Mitchell B. Schaffler

Mitchell B. Schaffler

Education

B.S., 1978, Stony Brook University (Biological Sciences); Ph.D., 1985, West Virginia University (Anatomy/Orthopaedics); Post-doc, 1987, University of Utah/U.S. Department of Energy (Radiobiology)

Awards & Honors

American Society for Biomechanics, Orthopaedic Research Society, American Society for Bone and Mineral Research, American Association of Anatomists, Sigma Xi, Phi Kappa Phi, AcroMed Award for Outstanding Research, North American Spine, Fellow, American Association of Anatomist, Fellow, American Institute of Medical and Biological Engineering Society, Editorial Boards, Journal of Orthopaedic Research, BONE, Anatomical Record; Grant review panels: NSF, The Wellcome Trust (UK), Medical Research Council (Canada), Orthopaedic Research Society, NIH-National Institute of Arthritis, Musculoskeletal and Skin Diseases

Research Interests

Bone biomechanics, tendon biomechanics, Skeletal fragility and aging, Bone physiology, Osteocyte function, Osteoporosis, Quantitative methods in analysis of skeletal structure

The major research emphasis of the Bone and Joint Laboratory is to understand how skeletal tissues (bone, ligament, tendon, cartilage) develop, maintain and repair themselves in order to meet mechanical demands throughout life. We focus on the cellular and integrative processes that control the architectural features of bone and tendon, and govern how they responds to physical challenges normally and in aging and in diseases such as osteoporosis, genetic defects and diabetes. Our current research efforts focus on fatigue and repair in bone and tendon, with specific emphasis on discovering how living cells in these tissues detect and repair wear and tear damage before it accumulates to the point of mechanical failure. We also examinie how osteocytes (the tissue-resident bone cells) influence bone mechanical function, both directly by modulating local matrix composition, and indirectly by controlling local bone remodeling activities. In related studies, we are examining how osteocytes function as mechanical sensors that allow bone to perceive and react to mechanical loading. Experimental approaches used in the Bone and Joint Laboratory focus on the cell and tissue levels, and include in vivo and tissue mechanical loading studies, mechanical and biomaterials testing, microscopy, microcomputed tomography and secondary harmonic imaging modalities, cell culture and molecular biology.

Selected Publications

Bentolila V., T.M. Boyce, D.P. Fyhrie, T.M. Skerry and M.B. Schaffler. Intracortical remodeling in adult rat long bones after fatigue loading. Bone 23:275-281, 1998.

Boyce, T.M., D.P. Fyhrie, E.L. Radin and M.B. Schaffler. Damage and strain mode associations in human compact bone bending fatigue. Journal of Orthopaedic Research 16:322-329, 1998.

Vashishth D., J. Koontz, S-J Qiu, D Lundin-Cannon, Y.N. Yeni, M.B. Schaffler and D.P. Fyhrie In vivo diffuse damage in human vertebral trabecular bone. Bone 26: 147-152, 2000.

Vashishth D., O. Verborgt, G. Divine, M.B. Schaffler and D.P. Fyhrie Decline in osteocyte lacunar density in human cortical bone is associated with the accumulation of microcracks with age Bone 26:375-380, 2000.

Verborgt O., G.J. Gibson and M.B. Schaffler Loss of osteocyte integrity in association with microdamage and bone remodeling after fatigue in vivo. Journal of Bone and Mineral Research 15: 60-67, 2000.

Schaffler M.B. and K.J Jepsen Fatigue and repair in bone. International Journal of Fatigue 22:839-846, 2000.

You L. S.C. Cowin, M.B. Schaffler and S Weinbaum. A model for strain amplification in the cytoskeleton of osteocytes due to fluid drag on pericellular matrix. Journal of Biomechanics 34:1375-1386, 2001.

Verborgt O., N.A. Tatton, R.J Majeska and M.B. Schaffler. Differential expression of Bax and Bcl-2 in osteocytes after bone fatigue: Complementary roles in bone remodeling regulation? Journal Bone and Mineral Research 17: 907-914, 2002.

Tami A., P. Nasser, O. Verborgt, M.B. Schaffler and M.L. Knothe Tate The role of interstitial fluid flow in the remodeling response to fatigue loading. Journal Bone and Mineral Research 17:2030-2037, 2002.

Akkus, O., A. Polyakova-Akkus, F. Adar and M.B. Schaffler. Aging of microstructural compartments in human compact bone. Journal Bone and Mineral Research 18:1012-1019, 2003.

Schaffler MB. Role of bone turnover in microdamage. Osteoporosis International 14, Suppl 5:73-80, 2003.

Akkus, O., F. Adar and M.B. Schaffler. Age-related changes in physicochemical properties of mineral crystals are related to impaired mechanical function of cortical bone. Bone 34:443-453, 2004.

You, L-D, S. Weinbaum, S.C. Cowin and M.B. Schaffler. Ultrastructure of the osteocyte process. Anatomical Record 278A: 505-513, 2004.

Hernandez, C.J., R.J. Majeska and M.B. Schaffler. Osteocyte density in woven bone. Bone 35:1095-1099, 2004.

Han Y-F, S.C. Cowin, M.B. Schaffler and S. Weinbaum Mechanotransduction and strain amplification in osteocyte cell processes. Proceedings, National Academy of Sciences 101:16689-94, 2004.

Tommasini, S.M,. P. Nasser, M.B. Schaffler and K.J Jepsen. The relationship between bone morphology and bone quality in male tibiae: Implications for stress fracture risk. Journal of Bone and Mineral Research 20: 1372-1380, 2005.

Li, C-Y C. Price; K. Delisser, P. Nasser, D. Laudier, M.O. Clement, K.J. Jepsen and M.B. Schaffler. Long-term disuse osteoporosis appears less sensitive to bisphosphonate treatment than other osteoporosis Journal of Bone and Mineral Research 20:117-124, 2005.

Wang, L, R.J. Majeska, Y. Wang, S. Henderson, Y. Han, S. Weinbaum and M.B. Schaffler. In situ measurement of solute transport in the bone lacunar-canalicular system PNAS 102: 11911-16, 2005.

Li, C.Y, K.J. Jepsen; R.J. Majeska, J. Zhang; R. Ni; B.D. Gelb and M.B. Schaffler. Mice lacking cathepsin K maintain bone remodeling but develop bone fragility despite high bone mass. Journal of Bone and Mineral Research 21: 865-875, 2006.

Wang Y., L. McNamara, M.B. Schaffler and S Weinbaum. A model for the role of integrins in flow induced mechanotransduction in osteocytes. PNAS 104: 15941-46, 2007.

Fung, D.P., V.M. Wang, K.J. Jepsen, M.B. Schaffler and E.L. Flatow. Subrupture tendon fatigue damage. Journal of Orthopaedic Research 27:264-273, 2009.

Cardoso L., B.C. Herman, O. Verborgt, D.M. Laudier, R.J. Majeska and M.B. Schaffler, Osteocyte apoptosis controls activation of intracortical resorption in response to bone fatigue. Journal of Bone and Mineral Research 24:597-605. 2009.

Fung D.T., V.M. Wang, J. Basta-Pljakic, Y. Li, D.M. Laudier, H.B. Sun, K.J. Jepsen, M.B Schaffler and E.L. Flatow. Early response to tendon fatigue damage accumulation in a novel in vivo model. Journal of Biomechanics 43:274-79, 2010.

Fung, D.T., J. Basta-Pljakic, J.B. Sereysky, D.M. Laudier, R. Huq, K.J. Jepsen, M.B. Schaffler and E.L. Flatow. Second harmonic generation imaging and Fourier transform spectral analysis reveal damage in fatigue-loaded tendons. Annals of Biomedical Engineering 38(5):1741-51, 2010.

Gu X.I., D.J. Leong, F. Guzman, R. Mahamud, Y.H. Li, R.J. Majeska, M.B. Schaffler, H.B. Sun and L. Cardoso. Development and validation of a motion and loading system for a rat knee joint in vivo. Annals of Biomedical Engineering 38(3): 621-31, 2010.

Leong, D.J., X.I. Gu, Y. Li, J.Y. Lee, D.M. Laudier, R.J. Majeska, M.B. Schaffler, L. Cardoso and H.B. Sun. Matrix metalloproteinase-3 in articular cartilage Is up-regulated by joint immobilization and suppressed by passive joint motion. Matrix Biology 29(5):420-6, 2010

Herman B.C., L. Cardoso, R.J. Majeska RJ, K.J. Jepsen and M.B. Schaffler. Activation of bone remodeling after fatigue: Differential response to linear microcracks and diffuse damage. Bone. 766-72, 2010.

Kennedy O.D., B.C. Herman , D.M. Laudier, R.J Majeska, H.B. Sun, M.B. Schaffler . . Activation of resorption in fatigue-loaded bone involves both apoptosis and active pro-osteoclastogenic signaling by distinct osteocyte populations. Bone 50(5):1115-22, 2012

Schaffler M.B. and O.D. Kennedy. Osteocytes in bone signaling. Current Osteoporosis Reports 10(2):118-25, 2012

Wu D, Schaffler MB, Weinbaum S, Spray DC. Matrix-dependent adhesion mediates network responses to physiological stimulation of the osteocyte cell process. Proceedings, National Academy of Sciences. 16;110(29):12096-101, 2013.

Mitchell B. Schaffler
CUNY and Wallace Coulter Distinguished Professor of Biomedical Engineering, Chairman, Department of Biomedical Engineering The City College of New York, City University of New York
Steinman Hall 564
212-650-5070
212-650-6727
mschaffler@ccny.cuny.edu
Schaffler Lab [..]