Qualitatively, the effects of mechanical loading acting onto bone on the bone metabolism are well-known. A certain "normal" load level is needed in order to maintain the amount of bone tissue required for providing a sufficient load-carrying capacity. If the actual load level is too low, bone tissue is lost (leading to thinner and/or more porous bones), whereas additional bone tissue may accumulate if the load level consistently exceeds the normal level. However, the bone research community has been pondering for decades over the question which mechanisms are eventually responsible for this behavior; and in particular which mechanical stimulus is able to steer the biology of bone towards anabolic or catabolic regimes. In this respect, several hypotheses were brought forward - however, their relevance has long remained unclear because of the impossibility of testing them in vivo. This contribution presents continuum microporomechanics-inspired modeling approaches, developed over the past few years, which allow for computing, quantitatively, the magnitudes of several of the proposed mechanobiological stimuli, including mechanical excitation of cells and other biological factors in bone by means of hydrostatic pressure, fluid flow-induced shear stresses, and piezoelectric effects. Rigorously considering to that end the hierarchical organization of bone tissue, it has turned out that hydrostatic pressure appears to be of major importance for the mechanobiology of bone, whereas the other stimuli probably play less prominent roles. Notably, the presented models can be (and have already been) straightforwardly utilized, e.g. for integration in structural simulations of bone organs. This has been recently demonstrated via the European project SGABU, where a publicly accessible computational platform has been developed, integrating micromechanics-based models of biological tissues. The general functioning of this platform is briefly presented as well.