Gregory Wohl, McMaster University
Department of Mechanical Engineering
Professor
Hamilton, Ontario
wohlg@mcmaster.ca
Office:
(905) 525-9140 ext. 21195
Expert In
Bio/Research
As part of my research, I am interested in the biological mechanisms that mediate bone formation in response to loading and injury. Mechanical stimuli (e.g., exercise) can induce bone formation (osteogenesis). Osteogenesis in response to moderate bone loading results in a highly organized, aniso...
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Bio/Research
As part of my research, I am interested in the biological mechanisms that mediate bone formation in response to loading and injury. Mechanical stimuli (e.g., exercise) can induce bone formation (osteogenesis). Osteogenesis in response to moderate bone loading results in a highly organized, anisotropic, “lamellar” bone structure that can modestly increase bone structural strength. In comparison, osteogenesis in response to mechanical fatigue injury and stress fractures can take the form of disorganized “woven” bone. In athletes and soldiers, long distance running or marching causes a cyclic loading of bones in the foot and leg and can induce fatigue damage including formation of cracks in the bone matrix. Unlike endochondral bone formation in fracture repair, which forms by calcification of an initial cartilage callous, the woven bone following fatigue injury is intramembranous in nature and forms rapidly without the need of a callous. Although the woven bone is a relatively “poor” material, the repair process is much faster than lamellar bone formation, and structural integrity of the bone can be rapidly restored. Molecular biology techniques such as quantitative real-time polymerase chain reaction (RT-qPCR) and in-situ hybridization are used to characterize gene expression associated with bone biological repair following mechanical loading and fatigue injury. The influence of genes on bone repair will be further explored by inhibiting molecular pathways (e.g., angiogenesis or Hedgehog signaling), and using transgenic or conditional knock-out models. Understanding the molecular mechanisms of bone adaptation will serve as a basis for development of novel strategies to enhance tissue engineering and the development of therapies to promote bone formation in patients at risk for skeletal fragility fractures.
I am also interested in the role of nutrition on bone adaptation. For example, dietary fatty acids can affect the mechanical properties of bone and can also alter the ability of bone cells to respond to mechanical stimuli through activation of synthetic molecules (e.g., prostanoids). Prostaglandins (PGs) play a role in bone formation and remodeling and are synthesized through cyclo-oxygenase-2 (Cox2) from fatty acids stored locally in the cells. Diet can influence the type of fatty acids stored in the cells. The consumption of saturated fatty acids (e.g., from animal fats) can alter the cellular balance of unsaturated fatty acids such as n-3 (e.g., fish oils) and n-6 (e.g., soybean and sunflower oils), and can impair the production of prostaglandins in response to injury or mechanical stimuli. High-fat diets of Western cultures with an emphasis on saturated fats may play a role in increased incidence of age-related metabolic bone disease (e.g., osteoporosis). In the aging skeleton, an inhibited cellular response to mechanical loading might exacerbate the age-related decline in bone mass and contribute to skeletal fragility.
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I am also interested in the role of nutrition on bone adaptation. For example, dietary fatty acids can affect the mechanical properties of bone and can also alter the ability of bone cells to respond to mechanical stimuli through activation of synthetic molecules (e.g., prostanoids). Prostaglandins (PGs) play a role in bone formation and remodeling and are synthesized through cyclo-oxygenase-2 (Cox2) from fatty acids stored locally in the cells. Diet can influence the type of fatty acids stored in the cells. The consumption of saturated fatty acids (e.g., from animal fats) can alter the cellular balance of unsaturated fatty acids such as n-3 (e.g., fish oils) and n-6 (e.g., soybean and sunflower oils), and can impair the production of prostaglandins in response to injury or mechanical stimuli. High-fat diets of Western cultures with an emphasis on saturated fats may play a role in increased incidence of age-related metabolic bone disease (e.g., osteoporosis). In the aging skeleton, an inhibited cellular response to mechanical loading might exacerbate the age-related decline in bone mass and contribute to skeletal fragility.
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