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World J Orthop. Jun 18, 2017; 8(6): 461-464
Published online Jun 18, 2017. doi: 10.5312/wjo.v8.i6.461
Role of fetuin A in the diagnosis and treatment of joint arthritis
Eleni Pappa, Despina S Perrea, Spiridon Pneumaticos, Vasileios S Nikolaou
Eleni Pappa, Despina S Perrea, Laboratory of Experimental Surgery “N.S. Christeas”, National and Kapodistrian University of Athens, School of Medicine, 11527 Athens, Greece
Spiridon Pneumaticos, 3rd Department of Orthopaedics, KAT Hospital, National and Kapodistrian University of Athens, School of Medicine, 11527 Athens, Greece
Vasileios S Nikolaou, 2nd Department of Orthopaedics, Agia Olga Hospital, National and Kapodistrian University of Athens, School of Medicine, 11527 Athens, Greece
Author contributions: Pappa E wrote the manuscript; Perrea DS and Pneumaticos S contributed to the writing of the manuscript; Nikolaou VS contributed to the writing of the manuscript and did the final proof editing.
Conflict-of-interest statement: Τhere is no conflict of interest associated with any of the senior author or other co-authors contributed their efforts in this manuscript.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Vasileios S Nikolaou, MD, PhD, MSc, Orthopaedic Surgeon, Assistant Professor of Orthopaedics, 2nd Department of Orthopaedics, Agia Olga Hospital, National and Kapodistrian University of Athens, School of Medicine, 21 Dimitriou Ralli Str, 11527 Athens, Greece. bniko@med.uoa.gr
Telephone: +30-693-2543400 Fax: +30-210-8020671
Received: January 20, 2017
Peer-review started: January 21, 2017
First decision: March 8, 2017
Revised: April 23, 2017
Accepted: May 3, 2017
Article in press: May 5, 2017
Published online: June 18, 2017
Abstract

Osteoarthritis is a slowly progressive disease which includes the intervention of several cytokines, macrophage metalleinoproteinases reaction, leading to the degradation of the local cartilage but also having an impact on the serum acute phase proteins (APPs). Subsequently, biomarkers seem to be essential to estimate its progression and the need for any surgical intervention such as total arthroplasty, but also can be used as therapeutic agents. Recently, among APPs, fetuin A drew attention regarding its possible anti-inflammatory role in animal models but also as a therapeutic agent in the inflammatory joint disease in clinical trials. In contrast with other APPs such as C-reactive protein, fetuin A appears to be lower in the serum of patients with degenerative joint disease in comparison with the healthy ones, and also acts as an antagonist of the anti-proliferative potential of transforming growth factor-β (TGF-β) cytokines. Because of its lower serum levels in arthritis, an unregulated binding of TGF-β and bone morphogenetic proteins takes place leading to further arthritic lesions. The purpose of the present review is to assess the current evidence regarding the multipotent role of the alpha-2-HS-glycoprotein or as also known Fetuin-a in animal models but also as a biomarker of the degenerative joint arthritis in clinical trials.

Keywords: Fetuin A, Arthritis, Alpha-2-HS-glycoprotein, Bone morphogenetic protein, Inflammation, Glycoprotein, Treatment

Core tip: Fetuin A, an acute phase glycoprotein, recently drew scientific attention regarding its anti-inflammatory role. In the case of arthritis, clinical studies have shown its therapeutic potential as well as its anti-inflammatory role as it has been indicated by animal models. In this manuscript, we intend to review the current evidence concerning its anti-inflammatory and therapeutic role in degenerative joint disease.