Last year marked the 80th anniversary of the first report of an association between hypermobility and articular manifestations by Finkelstein1 and this year the 30th anniversary since the definitive description of the hypermobility syndrome (HMS) by Kirk, et al.2 In the years since these landmark publications much has been written about hypermobility and reports can broadly be categorised as those dealing with its epidemiology, measurement, clinical associations, and the mechanisms causing them. Despite this our understanding of the role of hypermobility in articular and extra-articular manifestations remains confused. Agreement on a standard method of measurement has yet to be reached and proposed associations continue to be debated. It is perhaps timely to review the current status in the light of the conflicting reports, to highlight the importance of consistency in measurement and methodology so that valid comparisons can be made between studies, and to speculate on new developments that may play a part in unravelling the confusion that presently exists.

Investigation of the clinical relevance of hypermobility has to take into account that it can be generalised^2 3 or localised,4-7 genetically determined⁸ or acquired.9 ,10 It is also influenced by age,3 ,4 ,7 ,11-13 sex,3 ,12-16 and ethnicity,3 ,5 ,6 ,14 and some diseases such as acromegaly, hyperparathyroidism, and rheumatic fever are thought to predispose to joint laxity.9 While the majority of hypermobile people suffer no ill effects^5 8 some will develop features of HMS. In young children hypermobility is so common as to be of little predictive value in determining who will develop HMS.17Mobility decreases with age and introduces the problem of defining cut off points for different age groups. There are pronounced ethnic differences in the frequency of hypermobility …