage
Published on: February 10, 2014
Chemical modification of an implant surface increases osteogenesis and simultaneously reduces osteoclastogenesis: an
Anastasios A Mamalis1, Cleopatra Markopoulou, Ioannis Vrotsos
1Department of Periodontics, Health Science Center at San Antonio, University Of Texas, San Antonio, TX 78229-3900, USA. mamalis@uthscsa.edu
Objectives:
The present study investigated the effect of a chemical modification of the SLA surface (SLActive surface) on human periodontal ligament (hPDL) cell (1) adhesion, (2) proliferation, (3) osteogenic differentiation (core binding factor α-1 [Cbfa-1], bone morphogenetic protein-7 [BMP-7] gene expression and alkaline phosphatase [ALP] activity) and (4) osteoclast formation and activity (osteoprotegerin [OPG] and receptor activator of nuclear factor-κ B ligand [RANKL] gene expression). The above activities were based on the hypothesis that the expression of such molecules might be dependent on the characteristics of the implant surface.
Material And Methods:
hPDL cells were isolated and characterized for their mesenchymal origin, fibroblastic and osteoblastic phenotype. hPDL cells were cultured on smooth, SLA and SLActive implant surfaces (chemically modified). Cell attachment and proliferation were assessed for 5, 24, 72 h, 5 and 7 days. Cbfa-1, BMP-7, OPG and RANKL gene expression was assessed by RT-PCR and a colorimetric assay for ALP activity was applied.
Results:
hPDL cells grown on SLActive surfaces demonstrated increased proliferation rates (24 h, 5 and 7 days of the incubation period), and ALP activity was found to be significantly upregulated (5, 72 h and 7 days) as compared with the SLA surfaces. After 7 days of culture, the gene expression of BMP-7, Cbfa-1 and OPG by hPDL cells was significantly upregulated, while RANKL gene expression was significantly downregulated in response to the SLActive surface.
Conclusion:
Chemical modification of a previously roughened implant surface increases hPDL proliferation and upregulates osteoblastic differentiation. It can also suppress osteoclastogenesis regulating the RANKL-RANK-OPG axis. Hence, an osteoprotective microenvironment is created around chemically modified implants that may enhance osseointegration.
