Table 1.

In vitro animal studies included.

Reference	Author	Subjects	Pathway involved	Results
[3]	J. Wu et al. (2018)	New Zealand white rabbit chondrocytes	PRP and Wnt/ β-catenin	A lower expression level of WNT1 and β-catenin than in another group treated with IL-1β was observed
[4]	C.Lietman et al. (2018)	OA-induced murine model synovial fibroblasts and chondrocytes	XAV-939	After it was injected inside the joint, a reduction of the cartilage degradation and synovial inflammation was observed
[6]	L. Lodewyckx et al. (2012)	Cell culture (ATDC5) and mouse ribcage and tibial plateau chondrocytes from Frzb−/− and wild type mices	Wnt/β-catenin	Overexpression of FRZB coupled with an up-regulation of aggrecan and Col2a1 and down-regulation of Col3a1 and Col5a1. FRZB is in strict relationship to Wnt pathway
[7]	T. Yuasa et al. (2008)	New Zealand rabbit articular chondrocytes and guinea pig knee chondrocytes	Wnt/β-catenin	Wnt/beta-catenin signalling is a powerful stimulator of chondrocyte matrix catabolic action and may be part of mechanisms leading to excessive remodelling and degradation of cartilage matrix in age-associated joint pathologies
[8]	M. Zhu et al. (2009)	Adult Col2a1-CreERT2 transgenic mice chondrocytes	β-catenin	Activation of beta-catenin signalling in articular chondrocytes in adult mice leads to the premature chondrocyte differentiation and the development of an OA-like phenotype.
[10]	Y. Tamamura et al. (2005)	transgenic mice expressing a fusion mutant protein of β-catenin and LEF (CA-LEF) in nascent chondrocytes	δ-β-Catenin	Increase of proteins involved in cartilage matrix degradation (MMP-13, ADAMTS-4, ADAMTS-5 and RUNX-2)
[11]	Shi et al. (2016)	Sprague-Dawley rats (n=24) articular chondrocytes	WNT5A	Silencing WNT5A mRNA prevented degradation of COL2
[15]	Wang D. et al (2018)	100 BALB/c transgenic mice osteoclasts	PRP/RANKL/Wnt	The study indicated that PRP inhibits osteoclast differentiation through activation of the Wnt pathway and inhibiting RANKL