| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Articles in PresS, published online ahead of print December 11, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00234.2002
Submitted on May 21, 2002
Accepted on September 30, 2002
1 Department of Veterinary Basic Science, Royal Veterinary College, London, United Kingdom; University Department of Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom
2 Department of Biology, University of York, York, United Kingdom
3 Department of Veterinary Basic Science, Royal Veterinary College, London, United Kingdom
4 University Department of Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom
* To whom correspondence should be addressed. E-mail: Brendon.Noble{at}ed.ac.uk.
Bone is removed or replaced in defined locations by targeting osteoclasts and osteoblasts in response to its local history of mechanical loading. There is increasing evidence that osteocytes modulate this targeting by their apoptosis, which is associated with locally increased bone resorption. To investigate the role of osteocytes in the control of loading-related modelling or remodelling, we studied the effects on osteocyte viability of short periods of mechanical loading applied to the ulnae of rats. Loading, that produced peak compressive strains of -0.003 or -0.004, was associated with a 78% reduction in the resorption surface at the midshaft. The same loading regimen resulted in a 40% relative reduction in osteocyte apoptosis at the same site 3 days after loading compared with the contralateral side (p=0.01). The proportion of osteocytes that were apoptotic was inversely related to the estimated local strain (P<0.02). In contrast, a single short period of loading resulting in strains of -0.008 engendered both tissue micro damage and subsequent bone remodelling; and was associated with an eight-fold increase in the proportion of apoptotic osteocytes (P=0.02) at 7 days. This increase in osteocyte apoptosis was transient and preceded both intracortical remodelling and death of half of the osteocytes (P<0.01). The data suggest that osteocytes might use their U-shaped survival response to strain as a mechanism to influence bone remodelling. We hypothesise that this relationship reflects a causal mechanism by which osteocyte apoptosis regulates bone's structural architecture.
This article has been cited by other articles:
|
|
 |
|
  C. Dufour, X. Holy, and P. J. Marie Transforming growth factor-{beta} prevents osteoblast apoptosis induced by skeletal unloading via PI3K/Akt, Bcl-2, and phospho-Bad signaling Am J Physiol Endocrinol Metab, April 1, 2008; 294(4): E794 - E801. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Schipani, S. Ferrari, N. S. Datta, L. K. McCauley, A. Vignery, T. Bellido, G. J. Strewler, C. H. Turner, Y. Jiang, and E. Seeman Meeting Report from the 28th Annual Meeting of the American Society for Bone and Mineral Research IBMS BoneKEy, November 1, 2006; 3(11): 14 - 50. [Full Text] [PDF]
|
|
|
|
|
|
L. F. Bonewald Mechanosensation and Transduction in Osteocytes. IBMS BoneKEy, October 1, 2006; 3(10): 7 - 15. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. G. Hazenberg, T. C. Lee, and D. Taylor The Role of Osteocytes in Functional Bone Adaptation IBMS BoneKEy, February 1, 2006; 3(2): 10 - 16. [Full Text] [PDF]
|
|
|
|
|
|
S. C. Manolagas Choreography from the Tomb: An Emerging Role of Dying Osteocytes in the Purposeful, and Perhaps Not So Purposeful, Targeting of Bone Remodeling IBMS BoneKEy, January 1, 2006; 3(1): 5 - 14. [Full Text] [PDF]
|
|
|
|
 |
|
 T. Matsumoto, M. Yoshino, T. Asano, K. Uesugi, M. Todoh, and M. Tanaka Monochromatic synchrotron radiation {micro}CT reveals disuse-mediated canal network rarefaction in cortical bone of growing rat tibiae J Appl Physiol, January 1, 2006; 100(1): 274 - 280. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. I. Plotkin, I. Mathov, J. I. Aguirre, A. M. Parfitt, S. C. Manolagas, and T. Bellido Mechanical stimulation prevents osteocyte apoptosis: requirement of integrins, Src kinases, and ERKs Am J Physiol Cell Physiol, September 1, 2005; 289(3): C633 - C643. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
