Elsevier

Joint Bone Spine

Volume 79, Issue 2, March 2012, Pages 160-165
Joint Bone Spine

Original article
Serum resistin level is associated with radiographic changes in hand osteoarthritis: Cross-sectional study

https://doi.org/10.1016/j.jbspin.2011.04.009Get rights and content

Abstract

Objective

The aim of this study was to determine whether adipokines such as adiponectin and resistin were related to radiographic outcomes in patients with hand osteoarthritis (OA).

Methods

A total of 156 female subjects (46 controls, 60 non-radiographic hand OA, and 50 radiographic hand OA) were enrolled. We measured serum adiponectin and resistin concentrations using an enzyme-linked immunosorbent assay (ELISA). Radiographic hand OA was defined by the presence of a ≥ 2 Kellgren-Lawrence radiological grade after assessment for 20 joints of both hands. The association between radiographic hand OA and each adipokine was assessed using multivariate logistic regression models controlling for confounding clinical parameters.

Results

Serum resistin levels in radiographic hand OA patients were higher than in non-radiographic hand OA and controls (padj = 0.020 and padj = 0.019, respectively), whereas there were no significant differences in serum adiponectin levels. The presence of radiographic changes in hand OA was shown to be dependent on serum resistin levels (padj = 0.028). Specifically, subchondral erosion in radiographic hand OA was associated with serum resisitin (padj = 0.028). However, there were no associations of serum adipokines with joint space narrowing, bony ankylosis, and cortical destruction.

Conclusions

This study suggests that resistin is involved in radiographic changes in hand OA, and that adipokines contribute to pathogenesis in radiographic outcomes in hand OA.

Introduction

Hand osteoarthritis (OA), involving in interphalangeal joints and/or thumb base, is more prevalent form than knee and hip OA [1], [2]. Although the pathogenesis of hand OA remains unclear, evidences suggests that diverse immunological and inflammatory mechanisms contribute to the development and progression of OA have been accumulated. Recent studies have demonstrated that various adipokines such as leptin, adiponectin, and resistin may act as immune-inflammatory mediators during cartilage degeneration and synovial inflammation of OA, in addition to their traditional functions in fat storage and glucose metabolism. Adiponectin appears to have dual effects in the pathogenesis of OA: a protective role through dysregulation of matrix-regulating molecules such as matrix metalloproteinase-13 (MMP-13) [3]; and a pro-inflammatory effect on expression of nitric oxide synthase 2 and release of interleukin-6 (IL-6), MMP-3, and MMP-9 in chondrocytes [4]. In addition, resistin appears to be involved in the inhibition of proteoglycan production from articular cartilage in vitro [5] and is highly expressed in serum and synovial fluid in knee OA patients [6]. Recent clinical data revealed that adiponectin levels are much higher in erosive hand OA than non-erosive OA [7].

It has been focused on early prediction of disease severity and prognosis in OA to prevent poor clinical outcomes. Especially, radiographic progression in hand OA is also considered as a determinant of disease outcome and prognosis. Some studies demonstrated close relationships between radiographic changes and clinical measure tools [8], [9]. Clinical characteristics such as age, sex, pain severity, and presence of osteophytes were also suggested as risk factors of radiographic changes in hand OA [10], [11]. However, risk factors for radiographic changes have not been determined yet. Inflammatory biomarkers for radiographic outcomes in hand OA should be needed to predict progression or development of radiographic changes.

Although evidences exist for roles of adiponectin and resistin in the inflammatory response of OA, the involvement of adipokines in the pathogenesis of radiographic changes in hand OA needs to be investigated. We, therefore, measured serum adiponectin and resistin concentrations and assessed the presence of radiographic changes and their morphological patterns in hand OA patients. The aim of our study was to determine the association of two adipokines, adiponectin and resistin, with the radiographic changes of hand OA.

Section snippets

Subjects

We consecutively enrolled 110 OA patients who fulfilled the American College of Rheumatology criteria for the classification of hand OA [12] at the outpatient rheumatic clinic at Daegu Catholic University Medical Center. Forty-six control subjects who visited the clinic for evaluation of hand joint discomfort or stiffness were also enrolled without definite evidence of hand OA or other arthritis. Their joint discomforts were diagnosed transient and non-specific in the evaluation using physical

General characteristics and difference of adipokine levels in study population

General and clinical characteristics in enrolled subjects are shown in Table 1. Parameters such as weight, BMI, and age at menopause were similar among the three groups. However, subject age at the time of study enrollment and height were significantly different among the three groups (P < 0.0001 and P = 0.018, respectively). There was no statistically significant difference in history of diabetes among the three groups (P > 0.05). Parameters such as disease duration, VAS, CRP, ESR, and tender joint

Discussion

The pathogenesis of OA is multifactorial and consists of complicated mechanisms including the aging process, degenerative changes, and aberrant inflammatory or immune responses [1], [2]. Cartilage is the major target tissue in affected joints, but synovial tissues and subchondral bone also show inflammatory changes as enhanced expression of diverse inflammatory cytokines and proteolytic enzymes including tumor necrosis factor-α (TNF-α), IL-1, and some MMPs [16], [17], [18]. The understanding of

Disclosure of interest

The authors declare that they have no conflicts of interest concerning this article.

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    Two authors equally contributed to this manuscript.

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