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This content is taken from the The University of Sheffield, University of Liverpool, Newcastle University & CIMA (Centre for Research into Muscoskeletal Ageing)'s online course, The Musculoskeletal System: The Science of Staying Active into Old Age. Join the course to learn more.
A graphical representation of a human skull

How do our bones age?

Bone is a living tissue which is constantly remodelling itself. The human skeleton continues to develop after reaching adult height and highest bone mass (density) is attained at around the age of 30. Bone is then lost as part of the normal ageing process at rates between 3-11% per decade.

The major factor leading to bone loss in postmenopausal women is a lower production of hormones. However, other inherent factors of biological sex, genetics and ethnicity can predispose individuals to thinning of bones at a higher rate than normal. Smoking, a diet lacking in nutrients such as calcium and a lack of weight-bearing exercise have similar effects.

The bone loss that occurs with age results in changes to the bone’s structure. There is a thinning of the trabeculae (the thin columns and plates of bone that create a spongy structure inside bone) in both men and women after the age of 30 which is accelerated in women after the menopause. Trabecular bone is important because it gives strength to the bone whilst still maintaining its light weight.

The video below show inside the bone of a young and an old mouse. Notice how the trabeculae have begun to thin in the ageing bone.

This is an additional video, hosted on YouTube.

Later in life, particularly in post-menopausal women, there is also a thinning of the bone cortex and an increase in its porosity. These changes are due to an increased ability of osteoclast to remove bone coupled with a decreased ability of osteoblasts to replace it.

It is not currently known why there are more osteoclasts and less osteoblasts as we age. Recent research has shown that stem cells in bone which are responsible for the production of osteoblasts accumulate DNA damage and become senescent as we get older. Senescence is the process by which cells irreversibly stop dividing and enter a state of permanent growth arrest without undergoing cell death.

This is likely to affect their ability to produce more osteoblasts. Moreover, osteoblasts themselves also accumulate damage in their DNA and become senescent. This is thought to be responsible for the decreased ability to produce new bone.

For example, osteoblasts produce many factors including collagen. Collagen is a protein which is produced by osteoblasts as fibres and, when coupled with minerals, provides bone with its strong structure. Collagen production decreases with age. In addition senescent cells produce many inflammatory factors and these are thought to promote the activity of osteoclasts to remove bone.

All of these changes make the bone more brittle and fragile, increasing the chances of fracture.

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This article is from the free online course:

The Musculoskeletal System: The Science of Staying Active into Old Age

The University of Sheffield