Matthew Silva, PhD
Julia and Walter R. Peterson Orthopaedic Research Professor
- Phone: 314-747-3772
- Fax: Institute of Health | 11th floor | #11619
- Email: firstname.lastname@example.org
Department of Orthopaedics
Post-Doctoral Research Associate
The Silva lab in the Department of Orthopaedic Surgery at Washington University School in St Louis has an opening for a post-doctoral research associate in the field of Skeletal Mechanobiology & Osteoporosis. The associate will work on studies that utilize mice to study how mechanical loading stimulates bone formation, and how to enhance the response to loading in conditions of osteoporosis and aging.
You will join a multidisciplinary orthopaedic research laboratory, part of the dynamic community of the Washington University Musculoskeletal Research Center (https://musculoskeletal.wustl.edu).
Our focus is bone. Bone is a living material filled with cells that, when healthy, allow the skeleton to adapt to its physical loading environment, maintain itself over 70+ years of use, and self-repair after injury. Despite these remarkable qualities, with advancing age the skeleton’s abilities to respond to physical stimuli and to self-repair are diminished. Many people suffer from age-related osteoporosis – a loss of bone mass that leads to weak bones and a high risk of fracture. In fact, after age 50, one-half of women and one-quarter of men will suffer an osteoporotic fracture in their remaining lifetime, significantly diminishing quality of life and often lifespan. We are motivated by the problems of diminished bone mass and strength with age/osteoporosis, and by the negative influence of age on bone’s ability to respond to mechanical stimuli and to self-repair. We use approaches rooted in biomechanics, mechanobiology and bone biology to address these problems.
Our lab focuses on two main questions. 1) How does mechanical loading stimulate bone formation? Mechanical (physical) loading is a powerful stimulus to increase bone formation, whereby new layers of bone tissue are added onto existing bone surfaces, resulting in increased bone mass and strength. But the mechanisms for how the skeleton converts a mechanical stimulus to increased bone formation are not fully understood. We are studying the origin of the bone-forming cells (osteoblasts) and the role of the Wnt signaling pathway in loading-induced bone formation. We are also studying how aging affects each of these processes. The second question is: 2) How do bones heal after injury? The skeleton has a tremendous capacity for self-repair after stress fracture and full fracture. But under some conditions the native ability for repair is inadequate and a surgical intervention is required. Stress fractures heal by a combination of internal remodeling and external woven bone formation, also known as periosteal hard callus. Full fractures heal by these processes plus the formation of a temporary cartilage (soft) callus that is eventually replaced by bone. We are studying the role of bone cells in coordinating the complex fracture healing response, which also involves immune cells and the formation of new blood vessels (angiogenesis).
By studying how the skeleton responds to mechanical stimulation and how it heals after injury, we aim to contribute to the discovery of new approaches to treat reduced bone mass and strength in aging/osteoporosis, and to enhance bone repair in patients who suffer from non-healing fractures.