BONE FORMATION AND INHIBITION OF BONE LOSS BY DYNAMIC MUSCLE STIMULATION WITH ALTERED INTERSTITIAL FLUID PRESSURE

摘要

Tissue-level mechanisms and functions, including bone strain and muscle, are the potential key players in bone physiology and adaptation [1,2,3]. However, the mechanisms are not yet fully understood. Exercise such as muscle contraction appears to increase blood flow to the skeletal tissues, i.e., bone and muscle. These evidences imply that bone fluid flow induced by muscle dynamics may be an important role in regulating fluid flow through coupling of muscle and bone via microvascular system. To evaluate the mechanism that mechanical signals regulate skeletal tissue adaptation can potentially contribute to the design of new non-pharmacologic strategy to combat osteoporotic bone loss. Among many signaling candidates, load induced fluid flow in bone has been proposed and demonstrated as a promising regulatory component in the argument of bone adaptation [4]. Microvascular circulations in the skeletal system supply nutrients, oxygen and physiological flow to and move waste from muscle and bone. Exercise such as muscle contraction appears to increase blood flow to the skeletal tissues, i.e., bone and muscle. These evidences imply that bone fluid flow induced by muscle dynamics may play an important role in regulating fluid flow through the microvascular system in the musculo-skeleton. While fluid flow in bone is closely influenced by adjacent musculo-dynamics, evaluation of the interaction between musculo-circulation and fluid flow in bone may strengthen our understanding for the fluid flow mechanism in controlling of such skeletal diseases and developing treatment strategy. We propose that musculo-dynamics induced by physiologic muscle contraction can significantly induce fluid flow and enhance perfusion in bone, which may act as a mediator in initiating and regulating osteonal adaptation. Using oscillatory pressurized marrow fluid flow stimuli, the physiological fluid stimulus was found to initiate new bone formation and reduce intracortical bone porosities caused by disuse, even in the absence of direct tissue strain [4]. The objectives for this work were to evaluate (a) the role of dynamic muscle contraction served as a dynamic pump in regulation of intramedullary pressure (ImP), and (b) the in vivo adaptive response to dynamic skeletal muscle contraction adjacent to bone. We used a hindlimb suspension (HLS) model for this study.