Adipokines: Biomarkers for osteoarthritis?

Abstract

Osteoarthritis (OA) is one of the most common degenerative joint diseases in aging population. Obesity is an important risk factor for initiation and progression of OA. It is accepted that excess body weight may lead to cartilage degeneration by increasing the mechanical forces across weight-bearing joints. However, emerging data suggest that additional metabolic factors released mainly by white adipose tissue may also be responsible for the high prevalence of OA among obese people. Adipocyte-derived molecules ''adipokines'' have prompt much interest in OA pathophysiological research over the past decade since they play an important role in cartilage and bone homeostasis. Therefore, the aim of this review is to summarize the current knowledge on the role of adipokines including leptin, adiponectin, visfatin and resistin in OA and their potential to be used as biomarkers for earlier diagnosis, classifying disease severity, monitoring disease progression, and testing pharmacological interventions for OA. In OA patients, leptin, visfatin and resistin showed increased production whereas adiponectin showed decreased production. Leptin and adiponectin are far more studied than visfatin and resistin. Importantly, altered adipokine levels also contribute to a wide range of diseases. Further experiments are still crucial for understanding the relationship between adipokines and OA.

Section of the anterior cruciate ligament in the rabbit as animal model for osteoarthritis progression

“…Obesity has long been considered as a risk factor for OA initiation as well as the disease progression. Particularly, adipokines might be a potential biomarker for OA progression and classify the disease severity [16]. However, Harvey et al [17] explored the association of leg-length inequality with knee OA, whereby the result for progressive knee OA was less clear compared with incident knee OA.…”

Revealed aspect of metabolic osteoarthritis

“…In addition, adiponectin levels in OA synovial fluid was correlated with aggrecan degradation. 20 Hence from above it is clearly indicated that adiponectin plays crucial role in providing inflammatory environment in OA. Franchin et al, produced similar results where authors have shown link between adiponectin and cartilage degradation.…”

“…Researchers have started believing that adipokines plays a crucial role in homeostasis of cartilage and bone. 20 …”

“…Leptin, alone or in synergy with IL-1b, has also been reported to enhance the production of inducible nitric oxide synthase (iNOS), prostaglandin E2 (PGE2) and cyclooxygenasse (COX)-2 in human OA cartilage and chondrocytes. 20 …”

“…Leptin reduced proliferation of OA chondrocytes after the 48-h treatment. 20 Nitric oxide (NO) is a proinflammatory mediator which promotes apoptosis, chondrocyte phenotype loss, as well as MMPs activation. The combination of leptin and interferon-g can activate the production of type 2 nitric oxide synthase (NOS2) in cultured chondrocytes.…”