title: Nerve growth factor induced after temporomandibular joint inflammation decelerates chondrocyte differentiation.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  We employed the Col1-IL1β(XAT) 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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Orthodontics and Pediatric Dentistry, School of Dental Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.
authors.forename: H
authors.initials: H
authors.lastname: Huang
authors.forename: G
authors.initials: G
authors.lastname: Shank
authors.forename: L
authors.initials: L
authors.lastname: Ma
authors.forename: R H
authors.initials: RH
authors.lastname: Tallents
authors.forename: S
authors.initials: S
authors.lastname: Kyrkanides
mesh_terms: D000469:Alkaline Phosphatase / Q000032:analysis; D000818:Animals; D001168:Arthritis / Q000473:pathology*; D002358:Cartilage, Articular / Q000473:pathology; D018929:Cell Culture Techniques; D002454:Cell Differentiation / Q000187:drug effects / Q000502:physiology; D002460:Cell Line; D049109:Cell Proliferation; D019902:Chondrocytes / Q000187:drug effects / Q000502:physiology*; D024042:Collagen Type I / Q000235:genetics; D024043:Collagen Type II / Q000032:analysis; D004195:Disease Models, Animal; D006984:Hypertrophy; D053583:Interleukin-1beta / Q000235:genetics; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D020932:Nerve Growth Factor / Q000032:analysis* / Q000494:pharmacology; D020917:Receptor, trkA / Q000032:analysis / Q000494:pharmacology; D015398:Signal Transduction / Q000502:physiology; D013705:Temporomandibular Joint Disorders / Q000473:pathology*; D016212:Transforming Growth Factor beta / Q000032:analysis; D019076:Transgenes / Q000235:genetics
chemical_list: D024042:Collagen Type I; D024043:Collagen Type II; C587672:IL1B protein, mouse; D053583:Interleukin-1beta; D016212:Transforming Growth Factor beta; D020932:Nerve Growth Factor; D020917:Receptor, trkA; D000469:Alkaline Phosphatase