Advanced prostate, breast, and lung cancer can metastasise to bone. In pathological bone, the highly regulated bone remodelling signalling pathway is disrupted leading to irregular bone formation. A particularly painful symptom is net bone formation in some regions and simultaneous weakening in other areas. We present a stochastic agent-based model for bone formation incorporating osteoblasts (bone secreting cells) and dendritic osteocytes (bone regulatory cells). The dendritic osteocytes form a spatial network allowing communication between osteocytes and the osteoblasts located on the bone surface. This communication network facilitates coordinated bone formation. In the presence of a cancerous microenvironment, the morphology of this network changes. Commonly osteocytes appear to be either overdifferentiated (i.e., there are more dendrites) or underdeveloped (i.e., dendrites do not fully form). Our model both allows for the simulation of our spatial network model and analysis of mean-field equations in the form of integro-partial differential equations. We consider variations of our model to test specific physiological hypotheses related to osteoblast differentiation. We can therefore predict how changing measurable biological parameters, such as rates of bone secretion, rates of dendrite growth and rates of osteoblast differentiation can allow for qualitatively different network morphologies. We also plan to use experimental data in the form of pathology slides and suggest driver mutations that may result in the observed network morphology.