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The Validity and Heritability of Self-Report Osteoarthritis in an Australian Older Twin Sample

Published online by Cambridge University Press:  21 February 2012

Katherine M. Kirk
Affiliation:
Psychiatry Department, University of Queensland; Genetic Epidemiology, Queensland Institute of Medical Research.
Nicholas Bellamy
Affiliation:
Centre of National Research on Disability and Rehabilitation Medicine (CONROD),The University of Queensland.
Louise E. O'Gorman
Affiliation:
Genetic Epidemiology, Queensland Institute of Medical Research.
Petra M. Kuhnert
Affiliation:
Genetic Epidemiology, Queensland Institute of Medical Research.
Alex Klestov
Affiliation:
Royal Brisbane Hospital.
Ken Muirden
Affiliation:
University of Melbourne.
Paul Tesar
Affiliation:
Royal Brisbane Hospital.
Duncan Walker
Affiliation:
Royal Brisbane Hospital.
Nicholas G. Martin*
Affiliation:
Genetic Epidemiology, Queensland Institute of Medical Research. [email protected]
*
*Address for correspondence: Professor N. Martin, Queensland Institute of Medical Research, PO Royal Brisbane Hospital, Brisbane QLD 4029, Australia.

Abstract

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In order to investigate the genetic and environmental antecedents of osteoarthritis (OA), self-report measures of joint pain, stiffness and swelling were obtained from a popula-tion-based sample of 1242 twin pairs over 50 years of age. In order to provide validation for these self-report measures, a subsample of 118 twin pairs were examined according to the American College of Rheumatology clinical and radiographic criteria for the classification of osteoarthritis. A variety of statistical methods were employed to identify the model derived from self-report variables which would provide optimal prediction of these standardised assessments, and structural equation modelling was used to determine the relative influences of genetic and environmental influences on the development of osteoarthritis. Significant genetic effects were found to contribute to osteoarthritis of the hands, hips and knees in women, with heritability estimates ranging from 30–46% depending on the site. In addition, the additive genetic effects contributing to osteoarthritis in various parts of the body were confirmed to be the same. Statistically significant familial aggregation of osteoarthritis in men was also observed, but it was not possible to determine whether this was due to genetic or shared environmental effects.

Type
Articles
Copyright
Copyright © Cambridge University Press 2002