{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T07:56:10Z","timestamp":1790754970978,"version":"4.1.0"},"reference-count":39,"publisher":"Walter de Gruyter GmbH","issue":"1","license":[{"start":{"date-parts":[[2015,1,1]],"date-time":"2015-01-01T00:00:00Z","timestamp":1420070400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.elsevier.com\/tdm\/userlicense\/1.0\/"}],"content-domain":{"domain":["scandinavianjournalpain.com","elsevier.com","sciencedirect.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2015,1,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec id=\"j_j.sjpain.2014.10.002_s_001\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>It is unknown why an acute pain condition under various circumstances can transition into a chronic pain condition.<\/jats:p>\n                    <jats:p>There has been a shift towards neuroinflammation and hence glial cell activations specifically in the dorsal root ganglion and spinal cord as a mechanism possibly driving the transition to chronic pain. This has led to a focus on non-neuronal cells in the peripheral and central nervous system. Besides infiltrating macrophages, Schwann cells and satellite glial cells release cytokines and therefore important mechanisms in the maintenance of pain. Activated Schwann cells, satellite glial cells, microglia, and astrocytes may contribute to pain sensitivity by releasing cytokines leading to altered neuronal function in the direction of sensitisation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_j.sjpain.2014.10.002_s_002\">\n                    <jats:title>Aims of this perspective paper<\/jats:title>\n                    <jats:p>1) Highlight the complex but important recent achievement in the area of neuroinflammation and pain at spinal cord level and in the dorsal root ganglion.<\/jats:p>\n                    <jats:p>2) Encourage further research which hopefully may provide better understanding of new key elements driving the transition from acute to chronic pain.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_j.sjpain.2014.10.002_s_003\">\n                    <jats:title>Recent results in the area of neuroinflammation and pain<\/jats:title>\n                    <jats:p>Following a sciatic nerve injury, local macrophages, and Schwann cells trigger an immune response immediately followed by recruitment of blood-derived immune cells. Schwann cells, active resident, and infiltrating macrophages release proinflammatory cytokines. Proinflammatory cytokines contribute to axonal damage and also stimulate spontaneous nociceptor activity. This results in activation of satellite glial cells leading to an immune response in the dorsal root ganglia driven by macrophages, lymphocytes and satellite cells. The anterograde signalling progresses centrally to activate spinal microglia with possible up regulation of glial-derived proinflammatory\/pronociceptive mediators.<\/jats:p>\n                    <jats:p>An important aspect is extrasegmental spreading sensitisation where bilateral elevations in TNF-\u03b1, IL-6, and IL-10 are found in dorsal root ganglion in neuropathic models. Similarly in inflammatory pain models, bilateral up regulation occurs for TNF-\u03b1, IL-1 \u03b2, and p38 MAPK. Bilateral alterations in cytokine levels in the DRG and spinal cord may underlie the spread of pain to the uninjured side.<\/jats:p>\n                    <jats:p>An important aspect is how the opioids may interact with immune cells as opioid receptors are expressed by peripheral immune cells and thus can induce immune signaling changes. Furthermore, opioids may stimulate microglia cells to produce proinflammatory cytokines such as IL-1.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_j.sjpain.2014.10.002_s_004\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>The present perspective paper indicates that neuroinflammation and the associated release of pro-inflammatory cytokines in dorsal root ganglion and at the spinal cord contribute to the transition from acute to chronic pain. Neuroinflammatory changes have not only been identified in the spinal cord and brainstem, but more recently, in the sensory ganglia and in the nerves as well. The glial cell activation may be responsible for contralateral spreading and possible widespread sensitisation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_j.sjpain.2014.10.002_s_005\">\n                    <jats:title>Implications<\/jats:title>\n                    <jats:p>Communication between glia and neurons is proposed to be a critical component of neuroinflammatory changes that may lead to chronic pain. Sensory ganglia neurons are surrounded by satellite glial cells but how communication between the cells contributes to altered pain sensitivity is still unknown. Better understanding may lead to new possibilities for (1) preventing development of chronic pain and (2) better pain management.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1016\/j.sjpain.2014.10.002","type":"journal-article","created":{"date-parts":[[2014,11,24]],"date-time":"2014-11-24T13:16:13Z","timestamp":1416834973000},"page":"3-6","update-policy":"https:\/\/doi.org\/10.1016\/elsevier_cm_policy","source":"Crossref","is-referenced-by-count":51,"title":["Perspectives in Pain Research 2014: Neuroinflammation and glial cell activation: The cause of transition from acute to chronic pain?"],"prefix":"10.1515","volume":"6","author":[{"given":"Brian E.","family":"Cairns","sequence":"first","affiliation":[{"name":"Faculty of Pharmaceutical Sciences , University of British Columbia , 2405 Wesbrook Mall , Vancouver, BC , Canada V6T 1Z3"},{"name":"Center for Sensory-Motor Interaction, Department of Health Science and Technology, Faculty of Medicine , Aalborg University, Frederik Bajers Vej 7D3, 9220 Aalborg East , Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lars","family":"Arendt-Nielsen","sequence":"additional","affiliation":[{"name":"Center for Sensory-Motor Interaction, Department of Health Science and Technology, Faculty of Medicine , Aalborg University, Frederik Bajers Vej 7D3, 9220 Aalborg East , Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paola","family":"Sacerdote","sequence":"additional","affiliation":[{"name":"Dipartimento di Scienze farmacologiche e biomolecolari , Universit\u00e0 degli Studi di Milano , Via Vanvitelli 32, 20129 Milano , Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"374","published-online":{"date-parts":[[2015,1,1]]},"reference":[{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_001","doi-asserted-by":"crossref","unstructured":"Martucci C, Trovato AE, Costa B, Borsani E, Franchi S, Magnaghi V, Panerai AE, Rodella LF, Valsecchi AE, Sacerdote P, Colleoni M. The purinergic antagonist PPADS reduces pain related behaviours and interleukin-1 beta, interleukin-6, iNOS and nNOS overproduction in central and peripheral nervous system after peripheral neuropathy in mice. Pain 2008;137:81\u201395.","DOI":"10.1016\/j.pain.2007.08.017"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_002","doi-asserted-by":"crossref","unstructured":"Campana WM. Schwann cells: activated peripheral glia and their role in neuropathic pain. Brain Behav Immun 2007;21:522\u20137.","DOI":"10.1016\/j.bbi.2006.12.008"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_003","doi-asserted-by":"crossref","unstructured":"Grace PM, Hutchinson MR, Maier SF, Watkins LR. Pathological pain and the neuroimmune interface. Nat Rev Immunol 2014, http:\/\/dx.doi.org\/10.1038\/nri3621.","DOI":"10.1038\/nri3621"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_004","doi-asserted-by":"crossref","unstructured":"Sacerdote P, Franchi S, Moretti S, Castelli M, Procacci P, Magnaghi V, Panerai AE. Cytokine modulation is necessary for efficacious treatment of experimental neuropathic pain. J Neuroimmune Pharmacol 2013;8:202\u201311.","DOI":"10.1007\/s11481-012-9428-2"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_005","doi-asserted-by":"crossref","unstructured":"Sacerdote P, Niada S, Franchi S, Arrigoni E, Rossi A, Yenagi V, de Girolamo L, Panerai AE, Brini AT. Systemic administration of human adipose-derived stem cells reverts nociceptive hypersensitivity in an experimental model of neuropathy. Stem Cells Dev 2013;22:1252\u201363.","DOI":"10.1089\/scd.2012.0398"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_006","doi-asserted-by":"crossref","unstructured":"Sacerdote P, Franchi S, Panerai AE. Non-analgesic effects of opioids: mechanisms and potential clinical relevance of opioid-induced immunodepression. Curr Pharm Des 2012;18:6034\u201342.","DOI":"10.2174\/138161212803582496"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_007","doi-asserted-by":"crossref","unstructured":"Austin PJ, Moalem-Taylor G. The neuro-immune balance in neuropathic pain: involvement of inflammatory immune cells, immune-like glial cells and cytokines. J Neuroimmunol 2010;229:26\u201350.","DOI":"10.1016\/j.jneuroim.2010.08.013"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_008","doi-asserted-by":"crossref","unstructured":"Koltzenburg M, Wall PD, McMahon SB. Does the right side know what the left is doing? Trends Neurosci 1999;22:122\u20137.","DOI":"10.1016\/S0166-2236(98)01302-2"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_009","doi-asserted-by":"crossref","unstructured":"Dubovy P, Tuckova L, Jancalek R, Svizenska I, Klusakova I. Increased invasion of ED-1 positive macrophages in both ipsiand contralateral dorsal root ganglia following unilateral nerve injuries. Neurosci Lett 2007;427:88\u201393.","DOI":"10.1016\/j.neulet.2007.09.012"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_010","doi-asserted-by":"crossref","unstructured":"Dubovy P, Jancalek R, Klusakova I, Svizenska I, Pejchalova K. Intra- and extra-neuronal changes of immunoXuorescence staining for TNF-alpha and TNFR1 in the dorsal root ganglia of rat peripheral neuropathic pain models. Cell Mol Neurobiol 2006;26:1205\u201317.","DOI":"10.1007\/s10571-006-9006-3"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_011","doi-asserted-by":"crossref","unstructured":"Kleinschnitz C, Brinkho VJ, Sommer C, Stoll G. Contralateral cytokine gene induction after peripheral nerve lesions: dependence on the mode of injury and NMDA receptor signaling. Brain Res Mol Brain Res 2005;136:23\u20138.","DOI":"10.1016\/j.molbrainres.2004.12.015"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_012","doi-asserted-by":"crossref","unstructured":"Pitcher GM, Henry JL. Cellular mechanisms of hyperalgesia and spontaneous pain in a spinalized rat model of peripheral neuropathy: changes in my elinated afferent inputs implicated. Eur J Neurosci 2000;12:2006\u201320.","DOI":"10.1046\/j.1460-9568.2000.00087.x"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_013","doi-asserted-by":"crossref","unstructured":"Janc\u00e1lek R, Dubovy P, Sv\u00edzensk\u00e1 I, Klus\u00e1kov\u00e1 I. Bilateral changes of TNF-alpha and IL10 protein in the lumbar and cervical dorsal root ganglia following a unilateral chronic constriction injury of the sciatic nerve. J Neuroinflamm 2010;7:11.","DOI":"10.1186\/1742-2094-7-11"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_014","doi-asserted-by":"crossref","unstructured":"Jancalek R, Svizenska I, Klusakova I, Dubovy P. Bilateral changes of IL10 protein in lumbar and cervical dorsal root ganglia following proximal and distal chronic constriction injury of peripheral nerve. Neurosci Lett 2011;501:86\u201391.","DOI":"10.1016\/j.neulet.2011.06.052"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_015","doi-asserted-by":"crossref","unstructured":"Wagner R, Janjigian M, Myers RR. Anti-inflammatory interleukin-10 therapy in CCI neuropathy decreases thermal hyperalgesia, macrophage recruitment, and endoneurial TNF-alpha expression. Pain 1998;74:35\u201342.","DOI":"10.1016\/S0304-3959(97)00148-6"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_016","doi-asserted-by":"crossref","unstructured":"Dubovy P, Br\u00e1zda V, Klus\u00e1kov\u00e1 I, Hradilov\u00e1-Sv\u00edzensk\u00e1 I. Bilateral elevation of interleukin-6 protein and mRNA in both lumbar and cervical dorsal root ganglia following unilateral chronic compression injury of the sciatic nerve. J Neuroinflamm 2013;10:55.","DOI":"10.1186\/1742-2094-10-55"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_017","doi-asserted-by":"crossref","unstructured":"Beloeil H, Ji RR, Berde CB. Effects of bupivacaine and tetrodotoxin on carrageenan-induced hind paw inflammation in rats (Part 2): cytokines and p38 mitogen-activated protein kinases in dorsal root ganglia and spinal cord. Anesthesiology 2006;105:139\u201345.","DOI":"10.1097\/00000542-200607000-00023"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_018","doi-asserted-by":"crossref","unstructured":"Arguis MJ, Perez J, Mart\u00ednez G, Ubre M, Gomar C. Contralateral neuropathic pain following a surgical model of unilateral nerve injury in rats. Reg Anesth Pain Med 2008;33:211\u20136.","DOI":"10.1136\/rapm-00115550-200805000-00004"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_019","doi-asserted-by":"crossref","unstructured":"Dubovy P, Klus\u00e1kov\u00e1 I, Sv\u00edzensk\u00e1 I, Br\u00e1zda V. Satellite glial cells express IL-6 and corresponding signal-transducing receptors in the dorsal root ganglia of rat neuropathic pain model. Neuron Glia Biol 2010;6:73\u201383.","DOI":"10.1017\/S1740925X10000074"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_020","doi-asserted-by":"crossref","unstructured":"Hirota H, Kiyama H, Kishimoto T, Taga T. Accelerated nerve regeneration in mice by upregulated expression of interleukin (IL) 6 and IL-6 receptor after trauma. J Exp Med 1996;183:2627\u201334.","DOI":"10.1084\/jem.183.6.2627"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_021","doi-asserted-by":"crossref","unstructured":"DeLeo JA, Colburn RW, Nichols M, Malhotra A. Interleukin-6-mediatedhyperal-gesia\/allodynia and increased spinal IL-6 expression in a rat mononeuropathy model. J Interferon Cytokine Res 1996;16:695\u2013700.","DOI":"10.1089\/jir.1996.16.695"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_022","doi-asserted-by":"crossref","unstructured":"Tal M, Bennett GJ. Extra-territorial pain in rats with a peripheral mononeuropathy: mechano-hyperalgesia and mechano-allodynia in the territory of the uninjured nerve. Pain 1994;57:375\u201382.","DOI":"10.1016\/0304-3959(94)90013-2"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_023","doi-asserted-by":"crossref","unstructured":"Ringkamp M, Meyer RA. Injured versus uninjured afferents - who is to blame for neuropathic pain? Anesthesiology 2005;103:221\u20133.","DOI":"10.1097\/00000542-200508000-00002"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_024","doi-asserted-by":"crossref","unstructured":"Jang JH, Kim KH, Nam TS, Lee WT, Park KA, Kim DW, Leem JW. The role of uninjured C-afferents and injured afferents in the generation of mechanical hypersensitivity after partial peripheral nerve injury in the rat. Exp Neurol 2007;204:288\u201398.","DOI":"10.1016\/j.expneurol.2006.11.004"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_025","doi-asserted-by":"crossref","unstructured":"Schreiber KL, Beitz AJ, Wilcox GL. Activation of spinal microglia in a murine model of peripheral inflammation-induced, long-lasting contralateral allodynia. Neurosci Lett 2008;440:63\u20137.","DOI":"10.1016\/j.neulet.2008.05.044"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_026","doi-asserted-by":"crossref","unstructured":"Winkelstein BA, Rutkowski MD, Sweitzer SM, Pahl JL, DeLeo JA. Nerve injury proximal or distal to the DRG induces similar spinal glial activation and selective cytokine expression but differential behavioral responses to phar-macologic treatment. J Comp Neurol 2001;439:127\u201339.","DOI":"10.1002\/cne.2000.abs"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_027","doi-asserted-by":"crossref","unstructured":"Winkelstein BA, DeLeo JA. Nerve root injury severity differentially modulates spinal glial activation in a rat lumbar radiculopathy model: considerations for persistent pain. Brain Res 2002;956:294\u2013301.","DOI":"10.1016\/S0006-8993(02)03560-6"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_028","doi-asserted-by":"crossref","unstructured":"Ledeboer A, Sloane EM, Milligan ED, Frank MG, Mahony JH, Maier SF, Watkins LR. Minocycline attenuates mechanical allodynia and proinflammatory cytokine expression in rat models of pain facilitation. Pain 2005;115:71\u201383.","DOI":"10.1016\/j.pain.2005.02.009"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_029","doi-asserted-by":"crossref","unstructured":"Fu KY, Light AR, Maixner W. Relationship between nociceptor activity, peripheral edema, spinal microglial activation and long-term hyperalgesia induced by formalin. Neuroscience 2000;101:1127\u201335.","DOI":"10.1016\/S0306-4522(00)00376-6"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_030","doi-asserted-by":"crossref","unstructured":"Chang YW, Tan A, Saab C, Waxman S. Unilateral focal burn injury is followed by long-lasting bilateral allodynia and neuronal hyperexcitability in spinal cord dorsal horn. J Pain V 11 2010:119\u201330.","DOI":"10.1016\/j.jpain.2009.06.009"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_031","doi-asserted-by":"crossref","unstructured":"Laursen JC, Cairns BE, Dong XD, Kumar U, Somvanshi RK, Arendt-Nielsen L, Gazerani P. Glutamate dysregulation in the trigeminal ganglion: a novel mechanism for peripheral sensitization of the craniofacial region. Neuroscience 2014;256:23\u201335.","DOI":"10.1016\/j.neuroscience.2013.10.009"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_032","doi-asserted-by":"crossref","unstructured":"de Goeij M, van Eijk LT, Vanelderen P, Wilder-Smith OH, Vissers KC, van der Hoeven JG, Kox M, Scheffer GJ, Pickkers P. Systemic inflammation decreases pain threshold in humans in vivo. PLoS ONE 2013;8:e84159.","DOI":"10.1371\/journal.pone.0084159"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_033","doi-asserted-by":"crossref","unstructured":"Kwok YH, Hutchinson MR, Gentgall MG, Rolan PE. Increased responsiveness of peripheral blood mononuclear cells to in vitro TLR 2, 4 and 7 ligand stimulation in chronic pain patients. PLoS ONE 2012;7:e44232.","DOI":"10.1371\/journal.pone.0044232"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_034","doi-asserted-by":"crossref","unstructured":"Hutchinson MR, Zhang Y, Shridhar M, Evans JH, Buchanan MM, Zhao TX, Slivka PF, Coats BD, Rezvani N, Wieseler J, Hughes TS, Landgraf KE, Chan S, Fong S, Phipps S, Falke JJ, Leinwand LA, Maier SF, Yin H, Rice KC, Watkins LR. Evidence that opioids may have toll-like receptor4 and MD-2 effects. Brain Behav Immun 2010;24:83\u201395.","DOI":"10.1016\/j.bbi.2009.08.004"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_035","doi-asserted-by":"crossref","unstructured":"Habibi-Asl B, Hassanzadeh K, Charkhpour M. Central administration of minocycline and riluzole prevents morphine-induced tolerance in rats. Anesth Analg 2009;109:936\u201342.","DOI":"10.1213\/ane.0b013e3181ae5f13"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_036","doi-asserted-by":"crossref","unstructured":"Mika J, Wawrzczak-Bargiela A, Osikowicz M, Makuch W, Przewlocka B. Attenuation of morphine tolerance by minocycline and pentoxifylline in naive and neuropathic mice. Brain Behav Immun 2009;23:75\u201384.","DOI":"10.1016\/j.bbi.2008.07.005"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_037","doi-asserted-by":"crossref","unstructured":"Fukagawa H, Koyama T, Kakuyama M, Fukuda K. Microglial activation involved in morphine tolerance is not mediated by toll-like receptor 4. J Anesth 2013;27:93\u20137.","DOI":"10.1007\/s00540-012-1469-4"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_038","doi-asserted-by":"crossref","unstructured":"Kavelaars A, Eijkelkamp N, Willemen HL, Wang H, Carbajal AG, Heijnen CJ. Microglial GRK2: a novel regulator of transition from acute to chronic pain. Brain Behav Immun 2011;25:1055\u201360.","DOI":"10.1016\/j.bbi.2011.03.019"},{"key":"2025120910053090236_j_j.sjpain.2014.10.002_ref_039","doi-asserted-by":"crossref","unstructured":"Wang H, Heijnen CJ, van Velthoven CT, Willemen HL, Ishikawa Y, Zhang X, Sood AK, Vroon A, Eijkelkamp N, Kavelaars A. Balancing GRK2 and EPAC1 levels prevents and relieves chronic pain. J Clin Invest 2013;123:5023\u201334.","DOI":"10.1172\/JCI66241"}],"container-title":["Scandinavian Journal of Pain"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.degruyter.com\/view\/journals\/sjpain\/6\/1\/article-p3.xml","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/api.elsevier.com\/content\/article\/PII:S187788601400161X?httpAccept=text\/xml","content-type":"text\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/api.elsevier.com\/content\/article\/PII:S187788601400161X?httpAccept=text\/plain","content-type":"text\/plain","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.degruyterbrill.com\/document\/doi\/10.1016\/j.sjpain.2014.10.002\/xml","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.degruyterbrill.com\/document\/doi\/10.1016\/j.sjpain.2014.10.002\/pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,12,9]],"date-time":"2025-12-09T12:56:25Z","timestamp":1765284985000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.degruyterbrill.com\/document\/doi\/10.1016\/j.sjpain.2014.10.002\/html"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2015,1,1]]},"references-count":39,"journal-issue":{"issue":"1","published-online":{"date-parts":[[2015,1,1]]},"published-print":{"date-parts":[[2015,1,1]]}},"alternative-id":["10.1016\/j.sjpain.2014.10.002"],"URL":"https:\/\/doi.org\/10.1016\/j.sjpain.2014.10.002","relation":{},"ISSN":["1877-8860","1877-8879"],"issn-type":[{"value":"1877-8860","type":"print"},{"value":"1877-8879","type":"electronic"}],"subject":[],"published":{"date-parts":[[2015,1,1]]},"assertion":[{"value":"Elsevier","name":"publisher","label":"This article is maintained by"},{"value":"Perspectives in Pain Research 2014: Neuroinflammation and glial cell activation: The cause of transition from acute to chronic pain?","name":"articletitle","label":"Article Title"},{"value":"Scandinavian Journal of Pain","name":"journaltitle","label":"Journal Title"},{"value":"http:\/\/dx.doi.org\/10.1016\/j.sjpain.2014.10.002","name":"articlelink","label":"CrossRef DOI link to publisher maintained version"},{"value":"http:\/\/dx.doi.org\/10.1016\/j.sjpain.2014.10.004","name":"associatedlink","label":"CrossRef DOI link to the associated document"},{"value":"article","name":"content_type","label":"Content Type"},{"value":"Copyright \u00a9 2014 Scandinavian Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.","name":"copyright","label":"Copyright"}]}}