15:00〜16:00
Speaker: Prof. Taiji Adachi (Kyoto University, Japan)
Title: Structural Optimality in Bone: Modeling Osteocyte Network as a Mechanosensory System
Abstract: Ever since Julius Wolff proposed the Law of Bone Transformation in the 19th century, it has been widely accepted that the bone structure adapts function¬ally to the mechanical environment. There seems to be a mathematical correspondence between bone structure and stress trajectories as if trabecular/osteonal bone remodels toward its optimal structure. However, the mechanism by which bone remodels its microstructure to meet macro¬scopic functional demands as a load- bearing structure is not clear, because of the complex hierarchical system from molecular/cellular to tissue/organ levels with a variety of mechano-biochemical couplings. The process of bone remodeling is regulated by cellular activities. While osteoclasts and osteoblasts are responsible for bone resorption and formation, respectively, activities of these cells are believed to be controlled by a mechanosensory system of osteocytes embedded in the bone matrix. Under dynamic loading, the bone matrix deformation induces fluid flow in the lacuno-canalicular system that stimulates the osteocyte process membrane. In addition, intercellular network in the system may serve as a pathway to deliver mechanical signals to neighboring cells regulating their remodeling activities. Therefore, in this study, focusing on osteocyte mech¬anosensing and communication, we discuss how macroscopic well-organized bone structure is formed from microscopic cellular activities, based on multiscale modeling and simulation. 

16:00〜17:00
Speaker: Prof. Peter Vee Sin Lee (The University of Melbourne, Australia)
Title: Using A Hierarchical Approach to Investigate Cartilage and Subchondral Bone Responses Under Impact Load
Abstract: Osteoarthritis (OA) is a condition affecting the joints, and is a leading cause of chronic pain and disability worldwide. OA leads to cartilage and bone damage and is still not clearly understood. It is well known that micro damage in bone or cartilage due to impact load can trigger bone remodelling. In the repair process, bone resorption and bone formation are closely coupled and well balance. In the OA joint, imbalance can cause articular cartilage thinning. Any attempt to halt the progression of OA through physical rehabilitation or drug therapies, or reparative surgery using new implant materials, will require quantitative knowledge of bone and cartilage micro structure. Our overall focus is therefore to understand the structural integrity of cartilage and bone. We have developed multi-scale techniques to apply physiological loads on cartilage and bone via human motion experiments and mechanical testing systems. Damage to the cartilage and bone was studied using high resolution imaging techniques. In addition, computation models were used to probe the load bearing abilities of cartilage/bone affected by OA, to help advance our understanding of the disease process.