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Editorial

The interaction of canonical bone morphogenetic protein- and Wnt-signaling pathways may play an important role in regulating cartilage degradation in osteoarthritis

Benjamin Y Chan and Christopher B Little

Author affiliations

Raymond Purves Bone and Joint Research Laboratories, University of Sydney at The Royal North Shore Hospital, Kolling Institute of Medical Research, Level 10 Kolling Building - B6, St Leonards NSW 2065, Australia

Citation and License

Arthritis Research & Therapy 2012, 14:119  doi:10.1186/ar3837


See related research by Papathanasiou et al., http://arthritis-research.com/content/14/2/R82

Published: 6 June 2012

Abstract

Bone morphogenetic proteins (BMPs) and Wnts are important signaling protein families with key roles in embryologic, patterning, development, and tissue remodeling in growth. BMP and Wnt-β-catenin are highly evolutionarily conserved pathways that, though often regulating similar cellular events, are independent signaling mechanisms that can have complementary or antagonistic effects depending on various factors, including cell type and developmental stage. Although BMP and Wnt-β-catenin have the ability to act entirely independently, there is a developing body of evidence for specific extra- and intra-cellular molecular interactions and crosstalk that occur between BMP and Wnt-β-catenin signaling and that again this may be cell type-specific. In the previous issue of Arthritis Research & Therapy, Papathanasiou and colleagues provide novel insights into the role and direct interaction of BMP2 and canonical Wnt-β-catenin signaling in regulating chondrocyte hypertrophy and matrix metalloproteinase/a disintegrin like and metalloproteinase with thrombospondin type I motif (MMP/ADAMTS) synthesis in osteoarthritis.