The Role of Wnt Pathway in the Pathogenesis of OA and Its Potential Therapeutic Implications in the Field of Regenerative Medicine.

Biomed Res Int 2018 15;2018:7402947. Epub 2018 Oct 15.

Humanitas University Department of Biomedical Sciences, Via Manzoni 113, 20089 Rozzano, Milan, Italy.

Introduction: Osteoarthritis (OA) is a degenerative joint disease characterized by articular cartilage degradation, subchondral damage, and bone remodelling, affecting most commonly weight-bearing joints, such as the knee and hip. The loss of cartilage leads to joint space narrowing, pain, and loss of function which could ultimately require total joint replacement. The Wnt/ catenin pathway is involved in the pathophysiology of OA and has been proposed as a therapeutic target. Endogenous and pharmacological inhibitors of this pathway were recently investigated within innovative therapies including the use of platelet-rich plasma (PRP) and mesenchymal stem cells (MSCs).

Methods: A review of the literature was performed on the PubMed database based on the following inclusion criteria: article written in English language in the last 20 years and dealing with (1) the role of Wnt- catenin pathway in the pathogenesis of osteoarthritis and (2) pharmacologic or biologic strategies modulating the Wnt- catenin pathway in the OA setting.

Results: Evidences support that Wnt signalling pathway is likely linked to OA progression and severity. Its inhibition through natural antagonists and new synthetic or biological drugs shares the potential to improve the clinical condition of the patients by affecting the pathological activity of Wnt/-catenin signalling.

Conclusions: While further research is needed to better understand the mechanisms regulating the molecular interaction between OA regenerative therapies and Wnt, it seems that biologic therapies for OA exert modulation on Wnt/ catenin pathway that might be relevant in achieving the beneficial clinical effect of those therapeutic strategies.

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Source
https://www.hindawi.com/journals/bmri/2018/7402947/
Publisher Site
http://dx.doi.org/10.1155/2018/7402947DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6205317PMC
February 2019
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