Abstract
In order to determine whether there is a genetic component to hip or knee joint failure due to idiopathic osteoarthritis (OA), we invited patients (probands) undergoing hip or knee arthroplasty for management of idiopathic OA to provide detailed family histories regarding the prevalence of idiopathic OA requiring joint replacement in their siblings. We also invited their spouses to provide detailed family histories about their siblings to serve as a control group. In the probands, we confirmed the diagnosis of idiopathic OA using American College of Rheumatology criteria. The cohorts included the siblings of 635 probands undergoing total hip replacement, the siblings of 486 probands undergoing total knee replacement, and the siblings of 787 spouses. We compared the prevalence of arthroplasty for idiopathic OA among the siblings of the probands with that among the siblings of the spouses, and we used logistic regression to identify independent risk factors for hip and knee arthroplasty in the siblings. Familial aggregation for hip arthroplasty, but not for knee arthroplasty, was observed after controlling for age and sex, suggesting a genetic contribution to end-stage hip OA but not to end-stage knee OA. We conclude that attempts to identify genes that predispose to idiopathic OA resulting in joint failure are more likely to be successful in patients with hip OA than in those with knee OA.
Highlights
Data Hip arthroplasty probands and the total hip replacement (THR) proband sibling cohort We invited 763 individuals who were scheduled for hip arthroplasty to participate in the study, and 710 individuals agreed to participate
In order to evaluate the familial aggregation of hip arthroplasty independent of replacements involving other joints, we excluded from this cohort 75 individuals (10.5%) who were scheduled for hip arthroplasty and had either a history of prior knee arthroplasty or were scheduled for concurrent hip and knee replacement
We sought to determine whether the phenotypic traits of having a hip or knee arthroplasty for idiopathic OA were under genetic influence by comparing the prevalence of arthroplasty in siblings of affected individuals with that in control individuals
Summary
Environmental, hormonal, obesity, mechanical, and genetic factors have been implicated in its onset and progression [1]. OA is clinically heterogeneous because it can affect large or small joints, can be monoarticular or polyarticular, and can be associated with subtle or obvious physical and/or radiographic changes. Substantial efforts have been made to identify factors that can affect the incidence and progression of OA. Mendelian genetic disorders that have precocious joint failure as a component feature are an uncommon cause of OA [3], but their existence suggests that other genetic variants may contribute to common forms. Further evidence supporting a genetic contribution to common OA derives from studies looking at aggregation of OA within families [4,5,6,7,8,9,10] and within ethnic/geographic groups [11,12,13,14], and in twins [15,16,17]
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