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Manuel Mata [1; 2; 3] and Lara Milian [1; 3] and Maria Oliver [1; 3] and Javier Zurriaga [4] and Maria Sancho-Tello [1; 3] and Jose Javier Martin de Llano [1; 3] and Carmen Carda [1; 3; 5]

Academic Editor: Víctor Carriel

1, Department of Pathology, Faculty of Medicine and Odontology, University of Valencia, Blasco Ibáñez Avenue 15, 46010 Valencia, Spain, uv.es

2, Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES), Monforte de Lemos Avenue, 3-5, Pabellón 11, 28029 Madrid, Spain, ciberes.org

3, Fundación para la Investigación del Hospital Clínico de la Comunidad Valenciana (INCLIVA), Blasco Ibañez Avenue 15, 46010 Valencia, Spain, incliva.es

4, Hospital Clinico Universitario de Valencia, Blasco Ibañez Avenue 17, 46010 Valencia, Spain

5, Centro de Investigación Biomédica en Red en Bioingeniería Biomateriales y Nanomedicina (CIBERBBN), Monforte de Lemos Avenue, 3-5, Pabellón 11, 28029 Madrid, Spain

Received Apr 27, 2017; Accepted Jul 4, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Osteoarthritis (OA) is a complex systemic disease in which the whole joint, including the synovium, articular cartilage, subchondral bone, tendons, and muscles, is affected [1]. OA can be idiopathic or initiated by aging, trauma, malformations, or inflammatory disease [2, 3]. As it affects up to 10% of males and 18% of females greater than 48 yr of age, OA is becoming a serious health problem, and currently established therapies for OA insufficiently address the clinical need [1].

The loss of articular cartilage distinctive of OA is characterized by proteolytic degradation of the chondral matrix, which induces the release of cytokines including interleukin 6 (IL-6), IL-1β, and tumor necrosis factor alpha (TNF-α), leading to secretion of matrix-degrading enzymes from chondrocytes, further propagating tissue breakdown [4, 5]. The limited regeneration capacity of articular cartilage generally leads to formation of fibrocartilage-like scar tissue, which replaces the native hyaline cartilage matrix [6].

Current pharmacological agents for the treatment of OA involve anti-inflammatory drugs including cyclooxygenase 2-selective or nonselective nonsteroidal anti-inflammatory drugs as well as TNF-α-binding antibodies or IL-1 inhibitors [7–9]. However, the potential for these compounds to improve the structural damage is limited,...

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