Osteoporosis features reduced bone mass and damaged microarchitecture, yet some individuals sustain fragility fractures despite normal bone mineral density (BMD), showing that BMD alone cannot capture fracture resistance. Bone strength is governed by bone quality, integrating mass, microarchitecture, matrix material properties, and osteocyte activity. The osteocyte lacunar–canalicular network (LCN) is the central microanatomical pathway for mechanotransduction and metabolic exchange: it converts mechanical loading into interstitial fluid–flow–mediated cues and propagates signals that tune bone formation and resorption. Studies indicate that aging and disease can reduce LCN connectivity and disturb its geometry, leading to inefficient transport and blunted cellular responses; consequently, microdamage repair and mechanical adaptation decline even when bone mass appears preserved. This review summarizes LCN-centered, multi-physics mechanisms underlying osteoporosis heterogeneity and highlights opportunities for improved risk stratification and targeted interventions.