Adiponectin in Osteoarthritis: Pathophysiology, Relationship with Obesity and Presumptive Diagnostic Biomarker Potential.

Iosif Ilia,Diana Nitusca,Catalin Marian

doi:10.3390/diagnostics12020455

Iosif Ilia, Diana Nitusca + Show 1 more

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https://doi.org/10.3390/diagnostics12020455

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Abstract

Osteoarthritis (OA) is a multifactorial, irreversible age- and obesity-induced joint degenerative disease, with an increasing incidence in developed countries. With a pathophysiology and etiology that are currently under-investigated, the only available disease-modifying treatment relies solely on total joint arthroplasty, which entails major economic burdens. Recently, the research focus has shifted towards the evaluation of metabolically active mediators secreted by the adipose tissue, which could be potential targets for a better understanding of the mechanisms involved in OA onset and development. Of note, adiponectin has drawn a great deal of attention, since it is the most abundant type of circulating adipokine and has been highly associated with OA occurrence. Thus far, studies have been controversial in establishing whether adiponectin possesses a destructive or protective role in OA development. Therefore, we critically and systematically reviewed, herein, the roles of adiponectin in the pathophysiology of OA, the link between obesity, adiponectin expression and the progression of OA, as well as its potential role as a future biomarker for a more optimized and reliable diagnosis of this degenerative disorder.

Highlights

Osteoarthritis (OA) is a very common type of age-related, injury-induced joint degenerative disorder, being undoubtedly the most common form of arthritis [1]
At the AdipoR1 level, from both the chondrocytes and the osteoarthritis synovial fibroblasts (OASFs), high adiponectin levels stimulate via the AMPK and nuclear factor (NF-κB) signaling pathways for the release of proinflammatory interleukins, matrix metalloproteases (MMP-1 and -3), and
At the AdipoR1 level, from both the chondrocytes and the osteoarthritis synovial fibroblasts (OASFs), high adiponectin levels stimulate via the AMPK and nuclear factor (NF-κB) signaling pathways for the release of pro-inflammatory interleukins, matrix metalloproteases (MMP-1 and -3), and the production of inducible nitric oxide synthase, generating pain, inflammation, and matrix degradation [24,25]

Summary

Introduction

Osteoarthritis (OA) is a very common type of age-related, injury-induced joint degenerative disorder, being undoubtedly the most common form of arthritis [1]. One of the primary risk factors for OA development is age; the increase in global lifespan can, at least partly, explain the age-related increase in incidence (OA is more common over the age of 65). It is one of the leading causes of chronic pain, loss of function and global disability, due to its irreversible nature [6]. Bodyweight is highly correlated with OA occurrence and progression, increasing both mechanical stress on the cartilage and the production of inflammatory factors arising from the adipose tissue, such as metabolically active mediators (chemokines, pro-inflammatory cytokines, and adipokines) [7,8]. Adiponectin (a protein that has the following three isoforms: low-molecular-weight (LMW) trimers, medium-molecular-weight (MMW) hexamers, and high-molecular-weight (HMW) oligomers) appears to be a multifactorial key player in OA pathophysiology, and its levels can be detected in serum or synovial fluid sample specimens [9,10]

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