Co-variation of neuropeptide Y, calcitonin gene-related peptide, substance P and neurokinin A in joint fluid from patients with temporomandibular joint arthritis

Alstergren, Per; Appelgren, Anna; Appelgren, Björn; Kopp, Sigvard; Lundeberg, Thomas; Theodorsson, Elvar

doi:10.1016/0003-9969(94)00141-w

Cited by 60 publications

(42 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the analysis of SF, inflammatory chemical mediators, metabolites of the arachidonic acid cascade [1], neuropeptides [6], and cytokines [2,3], have been detected in patients with TMD. These cytokines stimulate to produce active matrix-degrading enzymes.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

The Redox States of Serum and Synovial Fluid of Patients with Temporomandibular Joint Disorders

Tomida

Ishimaru²,

Hayashi³

et al. 2003

Jpn.J.Physiol

View full text Add to dashboard Cite

[6] have been detected in the synovial fluid (SF) of the temporomandibular joint (TMJ). These findings may indicate that newly synthesized protein molecules tend to appear or increase in SF of the patient with TMDs. Recent studies have proposed that reactive free radicals, which were induced by mechanical stress, are responsible for the initiation of molecular events. Milam et al. [7] have hypothesized that free radicals might be produced in the intraarticular space by mechanical stresses in the TMJ, which may be provoked by masticatory muscle hyperactivity in malocclusion, dental irritation, physical stress, anxiety, and bad oral habits. Nitzen [8] has hypothesized that free radicals might result in disk displacement. Tomida et al. [9] have reviewed the possible source and mechanism of free radical interaction in the

show abstract

Section: Discussionmentioning

confidence: 99%

“…

…”

mentioning

confidence: 99%

The Redox States of Serum and Synovial Fluid of Patients with Temporomandibular Joint Disorders

Tomida

Ishimaru²,

Hayashi³

et al. 2003

Jpn.J.Physiol

View full text Add to dashboard Cite

show abstract

“…A correlation between the concentration of NK-A in the synovial fluid and the degree of arthritis in joints has been indicated in humans. (20)(21)(22) Moreover, tachykinin antagonist inhibits plasma extravasation induced by tachykinin, which was described to play an important role in neurogenic inflammation. (23,24) Although this is the first report on NK-A in arthritic joints, SP has been extensively studied in conjunction with AA.…”

Section: Nk-a In Bone Tissue and Adjuvant Arthritis 77mentioning

confidence: 99%

Neurokinin-A in Bone and Joint Tissues: Changes in Adjuvant Arthritis

Elhassan¹,

Lindgren²,

Hultenby³

et al. 1999

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

The localization of neurokinin A (NK-A) in the normal ankle joint of rats was investigated by an immunoelectron microscopic technique with specific antisera to NK-A. Immunoreactivity was detected in bone matrix, myelinated nerve fiber in the periosteum, and bone marrow and synovial cells. No immunoreactivity was observed in osteoblasts, osteocytes, and osteoclasts. Using radioimmunoassay (RIA), a detectable concentration of NK-A was observed in the bone marrow, periosteum, cortical bone, and ankle of normal rats. In rats with chronic adjuvant arthritis, induced by intradermal injection of mycobacterium butyricum in paraffin oil into the base of the tail, the concentrations of NK-A using RIA in ankles and spinal cords were found to be significantly increased compared with acute or control rats. There were no significant differences between the latter two. Similarly, increased NK-A labeling was observed using immunoelectron microscopy in bone matrix and bone marrow monocyte cells of the chronic arthritic rats. These findings indicate the existence of as well as a biological role of NK-A in bone and joint tissues. (J Bone Miner Res 1999;14:73-79)

show abstract

“…For instance, increased NPY levels were found in the synovial fluid of arthritic patients [3]. Other pro-algesic mediators such as nerve growth factor (NGF), protons, histamine, cytokines, prostaglandins, neurokinins, chemokines, glutamate and ATP also contribute to neurogenic inflammation [34,75,76].…”

Section: Introductionmentioning

confidence: 98%

Functional aspects and mechanisms of TRPV1 involvement in neurogenic inflammation that leads to thermal hyperalgesia

Planells-Cases

García-Sanz

Morenilla‐Palao

et al. 2005

Pflugers Arch - Eur J Physiol

136

107

View full text Add to dashboard Cite

Neurogenic inflammation is produced by overstimulation of peripheral nociceptor terminals by injury or inflammation of tissues. Excessive activity of sensory neurons produces vasodilation, plasma extravasation and hypersensitivity. Mechanistically, neurogenic inflammation is due to the release of substances from primary sensory nerve terminals that act directly or indirectly at the peripheral terminals, either activating or sensitizing nociceptors, endothelial cells and immunocytes. Notably, small-diameter sensory neurons that are sensitive to capsaicin play a key role in the generation of neurogenic inflammation. The cloning of the vanilloid receptor 1 (TRPV1) has been a breakthrough that has propelled our understanding of the molecular mechanisms involved in neurogenic inflammation. TRPV1 pivotally contributes to the integration of various stimuli and modulates nociceptor excitability, thus making it a true gateway for pain transduction. In addition, TRPV1 is the endpoint target of intracellular signalling pathways triggered by inflammatory mediators. Phosphorylation-induced potentiation of TRPV1 channel activity, along with an incremented TRPV1 surface expression are major events underlying the nociceptor activation and sensitization that leads to thermal hyperalgesia. The important contribution of TRPV1 receptor to the onset and maintenance of neurogenic inflammation has validated it as a therapeutic target for inflammatory pain management. As a result, the development of specific TRPV1 antagonists is a central focus of current drug discovery programs.

show abstract

Co-variation of neuropeptide Y, calcitonin gene-related peptide, substance P and neurokinin A in joint fluid from patients with temporomandibular joint arthritis

Cited by 60 publications

References 21 publications

The Redox States of Serum and Synovial Fluid of Patients with Temporomandibular Joint Disorders

The Redox States of Serum and Synovial Fluid of Patients with Temporomandibular Joint Disorders

Neurokinin-A in Bone and Joint Tissues: Changes in Adjuvant Arthritis

Functional aspects and mechanisms of TRPV1 involvement in neurogenic inflammation that leads to thermal hyperalgesia

Contact Info

Product

Resources

About