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This review describes the role of bone cells and their surrounding matrix in maintaining bone strength through the process of bone remodeling. Subsequently, this work focusses on how bone formation is guided by mechanical forces and fluid shear stress in particular. It has been demonstrated that mechanical stimulation is an important regulator of bone metabolism. Shear stress generated by interstitial fluid flow in the lacunar-canalicular network influences maintenance and healing of bone tissue. Fluid flow is primarily caused by compressive loading of bone as a result of physical activity. Changes in loading, e.g., due to extended periods of bed rest or microgravity in space are associated with altered bone remodeling and formation in vivo. In vitro, it has been reported that bone cells respond to fluid shear stress by releasing osteogenic signaling factors, such as nitric oxide, and prostaglandins. This work focusses on the application of in vitro models to study the effects of fluid flow on bone cell signaling, collagen deposition, and matrix mineralization. Particular attention is given to in vitro set-ups, which allow long-term cell culture and the application of low fluid shear stress. In addition, this review explores what mechanisms influence the orientation of collagen fibers, which determine the anisotropic properties of bone. A better understanding of these mechanisms could facilitate the design of improved tissue-engineered bone implants or more effective bone disease models.

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Bone regeneration is a common biological process occurring, for example, during fracture healing or osseo-integration of prostheses. Computer simulation of bone regeneration is difficult to carry out because it is a complex sequence of cell-mediated processes regulated by mechanobiological stimuli. An algorithm to predict the time-course of intramembranous and endochondral ossification has been developed. The algorithm assumes that there are precursor cells in the undifferentiated tissue and that these cells differentiate into either fibroblasts (to form fibrous connective tissue), chondrocytes (to form cartilaginous tissue) or osteoblasts (to form bone), based on a combination of biophysical stimuli derived from strain in the collagenous matrix and flow of the interstitial fluid. Both these stimuli are known to deform the precursor cells, and the authors hypothesise that this causes activation of cell differentiation pathways. The observation that precursor cells take time to spread throughout the fracture callus has been included in the algorithm. The algorithm was tested in an investigation of the fracture healing of a long bone using an axi-symmetric finite element model. The spatio-temporal sequence of tissue phenotypes that appear in the course of fracture healing was successfully simulated. Furthermore, the origin of the precursor cells (either surrounding muscle, bone marrow or periosteum) was predicted to have a fundamental effect on the healing pattern and on the rate of reduction of the interfragmentary strain (IFS). The initial IFS = 0.15 drops to 0.01 within seven iterations if cells originated from the surrounding soft tissue, but took more than 50% longer if cells originated in the inner cambium layer of the periosteum, and four times longer if precursor cells originated from the bone marrow only.

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