Bone remodeling is a complex and critical process for maintaining bone health and preventing age-related diseases like osteoporosis. In silico models are powerful tools for understanding the cellular and protein properties that regulate bone remodeling, especially in aging conditions. For this purpose, we recently established a 3D multiscale micro-MPA model of trabecular bone remodeling using longitudinal in vivo data from PolgA mice, a mouse model of premature aging. Our model includes receptor-ligand kinetics, mechanomics, diffusion, and decay of cytokines that regulate cell behavior. We simulated trabecular bone remodeling in the sixth caudal vertebra of five mice over four weeks and evaluated the static and dynamic morphometry of the trabecular bone microarchitecture. We identified a configuration of the model parameters to simulate homeostatic trabecular bone remodeling, here named basal. Additionally, we produced anabolic, anti-anabolic, catabolic, and anti-catabolic responses with an increase or decrease in the levels of osteoprotegerin (OPG), receptor activator of nuclear factor kB ligand (RANKL), and sclerostin (Scl) produced by the osteocytes. We found that changes in OPG and RANKL levels were positively and negatively correlated with the average trabecular bone volume fraction (BV/TV) values, respectively. Conversely, changes in Scl levels produced small fluctuations in BV/TV in comparison to the basal state. Scl was deemed to be the main driver of equilibrium, while RANKL and OPG were shown to be involved in changes in bone volume fraction with potential relevance for age-related bone features. Moreover, bone remodeling is regulated by the interaction between different cells and tissues across many spatial and temporal scales. However, quantifying cellular and protein properties in vivo, particularly in aging conditions, presents challenges. To address this, we adapted the previously developed micro-MPA model to investigate the effects of aging and mechanical loading on bone remodeling in aging mice using in vivo micro-CT images and micro-FE models. Our results showed that the mechanoregulation of remodeling was altered due to aging, and the anabolic effect of an increase in bone mass with mechanical loading was no longer present in aged mice. We also demonstrated the importance of single-cell mechanomics in simulating bone anabolic response and the disruption of this response with aging. Higher numbers of osteoblasts and mineralization rate along with single-cell mechanomics successfully correctly simulated the anabolic response in young mice, while their disruption led to no anabolic response with loading in aged mice. In summary, our study shows the potential of micro-MPA modeling to advance our understanding of bone remodeling mechanisms in different physiological and age-related conditions and guide the development of new therapies for bone diseases.