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<article xlink="http://www.w3.org/1999/xlink" dtd-version="1.0" article-type="dentistry" lang="en">
  <front>
    <journal-meta>
      <journal-id journal-id-type="publisher">JOHS</journal-id>
      <journal-id journal-id-type="nlm-ta">Journ of Health Scien</journal-id>
      <journal-title-group>
        <journal-title>Journal of HealthCare Sciences</journal-title>
        <abbrev-journal-title abbrev-type="pubmed">Journ of Health Scien</abbrev-journal-title>
      </journal-title-group>
      <issn pub-type="ppub">2231-2196</issn>
      <issn pub-type="opub">0975-5241</issn>
      <publisher>
        <publisher-name>Radiance Research Academy</publisher-name>
      </publisher>
    </journal-meta>
    <article-meta>
      <article-id pub-id-type="publisher-id">532</article-id>
      <article-id pub-id-type="doi">http://dx.doi.org/10.52533/JOHS.2026.60604</article-id>
      <article-id pub-id-type="doi-url"/>
      <article-categories>
        <subj-group subj-group-type="heading">
          <subject>Dentistry</subject>
        </subj-group>
      </article-categories>
      <title-group>
        <article-title>Orthodontically Induced Inflammatory Root Resorption Cellular Mechanisms and Preventive Protocols&#13;
</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Farran</surname>
            <given-names>Waleed Hashim</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alwayel</surname>
            <given-names>Ali Naji</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alesawi</surname>
            <given-names>Alhanoof Hasan</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alghamdi</surname>
            <given-names>Hatoon Saleh</given-names>
          </name>
        </contrib>
      </contrib-group>
      <pub-date pub-type="ppub">
        <day>14</day>
        <month>06</month>
        <year>2026</year>
      </pub-date>
      <volume>6</volume>
      <issue>6</issue>
      <fpage>349</fpage>
      <lpage>354</lpage>
      <permissions>
        <copyright-statement>This article is copyright of Popeye Publishing, 2009</copyright-statement>
        <copyright-year>2009</copyright-year>
        <license license-type="open-access" href="http://creativecommons.org/licenses/by/4.0/">
          <license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 4.0) Licence. You may share and adapt the material, but must give appropriate credit to the source, provide a link to the licence, and indicate if changes were made.</license-p>
        </license>
      </permissions>
      <abstract>
        <p>Orthodontically induced inflammatory root resorption is a common adverse effect associated with orthodontic tooth movement and represents a significant clinical concern due to its potential to compromise root integrity and long-term dental stability. Although mild resorption is frequently observed and often considered an unavoidable consequence of treatment, severe forms may result in substantial root shortening and permanent structural damage. The biological basis of this phenomenon involves a complex interplay between mechanical forces, cellular responses, inflammatory mediators, and individual susceptibility factors. Mechanical loading applied during orthodontic treatment initiates a cascade of biological events within the periodontal ligament and surrounding alveolar bone. Cellular deformation, vascular alterations, and extracellular matrix remodeling stimulate the release of cytokines, chemokines, and growth factors that regulate bone remodeling and clastic cell activity. Key molecular pathways, including the receptor activator of nuclear factor kappa-B ligand (RANKL)/osteoprotegerin (OPG) system, play a central role in osteoclast and odontoclast differentiation, ultimately influencing the extent of root surface resorption. Emerging evidence has further highlighted the contribution of immune regulation, oxidative stress, hypoxia-related signaling, and regulated cell death pathways in the progression of resorptive lesions. The severity of root resorption varies considerably among individuals, reflecting the influence of multiple biological determinants. Genetic predisposition, root morphology, previous dental trauma, age-related tissue characteristics, and local periodontal conditions have all been associated with differences in susceptibility. These factors may alter the balance between tissue injury and repair, affecting the capacity of periodontal structures to withstand orthodontic forces. Preventive approaches focus on minimizing unnecessary tissue damage while maintaining efficient tooth movement. Contemporary strategies emphasize the application of controlled force systems, individualized treatment planning, periodic radiographic monitoring, and the use of adjunctive modalities aimed at supporting tissue preservation. Advances in imaging and molecular research continue to improve understanding of the mechanisms governing root resorption, providing opportunities for more targeted and biologically informed interventions that support both treatment efficiency and long-term dental health.&#13;
</p>
      </abstract>
      <kwd-group>
        <kwd>orthodontic tooth movement</kwd>
        <kwd> inflammatory root resorption</kwd>
        <kwd> mechanotransduction</kwd>
        <kwd> osteoclastogenesis</kwd>
        <kwd> cytokines</kwd>
        <kwd> root preservation</kwd>
        <kwd> orthodontics</kwd>
      </kwd-group>
    </article-meta>
  </front>
</article>