Vol 68, No 3 (2017)
Original paper
Published online: 2017-06-21

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Venopunction of the cubital vein as an alternative approach for CGRP plasma level evaluation in TMD patients

Aleksandra Nitecka-Buchta1, Bogdan Marek2, Jolanta Batko Kapustecka1, Stefan Baron1
Pubmed: 28660990
Endokrynol Pol 2017;68(3):326-333.

Abstract

Introduction: Calcitonin gene-related peptide is an important vasodilator. It plays an important role in the metabolism of chewing muscles. The aim of the study was to evaluate the plasma level of CGRP in patients with myofascial pain (RDC/TMD Ia) and myofascial pain with limited opening (RDC/TMD Ib) before and after occlusal splint therapy (Michigan splint).

Material and methods: A randomised trial was performed including 39 patients (males = 3, females = 36). Blood samples were taken from the external jugular vein (JUG) and cubital vein (CUB) before and after 30 days of occlusal splint therapy. Plasma levels of CGRP were measured with ELISA KIT for Human Calcitonin Gene Related Peptide (CGRP) 96T (USCNK Business Co. Ltd.).

Results: The results of the study show that the plasma CGRP level was higher in the external jugular vein (JUG1 = 5.07pg/mL [SD = 1.99]) than in cubital vein (CUB1 = 4.3 pg/mL [SD = 1.6]). After 30 days of the occlusal splint therapy the levels in both veins increased: JUG2 = 6.07 pg/mL (SD = 2.19), and CUB2 = 4.9 pg/mL (SD = 1.4). The CGRP plasma level increase was statistically significant only in the external jugular vein (JUG) (p < 0.05). Statistically significant pain intensity reduction was observed: VAS1 = 5.4 (SD = 2.08) decreased to VAS2 = 1.7 (SD = 2.07) after splint therapy (p < 0.05).

Conclusions: Venepuncture of an external jugular vein is more precise, than venepuncture of a cubital vein in evaluating CGRP plasma level changes in patients with TMD.

References

  1. Assas BM, Pennock JI, Miyan JA. Calcitonin gene-related peptide is a key neurotransmitter in the neuro-immune axis. Front Neurosci. 2014; 8: 23.
  2. Romero-Reyes M, Pardi V, Akerman S. A potent and selective calcitonin gene-related peptide (CGRP) receptor antagonist, MK-8825, inhibits responses to nociceptive trigeminal activation: Role of CGRP in orofacial pain. Exp Neurol. 2015; 271: 95–103.
  3. R.King, S.D.Brain, Handbook of biologically Active Peptides, 2013, Elsevier Inc., http://dx.doi.org/10.1016/B978-0-12-385095-9.00189-5
  4. Bigal ME, Walter S, Rapoport AM. Calcitonin gene-related peptide (CGRP) and migraine current understanding and state of development. Headache. 2013; 53(8): 1230–1244.
  5. Villalón CM, Olesen J. The role of CGRP in the pathophysiology of migraine and efficacy of CGRP receptor antagonists as acute antimigraine drugs. Pharmacol Ther. 2009; 124(3): 309–323.
  6. Huang R, Karve A, Shah I, et al. Deletion of the mouse alpha-calcitonin gene-related peptide gene increases the vulnerability of the heart to ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2008; 294(3): H1291–H1297.
  7. Smillie SJ, Brain SD. Calcitonin gene-related peptide (CGRP) and its role in hypertension. Neuropeptides. 2011; 45(2): 93–104.
  8. Schiffman E, Ohrbach R, Truelove E, et al. International RDC/TMD Consortium Network, International association for Dental Research, Orofacial Pain Special Interest Group, International Association for the Study of Pain. Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) for Clinical and Research Applications: recommendations of the International RDC/TMD Consortium Network* and Orofacial Pain Special Interest Group†. J Oral Facial Pain Headache. 2014; 28(1): 6–27.
  9. Griner T. Muscle Metabolism: Aerobic vs. Anaerobic Dynamic Chiropractic – March 20, 2000, Vol. ; 18: Issue.
  10. Cernuda-Morollón E, Larrosa D, Ramón C, et al. Interictal increase of CGRP levels in peripheral blood as a biomarker for chronic migraine. Neurology. 2013; 81(14): 1191–1196.
  11. Sarchielli P, Alberti A, Vaianella L, et al. Chemokine levels in the jugular venous blood of migraine without aura patients during attacks. Headache. 2004; 44(10): 961–968.
  12. Appelgren A, Appelgren B, Kopp S, et al. Neuropeptides in the arthritic TMJ and symptoms and signs from the stomatognathic system with special consideration to rheumatoid arthritis. J Orofac Pain. 1995; 9(3): 215–225.
  13. Vause CV, Durham PL. CGRP stimulation of iNOS and NO release from trigeminal ganglion glial cells involves mitogen-activated protein kinase pathways. J Neurochem. 2009; 110(3): 811–821.
  14. Kopp S. Neuroendocrine, immune, and local responses related to temporomandibular disorders. J Orofac Pain. 2001; 15(1): 9–28.
  15. Ashina M, Bendtsen L, Jensen R, et al. Evidence for increased plasma levels of calcitonin gene-related peptide in migraine outside of attacks. Pain. 2000; 86(1-2): 133–138.
  16. Tvedskov JF, Lipka K, Ashina M, et al. No increase of calcitonin gene-related peptide in jugular blood during migraine. Ann Neurol. 2005; 58(4): 561–568.
  17. Friberg L, Olesen J, Olsen TS, et al. Absence of vasoactive peptide release from brain to cerebral circulation during onset of migraine with aura. Cephalalgia. 1994; 14(1): 47–54.
  18. Parlapiano C, Paoletti V, Campana E, et al. CGRP and ET-1 plasma levels in normal subjects. Eur Rev Med Pharmacol Sci. 1999; 3(3): 139–141.
  19. Joyce CD, Fiscus RR, Wang X, et al. Calcitonin gene-related peptide levels are elevated in patients with sepsis. Surgery. 1990; 108(6): 1097–1101.
  20. Cady RJ, Glenn JR, Smith KM, et al. Calcitonin gene-related peptide promotes cellular changes in trigeminal neurons and glia implicated in peripheral and central sensitization. Mol Pain. 2011; 7: 94.
  21. Sato J, Segami N, Nishimura M, et al. Correlation between the arthroscopic diagnosis of synovitis and microvessel density in synovial tissues in patients with internal derangement of the temporomandibular joint. J Craniomaxillofac Surg. 2003; 31(2): 101–106.
  22. Bick R, Mann M, Poindexter B, et al. Calcium Movements in CGRP-treated Cultured Skeletal Muscle Cells: Is There a Role for CGRP in Tension Headaches? International Journal of Peptide Research and Therapeutics. 2008; 14(2): 193–199.
  23. Homonko DA, Theriault E. Downhill running preferentially increases CGRP in fast glycolytic muscle fibers. J Appl Physiol (1985). 2000; 89(5): 1928–1936.
  24. Jonhagen S, Ackermann P, Saartok T, et al. Calcitonin gene related peptide and neuropeptide Y in skeletal muscle after eccentric exercise: a microdialysis study. Br J Sports Med. 2006; 40(3): 264–7; discussion 264.
  25. Allen DG. Why stretched muscles hurt--is there a role for half-sarcomere dynamics? J Physiol. 2006; 573(Pt 1): 4.
  26. Dessem D, Lovering RM. Repeated muscle injury as a presumptive trigger for chronic masticatory muscle pain. Pain Res Treat. 2011; 2011: 647967.
  27. McDaniel J, Ives SJ, Richardson RS. Human muscle length-dependent changes in blood flow. J Appl Physiol (1985). 2012; 112(4): 560–565.
  28. Tfelt-Hansen P, Le H. Calcitonin gene-related peptide in blood: is it increased in the external jugular vein during migraine and cluster headache? A review. J Headache Pain. 2009; 10(3): 137–143.
  29. Ambalavanar R, Dessem D, Moutanni A, et al. Muscle inflammation induces a rapid increase in calcitonin gene-related peptide (CGRP) mRNA that temporally relates to CGRP immunoreactivity and nociceptive behavior. Neuroscience. 2006; 143(3): 875–884.
  30. Benarroch EE. CGRP: sensory neuropeptide with multiple neurologic implications. Neurology. 2011; 77(3): 281–287.
  31. Brain SD. Calcitonin gene-related peptide (CGRP) antagonists: blockers of neuronal transmission in migraine. Br J Pharmacol. 2004; 142(7): 1053–1054.
  32. Guarda-Nardini L, Manfredini D, Salamone M, et al. Efficacy of botulinum toxin in treating myofascial pain in bruxers: a controlled placebo pilot study. Cranio. 2008; 26(2): 126–135.
  33. Donnerer J, Schuligoi R, Stein C. Increased content and transport of substance P and calcitonin gene-related peptide in sensory nerves innervating inflamed tissue: evidence for a regulatory function of nerve growth factor in vivo. Neuroscience. 1992; 49(3): 693–698.