Literature DB >> 15779537

Temporal changes in inflammatory mediator concentrations in an adjuvant model of temporomandibular joint inflammation.

Robert Spears1, Lori A Dees, Masha Sapozhnikov, Larry L Bellinger, Bob Hutchins.   

Abstract

AIMS: To determine temporal changes in the concentrations found in the temporomandibular joint (TMJ) and trigeminal ganglion of 3 specific classes of inflammatory mediators commonly linked with conditions of joint inflammation. The intent was to determine whether concentrations of the neuropeptide calcitonin gene-related peptide (CGRP), the neurotrophin nerve growth factor (NGF), and the proinflammatory cytokines interleukin-1beta (IL1beta) and tumor necrosis factor-alpha (TNF-alpha) are altered in the trigeminal ganglion and TMJ tissues during various stages of adjuvant-induced inflammation of the rat TMJ.
METHODS: Adult male rats received bilateral TMJ injection of complete Freund's adjuvant (CFA), while control rats did not receive CFA treatment. The trigeminal ganglion and TMJ tissues were collected at 2 days, and 2, 4, and 6 weeks postinjection and analyzed using either radioimmunoassay or enzyme-linked immunosorbent assay.
RESULTS: In the trigeminal ganglion, both CGRP and NGF concentrations were significantly elevated in comparison to controls from 2 days to 4 weeks; however, the patterns of increase differed. Concentrations of each inflammatory mediator were significantly elevated in the TMJ tissues of CFA-injected animals at 2 days and continued to be significantly elevated throughout the 6-week period. CGRP content remained at peak levels from 2 days through 6 weeks, while peak content for NGF, IL-1beta, and TNF-alpha was found at 2 days through 2 weeks.
CONCLUSION: The results suggest that the development of CFA-induced inflammation of the TMJ was accompanied by a variable increase in the concentration of different classes of inflammatory mediators in both the trigeminal ganglion and TMJ tissues, which implies that each class of inflammatory mediator may play a significant role during different stages in the onset and exacerbation of the inflammatory process.

Entities:  

Mesh:

Substances:

Year:  2005        PMID: 15779537

Source DB:  PubMed          Journal:  J Orofac Pain        ISSN: 1064-6655


  16 in total

1.  Central Role of Protein Kinase A in Promoting Trigeminal Nociception in an In Vivo Model of Temporomandibular Disorders.

Authors:  Lindsey K Koop; Jordan L Hawkins; Lauren E Cornelison; Paul L Durham
Journal:  J Oral Facial Pain Headache       Date:  2017 Summer

2.  Sustained inflammation induces degeneration of the temporomandibular joint.

Authors:  X D Wang; X X Kou; J J Mao; Y H Gan; Y H Zhou
Journal:  J Dent Res       Date:  2012-03-15       Impact factor: 6.116

3.  Dysregulated TNFα promotes cytokine proteome profile increases and bilateral orofacial hypersensitivity.

Authors:  F Ma; L Zhang; H S Oz; M Mashni; K N Westlund
Journal:  Neuroscience       Date:  2015-05-29       Impact factor: 3.590

4.  Modulation of temporomandibular joint nociception and inflammation in male rats after administering a physiological concentration of 17β-oestradiol.

Authors:  P R Kramer; L L Bellinger
Journal:  Eur J Pain       Date:  2012-06-19       Impact factor: 3.931

5.  Tumor necrosis factor-Alpha stimulates cytokine expression and transient sensitization of trigeminal nociceptive neurons.

Authors:  Zachary L Durham; Jordan L Hawkins; Paul L Durham
Journal:  Arch Oral Biol       Date:  2016-11-04       Impact factor: 2.633

6.  Repression of calcitonin gene-related peptide expression in trigeminal neurons by a Theobroma cacao extract.

Authors:  Marcie J Abbey; Vinit V Patil; Carrie V Vause; Paul L Durham
Journal:  J Ethnopharmacol       Date:  2007-10-05       Impact factor: 4.360

7.  The effects of cycling levels of 17beta-estradiol and progesterone on the magnitude of temporomandibular joint-induced nociception.

Authors:  P R Kramer; L L Bellinger
Journal:  Endocrinology       Date:  2009-04-09       Impact factor: 4.736

Review 8.  Emerging peripheral receptor targets for deep-tissue craniofacial pain therapies.

Authors:  R Ambalavanar; D Dessem
Journal:  J Dent Res       Date:  2009-03       Impact factor: 6.116

9.  Low-level laser therapy stimulates tissue repair and reduces the extracellular matrix degradation in rats with induced arthritis in the temporomandibular joint.

Authors:  George Azevedo Lemos; Renato Rissi; Ivan Luiz de Souza Pires; Letícia Prado de Oliveira; Andrea Aparecida de Aro; Edson Rosa Pimentel; Evanisi Teresa Palomari
Journal:  Lasers Med Sci       Date:  2016-05-04       Impact factor: 3.161

10.  Nociceptive Response to L-DOPA-Induced Dyskinesia in Hemiparkinsonian Rats.

Authors:  G C Nascimento; K Bariotto-Dos-Santos; C R A Leite-Panissi; E A Del-Bel; M Bortolanza
Journal:  Neurotox Res       Date:  2018-04-02       Impact factor: 3.911

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.