IntroductionMechanical loading of bone tissue is a prerequisite for the maintenance of bone structure. Experimental and clinical observations demonstrate that immobilisation of healthy individuals disturbs bone metabolism leading to increased bone resorption, decreased bone formation, and loss of bone mass mainly in weight bearing skeletal regions Dehority et al., 1999;Vico et al., 1987). Mechanical strain, transmitted into bone tissue via muscle force interacts with the impact of gravity (g) in an osteoanabolic manner. Therefore, bone loss occurs during long term periods of living in a micro-g environment, e.g. during space flights (Carmeliet and Bouillon, 1999) although the functional integrity of the neuro-muscular-skeletal system is not impaired. It is unclear how bone tissue perceives mechanical loading and whether gravitation exerts its anabolic effects directly on bone cells or indirectly on bone tissue by increasing the impact of muscle-and weight-induced forces on bone.Mechanical forces are absorbed by the bone matrix and transformed into deformation. Deformation of the bone matrix is perceived by bone cells via adhesion molecules which modulates osteoblast metabolism (Liegibel et al., 2002). Deformation of the interconnecting porous bone tissue also induces fluid shifts within the osteocytic lacunae and canaliculi. There is evidence that fluid flow may be more important for an osteocytic response AbstractDeformation of the bone matrix by mechanical strain causes fluid shifts within the osteocytic canaliculi which affect osteocytic cell metabolism. We applied low fluid shear (1 ± 63 Pa for 10 ± 48 h) to human osteoblastic cells (HOB) in vitro to study its impact on cell proliferation and differentiated functions. Proteins involved in translating the physical force into a cellular response were characterised. Low fluid shear stress stimulated proliferation of HOB 1.2-fold when stress was applied intermittently for 24 h. Shear stress also increased differentiated cellular properties such as alkaline phosphatase (ALP) activity (121% of control), fibronectin (FN) and fibronectin receptor (FNR) expression (290 % and 200%, respectively). Prostaglandin E 2 (PGE 2 ) and TGFb1 release into the medium were significantly stimulated when shear stress was applied for 6 ± 12 h and 24 ± 48 h, respectively. TGFb1 + 2 neutralising antibodies or the presence of indomethacine inhibited the mitogenic effect of fluid shear and reduced ALP activity to its control level. Furthermore, TGFb treatment induced a dose-dependent increase in FN and FNR expression. Therefore, fluid shear stress of low magnitude (a) suffices to affect HOB metabolism and (b) regulates anchorage of HOB via FN and FNR by stimulating osteoblastic PGE 2 and TGFb secretion.