These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Fatigue microdamage as an essential element of bone mechanics and biology.
    Author: Martin RB.
    Journal: Calcif Tissue Int; 2003 Aug; 73(2):101-7. PubMed ID: 14565590.
    Abstract:
    The fossil record shows that bone remodeling has existed since the earliest large vertebrates became weight-bearing on land, but the functions of remodeling have long been debated. The principal protagonists in this debate have been those favoring a mechanical function and those asserting that remodeling serves to move calcium in and out of the skeleton. In recent years the arguments of the former school have included not only the adaptation of internal structure to specific kinds of stresses, but the need to remove fatigue damage. It has become clear that (1) physiologic strains continually produce fatigue damage in bone; (2) this damage weakens bone and is associated with both osteocyte apoptosis and the activation of remodeling; and (3) remodeling is the only means by which this damage can be removed. The significance of these observations is increased by the fact that fatigue failure is more likely in larger structures. This "volume effect," along with the advantages of enhanced mobility and metabolic efficiency, may have selected for bone remodeling as a means of controlling fatigue damage as it occurs, allowing larger vertebrates to maintain a relatively light skeleton over an extended lifetime. In this view, bone remodeling is not primarily a mechanism for calcium transport, but is intimately related to other inflammatory repair responses.
    [Abstract] [Full Text] [Related] [New Search]