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Modeling Musculoskeletal Mechanobiology
Sandra Shefelbine, Northeastern University Chair: Shu-Wei Chang Time: 2019/12/19 13:20-14:00 (101C, 1F, TICC) |
Abstact:
The musculoskeletal system has the unique ability to sense and respond to mechanical stimuli. As mechanical loading increases, bone formation occurs in order to make the bone stronger. We use a combination of experiments and computational modeling to understand mechano-adaptation during joint formation, skeletal growth and aging.
Joint morphogenesis occurs early in development and is regulated by biological and mechanical factors. We use limb regeneration in an axolotl salamander to determine the effects of mechanical forces on joint formation. By modeling the forces and biochemical signaling we simulate the effect of mechanical stresses on joint development and validate our models with experimental results of joint shape and cellular expression. This project links tissue level stresses with cellular biochemical signaling in a multi-scale model of joint morphogenesis.
During post-natal growth the skeletal system is particularly responsive to mechanical forces, and bone deformities result when the loading is significantly altered. For example in children with cerebral palsy walk with an altered gait and have multiple bony deformities. We use musculoskeletal modeling to determine joint and muscle forces during gait and finite element modeling to determine tissue stresses and predict growth patterns. Understanding the loading patterns that are necessary for healthy bone growth will help therapists develop appropriate physical therapy regimes. In aging, the skeleton becomes less responsive to mechanical loading. We use a murine tibial loading model to explore how we can reactivate mechanosensitivity in the aged skeleton. Finite element modeling allows us to compare physical stimuli in the bone with regions of bone formation and to design loading regimes that are appropriate to stimulate old bone.
Understanding how bones respond to load provides new avenues for therapy to treat bone pathologies. Eventually we may be able to direct bone to form where it is needed with appropriate loading regimes.
The musculoskeletal system has the unique ability to sense and respond to mechanical stimuli. As mechanical loading increases, bone formation occurs in order to make the bone stronger. We use a combination of experiments and computational modeling to understand mechano-adaptation during joint formation, skeletal growth and aging.
Joint morphogenesis occurs early in development and is regulated by biological and mechanical factors. We use limb regeneration in an axolotl salamander to determine the effects of mechanical forces on joint formation. By modeling the forces and biochemical signaling we simulate the effect of mechanical stresses on joint development and validate our models with experimental results of joint shape and cellular expression. This project links tissue level stresses with cellular biochemical signaling in a multi-scale model of joint morphogenesis.
During post-natal growth the skeletal system is particularly responsive to mechanical forces, and bone deformities result when the loading is significantly altered. For example in children with cerebral palsy walk with an altered gait and have multiple bony deformities. We use musculoskeletal modeling to determine joint and muscle forces during gait and finite element modeling to determine tissue stresses and predict growth patterns. Understanding the loading patterns that are necessary for healthy bone growth will help therapists develop appropriate physical therapy regimes. In aging, the skeleton becomes less responsive to mechanical loading. We use a murine tibial loading model to explore how we can reactivate mechanosensitivity in the aged skeleton. Finite element modeling allows us to compare physical stimuli in the bone with regions of bone formation and to design loading regimes that are appropriate to stimulate old bone.
Understanding how bones respond to load provides new avenues for therapy to treat bone pathologies. Eventually we may be able to direct bone to form where it is needed with appropriate loading regimes.
