Shear force modulates osteoblast response to surface roughness

Previous studies have shown that osteoblasts are sensitive to surface roughness. When cultured on Ti, MG63 osteoblast-like cells exhibit decreased proliferation and increased differentiation with increasing surface roughness. In vivo, osteoblasts also are subjected to shear force during osseointegration. To examine how shear force modulates osteoblast response to surface roughness, MG63 cells were cultured on glass disks or Ti disks with three different R, values and topographies (PT: R(a) = 0.60 mum; SLA: R(a) = 3.97 mum; TPS: R(a) = 5.21 mum) in a continuous flow device, resulting in shear forces of 0, 1, 5, 14, and 30 dynes/cm(2). Confluent cultures were exposed to fluid flow for 1 h. After an additional 23 h, cell number, alkaline-phosphatase-specific activity, and levels of osteocalcin, TGF-beta1, and PGE(2) in the conditioned media were determined. Cell numbers on smooth surfaces (glass and PT) were unaffected by shear force. In contrast, shear force caused a dose-dependent reversal of the decrease in cell numbers seen on rough SLA and TPS surfaces. Alkaline-phosphatase-specific activity was unaffected on glass or PT, but shear force caused a biphasic reduction in the roughness-dependent increase on SLA and TPS that was maximal at 14 dynes/cm(2). There was a similar effect seen with TGF-beta1 levels. Osteocalcin was unaffected on smooth surfaces; shear force caused a dose-dependent reduction in the roughness-stimulated increase seen on SLA and TPS. PGE(2) production was increased by shear force on all surfaces. There was a twofold increase in PGE(2) levels in the media of MG63 cells cultured on glass and PT in response to 14 dynes/cm(2), but on SLA and TPS, 14 dynes/cm(2) shear force caused a 9-10-fold increase. These results show that osteoblastic response to shear force is modulated by surface topography. The shear-force-mediated decrease in osteoblast differentiation seen in cultures on rough surfaces may be due to increased production of PGE(2). (C) 2002 John Wiley Sons, Inc.