Nerve growth factor induced after temporomandibular joint inflammation decelerates chondrocyte differentiation
Article first published online: 12 DEC 2012
© 2012 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
Volume 19, Issue 6, pages 604–610, September 2013
How to Cite
Oral Diseases (2013) 19, 604–610
- Issue published online: 10 JUL 2013
- Article first published online: 12 DEC 2012
- Accepted manuscript online: 24 NOV 2012 06:08AM EST
- Manuscript Accepted: 11 NOV 2012
- Manuscript Revised: 31 OCT 2012
- Manuscript Received: 1 OCT 2012
The goal of this study was to investigate changes in nerve growth factor (NGF) and its high-affinity receptor-tropomyosin receptor kinase A (TrkA) expression in the TMJ after intra-articular inflammation.
Materials and Methods
We employed the Col1-IL1βXAT inducible model of joint inflammation. Changes in NGF and TrkA expression were evaluated by immunohistochemistry. The function of NGF on cell differentiation was assessed in vitro employing the ATDC5 chondrocyte cell line.
NGF expression was observed in articular chondrocytes only after TMJ inflammation, whereas TrkA expression was detected in articular chondrocytes under both naïve as well as inflamed conditions. The potential effect of NGF on articular chondrocytes was studied on the ATDC5 cell line, whereby NGF decelerated the maturation rate of this chondrogenic cell line, presumably by arresting cell differentiation at the prehypertrophic stage of chondrocyte maturation.
NGF-TrkA signaling in the TMJ provides potentially a means of protection against the development of osteoarthritis by decelerating chondrocyte differentiation. This discovery may lead to the development of novel therapies for osteoarthritis of the TMJ and other joints.