{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T06:57:39Z","timestamp":1779173859512,"version":"3.51.4"},"reference-count":162,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2025,11,18]],"date-time":"2025-11-18T00:00:00Z","timestamp":1763424000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2025,11,18]],"date-time":"2025-11-18T00:00:00Z","timestamp":1763424000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Int Endodontic J"],"published-print":{"date-parts":[[2026,3]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Inflammatory radicular cysts (IRCs) arise from periapical granulomas (PGs). IRCs originate from Malassez epithelial remnants (ERMs), which can proliferate under specific biological stimuli. Although ERMs are common within PGs, only a subset of lesions evolves into IRCs, suggesting that specific molecular and immunoregulatory mechanisms govern this selective transformation.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>Molecular mechanisms and cellular signalling pathways modulating the epithelial proliferation of the ERM represent an inflexion point in the progression from PG to IRC. The objective of this review is to analyse the mechanisms and pathways involved in uncontrolled ERM proliferation, intending to elucidate why only a subset of epithelium\u2010containing PGs progress to IRCs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A systematic literature search was conducted across MEDLINE (PubMed), Web of Science and Scopus from inception to July 2025. Sixty\u2010one articles met the inclusion criteria for narrative analysis and synthesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>ERM proliferation emerges from a coordinated interplay between immune, stromal and epithelial compartments. Fibroblast growth factor\u20107 (FGF\u20107\/KGF) activates the FGFR2\u2010IIIb\u2013MAPK\/PI3K\u2013AKT pathways, maintaining homeostasis of ERM proliferation. Transforming growth factor\u2010\u03b2 (TGF\u2010\u03b21\/\u03b22) and Smad2\/3 signalling sustain epithelial quiescence. IGF\u2010BP\u20106 sequesters bioavailable insulin growth factor (IGF\u2010II), avoiding mitogenic signalling. Proteolytic cleavage of IGF\u2010BP\u20106 releases bioactive IGF\u2010II, enhancing ERM pathological proliferation. Intense AP upregulates epidermal growth factor (EGF) and its receptor (EGF\u2010R), promoting uncontrolled ERM proliferation. IL\u20101\u03b2 antagonises TGF\u2010\u03b2\/Smad2 suppression through NF\u2010\u03baB (p65) activation. IL\u20106 promotes pathological ERM proliferation and migration via classic and trans\u2010signalling. Persistent M1 macrophage polarisation and Th1\/Th17 dominance reinforce this microenvironment. Activated dendritic cells potentiate T\u2010cell responses and cytokine release.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Not all PGs progress to IRCs because cystic transformation requires the convergence of epithelial, stromal and immune thresholds that override ERM quiescence. This review proposes an integrative theoretical model that redefines ERMs as dynamic, inflammation\u2010responsive progenitors whose activation depends on immune\u2013epithelial cross\u2010talk rather than infection alone. By delineating specific biomarker clusters\u2014epithelial, immune\/co\u2010stimulatory and stromal\/remodelling\u2014this work proposes a mechanistic framework capable of predicting lesion behaviour. It may establish the foundation for molecularly guided diagnosis and the rational design of targeted therapeutic strategies aimed at preventing or reversing cystic transformation, ultimately bridging molecular insight with clinical endodontic practice.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/iej.70062","type":"journal-article","created":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T04:00:00Z","timestamp":1763524800000},"page":"396-425","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["From Quiescence to Proliferation: Molecular Mechanisms Driving Malassez Epithelial Cell Activation and Proliferation Into Inflammatory Radicular Cystic Transformation"],"prefix":"10.1111","volume":"59","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6675-6789","authenticated-orcid":false,"given":"Nestor","family":"R\u00edos\u2010Osorio","sequence":"first","affiliation":[{"name":"Endodontic Research Department CES University, School of Dentistry  Medellin Colombia"},{"name":"Faculty of Dentistry, Instituci\u00f3n Universitaria Visi\u00f3n de Las Am\u00e9ricas  Medell\u00edn Colombia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0407-9847","authenticated-orcid":false,"given":"Javier","family":"Caviedes\u2010Bucheli","sequence":"additional","affiliation":[{"name":"Centro de Investigaciones Odontol\u00f3gicas Pontificia Universidad Javeriana  Bogot\u00e1 Colombia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-9013-6872","authenticated-orcid":false,"given":"Juan","family":"Sosa\u2010Gutierrez","sequence":"additional","affiliation":[{"name":"School of Medicine and Life Sciences Universidad Escuela de Ingenieros de Antioquia (EIA)  Medell\u00edn Colombia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1431-8373","authenticated-orcid":false,"given":"Rafael","family":"Fern\u00e1ndez\u2010Grisales","sequence":"additional","affiliation":[{"name":"Endodontic Research Department CES University, School of Dentistry  Medellin Colombia"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2025,11,18]]},"reference":[{"key":"e_1_2_20_2_1","doi-asserted-by":"publisher","DOI":"10.1038\/oncsis.2016.71"},{"key":"e_1_2_20_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/35021228"},{"key":"e_1_2_20_4_1","doi-asserted-by":"publisher","DOI":"10.7717\/peerj.14949"},{"key":"e_1_2_20_5_1","doi-asserted-by":"publisher","DOI":"10.1111\/jop.12475"},{"key":"e_1_2_20_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.jobcr.2023.06.008"},{"key":"e_1_2_20_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.crmicr.2025.100443"},{"key":"e_1_2_20_8_1","doi-asserted-by":"publisher","DOI":"10.1590\/1678-775720140140"},{"key":"e_1_2_20_9_1","doi-asserted-by":"publisher","DOI":"10.1055\/s-2007-978723"},{"key":"e_1_2_20_10_1","doi-asserted-by":"publisher","DOI":"10.1038\/srep10721"},{"key":"e_1_2_20_11_1","doi-asserted-by":"publisher","DOI":"10.1152\/ajpendo.2000.278.6.E967"},{"key":"e_1_2_20_12_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrd2792"},{"issue":"2","key":"e_1_2_20_13_1","first-page":"419","article-title":"Radiological, Histological and Immunohistochemical Evaluation of Periapical Inflammatory Lesions","volume":"57","author":"Berar A. 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