**4. Conclusions**

Recent advances in animal experimentation and molecular biology have led to significant progress in our understanding of the mechanisms underlying the pathogenesis of arthritis pain. The concept that pain is a mere byproduct of joint damage and nociceptive response has become outdated. Aside from DAMPs produced from joint destruction, various nociceptive players, such as NGF- TrkA axis, CGRP, TRPV-1, and SASP, have been proposed as molecular mediators of OA pain. For RA, pain independent of inflammation has been correlated with ATF-3, TLR-4, and FcγR1. With the advances in cutting edge molecular techniques such as single cell polymerase chain reaction (PCR) and CRISPR/Cas9 mediated gene regulation, the knowledge base for pain pathogenesis would be significantly and rapidly expanded. Despite the inherent difficulty in extrapolating data gained in animal pain behavior studies to human arthritis, the critical assessment of various molecular mediators and translational studies would help to define the biological relevance of novel therapeutic targets for the treatment of arthritis pain.

**Author Contributions:** Acquisition and interpretation of data for the work, J.-I.H.; drafting the work, I.Y.P., J.-I.H. and H.A.K.; conception or design of the work, acquisition and interpretation of data for the work, H.A.K. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research was supported by a grant of the Basic Science Research Program through the National Research Foundation (NRF) of Korea funded by the Ministry of Education (2017R1A2B2001881), and by the Hallym University Research Fund.

**Conflicts of Interest:** The authors declare no conflict of interest.
