Trabecular-bone adaptation (TBA) is a continuous process that adjusts trabecular morphology in response to external loading. The external loading is sensed by osteocytes through multiple pathways, resulting in different mechanical stimuli. While the strain energy density (SED)-based measures and flow-related cues were both widely discussed [1], the coupled in silico assessment of solid and fluid stimuli at the single-trabecula scale remains underexplored, particularly considering separately the deviatoric and hydrostatic components of SED. The former component represents matrix distortion, while the latter correlates with deformation-induced fluid pumping. Applying the distinct calculation rules to the deviatoric and hydrostatic components within the bone matrix, and linking the hydrostatic response to an implicit flow proxy, provide a route to bridge solid- and fluid-based remodelling stimuli within a single framework. This study introduces a 3D finite-element trabecular-adaptation framework combining a mechanostat gate with a stimulus non-uniformity rule and extends it with an implicit fluid flow channel to represent osteocyte’s flow sensitivity. The framework is implemented in ABAQUS using user-defined subroutines to simulate trabecular evolution under compressive loading. Solid stimuli are quantified using decomposed SED components, while the fluid stimulus is represented by a flow proxy obtained from a coupled pore-pressure–displacement formulation with effective lacunar–canalicular permeability [2]. The evolving microstructure is characterised using standard trabecular morphometric parameters. The obtained results demonstrate that including a fluid flow channel redistributes remodelling activity towards the regions with elevated flow proxies and alters the final mass distribution compared to the solid-only simulations, while preserving the distinct trends associated with deviatoric and hydrostatic SED contributions. This work provides a systematic route to integrate decomposed solid stimuli and flow-related osteocyte sensing into microscale TBA simulations, revealing the joint remodelling mechanism driven by solid and fluid stimuli.