Mitchell B Schaffler, PhD
- ADJUNCT PROFESSOR | Orthopaedics
Skeletal biology, biomechanics, aging and skeletal fragility, and osteoporosis
Students: MSTP: Brad Herman, Kemesha Delisser
Postdoctoral Fellows: Vincent Wang, Luis Cardoso-Landa, Laoise McNamara
In order to maintain structural and functional integrity under the demands of mechanical usage, skeletal tissues (bone, cartilage, ligament, tendon) must develop and continually adapt throughout life to the rigors of those mechanical demands. Our research examines cellular and tissue processes underlying adaptations of skeletal tissues to mechanical usage and the mechanisms by which failures of those adaptive processes lead to skeletal disease. Specifically, we use a combination of quantitative morphological, histomorphometric and molecular techniques to examine:\r\n
Detection and repair of microscopic injury in the skeleton
These studies examine mechanisms by which repetitive mechanical use damages bone and tendon at the microscopic level and living cells detect and repair such wear and tear damage before it accumulates to the point of causing fracture.
Aging and skeletal fragility
Microscopic damage accumulates in human skeletal tissue with increasing age, contributing to the increased fragility of the aging skeletal tissues. Cellular, matrix composition and biomechanical studies are ongoing to determine the extent to which cellular factors versus changes in bone matrix composition and susceptibility to mechanical damage contribute to the functional deterioration of skeletal tissues with age.
Bone loss in space and in aging
Our studies of disuse osteoporosis reveal that this bone loss occurs through similar bone cellular and architectural processes as post-menopausal osteoporosis. These studies are also helping us to understand which features of bone's microarchitecture are critical for maintaining bone strength in osteoporosis. Based on this understanding of bone architecture, we are working to develop technologies to non-invasively examine bone strength and architecture.
Bentolila V, Boyce TM, Fyhrie DP, Skerry TM, Schaffler MB. Intracortical remodeling in adult rat long bones after fatigue loading. Bone 1998; 23: 275-281.
Vashishth D, Verborgt O, Divine G, Schaffler MB, Fyhrie DP. Decline in osteocyte lacunar density in human cortical bone is associated with the accumulation of microcracks with age. Bone 2000; 26: 375-380.
Verborgt O, Gibson GJ, Schaffler MB. Loss of osteocyte integrity in association with microdamage and bone remodeling after fatigue in vivo. J Bone Miner Res 2000; 15: 60-67.
Hausman MR, Schaffler MB, Majeska RJ. Prevention of fracture healing by inhibition of angiogenesis. Bone 2001; 29: 560-564.
You LC, Cowin SC, Schaffler MB, Weinbaum S. A model for strain amplification in the cytoskeleton of osteocytes due to fluid drag on pericellular matrix. Journal of Biomechanics 2001; 34: 1375-1386.
Verborgt O, Tatton NA, Majeska RJ, Schaffler MB. Differential expression of Bax and Bcl-2 in osteocytes after bone fatigue: Complementary roles in bone remodeling regulation. Journal Bone and Mineral Research 2002; 17: 907-914.
Schaffler MB. Role of bone turnover in microdamage. Osteoporosis Int 2003; 14(Suppl 5): 73-80.
Akkus O, Polyakova-Akkus A, Adar F, Schaffler MB. Aging of microstructural compartments in human compact bone. J Bone Miner Res 2003; 18: 1012-1019.
Akkus O, Adar F, Schaffler MB. Age-related changes in physicochemical properties of mineral crystals are related to impaired mechanical function of cortical bone. Bone 2004; 34: 443-453.
You LD, Weinbaum S, Cowin SC, Schaffler MB. Ultrastructure of the osteocyte process. Anatomical Record 2004; 278A(2): 505-513.