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      Microrough titanium surface affects biologic response in MG63 osteoblast-like cells.

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          Abstract

          The purpose of this study was to define the surface properties of prepared titanium (Ti) disks, which served as a model system, and to contrast the biologic response of MG63 cells exposed to Ti disks with different levels of surface roughness. The surface properties interact with each other, resulting in a change of other surface qualities in addition to roughness due to the surface roughening procedure. The machined Ti disks were roughened by sandblasting and electric glow discharging. The surface properties of the Ti specimens were inspected through a comprehensive surface analysis. MG63 cell behaviors were compared along with cell number, alkaline phosphatase (ALP) activity, Runx2 gene expression, and type I collagen production. Statistics were evaluated, using analysis of variance (ANOVA). The sandblasted Ti disks demonstrated well-controlled surface roughness features and meaningful average roughness ranges, including the surface roughness of the "modern" microrough implant, used clinically. With increasing Ti surface roughness, the cell number decreased, while the ALP activity, type I collagen production, and Runx2 gene expression increased significantly. The rougher the Ti surface was, the sooner the Runx2 gene was expressed. Based on these results, we suggest that the microrough Ti surfaces of the 1-3 mum range may contribute effectively to osteogenic differentiation and proliferation in MG63 cells.

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          Author and article information

          Journal
          J Biomed Mater Res A
          Journal of biomedical materials research. Part A
          Wiley-Blackwell
          1549-3296
          1549-3296
          Dec 15 2006
          : 79
          : 4
          Affiliations
          [1 ] Department of Prosthodontics, Graduate School, Seoul National University, Seoul, Korea.
          Article
          10.1002/jbm.a.31040
          17034031
          59707101-d910-4ead-897d-81f9a2a95591
          History

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