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How do our tendons age?

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© University of Liverpool/The University of Sheffield/Newcastle University
Tendons are bands of fibrous tissue which bind muscle to bone. They are designed to withstand bending, stretching and twisting, but can become injured due to a combination of factors including the effects of ageing, repetitive exercise and inflammation.
Persistent tendon diseases are highly incapacitating and increasingly frequent, accounting for a third of all GP consultations in the UK. Tendon disease of the shoulder is most frequent at 50 years of age and increases with age; Achilles tendon disease is most commonly observed in middle age; in people’s 40s and 50s.
Tendon can become damaged due to repetitive stressful movements and with increasing age when tendons lose their elasticity. It is not known exactly what causes this loss of elasticity. The structure and function of a tendon depend on the maintenance of cells called tenocytes and the production of extracellular matrix molecules; such as collagens and proteoglycans within the tendon tissue. These are produced by the tenocytes and give the tendon its elastic properties.
Recent research suggests that age-related changes occur at specific locations within the tendon which may be overlooked by measuring properties of the whole tendon.
For example, we recently conducted a study with young and old horses which are good models for studying tendons in humans. We investigated two substructural locations and found that with ageing, there were differences in the types of proteins produced in specific locations of the tendons
A graphical representation of a tendon which shows how the tendon is made up of different layers. These layers are called (starting with the smallest and working up to the largest) Tropocollagen, microfibril, fribil, crimping, fibre, crimp waveform, tenocyte, fascicle, interfascicular matrix and endotendon. The substructure of a tendon
A number of other mechanisms may contribute to tendon change with age. Stem cells which produce the tendon cells may become less good at doing so. In addition, tendon cells themselves become senescent. This causes a failure of the cells to divide and to produce more cells. In addition, senescent cells secrete inflammatory factors which may harm the structure of the tendons.
Aged cells may also produce more reactive oxygen species. These are highly reactive molecules which contain oxygen. They are part of the natural defenses of our immune system but can have a negative effect on a tissue if they are produced in excess.
More research in this area is needed to find new interventions for diseases of tendons.
© University of Liverpool/The University of Sheffield/Newcastle University
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The Musculoskeletal System: The Science of Staying Active into Old Age

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