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General Orthopaedics

ADIPOKINE PROFILE OF SYNOVIAL FLUID IN END-STAGE KNEE OSTEOARTHRITIS: AN INVESTIGATION ACROSS RACIAL GROUPS

Canadian Orthopaedic Association (COA) and Canadian Orthopaedic Research Society (CORS) Annual Meeting, June 2016; PART 1.



Abstract

In addition to mechanical stresses, an inflammatory mediated association between obesity and knee osteoarthritis (OA) is increasingly being recognised. Adipokines, such as adiponectin and leptin, have been postulated as likely mediators. Clinical and epidemiological differences in OA by race have been reported. What contributes to these differences is not well understood. In this study, we examined the profile of adipokines in knee synovial fluid (SF) and the gene expression profile of the infra-patellar fat pad (IFP) by race among patients with end-stage knee OA scheduled for knee arthroplasty.

Age, sex, weight and height (used to derive body mass index (BMI)) and race (White, Asian and Black) were elicited through self-report questionnaire prior to surgery. SF and IFP samples were collected at the time of surgery. Adipokines (adiponectin and leptin) were examined in the SF using MAGPIX Multiplex platform. IFP was profiled using Human Adipogenesis PCRArray and genes of interest were further validated via quantitative relative RT-PCR using Student's t-test. Overall differences in adiponectin and leptin concentrations were tested across race. Linear regression modeling was used to investigate the association between adiponectin and leptin concentrations (outcomes) and race (predictor; referent group: White), adjusting for age, sex and BMI.

67 patients (18 White, 33 Asian, 16 Black) were included. Mean SF adiponectin concentration was greatest in Whites (1175.05 ng/mL), followed by Blacks (868.53 ng/mL) and Asians (702.23 ng/mL) (p=0.034). The mean SF leptin concentration was highest in Blacks (44.88 ng/mL), followed by Whites (29.86 ng/mL) and Asians (20.18 ng/mL) (p=0.021). Regression analysis showed Asians had significantly lower adiponectin concentrations compared to Whites (p<0.05). However, leptin concentrations did not differ significantly by race after adjusting for covariates. Testing of the IFP, using the Adipogenesis PCRArray, showed significant higher expression of LEP gene (leptin, p=0.03) in Asians (n=4) compared to Whites (n=4).

There appears to be important racial differences in the SF adiponectin profile among individuals with end-stage knee OA. Differential gene expression in the IFP across racial groups could be a potential contributory source for the noted SF variations. Further work to determine the source and function of adipokines in knee OA pathophysiology across racial groups is warranted.


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