Display Settings:

Format

Send to:

Choose Destination
See comment in PubMed Commons below
Calcif Tissue Int. 1993;53 Suppl 1:S121-5; discussion S125-6.

Vertebral structure and strength in vivo and in vitro.

Author information

  • Department of Connective Tissue Biology, University of Aarhus, Denmark.

Abstract

The incidence of vertebral fragility fractures has increased 2-4-fold during the past 30 years and the rate of increase is the same for both men and women. To arrest or reverse this increase, thorough understanding of normal, age-related changes in bone structure and strength is crucial. The human vertebral body is constructed to provide maximum strength with minimum bone mass. The strength is the sum of bone size, cortical thickness, trabecular architecture, and bone mass. With age, all these factors change due to the remodeling process, but the decline in bone strength is much more pronounced than the decline in mass. In individuals with very low bone mass, this discrepancy between mass and strength is even more marked. Structural studies have all shown a disruption of the trabecular network with age--mainly caused by perforation of horizontal supporting struts. These changes begin in the vertebral center. Later, a decline in cortical thickness is disclosed. The biomechanical consequence of this is a 4-6-fold decrease in vertebral strength during normal aging. As the structural changes cannot be reversed, it is difficult to increase bone strength by therapeutic regimens. Focus should therefore be placed on prevention. Three avenues are suggested: (1) to use the vast amount of existing biological data in a computer model to increase the understanding of the relationship among bone structure, mass, and strength, and to help identify the intervention regimens offering the best prospects of success; (2) to investigate characteristics of load-bearing trabecular bone that does not fracture; and (3) to focus more on life-style factors.

PMID:
8275365
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Write to the Help Desk