Dolan, et al: Hypermobility, OA, and BMD 799
2002-256-1
From the Department of Rheumatology, Queen Elizabeth Hospital; Twin
Research and Genetic Epidemiology Unit, St. Thomas’ Hospital; Whipps
Cross Hospital; and University College London Hospitals, London, UK.
A.L. Dolan, MA, FRCP, Department of Rheumatology, Queen Elizabeth
Hospital; D.J. Hart, PhD; T.D. Spector, MD, FRCP, Twin Research and
Genetic Epidemiology Unit, St. Thomas’Hospital; D.V. Doyle, FRCP,
Whipps Cross Hospital; R. Grahame, MD, FRCP, University College
London Hospitals.
Address reprint requests to Dr. A.L. Dolan, Department of Rheumatology,
Queen Elizabeth Hospital, Stadium Road, London, SE18 4QH, UK.
E-mail: Ldolan@btinternet.com
Submitted March 20, 2002; revision accepted September 19, 2002.
A hypermobile joint is one whose range of movement
exceeds that which is normal for that individual, taking into
consideration age, sex, and ethnic background
1
. A joint’s
range is determined by the tightness or laxity of its liga-
ments, and joint laxity can be considered to be a prerequisite
for hypermobility.
In general, joint laxity is greatest at birth, declining
rapidly through childhood, less rapidly during the teens, and
more slowly during adult life
1
. Females are generally more
lax jointed than males at all ages and there is a wide ethnic
variation. Epidemiological studies using a variety of defini-
tions have suggested hypermobility is seen in up to 10% of
Western populations and may be up to 25% in other racial
groups
2-4
. The extent to which joint hypermobility is symp-
tomatic in the general population is unclear. Many studies of
symptomatic joint hypermobility have been based on clinic
populations, with likely attendant selection bias. In one such
study, 15% of a rheumatology clinic population were hyper-
mobile
5
. The prevalence of hypermobility and its conse-
quences in an older postmenopausal community population
has not previously been studied.
Hypermobility is seen as a common unifying feature in
the hereditary diseases of connective tissue (HDCT) such as
Ehlers Danlos syndrome (EDS)
6
, Marfan’s syndrome
7
, and
osteogenesis imperfecta
8
. It is also recognized as a feature of
the benign joint hypermobility syndrome (BJHS)
9
, said to
exist when a hypermobile joint (or joints) becomes sympto-
matic. It is not known whether women in the community
who manifest osteoarthritis (OA) and/or reduced bone
density have other features to suggest an underlying HDCT.
We examined the occurrence of hypermobility in a
general population to determine whether women with OA or
osteoporosis might share phenotypic features of a genetic
The Relationship of Joint Hypermobility, Bone Mineral
Density, and Osteoarthritis in the General Population:
The Chingford Study
A. LOUISE DOLAN, DEBBIE J. HART, DAVID V. DOYLE, RODNEYGRAHAME, and TIM D. SPECTOR
ABSTRACT. Objective. The prevalence of hypermobility and its consequence in an aging female population is
unknown. Case studies of patients with the benign joint hypermobility syndrome suggest both a
tendency toward osteopenia and an association with premature osteoarthritis (OA). We assessed
hypermobility and its relationship to bone mineral density (BMD) and OA in a postmenopausal
female community population.
Methods. Joint hypermobility was assessed by the Beighton and the (more quantitative)
Contompasis scores in 716 female subjects under followup in the Chingford Study (age range 53–72,
mean 61 yrs, SD 5.8).
Results. We found 79 of 716 subjects (11%) had a hypermobility score > 1/9 on the Beighton scale
(spine in 75/79); 82/716 had a Contompasis score > 22 (normal < 18). Only one had a 4/9 Beighton
score indicative of generalized joint hypermobility. Subjects with Contompasis > 22 were more
physically active and less likely to smoke. They had a reduced risk of knee OA (joint space
narrowing) (OR 0.48, 95% CI 0.27–0.83, after adjusting for age, height, weight, and activity), but
no change in risk of OA in spine or hands. Hip BMD was increased by 3% in this more hypermo-
bile subgroup (p < 0.05). A similar effect was seen for knee OA, but not BMD in those with a
Beighton score > 1.
Conclusion. Our data suggest that in this postmenopausal population the tendency to joint hyper-
mobility may be a marker for fitness, manifested by reduced knee OA and increased hip BMD. The
incidence of generalized hypermobility (Beighton > 4/9) was very low (0.14%) compared with the
localized form (seen in 11%) and other studies. Those with mild degrees of hypermobility showed
no evidence of premature OA or reduced BMD, as reported in some of the rarer heritable disorders
of connective tissue. (J Rheumatol 2003;30:799–803)
Key Indexing Terms:
HYPERMOBILITY OSTEOPOROSIS OSTEOARTHRITIS
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