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Rheumatology Advance Access originally published online on April 12, 2005
Rheumatology 2005 44(6):703-704; doi:10.1093/rheumatology/keh639
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© The Author 2005. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

EDITORIAL

Joint hypermobility in children

H. A. Bird

Academic Unit of Musculoskeletal Medicine, Chapel Allerton Hospital, Leeds, UK

Correspondence to: H. A. Bird, Academic Unit of Musculoskeletal Medicine, Chapel Allerton Hospital, Chapeltown Road, Leeds LS7 4SA, UK. E-mail: howard.bird@leedsth.nhs.uk

The first 150 words of the full text of this article appear below.

The late Dr Barbara Ansell frequently stated that ‘hypermobility is tricky in children’. That joint hypermobility should more frequently occur in children than in adults is undoubted. This is normally attributed to the stabilization of joint collagen that occurs as a result of increased cross-linking between adjacent molecules as disulphide bridges form with ageing. However, this is not the whole picture because most authorities agree that joint laxity increases up to a maximum at the time of adolescence, only decreasing thereafter. Presumably the stretching effect of growth on collagen predominates over decline, additional ‘spurts’ of hypermobility apparently accompanying each of the growth spurts in either sex and the onset of menstruation in females. The first seminal description of hypermobility as a syndrome and frequently recognized as a cause of symptoms, often severe, came from Dr Ansell and her colleagues in 1967 [1]. It has also long been recognized . . . [Full Text of this Article]


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