Artikel
Shear forces modulate the response of osteoblasts to implantat surfaces through prostaglandin E2-dependent mechanisms
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Veröffentlicht: | 28. September 2006 |
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Gliederung
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Introduction: Prior studies have shown that osteoblasts are sensitive to implant surface roughness. MG63 osteoblasts-like cells grown on titanium surfaces (Ti) exhibit an increased differentiation and realese of growth factors dependent on surface roughness. In vivo, osteoblasts are exposed to shear forces during and after osseointegration of the implant.
Hypothesis:This study investigates that shear forces modulate the response of osteoblasts to surface roughness and that this effect is mediated by prostaglandins.
Materials and methods:MG63 osteoblast-like cells were cultured on disks from glass or Ti with 3 different roughnesses (Ry values) and surface topography (PT: Ra = 0.60 µm; SLA: Ra = 3.97 µm; TPS: Ra = 5.21 µm) in an apparatus with a continuous flow of the culture media with shear forces of 0, 1, 5, 14, and 30 dynes/cm2. Additionally, the cultures were treated with or without 10-7 M of the general Cox-inhibitor Indomethacin (Indo) or 25µM Meloxicam (Mel), a Cox-2 inhibitor.
Results: Cell number, alkaline phosphatase specific acitivty, osteocalcin, TGF-ß1 and PGE2 were measured. The results showed that shear forces do not influence cell number, alkaline phosphatase, osteocalcin, and TGF-ß1 on smooth surfaces. On rough surfaces, the influence of shear forces induced an inhibition of alkaline phosphatase activity, osteocalcin and TGF-ß1-expression. PGE2 was increased by shear force on glass and PT by 100%, and on SLA and TPS by 9 – 10 fold. Those effects were inhibited by treatment with Indo. Mel also induced an inhibition of the effects of shear force, but to a lesser extent than Indo. Discussion: The results show that the response of osteoblasts to shear force may be modulated by surface topography. The most pronounced effects were induced at 14 dynes/cm2. The data of the present investigation show that the inhibition of osteoblastic differentiation by shear forces on rougher surfaces is mediated by PGE2. These effects are only partially mediated by Cox-2 dependent mechanisms