[1. Okiji T. Pulp As a Connective Tissue. In: Bywaters LC, ed. Seltzer and Bender’s Dental Pulp. 3rd ed. IL: Quintessence Publishing; 2002. p. 95-121.]Search in Google Scholar
[2. Haug SR, Heyeraas KJ. Modulation of dental inflammation by the sympathetic nervous system. J Dent Res. 2006; 85:488-95.10.1177/154405910608500602]Open DOISearch in Google Scholar
[3. Khayat BG, Byers MR, Taylor PE, Mecifi K, Kimberly CL. Responses of nerve fibers to pulpal inflammation and periapical lesions in rat molars demonstrated by calcitonin gene-related peptide immunocytochemistry. J Endod. 1988; 14:577-87.10.1016/S0099-2399(88)80054-2]Search in Google Scholar
[4. Byers MR, Taylor PE. Effect of sensory denervation on the response of rat molar pulp to exposure injury. J Dent Res. 1993; 72:613-8.10.1177/00220345930720031001]Open DOISearch in Google Scholar
[5. Rodd HD, Boissonade FM. Innervation of human tooth pulp in relation to caries and dentition type. J Dent Res. 2001; 80:389-93.10.1177/00220345010800011601]Open DOISearch in Google Scholar
[6. Byers MR. Dynamic plasticity of dental sensory nerve structure and cytochemistry. Arch Oral Biol. 1994; 39 Suppl:S13-S21.10.1016/0003-9969(94)90183-X]Open DOISearch in Google Scholar
[7. Kim S. Neurovascular interactions in the dental pulp in health and inflammation. J Endod. 1990; 16:48-53.10.1016/S0099-2399(06)81563-3]Search in Google Scholar
[8. Rodd HD, Boissonade FM. Immunocytochemical investigation of neurovascular relationships in human tooth pulp. J Anat. 2003; 202:195-203.10.1046/j.1469-7580.2003.00153.x157107712647869]Open DOISearch in Google Scholar
[9. Pashley DH. Dynamics of the pulpo-dentin complex. Crit Rev Oral Biol Med. 1996; 7:104-33.10.1177/104544119600700201018875027]Open DOISearch in Google Scholar
[10. Caviedes-Bucheli J, Munoz HR, Azuero-Holguin MM, Ulate E. Neuropeptides in dental pulp: the silent protagonists. J Endod. 2008; 34:773-88.10.1016/j.joen.2008.03.01018570980]Search in Google Scholar
[11. Byers MR, Schatteman GC, Bothwell M. Multiple functions for NGF receptor in developing, aging and injured rat teeth are suggested by epithelial, mesenchymal and neural immunoreactivity. Development. 1990; 109:461-71.10.1242/dev.109.2.4612169390]Search in Google Scholar
[12. Renton T, Yiangou Y, Plumpton C, Tate S, Bountra C, Anand P. Sodium channel Nav1.8 immunoreactivity in painful human dental pulp. BMC Oral Health. 2005; 5:5.10.1186/1472-6831-5-5]Open DOISearch in Google Scholar
[13. Warren CA, Mok L, Gordon S, Fouad AF, Gold MS. Quantification of neural protein in extirpated tooth pulp. J Endod. 2008; 34:7-10.10.1016/j.joen.2007.09.014]Search in Google Scholar
[14. Rodd HD, Boissonade FM. Comparative immunohistochemical analysis of the peptidergic innervation of human primary and permanent tooth pulp. Arch Oral Biol. 2002; 47:375-85.10.1016/S0003-9969(02)00012-2]Open DOISearch in Google Scholar
[15. Rodd HD, Boissonade FM. Substance P expression in human tooth pulp in relation to caries and pain experience. Eur J Oral Sci. 2000; 108:467-74.10.1034/j.1600-0722.2000.00924.x]Open DOISearch in Google Scholar
[16. Wells JE, Rose ET, Rowland KC, Hatton JF. Kv1.4 subunit expression is decreased in neurons of painful human pulp. J Endod. 2007; 33:827-9.10.1016/j.joen.2007.03.013]Search in Google Scholar
[17. Luo S, Perry GM, Levinson SR, Henry MA. Nav1.7 expression is increased in painful human dental pulp. Mol Pain. 2008; 4:16.10.1186/1744-8069-4-16]Open DOISearch in Google Scholar
[18. Johnsen D, Johns S. Quantitation of nerve fibres in the primary and permanent canine and incisor teeth in man. Arch Oral Biol. 1978; 23:825-9.10.1016/0003-9969(78)90163-2]Open DOISearch in Google Scholar
[19. Egan CA, Bishop MA, Hector MP. An immunohistochemical study of the pulpal nerve supply in primary human teeth: evidence for the innervation of deciduous dentine. J Anat. 1996; 188:623-31.]Search in Google Scholar
[20. Sari S, Aras S, Gunhan O. The effect of physiological root resorption on the histological structure of primary tooth pulp. J Clin Pediatr Dent. 1999 Spring; 23:221-5.]Search in Google Scholar
[21. Monteiro J, Day P, Duggal M, Morgan C, Rodd H. Pulpal status of human primary teeth with physiological root resorption. Int J Paediatr Dent. 2009; 19:16-25.10.1111/j.1365-263X.2008.00963.x19120506]Open DOISearch in Google Scholar
[22. Byers MR, Narhi MVO. Nerves Supply of the Pulpodentin Complex and Responses to Injury In: Bywaters LC, ed. Seltzer and Bender’s Dental Pulp. 3rd ed. IL: Quintessence Publishing; 2002. p. 151-80.]Search in Google Scholar
[23. Caviedes-Bucheli J, Camargo-Beltran C, Gomez-la- Rotta AM, Moreno SC, Abello GC, Gonzalez-Escobar JM. Expression of calcitonin gene-related peptide (CGRP) in irreversible acute pulpitis. J Endod. 2004; 30 :201-4.10.1097/00004770-200404000-0000415085045]Search in Google Scholar
[24. Awawdeh L, Lundy FT, Shaw C, Lamey PJ, Linden GJ, Kennedy JG. Quantitative analysis of substance P, neurokinin A and calcitonin gene-related peptide in pulp tissue from painful and healthy human teeth. Int Endod J. 2002; 35:30-6.10.1046/j.1365-2591.2002.00451.x11853236]Open DOISearch in Google Scholar
[25. Okiji T, Jontell M, Belichenko P, Dahlgren U, Bergenholtz G, Dahlstrom A. Structural and functional association between substance P- and calcitonin generelated peptide-immunoreactive nerves and accessory cells in the rat dental pulp. J Dent Res. 1997; 76: 1818-24.10.1177/00220345970760120301]Open DOISearch in Google Scholar
[26. Gazelius B, Brodin E, Olgart L. Depletion of substance P-like immunoreactivity in the cat dental pulp by antidromic nerve stimulation. Acta Physiol Scand. 1981; 111:319-27.10.1111/j.1748-1716.1981.tb06743.x]Open DOISearch in Google Scholar
[27. Olgart L, Kerezoudis NP. Nerve-pulp interactions. Arch Oral Biol. 1994; 39 Suppl:S47-S54.10.1016/0003-9969(94)90188-0]Open DOISearch in Google Scholar
[28. Wakisaka S. Neuropeptides in the dental pulp: distribution, origins, and correlation. J Endod. 1990; 16:67-9.10.1016/S0099-2399(06)81566-9]Search in Google Scholar
[29. Byers MR, Narhi MV. Dental injury models: experimental tools for understanding neuroinflammatory interactions and polymodal nociceptor functions. Crit Rev Oral Biol Med. 1999; 10:4-39.10.1177/10454411990100010101]Open DOISearch in Google Scholar
[30. Taylor PE, Byers MR, Redd PE. Sprouting of CGRP nerve fibers in response to dentin injury in rat molars. Brain Res. 1988; 461:371-6.10.1016/0006-8993(88)90270-3]Search in Google Scholar
[31. Byers MR, Suzuki H, Maeda T. Dental neuroplasticity, neuro-pulpal interactions, and nerve regeneration. Microsc Res Tech. 2003; 60:503-15.10.1002/jemt.10291]Open DOISearch in Google Scholar
[32. Byers MR, Taylor PE, Khayat BG, Kimberly CL. Effects of injury and inflammation on pulpal and periapical nerves. J Endod. 1990; 16:78-84.10.1016/S0099-2399(06)81568-2]Search in Google Scholar
[33. Goodman BE. Channels active in the excitability of nerves and skeletal muscles across the neuromuscular junction: basic function and pathophysiology. Adv Physiol Educ. 2008; 32:127-35.10.1152/advan.00091.200718539851]Open DOISearch in Google Scholar
[34. Eder C. Regulation of microglial behavior by ion channel activity. J Neurosci Res. 2005; 81:314-21.10.1002/jnr.2047615929071]Open DOISearch in Google Scholar
[35. Cummins TR, Sheets PL, Waxman SG. The roles of sodium channels in nociception: Implications for mechanisms of pain. Pain. 2007; 131:243-57.10.1016/j.pain.2007.07.026]Search in Google Scholar
[36. Amir R, Argoff CE, Bennett GJ, Cummins TR, Durieux ME, Gerner P, et al. The role of sodium channels in chronic inflammatory and neuropathic pain. J Pain. 2006; 7:S1-S29.10.1016/j.jpain.2006.01.444]Open DOISearch in Google Scholar
[37. Maingret F, Coste B, Padilla F, Clerc N, Crest M, Korogod SM, et al. Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism. J Gen Physiol. 2008; 131:211-25.10.1085/jgp.200709935]Search in Google Scholar
[38. Strickland IT, Martindale JC, Woodhams PL, Reeve AJ, Chessell IP, McQueen DS. Changes in the expression of NaV1.7, NaV1.8 and NaV1.9 in a distinct population of dorsal root ganglia innervating the rat knee joint in a model of chronic inflammatory joint pain. Eur J Pain. 2008; 12:564-72.10.1016/j.ejpain.2007.09.001]Search in Google Scholar
[39. Davidson RM. Neural form of voltage-dependent sodium current in human cultured dental pulp cells. Arch Oral Biol. 1994; 39:613-20.10.1016/0003-9969(94)90137-6]Open DOISearch in Google Scholar
[40. Allard B, Magloire H, Couble ML, Maurin JC, Bleicher F. Voltage-gated sodium channels confer excitability to human odontoblasts: possible role in tooth pain transmission. J Biol Chem. 2006; 281:29002-10.10.1074/jbc.M60102020016831873]Search in Google Scholar
[41. Henry MA, Luo S, Foley BD, Rzasa RS, Johnson LR, Levinson SR. Sodium channel expression and localization at demyelinated sites in painful human dental pulp. J Pain. 2009; 10:750-8.10.1016/j.jpain.2009.01.264275002719559391]Open DOISearch in Google Scholar
[42. Wells JE, Bingham V, Rowland KC, Hatton J. Expression of Nav1.9 channels in human dental pulp and trigeminal ganglion. J Endod. 2007; 33:1172-6.10.1016/j.joen.2007.05.02317889684]Search in Google Scholar
[43. Byers MR, Rafie MM, Westenbroek RE. Dexamethasone effects on Na(v)1.6 in tooth pulp, dental nerves, and alveolar osteoclasts of adult rats. Cell Tissue Res. 2009; 338:217-26.10.1007/s00441-009-0842-619763626]Search in Google Scholar
[44. Ichikawa H, Fukuda T, Terayama R, Yamaai T, Kuboki T, Sugimoto T. Immunohistochemical localization of gamma and beta subunits of epithelial Na+ channel in the rat molar tooth pulp. Brain Res. 2005; 1065: 138-41.10.1016/j.brainres.2005.10.01516297886]Search in Google Scholar
[45. Caldwell JH, Schaller KL, Lasher RS, Peles E, Levinson SR. Sodium channel Na(v)1.6 is localized at nodes of ranvier, dendrites, and synapses. Proc Natl Acad Sci U S A. 2000; 97:5616-20.10.1073/pnas.090034797]Search in Google Scholar
[46. Black JA, Renganathan M, Waxman SG. Sodium channel Na(v)1.6 is expressed along nonmyelinated axons and it contributes to conduction. Brain Res Mol Brain Res. 2002; 105:19-28.10.1016/S0169-328X(02)00385-6]Search in Google Scholar
[47. Luo S, Perry GM, Levinson SR, Henry MA. Pulpitis increases the proportion of atypical nodes of Ranvier in human dental pulp axons without a change in Na v 1.6 sodium channel expression. Neuroscience. 2010; 169:1881-7.10.1016/j.neuroscience.2010.06.044]Search in Google Scholar
[48. Staud R, Price DD, Janicke D, Andrade E, Hadjipanayis AG, Eaton WT, et al. Two novel mutations of SCN9A (Nav1.7) are associated with partial congenital insensitivity to pain. Eur J Pain [Internet]. 2010. Available from: doi:10.1016/j.ejpain.2010.07.003.]Search in Google Scholar
[49. Nilsen KB, Nicholas AK, Woods CG, Mellgren SI, Nebuchennykh M, Aasly J. Two novel SCN9A mutations causing insensitivity to pain. Pain. 2009; 143:155-8.10.1016/j.pain.2009.02.016]Search in Google Scholar
[50. Nassar MA, Stirling LC, Forlani G, Baker MD, Matthews EA, Dickenson AH, et al. Nociceptorspecific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain. Proc Natl Acad Sci U S A. 2004; 101:12706-11.10.1073/pnas.0404915101]Search in Google Scholar
[51. Beneng K, Renton T, Yilmaz Z, Yiangou Y, Anand P. Sodium channel Na v 1.7 immunoreactivity in painful human dental pulp and burning mouth syndrome. BMC Neurosci. 2010; 11:71.10.1186/1471-2202-11-71]Search in Google Scholar
[52. Renganathan M, Cummins TR, Waxman SG. Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons. J Neurophysiol. 2001; 86:629-40.10.1152/jn.2001.86.2.629]Search in Google Scholar
[53. Dib-Hajj S, Black JA, Cummins TR, Waxman SG. NaN/ Nav1.9: a sodium channel with unique properties. Trends Neurosci. 2002; 25:253-9.10.1016/S0166-2236(02)02150-1]Search in Google Scholar
[54. Amaya F, Wang H, Costigan M, Allchorne AJ, Hatcher JP, Egerton J, et al. The voltage-gated sodium channel Na(v)1.9 is an effector of peripheral inflammatory pain hypersensitivity. J Neurosci. 2006; 26:12852-60.10.1523/JNEUROSCI.4015-06.2006667496917167076]Search in Google Scholar
[55. Joshi SK, Mikusa JP, Hernandez G, Baker S, Shieh CC, Neelands T, et al. Involvement of the TTX-resistant sodium channel Nav 1.8 in inflammatory and neuropathic, but not post-operative, pain states. Pain. 2006; 123:75-82.10.1016/j.pain.2006.02.011]Search in Google Scholar
[56. Devor M. Sodium channels and mechanisms of neuropathic pain. J Pain. 2006; 7:S3-S12.10.1016/j.jpain.2005.09.006]Open DOISearch in Google Scholar
[57. Khasar SG, Gold MS, Levine JD. A tetrodotoxinresistant sodium current mediates inflammatory pain in the rat. Neurosci Lett. 1998; 256:17-20.10.1016/S0304-3940(98)00738-1]Search in Google Scholar
[58. Akopian AN, Souslova V, England S, Okuse K, Ogata N, Ure J, et al. The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways. Nat Neurosci. 1999; 2:541-8.10.1038/919510448219]Search in Google Scholar
[59. Tate S, Benn S, Hick C, Trezise D, John V, Mannion RJ, et al. Two sodium channels contribute to the TTX-R sodium current in primary sensory neurons. Nat Neurosci. 1998; 1:653-5.10.1038/365210196578]Open DOISearch in Google Scholar
[60. Dib-Hajj SD, Tyrrell L, Black JA, Waxman SG. NaN, a novel voltage-gated Na channel, is expressed preferentially in peripheral sensory neurons and down-regulated after axotomy. Proc Natl Acad Sci U S A. 1998; 95:8963-8.10.1073/pnas.95.15.8963211859671787]Open DOISearch in Google Scholar
[61. Henry MA, Sorensen HJ, Johnson LR, Levinson SR. Localization of the Nav1.8 sodium channel isoform at nodes of Ranvier in normal human radicular tooth pulp. Neurosci Lett. 2005; 380:32-6.10.1016/j.neulet.2005.01.01715854746]Search in Google Scholar
[62. Padilla F, Couble ML, Coste B, Maingret F, Clerc N, Crest M, et al. Expression and localization of the Nav1. 9 sodium channel in enteric neurons and in trigeminal sensory endings: implication for intestinal reflex function and orofacial pain. Mol Cell Neurosci. 2007; 35:138-52.10.1016/j.mcn.2007.02.00817363266]Search in Google Scholar
[63. Drummond HA, Grifoni SC, Jernigan NL. A new trick for an old dogma: ENaC proteins as mechanotransducers in vascular smooth muscle. Physiology (Bethesda). 2008; 23:23-31.10.1152/physiol.00034.200718268362]Open DOISearch in Google Scholar
[64. Kellenberger S, Schild L. Epithelial sodium channel/ degenerin family of ion channels: a variety of functions for a shared structure. Physiol Rev. 2002; 82:735-67.10.1152/physrev.00007.200212087134]Open DOISearch in Google Scholar
[65. Fricke B, Lints R, Stewart G, Drummond H, Dodt G, Driscoll M, et al. Epithelial Na+ channels and stomatin are expressed in rat trigeminal mechanosensory neurons. Cell Tissue Res. 2000; 299:327-34.]Search in Google Scholar
[66. Hitomi Y, Suzuki A, Kawano Y, Nozawa-Inoue K, Inoue M, Maeda T. Immunohistochemical detection of ENaCbeta in the terminal Schwann cells associated with the periodontal Ruffini endings of the rat incisor. Biomed Res. 2009; 30:113-9.10.2220/biomedres.30.11319420735]Open DOISearch in Google Scholar
[67. Scholz A, Kuboyama N, Hempelmann G, Vogel W. Complex blockade of TTX-resistant Na+ currents by lidocaine and bupivacaine reduce firing frequency in DRG neurons. J Neurophysiol. 1998; 79:1746-54.10.1152/jn.1998.79.4.17469535944]Search in Google Scholar
[68. Chevrier P, Vijayaragavan K, Chahine M. Differential modulation of Nav1.7 and Nav1.8 peripheral nerve sodium channels by the local anesthetic lidocaine. Br J Pharmacol. 2004; 142:576-84.10.1038/sj.bjp.0705796157496515148257]Search in Google Scholar
[69. Leffler A, Reiprich A, Mohapatra DP, Nau C. Usedependent block by lidocaine but not amitriptyline is more pronounced in tetrodotoxin (TTX)-Resistant Nav1.8 than in TTX-sensitive Na+ channels. J Pharmacol Exp Ther. 2007; 320:354-64.10.1124/jpet.106.10902517005919]Search in Google Scholar
[70. Kim HY, Kim K, Li HY, Chung G, Park CK, Kim JS, et al. Selectively targeting pain in the trigeminal system. Pain. 2010; 150:29-40.10.1016/j.pain.2010.02.016470411020236764]Search in Google Scholar
[71. Herold KF, Nau C, Ouyang W, Hemmings HC, Jr. Isoflurane inhibits the tetrodotoxin-resistant voltage-gated sodium channel Nav1.8. Anesthesiology. 2009; 111:591-9.10.1097/ALN.0b013e3181af64d4275608219672182]Search in Google Scholar
[72. Park CK, Li HY, Yeon KY, Jung SJ, Choi SY, Lee SJ, et al. Eugenol inhibits sodium currents in dental afferent neurons. J Dent Res. 2006; 85:900-4.10.1177/15440591060850100516998128]Open DOISearch in Google Scholar
[73. Park CK, Kim K, Jung SJ, Kim MJ, Ahn DK, Hong SD, et al. Molecular mechanism for local anesthetic action of eugenol in the rat trigeminal system. Pain. 2009; 144:84-94.10.1016/j.pain.2009.03.01619376653]Open DOISearch in Google Scholar
[74. Haeseler G, Foadi N, Ahrens J, Dengler R, Hecker H, Leuwer M. Tramadol, fentanyl and sufentanil but not morphine block voltage-operated sodium channels. Pain. 2006; 126:234-44.10.1016/j.pain.2006.07.00316949748]Open DOISearch in Google Scholar
[75. Ekberg J, Jayamanne A, Vaughan CW, Aslan S, Thomas L, Mould J, et al. muO-conotoxin MrVIB selectively blocks Nav1.8 sensory neuron specific sodium channels and chronic pain behavior without motor deficits. Proc Natl Acad Sci U S A. 2006; 103: 17030-5.10.1073/pnas.0601819103162908617077153]Search in Google Scholar
[76. Jarvis MF, Honore P, Shieh CC, Chapman M, Joshi S, Zhang XF, et al. A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat. Proc Natl Acad Sci U S A. 2007; 104:8520-5.10.1073/pnas.0611364104189598217483457]Search in Google Scholar
[77. Krafte DS, Chapman M, Marron B, Atkinson R, Liu Y, Ye F, et al. Block of Nav1.8 by small molecules. Channels (Austin). 2007; 1:152-3.10.4161/chan.476018690030]Search in Google Scholar
[78. Kort ME, Drizin I, Gregg RJ, Scanio MJ, Shi L, Gross MF, et al. Discovery and biological evaluation of 5-aryl-2-furfuramides, potent and selective blockers of the Nav1.8 sodium channel with efficacy in models of neuropathic and inflammatory pain. J Med Chem. 2008; 51:407-16. 10.1021/jm070637u18176998]Search in Google Scholar