A Unified Theory for Strain Related Modeling and Remodeling in Cortical and Trabecular Bone

Introduction: Trabecular bone adapts to external loading conditions in terms of mass and trabecular orientation. Mature trabecular bone is subject to continuous tissue remodeling by BMU’s of osteoblasts and osteoclasts, active mainly at the trabecular surfaces. The regulatory mechanisms that control osteoclast and osteoblast activities in bone modeling (growth or adaptation) and in remodeling (maintenance during adulthood) are not fully understood. It is widely assumed that osteocytes in the bone matrix serve as mechanosensors and send anabolic or catabolic signals through the osteocytic canalicular network to recruit osteoclasts and osteoblasts at the bone surface [1-3]. We have developed a strain based regulation theory for these processes [4]. The purpose of this work was to develop a similar regulatory theory for cortical bone, and to merge both in a ‘unified theory’. For this latter purpose, it turned out, we had to slightly adapt the original trabecular regulatory theory. Cortical bone is filled with osteons or Haversian systems of relatively young bone. These elongated cylindrical structures align to the dominant loading direction [5]. They are created by Basic Multi-cellular Units (BMU’s) that continuously remodel the tissue. In the tip – or cutting cone – of the BMU osteoclasts dig a circular tunnel. They are closely followed by the closing cone, where bone-forming osteoblasts fill the tunnel [6]. We investigated whether the proposed mechanical feedback mechanism based on osteocyte signaling explains: 1) how osteoclasts and osteoblasts shape and adapt the bone at the tissue structural level, relative to the external loads (modeling), and 2) how they collaborate at the BMU-level during remodeling in cortical and in trabecular bone (i.e. whether it explains how osteoclasts find their way in the loading direction and how osteoblast bone formation is coupled).