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Abstract Number: 926

Does a Family History of Total Knee Replacement for Knee Osteoarthritis Influence Knee Pain and Structural Progression? a Prospective Longitudinal Cohort Study

Feng Pan1, Hussain Khan1, Changhai Ding1, Tania Winzenberg2, Johanne Martel-Pelletier3, Jean-Pierre Pelletier3, Flavia Cicuttini4 and Graeme Jones1, 1Musculoskeletal Unit, Menzies Research Institute Tasmania, University of Tasmania, Hobart,7000, Australia, 2Menzies Research Institute Tasmania, University of Tasmania, Hobart,7000, Australia, 3Osteoarthritis Research Unit, University of Montreal Hospital Research Centre (CRCHUM), Notre-Dame Hospital, Montreal, QC, Canada, 4Department of Epidemiology and Preventive Medicine, School of Public Health and Preventive Medicine, Monash University, Melbourne, Australia

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: genetics, Knee, osteoarthritis and pain

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Session Information

Title: Pain: Basic and Clinical Aspects I

Session Type: Abstract Submissions (ACR)

Background/Purpose: Genetic factors appear to play an important role in the pathogenesis of both knee pain and radiographic osteoarthritis (OA) based on cross-sectional studies but there are limited studies on the role of genetic mechanisms in the development of these factors over time. The aims of this study were to describe whether offspring having at least one parent with a total knee replacement for severe primary knee OA have an increased risk of worsening knee pain and knee structural progression over 8 to 10 years as compared to randomly selected controls with no family history of knee OA.

Methods: A total of 219 participants (mean age 48 years, range 29 to 61) with 115 offspring and 104 controls participated in this study. Knee pain was respectively assessed using a simple knee pain questionnaire at baseline and Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) at 2 years and 10 years. T1 or T2-weighted fat saturated magnetic resonance imaging of the right knee was performed to assess knee cartilage defects, bone marrow lesions (BMLs), meniscal extrusion and tears.

Results: Compared with controls, the prevalence of knee pain for offspring was higher at baseline (45% versus 20%, P <0.001, assessed as yes/no), similar at 2 years (56% versus 54%, P = 0.764, WOMAC >0) and much higher at 10 years (74% versus 54%, P = 0.002, WOMAC >0). Over 8 years, offspring more frequently had an increase in knee pain (66% versus 41% ≥1 point increase, P = 0.003) and in all subscales apart from walking (all P <0.05). In addition, they also had a greater increase in cartilage defect score (1.03 versus 0.52, P =0.007), meniscal extrusion score (0.28 versus 0.10, P = 0.027), and meniscal tear score (0.40 versus 0.10, P = 0.012) in the medial tibiofemoral compartment. No significant difference in BML change was observed. In multivariable analysis, after adjustment for confounders and these structural factors, offspring still had an elevated risk of worsening knee pain (OR = 2.22, 95%CI = 1.17 to 4.22), as well as each subscale apart for walking and standing (OR = 2.01 to 3.36, all P <0.05).

Conclusion: Offspring with family history of knee OA have an increased risk of worsening knee pain and progression of knee cartilage and meniscal pathology but not bony structural changes suggesting that genetic factors may be independently involved in the pathogenesis of knee pain and facets of structural progression. Intriguingly, the change in knee pain was independent of structural factors suggesting this effect is mediated by factors outside the knee.


Disclosure:

F. Pan,
None;

H. Khan,
None;

C. Ding,
None;

T. Winzenberg,
None;

J. Martel-Pelletier,
None;

J. P. Pelletier,
None;

F. Cicuttini,
None;

G. Jones,
None.

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