Transduction of mechanical strain in bone.
One physiologic consequence of extended periods of weightlessness is the rapid loss of bone mass associated with skeletal unloading.  Conversely, mechanical loading has been shown to increase bone formation and stimulate osteoblastic function.  The mechanisms underlying mechanotransduction, or how the osteoblast senses and converts biophysical stimuli into cellular responses has yet to be determined.  For non-innervated mechanosensitive cells like the osteoblast, mechanotransduction can be divided into four distinct phases: 1) mechanocoupling, or the characteristics of the mechanical force applied to the osteoblast, 2) biochemical coupling, or the mechanism through which mechanical strain is transduced into a cellular biochemical signal, 3) transmission of signal from sensor to effector cell and 4) the effector cell response.  This review examines the characteristics of the mechanical strain encountered by osteoblasts, possible biochemical coupling mechanisms, and how the osteoblast responds to mechanical strain.  Differences in osteoblastic responses to mechanical strain are discussed in relation to the types of strain encountered and the possible transduction pathways involved.
Duncan
R L
RL
Department of Orthopaedic Surgery, Physiology and Biophysics, Indiana University Medical Center, Indianapolis 46202, USA.
D000818:Animals; D001696:Biomechanical Phenomena; D018488:Bone Demineralization, Pathologic / Q000503:physiopathology*; D001842:Bone and Bones / Q000166:cytology / Q000502:physiology* / Q000503:physiopathology; D016023:Integrins / Q000502:physiology; D015640:Ion Channel Gating / Q000502:physiology; D010006:Osteoblasts / Q000166:cytology / Q000502:physiology*; D051381:Rats; D015398:Signal Transduction / Q000502:physiology*; D013026:Space Flight; D013314:Stress, Mechanical; D014893:Weightlessness
D016023:Integrins