  The mechanical properties of vertebrate bone are largely determined by a
process which involves the complex interplay of three different cell types.
This process is called {\it bone remodeling}, and occurs asynchronously at
multiple sites in the mature skeleton. The cells involved are bone resorbing
osteoclasts, bone matrix producing osteoblasts and mechanosensing osteocytes.
These cells communicate with each other by means of autocrine and paracrine
signaling factors and operate in complex entities, the so-called bone
multicellular units (BMU). To investigate the BMU dynamics in silico, we
develop a novel mathematical model resulting in a system of nonlinear partial
differential equations with time delays. The model describes the osteoblast and
osteoclast populations together with the dynamics of the key messenger molecule
RANKL and its decoy receptor OPG. Scaling theory is used to address parameter
sensitivity and predict the emergence of pathological remodeling regimes. The
model is studied numerically in one and two space dimensions using finite
difference schemes in space and explicit delay equation solvers in time. The
computational results are in agreement with in vivo observations and provide
new insights into the role of the RANKL/OPG pathway in the spatial regulation
of bone remodeling.
