Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2003 Oct;12 Suppl 2(Suppl 2):S97-S103.
doi: 10.1007/s00586-003-0621-0. Epub 2003 Sep 9.

Biomechanics of the aging spine

Affiliations
Review

Biomechanics of the aging spine

Stephen J Ferguson et al. Eur Spine J. 2003 Oct.

Abstract

The human spine is composed of highly specific tissues and structures, which together provide the extensive range of motion and considerable load carrying capacity required for the physical activities of daily life. Alterations to the form and composition of the individual structures of the spine with increasing age can increase the risk of injury and can have a profound influence on the quality of life. Cancellous bone forms the structural framework of the vertebral body. Individual trabeculae are oriented along the paths of principal forces and play a crucial role in the transfer of the predominantly compressive forces along the spine. Age-related changes to the cancellous core of the vertebra includes a loss of bone mineral density, as well as morphological changes including trabecular thinning, increased intratrabecular spacing, and loss of connectivity between trabeculae. Material and morphological changes may lead to an increased risk of vertebral fracture. The vertebral endplate serves the dual role of containing the adjacent disc and evenly distributing applied loads to the underlying cancellous bone and the cortex of the vertebra. With aging, thinning of the endplate, and loss of bone mineral density increases the risk of endplate fracture. Ossification of the endplate may have consequences for the nutritional supply and hydration of the intervertebral disc. The healthy intervertebral disc provides mobility to the spine and transfers load via hydrostatic pressurization of the hydrated nucleus pulposus. Changes to the tissue properties of the disc, including dehydration and reorganization of the nucleus and stiffening of the annulus fibrosus, markedly alter the mechanics of load transfer in the spine. There is no direct correlation between degenerative changes to the disc and to the adjacent vertebral bodies. Furthermore, advancing age is not the sole factor in the degeneration of the spine. Further study is crucial for understanding the unique biomechanical function of the aging spine.

PubMed Disclaimer

Figures

Fig. 1.
Fig. 1.
Normal (top) and osteoporotic (bottom) vertebral bodies. Decreased structural strength is not only the result of reduced apparent bone density but also changes in the architecture of the trabecular bone. The increase in bone fragility is due to replacement of platelike close trabecular structures with more open, rodlike structures. The more porous cancellous bone appearance is the result of reduced horizontal cross-linking struts
Fig. 2.
Fig. 2.
Spatial distribution of endplate material properties, normalized to maximum values measured. Endplate strength is greatest towards the posterolateral and lowest at the center of the endplate. Regional variation in endplate properties is more pronounced with decreasing bone mineral density. (Adapted from [9])
Fig. 3.
Fig. 3.
Typical stress profiles for grade-1 disc (top) and for a grade 4 disc (bottom). In the healthy disc, a hydrostatic pressure is developed in the nucleus, as indicated by the plateau in the stress plot. For the degenerate disc, nuclear pressure is lower, and stress peaks in the annulus fibrosus are observed. A Anterior; P posterior. (Adapted from [2])

References

    1. Acaroglu Spine. 1995;20:2690. - PubMed
    1. Adams J Bone Joint Surg Br. 1996;78:965. - PubMed
    1. Ayotte J Biomech Eng. 2000;122:587. - PubMed
    1. Brinckmann Spine. 1989;14:606. - PubMed
    1. Cummings Am J Med. 1995;98:24S. - PubMed