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PAPERS: Peter Lanyon, Kenneth Muir, Sally Doherty, and Michael Doherty Assessment of a genetic contribution to osteoarthritis of the hip: sibling study BMJ 2000; 321: 1179-1183 [Abstract] [Full text]

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Genetic Link to Hip Osteoarthritis

Iain Chambers   (22 November 2000)

Assessment of a genetic contribution to osteoarthritis of the hip

John Lourie   (8 December 2000)

Genetic Link to Hip Osteoarthritis 22 November 2000
Iain Chambers Send response to journal: Re: Genetic Link to Hip Osteoarthritis	Editor - I read the article by Lanyon and colleagues initially with great enthusiasm, relating to the implication of genetic factors in hip osteoarthritis1. However, I am uncertain just how ethical it is to subject more than 600 healthy participants (siblings of their original cohort) to pelvic radiographs. The authors' only purpose of using radiographs was as a diagnostic tool. Rather than this, clinical examination using the Harris Hip Score would have more accurately obtained the diagnosis with the addition of information concerning loss of function and disease severity. Examination of the patient would have detected and excluded those patients with rheumatoid arthritis. Despite the use of radiographs in this study, a great opportunity was missed: no information concerning the morphology of the hip joints was given. It would have been fascinating to measure the degree of femoral head cover (CE angle), angle of acetabular inclination and femoral shaft offset, which govern the magnitude and direction of forces and degree of pressure concentration in the joint. Such morphological differences exist between races and are believed to account for differences in prevalence of OA and hip dysplasia2. If Lanyon and colleagues had undertaken a morphological analysis, finding no significant variations between the study and control groups (presuming a similar racial breakdown in both groups, although this information is not given), then rather than biomechanical and morphological factors being responsible, articular collagen composition (ie. biochemical factors) may be implicated. Obviously if collagen composition predominates in influencing susceptibility then this may focus treatment approaches in the future. Unfortunately the study only succeeds in measuring the point prevalence of OA in two selected groups, a figure more easily obtained by simply comparing the rate of total hip replacement between them. Did the ethics committee consult advice from specialists in musculoskeletal medicine before approval? References 1. Lanyon P et al. Assessment of a genetic contribution to osteoarthritis of the hip: sibling study. BMJ 2000; 321:1179-83. 2. Fuji G, Funayama K, Benson M. Radiological measurement of the hip joint: comparison between Japanese and British. British and Japanese Orthopaedic Associations Combined Congress, London, 3-6 Oct 2000. Iain Chambers Hip Research Fellow Department of Orthopaedics, Queen Elizabeth Hospital, Gateshead NE9 6SX. No competing interests. Correspondence to: Iain Chambers FRCS, 18 Cloverdale Gardens, High Heaton, Newcastle upon Tyne NE7 7QJ.
Assessment of a genetic contribution to osteoarthritis of the hip 8 December 2000
John Lourie, Consultant Orthopaedic Surgeon Saxon Clinic, Milton Keynes Send response to journal: Re: Assessment of a genetic contribution to osteoarthritis of the hip	The paper by Lanyon and colleagues1 adds further weight to the genetic contribution to "primary" osteoarthritis of the hip. In a 1983 study2 of 341 such patients of both sexes aged 39-86 undergoing total hip replacement in Oxford, matched with a control population of 7072 blood donors from the same geographical catchment area, the relative frequencies of blood groups O and A were found to be reversed in the two groups, Group A being commoner than Group O in the osteoarthritis patients. When Group O phenotype frequencies were compared with "non-O" (i.e. A, B and AB), patients and controls differed significantly (chi-squared = 3.87). All patients had radiological evidence of degenerative arthritis, with confirmatory histological evidence from examination of the excised femoral heads. All individuals within this clearly defined group were included, as blood was routinely taken for cross-matching pre-operatively in all cases. Lanyon and colleagues included both primary and revision hip replacement patients in their study population, whose composition also depended on response to a questionnaire. While their index participants were a comparable group to those in the above blood group study, their sibling and urography groups were only defined by radiographic and not clinical evidence of arthritis. Numerous insults to the hip such as trauma, infection, avascularity, rheumatoid disease, or congenital abnormality are known precursors of "secondary" arthritis. Such histories were excluded in the blood group study population. The pathogenesis of "primary" osteoarthritis of the hip remains elusive. Biochemical variations in cartilage metabolism under genetic control may be responsible for susceptibility to arthritic change in certain individuals, and the factors underlying the ABO polymorphism play a fundamental role in the organisation of cell membranes. Further large-scale studies will provide more information about the genetic contribution to this common condition, but populations must be carefully specified to include only those in whom there is no known predisposing factor for arthritis, and who have clinical (and ideally histolgical) as well as radiographic evidence of the disease. 1 Lanyon P, Muir K, Doherty S, Doherty M. Assessment of a genetic contribution to osteoarthritis of the hip: sibling study. BMJ 2000; 321:479-83 (11 November). 2 Lourie JA. Is there an association between ABO blood groups and primary osteoarthrosis of the hip? Ann Hum Biol 1983; 10:381-4.