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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">319</article-id>
      <article-id pub-id-type="doi">http://dx.doi.org/10.52533/JOHS.2024.41109</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>Genetic and Environmental Factors in Susceptibility to Oral Diseases&#13;
</article-title>
      </title-group>
      <contrib-group>
        <contrib contrib-type="author">
          <name>
            <surname>Munshi</surname>
            <given-names>Maha Assad</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alhabashi</surname>
            <given-names>Yousef Kh</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alshahrani</surname>
            <given-names>Norah Aedh</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Mushabab</surname>
            <given-names>Abdulaziz Abdullah</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alsaleh</surname>
            <given-names>Osama Saeed</given-names>
          </name>
        </contrib>
        <contrib contrib-type="author">
          <name>
            <surname>Alzahrani</surname>
            <given-names>Abdulrahman Hamed</given-names>
          </name>
        </contrib>
      </contrib-group>
      <pub-date pub-type="ppub">
        <day>25</day>
        <month>11</month>
        <year>2024</year>
      </pub-date>
      <volume>4</volume>
      <issue>11</issue>
      <fpage>616</fpage>
      <lpage>621</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>Oral diseases, such as dental caries, periodontitis, and oral cancers, are influenced by a combination of genetic, environmental, and epigenetic factors. Genetic predispositions, including polymorphisms in genes related to immune response and tissue repair, increase susceptibility to oral diseases. Variants in genes like interleukin-1 (IL-1) and matrix metalloproteinases (MMPs) have been associated with heightened inflammatory responses and tissue breakdown, contributing to the progression of periodontitis. Additionally, mutations in genes involved in enamel formation, such as AMELX, can lead to structural defects in teeth, increasing the risk of dental caries. Environmental factors, including diet, smoking, and lifestyle choices, further exacerbate oral disease risk. High sugar intake promotes the growth of acidogenic bacteria, leading to enamel demineralization and caries development. Smoking, in particular, accelerates periodontal disease progression and significantly raises the risk of oral cancer. The effects of environmental exposures are especially pronounced in individuals with underlying genetic vulnerabilities, highlighting the role of gene-environment interactions in oral disease susceptibility. Epigenetic modifications, including DNA methylation, histone acetylation, and microRNA regulation, add an additional layer of complexity to oral disease development. These modifications can alter gene expression without changing the DNA sequence, mediating the impact of environmental factors on genetic predispositions. Hypermethylation of tumor suppressor genes, such as CDKN2A, has been observed in oral cancer tissues, while altered histone acetylation patterns contribute to increased inflammation in periodontitis. Together, genetic predispositions, environmental exposures, and epigenetic modifications create a multifaceted risk profile for oral diseases. Understanding the interactions among these factors is crucial for developing personalized prevention and treatment strategies aimed at improving oral health outcomes. Future research focused on these molecular mechanisms holds promise for advancing early diagnosis and tailored therapeutic interventions in oral healthcare.&#13;
</p>
      </abstract>
      <kwd-group>
        <kwd>Genetic factors</kwd>
        <kwd> oral diseases</kwd>
        <kwd> environmental factors</kwd>
        <kwd> epigenetic modifications</kwd>
        <kwd> periodontitis</kwd>
      </kwd-group>
    </article-meta>
  </front>
</article>