Calcitonin gene-related peptide and other neuropeptides in the plasma of patients with soft tissue injury

Onuoha, Gracey N.; Alpar, E. K.

doi:10.1016/s0024-3205(99)00374-4

Cited by 50 publications

(30 citation statements)

References 25 publications

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“…Other studies on minor orthopaedic trauma, such as sprains and muscle injuries, have shown raised concentrations of CGRP in plasma, 9 and after tendon rupture in the rat there is extensive nerve ingrowth into the tendon, which is normally devoid of nerves, expressing CGRP. 23 Therefore these studies indicate that the peripheral nervous system initially reacts to exercise and injury by releasing regulatory neuronal mediators such as CGRP.…”

Section: Discussionmentioning

confidence: 89%

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Calcitonin gene related peptide and neuropeptide Y in skeletal muscle after eccentric exercise: a microdialysis study

Jönhagen

Ackermann²,

Saartok³

et al. 2006

Br J Sports Med

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Section: Discussionmentioning

confidence: 89%

“…8 An adaptive role for CGRP in pain and healing was also suggested in studies of minor orthopaedic trauma, in which raised concentrations of plasma CGRP were found. 9 The autonomic neuropeptide Y (NPY) seems to show opposite effects to CGRP-that is, it acts as a vasoconstrictor 8 and exerts antinociceptive 10 effects.…”

mentioning

confidence: 99%

Calcitonin gene related peptide and neuropeptide Y in skeletal muscle after eccentric exercise: a microdialysis study

Jönhagen

Ackermann²,

Saartok³

et al. 2006

Br J Sports Med

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“…When impulses arrive from C-fibre afferents, SP is released 16 and the plasma levels of neurotransmitter peptides are elevated 10 Our patients with an isolated whiplash injury had high plasma levels of pain neurotransmitters which fell to normal levels after decompression of the median nerve at the wrist. The plasma levels of SP are also raised in other painful conditions, [17][18][19][20] and those of CGRP are altered in soft-tissue injuries, 21 in chronic pain 22 and infection. 23 Carpal tunnel decompression is indicated in patients who have chronic neck, shoulder and arm pain after a whiplash injury.…”

Section: Discussionmentioning

confidence: 99%

Management of chronic pain in whiplash injury

Alpar

Onuoha

Kıllampallı

et al. 2002

The Journal of Bone and Joint Surgery. British volume

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We investigated the response of chronic neck and shoulder pain to decompression of the carpal tunnel in 38 patients with whiplash injury. We also determined the plasma levels of substance P (SP) and calcitonin gene-related peptide (CGRP), which are inflammatory peptides that sensitise nociceptors. Compared with normal control subjects, the mean concentrations of SP (220 v 28 ng/l; p < 0.0001) and CGRP (400 v 85 ng/l; p < 0.0005) were high in patients with chronic shoulder and neck pain before surgery. After operation their levels fell to normal. There was resolution of neurological symptoms with improvement of pain in 90% of patients. Only two of the 30 with chronic neck and shoulder pain who had been treated conservatively showed improvement when followed up at two years.In spite of having neuropathic pain arising from the median nerve, all these patients had normal electromyographic and nerve-conduction studies. Chronic pain in whiplash injury may be caused by 'atypical' carpal tunnel syndrome and responds favourably to surgery which is indicated in patients with neck, shoulder and arm pain but not in those with mild symptoms in the hand. Previously, the presence of persistent neurological symptoms has been accepted as a sign of a poor outcome after a whiplash injury, but our study suggests that it may be possible to treat chronic pain by carpal tunnel decompression.

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“…Both neuropeptides induce vasodilation (16), local blood flow increase (15), vascular permeability enhancement (17), and pain (18,19), thus modulating inflammation (20,21). CGRP and SP are present in pulpal and gingival tissues (17,22,23) and are increased markedly in human teeth exposing pulp due to advanced caries and/or those with painful pulpitis (24,25), which suggests a modulation of pulpal inflammation by these peptides.…”

mentioning

confidence: 99%

Neuropeptide Release from Dental Pulp Cells by RgpB via Proteinase-Activated Receptor-2 Signaling

Tancharoen

Sarker

Imamura

et al. 2005

The Journal of Immunology

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Dental pulp inflammation often results from dissemination of periodontitis caused mostly by Porphyromonas gingivalis infection. Calcitonin gene-related peptide and substance P are proinflammatory neuropeptides that increase in inflamed pulp tissue. To study an involvement of the periodontitis pathogen and neuropeptides in pulp inflammation, we investigated human dental pulp cell neuropeptide release by arginine-specific cysteine protease (RgpB), a cysteine proteinase of P. gingivalis, and participating signaling pathways. RgpB induced neuropeptide release from cultured human pulp cells (HPCs) in a proteolytic activity-dependent manner at a range of 12.5–200 nM. HPCs expressed both mRNA and the products of calcitonin gene-related peptide, substance P, and proteinase-activated receptor-2 (PAR-2) that were also found in dental pulp fibroblast-like cells. The PAR-2 agonists, SLIGKV and trypsin, also induced neuropeptide release from HPCs, and HPC PAR-2 gene knockout by transfection of PAR-2 antisense oligonucleotides inhibited significantly the RgpB-elicited neuropeptide release. These results indicated that RgpB-induced neuropeptide release was dependent on PAR-2 activation. The kinase inhibitor profile on the RgpB-neuropeptide release from HPC revealed a new PAR-2 signaling pathway that was mediated by p38 MAPK and activated transcription factor-2 activation, in addition to the PAR-2-p44/42 p38MAPK and -AP-1 pathway. This new RgpB activity suggests a possible link between periodontitis and pulp inflammation, which may be modulated by neuropeptides released in the lesion.

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Calcitonin gene-related peptide and other neuropeptides in the plasma of patients with soft tissue injury

Cited by 50 publications

References 25 publications

Calcitonin gene related peptide and neuropeptide Y in skeletal muscle after eccentric exercise: a microdialysis study

Calcitonin gene related peptide and neuropeptide Y in skeletal muscle after eccentric exercise: a microdialysis study

Management of chronic pain in whiplash injury

Neuropeptide Release from Dental Pulp Cells by RgpB via Proteinase-Activated Receptor-2 Signaling

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