Chemical modification of an implant surface increases osteogenesis and simultaneously reduces osteoclastogenesis: an in vitro study.
OBJECTIVE
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.


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.


CONCLUSIONS
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.
Department of Periodontics, Health Science Center at San Antonio, University Of Texas, San Antonio, TX 78229-3900, USA. mamalis@uthscsa.edu
Anastasios A
AA
Mamalis
Cleopatra
C
Markopoulou
Ioannis
I
Vrotsos
Michael
M
Koutsilirieris
D000134:Acid Etching, Dental / Q000379:methods; D000469:Alkaline Phosphatase / Q000032:analysis; D055419:Bone Morphogenetic Protein 7 / Q000032:analysis; D002448:Cell Adhesion / Q000502:physiology; D018929:Cell Culture Techniques; D002454:Cell Differentiation / Q000502:physiology; D049109:Cell Proliferation; D002469:Cell Separation; D050659:Core Binding Factor Alpha 1 Subunit / Q000032:analysis; D045662:Dental Etching / Q000379:methods; D015921:Dental Implants; D003764:Dental Materials / Q000737:chemistry*; D003775:Dental Polishing / Q000379:methods; D006801:Humans; D010010:Osteoclasts / Q000473:pathology* / Q000502:physiology; D010012:Osteogenesis / Q000502:physiology*; D053244:Osteoprotegerin / Q000032:analysis; D010513:Periodontal Ligament / Q000473:pathology*; D010641:Phenotype; D053245:RANK Ligand / Q000032:analysis; D013499:Surface Properties; D013997:Time Factors; D014025:Titanium / Q000737:chemistry*
C525819:BMP7 protein, human; D055419:Bone Morphogenetic Protein 7; D050659:Core Binding Factor Alpha 1 Subunit; D015921:Dental Implants; D003764:Dental Materials; D053244:Osteoprotegerin; D053245:RANK Ligand; C505688:TNFSF11 protein, human; D014025:Titanium; D000469:Alkaline Phosphatase