Abstract / Summary
Fluid shear stress is increasingly recognized as a central regulator of bone remodeling, with osteoblasts and periosteal progenitor cells responding to shear by increasing proliferation, differentiation, and osteogenic activity. Current models attribute this shear stress primarily to deformation-induced fluid flow generated within bone. Here I propose a complementary mechanism. I hypothesize that cyclic fluctuations in skeletal muscle compartment pressure, together with gravity-dependent fascial tension, generate pressure gradients that drive interstitial fluid flow along periosteal surfaces, producing shear stress that acts directly on periosteal osteogenic cells. Under this model, skeletal muscle is not only a force-generating organ but also a pressure-generating organ that maintains tissue fluid exchange, and bone remodeling is viewed not merely as a response to mechanical loading but as a consequence of pressure-driven fluid dynamics. Because muscle fascia, periosteum, and surrounding connective tissue form a mechanically continuous system, compartmental pressure changes may be transmitted to periosteal tissues even during low-intensity activity and rest. The hypothesis does not contradict the classical lacunar-canalicular mechanotransduction model but offers an additional, more continuous source of periosteal flow. It generates testable predictions and provides a unifying framework for the osteogenic effects of intermittent pneumatic compression, fracture healing, immobilization-induced bone loss, and microgravity-associated osteoporosis. If confirmed, the framework would reframe pressure oscillation, rather than skeletal strain alone, as a therapeutic target for preserving bone mass.