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      <title>Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</title>
      <link>https://onlinelibrary.wiley.com/journal/16000714?af=R</link>
      <description>Table of Contents for Journal of Oral Pathology &amp; Medicine. List of articles from both the latest and EarlyView issues.</description>
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      <copyright>© John Wiley &amp; Sons A/S. Published by John Wiley &amp; Sons Ltd</copyright>
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      <pubDate>Fri, 12 Jun 2026 07:38:15 +0000</pubDate>
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      <dc:title>Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</dc:title>
      <dc:publisher>Wiley-Online-Library</dc:publisher>
      <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
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         <title>Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</title>
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         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70158?af=R</link>
         <pubDate>Thu, 11 Jun 2026 23:54:18 -0700</pubDate>
         <dc:date>2026-06-11T11:54:18-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
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         <title>Bridging the Health Literacy Gap for Patients With Oral Cancer: Readability Enhancement With AI Chatbots</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Early diagnosis is crucial in improving oral cancer outcomes. Patient education materials support timely recognition and management. However, these resources are often written above recommended reading levels, beyond patients' health literacy and limiting accessibility.


Objectives
To assess the readability of available patient information on oral cancer by the NHS, to evaluate three large language models (LLMs; ChatGPT, Claude and Gemini) in simplifying texts while preserving their content, and to propose an improved leaflet based on UK materials, expert review and LLM adjustment to match average UK reading levels.


Methods
Materials were collected from NHS‐affiliated websites. Original and LLM‐simplified texts were assessed using validated readability tools (FRES, FKGL, GFI, CLI and SMOG). Content fidelity was assessed using character 3–5‐g cosine, sentence‐content retention and latent semantic analysis (LSA). An expert review was applied to the proposed leaflet.


Results
LLM‐revisions significantly improved readability across all five indices (p &lt; 0.0001). Mean FRES of original texts was 66.4 ± 7.7, while Claude (81.6 ± 6.2) was the only model to surpass the 80 benchmark. Semantic similarity to source text remained high (LSA means 0.97 ± 0.04, 0.94 ± 0.09 and 0.96 ± 0.08; character 3–5‐g cosine 0.85 ± 0.05, 0.80 ± 0.08 and 0.82 ± 0.08 for respective models). Baseline readability of the proposed leaflet was comparable to NHS materials (FRES 65.7); Claude increased this to 81.2.


Conclusions
LLM‐based simplification enhanced readability while preserving content fidelity. This approach can help enhance accessibility, particularly for populations disproportionately affected by oral cancer. With human oversight, it could be adopted at the policy level to standardise patient education and reduce health literacy disparities.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Early diagnosis is crucial in improving oral cancer outcomes. Patient education materials support timely recognition and management. However, these resources are often written above recommended reading levels, beyond patients' health literacy and limiting accessibility.&lt;/p&gt;
&lt;h2&gt;Objectives&lt;/h2&gt;
&lt;p&gt;To assess the readability of available patient information on oral cancer by the NHS, to evaluate three large language models (LLMs; ChatGPT, Claude and Gemini) in simplifying texts while preserving their content, and to propose an improved leaflet based on UK materials, expert review and LLM adjustment to match average UK reading levels.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Materials were collected from NHS-affiliated websites. Original and LLM-simplified texts were assessed using validated readability tools (FRES, FKGL, GFI, CLI and SMOG). Content fidelity was assessed using character 3–5-g cosine, sentence-content retention and latent semantic analysis (LSA). An expert review was applied to the proposed leaflet.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;LLM-revisions significantly improved readability across all five indices (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.0001). Mean FRES of original texts was 66.4 ± 7.7, while Claude (81.6 ± 6.2) was the only model to surpass the 80 benchmark. Semantic similarity to source text remained high (LSA means 0.97 ± 0.04, 0.94 ± 0.09 and 0.96 ± 0.08; character 3–5-g cosine 0.85 ± 0.05, 0.80 ± 0.08 and 0.82 ± 0.08 for respective models). Baseline readability of the proposed leaflet was comparable to NHS materials (FRES 65.7); Claude increased this to 81.2.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;LLM-based simplification enhanced readability while preserving content fidelity. This approach can help enhance accessibility, particularly for populations disproportionately affected by oral cancer. With human oversight, it could be adopted at the policy level to standardise patient education and reduce health literacy disparities.&lt;/p&gt;</content:encoded>
         <dc:creator>
Agata Baczynska, 
Umar Rehman, 
Shireen S. Gohari, 
Kelly Chu, 
Mohammad Sohaib Sarwar, 
Peter A. Brennan
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Bridging the Health Literacy Gap for Patients With Oral Cancer: Readability Enhancement With AI Chatbots</dc:title>
         <dc:identifier>10.1111/jop.70158</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70158</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70158?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70156?af=R</link>
         <pubDate>Tue, 09 Jun 2026 04:55:45 -0700</pubDate>
         <dc:date>2026-06-09T04:55:45-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70156</guid>
         <title>Rapamycin Targets Cancer Stem Cells to Decrease Cisplatin Resistance in a Head and Neck Cancer Mouse Xenograft Model</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Cisplatin is a common chemotherapeutic agent for advanced head and neck squamous cell carcinoma (HNSCC), but treatment success is often limited by resistance. Cancer stem cells (CSCs) are known contributors to this cisplatin chemoresistance in HNSCC. The mechanistic target of rapamycin (mTOR) pathway, which is frequently dysregulated in HNSCC, plays a crucial role via the PI3K/AKT/mTOR axis in maintaining CSC populations and promoting cancer proliferation. However, the specific effects of combining rapamycin, an mTOR pathway inhibitor, with chemotherapeutic agents on CSC maintenance and overall tumorigenicity remain unclear.


Methods
We examined CSC gene expression in HNSCC cell lines (HSC4, SCC25, OT‐1109) and evaluated the therapeutic potential of combining rapamycin, an mTOR pathway inhibitor, with cisplatin on CSC using a cell viability assay. The combination was further evaluated in an HSC4 mouse xenograft model. Tumor volume and animal weight were monitored throughout treatment. Xenograft tissue analysis via immunohistochemistry assessed stem cell markers (CD133 and ALDH1A1), proliferation markers (Ki‐67), and mTOR pathway inhibition (pS6).


Results
Administration of low‐dose cisplatin enriched the CD133+ cell population but failed to decrease the tumor mass in HNSCC xenografts. In contrast, the combination of cisplatin and rapamycin significantly impeded tumor growth and minimized toxicity, concurrently reducing the population of CD133+ tumor cells.


Conclusion
These findings suggest that rapamycin enhances the mechanistic efficacy of cisplatin by specifically targeting and reducing cisplatin‐induced stemness (CD133+ CSC population). This study proposes a viable combination therapy for HNSCC involving an mTOR inhibitor and a platinum‐based drug to overcome CSC‐mediated resistance.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Cisplatin is a common chemotherapeutic agent for advanced head and neck squamous cell carcinoma (HNSCC), but treatment success is often limited by resistance. Cancer stem cells (CSCs) are known contributors to this cisplatin chemoresistance in HNSCC. The mechanistic target of rapamycin (mTOR) pathway, which is frequently dysregulated in HNSCC, plays a crucial role via the PI3K/AKT/mTOR axis in maintaining CSC populations and promoting cancer proliferation. However, the specific effects of combining rapamycin, an mTOR pathway inhibitor, with chemotherapeutic agents on CSC maintenance and overall tumorigenicity remain unclear.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;We examined CSC gene expression in HNSCC cell lines (HSC4, SCC25, OT-1109) and evaluated the therapeutic potential of combining rapamycin, an mTOR pathway inhibitor, with cisplatin on CSC using a cell viability assay. The combination was further evaluated in an HSC4 mouse xenograft model. Tumor volume and animal weight were monitored throughout treatment. Xenograft tissue analysis via immunohistochemistry assessed stem cell markers (CD133 and ALDH1A1), proliferation markers (Ki-67), and mTOR pathway inhibition (pS6).&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Administration of low-dose cisplatin enriched the CD133&lt;sup&gt;+&lt;/sup&gt; cell population but failed to decrease the tumor mass in HNSCC xenografts. In contrast, the combination of cisplatin and rapamycin significantly impeded tumor growth and minimized toxicity, concurrently reducing the population of CD133&lt;sup&gt;+&lt;/sup&gt; tumor cells.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;These findings suggest that rapamycin enhances the mechanistic efficacy of cisplatin by specifically targeting and reducing cisplatin-induced stemness (CD133&lt;sup&gt;+&lt;/sup&gt; CSC population). This study proposes a viable combination therapy for HNSCC involving an mTOR inhibitor and a platinum-based drug to overcome CSC-mediated resistance.&lt;/p&gt;</content:encoded>
         <dc:creator>
Khin Swe Hlaing, 
Aung Phyo Shan, 
Eakapong Tamboon, 
Asada Leelahavanichkul, 
Panomwat Amornphimoltham
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Rapamycin Targets Cancer Stem Cells to Decrease Cisplatin Resistance in a Head and Neck Cancer Mouse Xenograft Model</dc:title>
         <dc:identifier>10.1111/jop.70156</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70156</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70156?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70157?af=R</link>
         <pubDate>Thu, 04 Jun 2026 23:41:17 -0700</pubDate>
         <dc:date>2026-06-04T11:41:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70157</guid>
         <title>Pg‐Induced ATR Activation Promotes ESCC Progression via M2 TAM Polarization</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Emerging evidence suggests that oral pathogens may contribute to the development of systemic malignancies. Porphyromonas gingivalis (Pg), a major periodontal pathogen, has been implicated in several cancers including esophageal squamous cell carcinoma (ESCC). However, the molecular mechanisms underlying this association remain unclear.


Objective
This study aimed to investigate the impact of Porphyromonas gingivalis (Pg) on the growth of esophageal squamous cell carcinoma (ESCC) and its potential mechanisms.


Methods
THP‐1 cells were differentiated into M0 macrophages with PMA and divided into control group, Pg group, and Pg + siATR group. THP‐1 cells were divided into three groups: control group, Pg group, and Pg + siATR group. The control and Pg groups were transfected with siNC, while the Pg + siATR group was transfected with siATR. After transfection, the Pg group and Pg + siATR group were incubated with 200 MOI pg. The control group was cultured normally. Cells and supernatants were collected, and macrophage polarization status was detected with qRT‐PCR, Western blot, and flow cytometry. Macrophages treated differently were co‐cultured with human esophageal squamous cell carcinoma cell line KYSE150. The proliferation, invasion, and apoptosis of KYSE150 were examined. KYSE150+shATR and KYSE150+shNC cell lines were constructed with a lentivirus system. Thirty male BALB/c mice aged 6–8 weeks were randomly divided into control group, pg group, and pg+shATR group, with 10 mice in each group. For the Pg and Pg+shATR groups, 200 μL Pg (1 × 107 CFU/mouse) was applied to the mandibular molars of mice four times a week for 1 month. The control group was treated with the vehicle (CMC) only. After 3 weeks of bacterial colonization, KYSE150+shATR cells (1 × 106 cells/mouse) were inoculated into the right axilla of mice in the Pg+shATR group, while KYSE150 + shNC (1 × 106 cells/mouse) were inoculated into the right axilla of mice in the control and Pg groups. Tumor volume was measured with calipers every 7 days. After 4 weeks of experimentation, D‐luciferin potassium salt was injected intraperitoneally at 150 mg/kg, and bioluminescence imaging was performed after sodium pentobarbital anesthesia. The mice were euthanized post‐imaging, and macrophage polarization in tumor tissues was examined with qRT‐PCR, histopathological examination, and Western blot.


Results
In this study, we found that Pg could promote the polarization of M0 macrophages into M2 macrophages, while also promoting the malignant progression of KYSE150 cells. The expression levels of ATR, phosphorylated ATR (p‐ATR), and M2 macrophage markers (CD206, Arg1, and VEGF) decreased when ATR was inhibited. In BALB/c mice, Pg‐induced ATR activation promoted the growth of subcutaneously implanted tumors by recruiting M2‐type TAMs. Experimental data also indicated an association between M2 polarization, decreased p‐chik, and ATR.


Conclusion
This study reveals that Pg can activate the ataxia‐telangiectasia and Rad3‐related protein (ATR) signaling pathway, inducing the polarization of M2 tumor‐associated macrophages (TAM), thereby promoting the growth of ESCC. This provides a new theoretical basis for the prevention and treatment of ESCC.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Emerging evidence suggests that oral pathogens may contribute to the development of systemic malignancies. &lt;i&gt;Porphyromonas gingivalis&lt;/i&gt; (Pg), a major periodontal pathogen, has been implicated in several cancers including esophageal squamous cell carcinoma (ESCC). However, the molecular mechanisms underlying this association remain unclear.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;This study aimed to investigate the impact of &lt;i&gt;Porphyromonas gingivalis&lt;/i&gt; (Pg) on the growth of esophageal squamous cell carcinoma (ESCC) and its potential mechanisms.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;THP-1 cells were differentiated into M0 macrophages with PMA and divided into control group, Pg group, and Pg + siATR group. THP-1 cells were divided into three groups: control group, Pg group, and Pg + siATR group. The control and Pg groups were transfected with siNC, while the Pg + siATR group was transfected with siATR. After transfection, the Pg group and Pg + siATR group were incubated with 200 MOI pg. The control group was cultured normally. Cells and supernatants were collected, and macrophage polarization status was detected with qRT-PCR, Western blot, and flow cytometry. Macrophages treated differently were co-cultured with human esophageal squamous cell carcinoma cell line KYSE150. The proliferation, invasion, and apoptosis of KYSE150 were examined. KYSE150+shATR and KYSE150+shNC cell lines were constructed with a lentivirus system. Thirty male BALB/c mice aged 6–8 weeks were randomly divided into control group, pg group, and pg+shATR group, with 10 mice in each group. For the Pg and Pg+shATR groups, 200 μL Pg (1 × 10&lt;sup&gt;7&lt;/sup&gt; CFU/mouse) was applied to the mandibular molars of mice four times a week for 1 month. The control group was treated with the vehicle (CMC) only. After 3 weeks of bacterial colonization, KYSE150+shATR cells (1 × 10&lt;sup&gt;6&lt;/sup&gt; cells/mouse) were inoculated into the right axilla of mice in the Pg+shATR group, while KYSE150 + shNC (1 × 10&lt;sup&gt;6&lt;/sup&gt; cells/mouse) were inoculated into the right axilla of mice in the control and Pg groups. Tumor volume was measured with calipers every 7 days. After 4 weeks of experimentation, D-luciferin potassium salt was injected intraperitoneally at 150 mg/kg, and bioluminescence imaging was performed after sodium pentobarbital anesthesia. The mice were euthanized post-imaging, and macrophage polarization in tumor tissues was examined with qRT-PCR, histopathological examination, and Western blot.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;In this study, we found that Pg could promote the polarization of M0 macrophages into M2 macrophages, while also promoting the malignant progression of KYSE150 cells. The expression levels of ATR, phosphorylated ATR (p-ATR), and M2 macrophage markers (CD206, Arg1, and VEGF) decreased when ATR was inhibited. In BALB/c mice, Pg-induced ATR activation promoted the growth of subcutaneously implanted tumors by recruiting M2-type TAMs. Experimental data also indicated an association between M2 polarization, decreased p-chik, and ATR.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This study reveals that Pg can activate the ataxia-telangiectasia and Rad3-related protein (ATR) signaling pathway, inducing the polarization of M2 tumor-associated macrophages (TAM), thereby promoting the growth of ESCC. This provides a new theoretical basis for the prevention and treatment of ESCC.&lt;/p&gt;</content:encoded>
         <dc:creator>
Yanhua Sun, 
Lin Yang, 
Xiaodong Wei
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Pg‐Induced ATR Activation Promotes ESCC Progression via M2 TAM Polarization</dc:title>
         <dc:identifier>10.1111/jop.70157</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70157</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70157?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70154?af=R</link>
         <pubDate>Thu, 28 May 2026 04:59:56 -0700</pubDate>
         <dc:date>2026-05-28T04:59:56-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70154</guid>
         <title>Implications of ADP‐Ribosylation Factor‐Like Protein 4C (ARL4C) in Human Neoplasia With Special Emphasis on Ameloblastoma: A Scoping Review</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
ADP‐ribosylation factor‐like protein 4C (ARL4C), a member of the ARF small GTP‐binding protein subfamily, has emerged from its role as an epithelial growth regulator to become a central molecule in cancer biology. This scoping review was conducted according to the PRISMA‐ScR framework, systematically maps literature from PubMed, Scopus and Web of Science up to December 2024 to synthesise evidence on ARL4C's regulatory mechanisms and its implications in tumourigenesis and relevance to ameloblastoma.


Findings
Originally recognised for its role in tissue morphogenesis, ARL4C is now known to drive cancer cell proliferation, migration and invasion when dysregulated. Its expression is modulated by major signalling cascades including Wnt/MAPK, PI3K/AKT and TGF‐β, as well as epigenetic factors. While primarily acting as an oncogenic driver, ARL4C exhibits context‐dependent roles, occasionally functioning as a tumour suppressor. In ameloblastoma, a locally aggressive odontogenic tumour, ARL4C expression correlates with invasion and bone resorption. Notably, this influence appears independent of BRAF mutation status, suggesting a unique pathological role in this setting.


Conclusion
ARL4C stands at the intersection of fundamental cell biology and clinical oncology. It holds promise as a biomarker for prognosis and recurrence and as a potential therapeutic target. However, its dual nature highlights the complexity of cancer signalling networks. Future research involving larger patient cohorts is essential to validate ARL4C's utility in precision oncology, particularly for the management of ameloblastoma.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;ADP-ribosylation factor-like protein 4C (ARL4C), a member of the ARF small GTP-binding protein subfamily, has emerged from its role as an epithelial growth regulator to become a central molecule in cancer biology. This scoping review was conducted according to the PRISMA-ScR framework, systematically maps literature from PubMed, Scopus and Web of Science up to December 2024 to synthesise evidence on ARL4C's regulatory mechanisms and its implications in tumourigenesis and relevance to ameloblastoma.&lt;/p&gt;
&lt;h2&gt;Findings&lt;/h2&gt;
&lt;p&gt;Originally recognised for its role in tissue morphogenesis, ARL4C is now known to drive cancer cell proliferation, migration and invasion when dysregulated. Its expression is modulated by major signalling cascades including Wnt/MAPK, PI3K/AKT and TGF-β, as well as epigenetic factors. While primarily acting as an oncogenic driver, ARL4C exhibits context-dependent roles, occasionally functioning as a tumour suppressor. In ameloblastoma, a locally aggressive odontogenic tumour, ARL4C expression correlates with invasion and bone resorption. Notably, this influence appears independent of BRAF mutation status, suggesting a unique pathological role in this setting.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;ARL4C stands at the intersection of fundamental cell biology and clinical oncology. It holds promise as a biomarker for prognosis and recurrence and as a potential therapeutic target. However, its dual nature highlights the complexity of cancer signalling networks. Future research involving larger patient cohorts is essential to validate ARL4C's utility in precision oncology, particularly for the management of ameloblastoma.&lt;/p&gt;</content:encoded>
         <dc:creator>
Muhammad Nazim Aiman Azhari, 
Chuey Chuan Tan, 
Lee Fah Yap, 
Siti Amalina Inche Zainal Abidin, 
Yet Ching Goh, 
Wanninayake Mudiyanselage Tilakaratne
</dc:creator>
         <category>REVIEW</category>
         <dc:title>Implications of ADP‐Ribosylation Factor‐Like Protein 4C (ARL4C) in Human Neoplasia With Special Emphasis on Ameloblastoma: A Scoping Review</dc:title>
         <dc:identifier>10.1111/jop.70154</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70154</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70154?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70150?af=R</link>
         <pubDate>Mon, 25 May 2026 17:25:27 -0700</pubDate>
         <dc:date>2026-05-25T05:25:27-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70150</guid>
         <title>Heterogeneity of miRNAs in Salivary Gland Neoplasms: An Exploratory Pilot Study</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Introduction
MicroRNAs (miRNAs) are small RNAs that have been associated with tumourigenesis and tumour progression and that play an important role in the pathogenesis of salivary gland neoplasms. The aim of this study was to evaluate the global miRNA expression profile in a sample of salivary gland neoplasms.


Methods
Cases of pleomorphic adenoma (n = 4), adenoid cystic carcinoma (n = 4) and mucoepidermoid carcinoma (n = 4) were studied by real‐time RT‐PCR.


Results
The main up‐regulated miRNAs were hsa‐miR‐373, hsa‐miR‐675, hsa‐miR‐508, hsa‐miR‐1290 and hsa‐miR−483‐3p, while hsa‐miR‐105 and hsa‐let‐7f‐1 were among the most down‐regulated miRNAs compared to the normal salivary gland. Hsa‐miR‐106b, hsa‐miR‐142‐5p, hsa‐miR‐622, hsa‐miR‐642, hsa‐miR‐574‐3p and hsa‐miR‐486 were significantly differentially expressed (p &lt; 0.05) when each neoplasm and normal glandular tissue were compared.


Conclusion
This study described the global molecular signature of miRNAs in benign and malignant salivary gland neoplasms and provided preliminary evidence of miRNA dysregulation, suggesting a potential association between specific miRNA signatures and molecular pathways implicated in tumour progression.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Introduction&lt;/h2&gt;
&lt;p&gt;MicroRNAs (miRNAs) are small RNAs that have been associated with tumourigenesis and tumour progression and that play an important role in the pathogenesis of salivary gland neoplasms. The aim of this study was to evaluate the global miRNA expression profile in a sample of salivary gland neoplasms.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Cases of pleomorphic adenoma (&lt;i&gt;n&lt;/i&gt; = 4), adenoid cystic carcinoma (&lt;i&gt;n&lt;/i&gt; = 4) and mucoepidermoid carcinoma (&lt;i&gt;n&lt;/i&gt; = 4) were studied by real-time RT-PCR.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The main up-regulated miRNAs were hsa-miR-373, hsa-miR-675, hsa-miR-508, hsa-miR-1290 and hsa-miR−483-3p, while hsa-miR-105 and hsa-let-7f-1 were among the most down-regulated miRNAs compared to the normal salivary gland. Hsa-miR-106b, hsa-miR-142-5p, hsa-miR-622, hsa-miR-642, hsa-miR-574-3p and hsa-miR-486 were significantly differentially expressed (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.05) when each neoplasm and normal glandular tissue were compared.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This study described the global molecular signature of miRNAs in benign and malignant salivary gland neoplasms and provided preliminary evidence of miRNA dysregulation, suggesting a potential association between specific miRNA signatures and molecular pathways implicated in tumour progression.&lt;/p&gt;</content:encoded>
         <dc:creator>
Dandara Andrade de Santana, 
Poliana Ramos Braga, 
Daniel Araki Ribeiro, 
Patricia Ramos Cury, 
Ana Carolina Velasco Pondé de Sena, 
Flávia Caló de Aquino Xavier, 
Fernando Augusto Soares, 
Iguaracyra Barreto de Araújo, 
Fabio Albuquerque Marchi, 
Valéria Souza Freitas, 
Cláudia Malheiros Coutinho‐Camillo, 
Jean Nunes dos Santos
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Heterogeneity of miRNAs in Salivary Gland Neoplasms: An Exploratory Pilot Study</dc:title>
         <dc:identifier>10.1111/jop.70150</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70150</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70150?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70153?af=R</link>
         <pubDate>Mon, 18 May 2026 17:49:17 -0700</pubDate>
         <dc:date>2026-05-18T05:49:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70153</guid>
         <title>Adjuvant Immune Checkpoint Inhibitors in Head and Neck Cancer: A Meta‐Analysis of Phase III Trials</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
This meta‐analysis evaluates the efficacy and safety of adjuvant immune checkpoint inhibitors (ICIs), specifically nivolumab and pembrolizumab, when combined with standard chemoradiotherapy (CRT) in patients with resected locally advanced head and neck squamous cell carcinoma (LA‐HNSCC). Despite the potential of ICIs in improving survival outcomes, variability in patient responses and adverse event profiles remains a challenge.


Methods
Data were pooled from two Phase III randomized controlled trials, NIVOPOSTOP and KEYNOTE‐689, involving 1394 high‐risk patients with advanced disease, positive surgical margins, and extranodal extension. The primary endpoints were disease‐free survival (DFS) and overall survival (OS). Secondary endpoints included treatment‐related adverse events. Hazard ratios (HR) and corresponding 95% confidence intervals (CI) were calculated for survival outcomes, and risk ratios (RR) for adverse events. Subgroup analyzes were performed based on PD‐L1 expression.


Results
The addition of ICIs to CRT resulted in significant improvements in DFS (HR: 0.75, 95% CI: 0.65–0.87) and OS (HR: 0.74, 95% CI: 0.65–0.85), representing a 25% reduction in the risk of recurrence and a 26% reduction in the risk of death. Subgroup analysis showed a greater benefit for patients with PD‐L1 expression (CPS ≥ 1), with a pooled HR of 0.66 (95% CI: 0.49–0.88). Adverse events were more frequent with ICIs, with 81% of patients reporting any‐grade adverse events and 42.9%–44.6% experiencing Grade 3 or higher events. The incidence of immune‐related adverse events was significantly higher in the immunotherapy groups (p = 0.008), with notable increases in hypothyroidism and immune‐mediated toxicities. Treatment discontinuation due to adverse events occurred in 12.4%–17.7% of patients.


Conclusions
Adjuvant ICIs significantly improve survival outcomes in high‐risk patients with resected LA‐HNSCC, especially in case of CPS ≥ 1, but are associated with an increased risk of adverse events, particularly immune‐related toxicities. These findings support the integration of ICIs into postsurgical treatment regimens, though careful patient selection and monitoring are essential. Further research is needed to optimize treatment regimens and manage toxicities effectively.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;This meta-analysis evaluates the efficacy and safety of adjuvant immune checkpoint inhibitors (ICIs), specifically nivolumab and pembrolizumab, when combined with standard chemoradiotherapy (CRT) in patients with resected locally advanced head and neck squamous cell carcinoma (LA-HNSCC). Despite the potential of ICIs in improving survival outcomes, variability in patient responses and adverse event profiles remains a challenge.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Data were pooled from two Phase III randomized controlled trials, NIVOPOSTOP and KEYNOTE-689, involving 1394 high-risk patients with advanced disease, positive surgical margins, and extranodal extension. The primary endpoints were disease-free survival (DFS) and overall survival (OS). Secondary endpoints included treatment-related adverse events. Hazard ratios (HR) and corresponding 95% confidence intervals (CI) were calculated for survival outcomes, and risk ratios (RR) for adverse events. Subgroup analyzes were performed based on PD-L1 expression.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The addition of ICIs to CRT resulted in significant improvements in DFS (HR: 0.75, 95% CI: 0.65–0.87) and OS (HR: 0.74, 95% CI: 0.65–0.85), representing a 25% reduction in the risk of recurrence and a 26% reduction in the risk of death. Subgroup analysis showed a greater benefit for patients with PD-L1 expression (CPS ≥ 1), with a pooled HR of 0.66 (95% CI: 0.49–0.88). Adverse events were more frequent with ICIs, with 81% of patients reporting any-grade adverse events and 42.9%–44.6% experiencing Grade 3 or higher events. The incidence of immune-related adverse events was significantly higher in the immunotherapy groups (&lt;i&gt;p&lt;/i&gt; = 0.008), with notable increases in hypothyroidism and immune-mediated toxicities. Treatment discontinuation due to adverse events occurred in 12.4%–17.7% of patients.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;Adjuvant ICIs significantly improve survival outcomes in high-risk patients with resected LA-HNSCC, especially in case of CPS ≥ 1, but are associated with an increased risk of adverse events, particularly immune-related toxicities. These findings support the integration of ICIs into postsurgical treatment regimens, though careful patient selection and monitoring are essential. Further research is needed to optimize treatment regimens and manage toxicities effectively.&lt;/p&gt;</content:encoded>
         <dc:creator>
Wala Ben Kridis, 
Afef Khanfir
</dc:creator>
         <category>REVIEW</category>
         <dc:title>Adjuvant Immune Checkpoint Inhibitors in Head and Neck Cancer: A Meta‐Analysis of Phase III Trials</dc:title>
         <dc:identifier>10.1111/jop.70153</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70153</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70153?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70147?af=R</link>
         <pubDate>Thu, 14 May 2026 19:40:01 -0700</pubDate>
         <dc:date>2026-05-14T07:40:01-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70147</guid>
         <title>Tempol Protects Against Radiation Injury in the Submandibular Gland Through the β‐Catenin Signaling Pathway</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Radiation damage severely impacts salivary gland function and cell survival, especially in head and neck radiotherapy. Tempol (TPL), a free radical scavenger, has shown protective effects against radiation damage. This research aimed to investigate the protective effects of TPL on radiation‐induced damage in Hs917.T cells and the submandibular gland (SMG) of C57BL/6 mice, along with the mechanisms involved.


Methods
Human parotid fibroblasts (Hs917.T) were pre‐treated with TPL and exposed to ionizing radiation (IR). Protective effects were evaluated using MTT, clonogenic survival assays, flow cytometry, and intracellular reactive oxygen species levels. In vivo, C57BL/6 mice were pre‐treated with TPL (275 mg/kg) and exposed to 15 gray (Gy). Effects were assessed by survival rates, body weight changes, histological analysis, and TUNEL staining. Changes in apoptosis‐related markers and β‐catenin signaling pathway were analyzed, and the role of TPL was verified using the β‐catenin inhibitor XAV939.


Results
TPL pre‐treatment increased cell survival, reduced apoptosis, alleviated cell cycle arrest, and decreased intracellular superoxide and hydrogen peroxide levels in Hs917. T cells. In C57BL/6 mice, pre‐treatment with TPL improved survival, mitigated weight loss, reduced SMG damage, and decreased apoptosis. TPL inhibited IR‐induced apoptosis by increasing Bcl‐2 expression and decreasing Bax and caspase‐9 levels. TPL exerted anti‐apoptotic and protective effects by upregulating the expression of β‐catenin, promoting its nuclear translocation, and inhibiting its phosphorylation. These protective effects of TPL were reversed by XAV939.


Conclusions
TPL exerted protective effects against IR‐induced damage in Hs917.T cells and the SMG of C57BL/6 mice through activating the β‐catenin signaling pathway, inhibiting cell apoptosis, and alleviating oxidative stress.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Radiation damage severely impacts salivary gland function and cell survival, especially in head and neck radiotherapy. Tempol (TPL), a free radical scavenger, has shown protective effects against radiation damage. This research aimed to investigate the protective effects of TPL on radiation-induced damage in Hs917.T cells and the submandibular gland (SMG) of C57BL/6 mice, along with the mechanisms involved.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Human parotid fibroblasts (Hs917.T) were pre-treated with TPL and exposed to ionizing radiation (IR). Protective effects were evaluated using MTT, clonogenic survival assays, flow cytometry, and intracellular reactive oxygen species levels. In vivo, C57BL/6 mice were pre-treated with TPL (275 mg/kg) and exposed to 15 gray (Gy). Effects were assessed by survival rates, body weight changes, histological analysis, and TUNEL staining. Changes in apoptosis-related markers and β-catenin signaling pathway were analyzed, and the role of TPL was verified using the β-catenin inhibitor XAV939.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;TPL pre-treatment increased cell survival, reduced apoptosis, alleviated cell cycle arrest, and decreased intracellular superoxide and hydrogen peroxide levels in Hs917. T cells. In C57BL/6 mice, pre-treatment with TPL improved survival, mitigated weight loss, reduced SMG damage, and decreased apoptosis. TPL inhibited IR-induced apoptosis by increasing Bcl-2 expression and decreasing Bax and caspase-9 levels. TPL exerted anti-apoptotic and protective effects by upregulating the expression of β-catenin, promoting its nuclear translocation, and inhibiting its phosphorylation. These protective effects of TPL were reversed by XAV939.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;TPL exerted protective effects against IR-induced damage in Hs917.T cells and the SMG of C57BL/6 mice through activating the β-catenin signaling pathway, inhibiting cell apoptosis, and alleviating oxidative stress.&lt;/p&gt;</content:encoded>
         <dc:creator>
Jinfeng Wang, 
Mingjun Xu, 
Jinghua Zhong, 
Kui Zhong, 
Zheng Chen, 
Chunyu Liu, 
Chao Liu
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Tempol Protects Against Radiation Injury in the Submandibular Gland Through the β‐Catenin Signaling Pathway</dc:title>
         <dc:identifier>10.1111/jop.70147</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70147</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70147?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70152?af=R</link>
         <pubDate>Wed, 13 May 2026 03:25:16 -0700</pubDate>
         <dc:date>2026-05-13T03:25:16-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70152</guid>
         <title>Exploring Career Prospects in Oral and Maxillofacial Pathology and Oral Medicine Among Final‐Year Brazilian Dental Students: A Multi‐institutional Study</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Oral and maxillofacial pathology (OP) and oral medicine (OM) are recognized specialties in Brazil and worldwide. Identifying dental students' intentions to pursue these fields and understanding the factors influencing their career choices may provide insights into the future of the specialties. Therefore, this study aimed to determine the intention of Brazilian final‐year dental students to pursue the professional career in OP and OM.


Methods
Final‐year undergraduate dental students, from various public and private institutions in Brazil, were invited to voluntarily complete a self‐administered and anonymous virtual questionnaire. The questionnaire consisted of 11 questions. The statistical analysis consisted of describing the absolute and relative numbers, and performing analytical statistics using Pearson's chi‐squared test for categorical variables.


Results
A total of 358 students participated of the study. The majority were female (75.1%), with a mean age of 25.27 years, mainly from public universities (52%). The main careers pursued were restorative dentistry (39.1%), dental implantology (37.7%), prosthodontics (33%), and orofacial harmonization (31.3%). The main reasons for choosing specialization were to stand out in the profession and to perform better in the profession with better clinical outcomes. OM was reported as a career choice by 17% of students and OP by 7.5%. The motivations for such choice were vocation and influence from professors, colleagues, or family members.


Conclusion
The results revealed a surprising and concerning finding: interest in the fields of OP and OM, which are fundamental for diagnosing and treating complex conditions of the oral cavity, was relatively low.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Oral and maxillofacial pathology (OP) and oral medicine (OM) are recognized specialties in Brazil and worldwide. Identifying dental students' intentions to pursue these fields and understanding the factors influencing their career choices may provide insights into the future of the specialties. Therefore, this study aimed to determine the intention of Brazilian final-year dental students to pursue the professional career in OP and OM.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Final-year undergraduate dental students, from various public and private institutions in Brazil, were invited to voluntarily complete a self-administered and anonymous virtual questionnaire. The questionnaire consisted of 11 questions. The statistical analysis consisted of describing the absolute and relative numbers, and performing analytical statistics using Pearson's chi-squared test for categorical variables.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;A total of 358 students participated of the study. The majority were female (75.1%), with a mean age of 25.27 years, mainly from public universities (52%). The main careers pursued were restorative dentistry (39.1%), dental implantology (37.7%), prosthodontics (33%), and orofacial harmonization (31.3%). The main reasons for choosing specialization were to stand out in the profession and to perform better in the profession with better clinical outcomes. OM was reported as a career choice by 17% of students and OP by 7.5%. The motivations for such choice were vocation and influence from professors, colleagues, or family members.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;The results revealed a surprising and concerning finding: interest in the fields of OP and OM, which are fundamental for diagnosing and treating complex conditions of the oral cavity, was relatively low.&lt;/p&gt;</content:encoded>
         <dc:creator>
Hélen Kaline Farias Bezerra, 
Fabrício Emanuel Soares de Oliveira, 
Daniella Reis Barbosa Martelli, 
Renato Assis Machado, 
Zêus Araújo Cunha, 
Fábio Ramoa Pires, 
Danyele Cambraia Franco de Souza, 
Silvia Regina de Almeida Reis, 
Giovanna Ribeiro Souto, 
Paulo Rogério Ferreti Bonan, 
Danyel Elias da Cruz Perez, 
Alan Roger dos Santos‐Silva, 
Luiz Evaristo Ricci Volpato, 
Janete Dias Almeida, 
Hercílio Martelli‐Júnior
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Exploring Career Prospects in Oral and Maxillofacial Pathology and Oral Medicine Among Final‐Year Brazilian Dental Students: A Multi‐institutional Study</dc:title>
         <dc:identifier>10.1111/jop.70152</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70152</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70152?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70149?af=R</link>
         <pubDate>Wed, 13 May 2026 03:22:02 -0700</pubDate>
         <dc:date>2026-05-13T03:22:02-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70149</guid>
         <title>Models of Oral Epithelial Dysplasia: A Systematic Review and Temporal Analysis</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Oral squamous cell carcinoma (OSCC) is the most common malignancy of the head and neck, associated with substantial morbidity and mortality worldwide. Oral epithelial dysplasia (OED) can precede OSCC, offering a critical window for preventive and therapeutic intervention. This review maps the historical and current landscape of in vitro and in vivo models of OED, providing insight into their strengths, limitations, and translational relevance.


Methods
A systematic review and temporal analysis were conducted following PRISMA guidelines, with literature searches performed across Medline, EMBASE, EBM Reviews, and Web of Science.


Results
From 4009 records, 292 studies from 26 countries were included, yielding 307 models of OED. Only a minority of studies (17.4%) focused primarily on dysplasia as a precancerous condition. In vivo models predominated (88.9%), while in vitro systems were comparatively scarce and largely limited to 2D cultures. Organoid‐based approaches were rarely reported, highlighting a gap in advanced model development. Reproducibility data were available for 125 studies (45.8%). The hamster emerged as the most frequently used animal [n = 96, 35%], and 4‐nitroquinoline‐1‐oxide (4‐NQO) remained the most common carcinogen, particularly in murine models. A strong sex bias was observed, with male animals heavily over‐represented.


Conclusion
Overall, models of OED remain under‐represented and under‐developed, particularly in comparison to innovations in other fields of cancer research. Despite the central role of OED in oral carcinogenesis, current models do not adequately reflect clinical diversity or exploit modern 3D and patient‐derived technologies. This review provides a critical reference point to guide future studies toward more accurate, reproducible, and clinically relevant models, with the potential to advance prevention, early detection, and targeted therapies for OSCC.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Oral squamous cell carcinoma (OSCC) is the most common malignancy of the head and neck, associated with substantial morbidity and mortality worldwide. Oral epithelial dysplasia (OED) can precede OSCC, offering a critical window for preventive and therapeutic intervention. This review maps the historical and current landscape of in vitro and in vivo models of OED, providing insight into their strengths, limitations, and translational relevance.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A systematic review and temporal analysis were conducted following PRISMA guidelines, with literature searches performed across Medline, EMBASE, EBM Reviews, and Web of Science.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;From 4009 records, 292 studies from 26 countries were included, yielding 307 models of OED. Only a minority of studies (17.4%) focused primarily on dysplasia as a precancerous condition. In vivo models predominated (88.9%), while in vitro systems were comparatively scarce and largely limited to 2D cultures. Organoid-based approaches were rarely reported, highlighting a gap in advanced model development. Reproducibility data were available for 125 studies (45.8%). The hamster emerged as the most frequently used animal [&lt;i&gt;n&lt;/i&gt; = 96, 35%], and 4-nitroquinoline-1-oxide (4-NQO) remained the most common carcinogen, particularly in murine models. A strong sex bias was observed, with male animals heavily over-represented.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Overall, models of OED remain under-represented and under-developed, particularly in comparison to innovations in other fields of cancer research. Despite the central role of OED in oral carcinogenesis, current models do not adequately reflect clinical diversity or exploit modern 3D and patient-derived technologies. This review provides a critical reference point to guide future studies toward more accurate, reproducible, and clinically relevant models, with the potential to advance prevention, early detection, and targeted therapies for OSCC.&lt;/p&gt;</content:encoded>
         <dc:creator>
Zilefac Brian Ngokwe, 
Satutya Wicaksono, 
Michael McCullough, 
Antonio Celentano, 
Tami Yap
</dc:creator>
         <category>REVIEW</category>
         <dc:title>Models of Oral Epithelial Dysplasia: A Systematic Review and Temporal Analysis</dc:title>
         <dc:identifier>10.1111/jop.70149</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70149</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70149?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70151?af=R</link>
         <pubDate>Wed, 13 May 2026 03:18:17 -0700</pubDate>
         <dc:date>2026-05-13T03:18:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70151</guid>
         <title>The Prognostic Significance of Tertiary Lymphoid Structures in Head and Neck Cancers: A Systematic Review and Meta‐Analysis</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Head and neck squamous cell carcinoma (HNSCC), particularly oral squamous cell carcinoma (OSCC), is associated with poor survival despite therapeutic advances. Tertiary lymphoid structures (TLSs) are emerging components of the tumor microenvironment, but their prognostic significance in HNSCC remains unclear.


Objective
To systematically review and meta‐analyze the prognostic impact of TLSs in HNSCC.


Methods
PubMed/MEDLINE, Scopus, ScienceDirect, and Embase were searched through August 2025. Eligible studies evaluated TLS presence, density, maturity, or spatial distribution in histologically confirmed HNSCC. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using fixed‐effects models. Risk of bias and certainty of evidence were assessed using QUIPS and GRADE, respectively.


Results
Seventeen studies involving more than 2309 patients were included. TLS‐positive tumors were significantly associated with improved overall and disease‐free survival (DFS) (p &lt; 0.001). Absence of TLSs was associated with worse overall survival (HR: 2.20, 95% CI: 1.74–2.78, I2 = 26%) and poorer DFS (HR: 2.21, 95% CI: 1.49–3.28, I2 = 0%). This adverse prognostic effect persisted in the OSCC subgroup (HR: 1.97, 95% CI: 1.42–2.73, I2 = 28%). Beyond quantitative presence, TLS maturation and spatial distribution influenced prognosis, with mature intratumoral TLSs associated with more favorable outcomes. Moreover, emerging evidence suggests that TLSs may also predict response to immunotherapy, particularly immune checkpoint blockade.


Conclusion
TLSs are strong prognostic biomarkers in HNSCC. Their presence, maturity, and spatial context significantly influence survival, supporting their role in prognostic stratification and future therapeutic strategies. TLS maturity emerges as a promising feature for standardized scoring systems and should be further explored in future studies.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Head and neck squamous cell carcinoma (HNSCC), particularly oral squamous cell carcinoma (OSCC), is associated with poor survival despite therapeutic advances. Tertiary lymphoid structures (TLSs) are emerging components of the tumor microenvironment, but their prognostic significance in HNSCC remains unclear.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;To systematically review and meta-analyze the prognostic impact of TLSs in HNSCC.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;PubMed/MEDLINE, Scopus, ScienceDirect, and Embase were searched through August 2025. Eligible studies evaluated TLS presence, density, maturity, or spatial distribution in histologically confirmed HNSCC. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using fixed-effects models. Risk of bias and certainty of evidence were assessed using QUIPS and GRADE, respectively.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Seventeen studies involving more than 2309 patients were included. TLS-positive tumors were significantly associated with improved overall and disease-free survival (DFS) (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001). Absence of TLSs was associated with worse overall survival (HR: 2.20, 95% CI: 1.74–2.78, &lt;i&gt;I&lt;/i&gt;
&lt;sup&gt;2&lt;/sup&gt; = 26%) and poorer DFS (HR: 2.21, 95% CI: 1.49–3.28, &lt;i&gt;I&lt;/i&gt;
&lt;sup&gt;2&lt;/sup&gt; = 0%). This adverse prognostic effect persisted in the OSCC subgroup (HR: 1.97, 95% CI: 1.42–2.73, &lt;i&gt;I&lt;/i&gt;
&lt;sup&gt;2&lt;/sup&gt; = 28%). Beyond quantitative presence, TLS maturation and spatial distribution influenced prognosis, with mature intratumoral TLSs associated with more favorable outcomes. Moreover, emerging evidence suggests that TLSs may also predict response to immunotherapy, particularly immune checkpoint blockade.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;TLSs are strong prognostic biomarkers in HNSCC. Their presence, maturity, and spatial context significantly influence survival, supporting their role in prognostic stratification and future therapeutic strategies. TLS maturity emerges as a promising feature for standardized scoring systems and should be further explored in future studies.&lt;/p&gt;</content:encoded>
         <dc:creator>
Everton Freitas de Morais, 
Bruno Cesar da Costa, 
Antti Mäkitie, 
Ricardo D. Coletta, 
Alhadi Almangush
</dc:creator>
         <category>REVIEW</category>
         <dc:title>The Prognostic Significance of Tertiary Lymphoid Structures in Head and Neck Cancers: A Systematic Review and Meta‐Analysis</dc:title>
         <dc:identifier>10.1111/jop.70151</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70151</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70151?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70121?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70121</guid>
         <title>Comment on “COVID‐19 Dry Mouth Induced by SARS‐CoV‐2 Not Binding Directly to ACE2 but Interacting Electrostatically With Lipid Raft in Salivary Glands”</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 509-510, May 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Hironori Tsuchiya
</dc:creator>
         <category>LETTER TO THE EDITOR</category>
         <dc:title>Comment on “COVID‐19 Dry Mouth Induced by SARS‐CoV‐2 Not Binding Directly to ACE2 but Interacting Electrostatically With Lipid Raft in Salivary Glands”</dc:title>
         <dc:identifier>10.1111/jop.70121</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70121</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70121?af=R</prism:url>
         <prism:section>LETTER TO THE EDITOR</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70144?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70144</guid>
         <title>Issue Information</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page i-iii, May 2026. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator/>
         <category>ISSUE INFORMATION</category>
         <dc:title>Issue Information</dc:title>
         <dc:identifier>10.1111/jop.70144</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70144</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70144?af=R</prism:url>
         <prism:section>ISSUE INFORMATION</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70109?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70109</guid>
         <title>Imbalance of Free Radicals and Antioxidants in Oral Potentially Malignant Disorders and Oral Squamous Cell Carcinoma: A Review</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 520-531, May 2026. </description>
         <dc:description>
ABSTRACT

Background
The dynamic interplay between reactive free radicals (FR) and antioxidants (AO) can lead to either redox homeostasis or oxidative stress. Disruption of redox balance contributes to oxidative stress, a key factor in the pathogenesis of various conditions, notably oral potentially malignant disorders (OPMDs) and oral squamous cell carcinoma (OSCC). At low to moderate levels, FRs trigger adaptive mutations that initiate carcinogenesis and support neoplastic cell survival. In contrast, high concentrations of FRs exert cytotoxic effects, a mechanism exploited in radiotherapy and chemotherapy. Antioxidants counteract FRs, mitigating cellular damage—a benefit demonstrated in several clinical trials involving OPMDs. However, their efficacy in OSCC remains contentious.


Methods and Finding
This review explores the multifaceted roles of FRs and AOs in OPMD and OSCC, with emphasis on their contributions to carcinogenesis and therapeutic strategies. Tracking the FR–AO ratio during treatment may offer predictive insights into malignant transformation and facilitate early OSCC detection.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;The dynamic interplay between reactive free radicals (FR) and antioxidants (AO) can lead to either redox homeostasis or oxidative stress. Disruption of redox balance contributes to oxidative stress, a key factor in the pathogenesis of various conditions, notably oral potentially malignant disorders (OPMDs) and oral squamous cell carcinoma (OSCC). At low to moderate levels, FRs trigger adaptive mutations that initiate carcinogenesis and support neoplastic cell survival. In contrast, high concentrations of FRs exert cytotoxic effects, a mechanism exploited in radiotherapy and chemotherapy. Antioxidants counteract FRs, mitigating cellular damage—a benefit demonstrated in several clinical trials involving OPMDs. However, their efficacy in OSCC remains contentious.&lt;/p&gt;
&lt;h2&gt;Methods and Finding&lt;/h2&gt;
&lt;p&gt;This review explores the multifaceted roles of FRs and AOs in OPMD and OSCC, with emphasis on their contributions to carcinogenesis and therapeutic strategies. Tracking the FR–AO ratio during treatment may offer predictive insights into malignant transformation and facilitate early OSCC detection.&lt;/p&gt;</content:encoded>
         <dc:creator>
Toniya Raut, 
Namrata G. R. Raut, 
Neetu Jain, 
Shashi Keshwar, 
Sunil Shrestha
</dc:creator>
         <category>REVIEW</category>
         <dc:title>Imbalance of Free Radicals and Antioxidants in Oral Potentially Malignant Disorders and Oral Squamous Cell Carcinoma: A Review</dc:title>
         <dc:identifier>10.1111/jop.70109</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70109</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70109?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70115?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70115</guid>
         <title>Papilliferous Keratoameloblastoma (PKA): Is It a Different Clinicopathological Entity or Histological Subtype of Conventional Ameloblastoma?</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 511-519, May 2026. </description>
         <dc:description>
ABSTRACT

Background
Papilliferous keratoameloblastoma (PKA) is an exceptionally rare variant of conventional ameloblastoma, marked by papilliferous epithelial projections and prominent keratinization within an ameloblastomatous framework. Because of its rarity and overlap with other keratinizing odontogenic tumours, PKA is often overlooked and is not recognised in the current WHO classification. Limited awareness and inconsistent terminology contribute to diagnostic uncertainty and may affect clinical management.


Objectives
This review critically analysed all published PKA cases to describe their clinical, radiographic and histopathological features, evaluating whether PKA should be regarded as a distinct clinicopathological entity or a histological subtype of conventional ameloblastoma.


Materials and Methods
A comprehensive search of PubMed, Scopus, Web of Science, and Google Scholar was performed to identify all English‐language reports of PKA. Extracted data included demographics, clinical presentation, radiographic findings, histopathology, treatment and outcomes. The information was synthesised and descriptively analysed.


Results
Seven cases of PKA were included. Patients ranged from 18 to 76 years (mean age: 50.4 years), with a male predominance. All lesions involved the right mandible. Clinically, most patients presented with slow‐growing mandibular swellings, occasionally accompanied by pain or mucosal changes. Radiographs most often show multilocular radiolucencies with buccolingual expansion or cortical perforation. Histopathology consistently reveals classic ameloblastomatous epithelium with squamous metaplasia, keratin pearl formation, and distinctive papilliferous projections lining cystic spaces.


Conclusion
The uniform histopathological pattern observed across reported cases supports recognising PKA as a distinct histopathological subtype of conventional ameloblastoma. Its formal inclusion in odontogenic tumour classification appears justified, although further molecular and clinicopathological studies are needed to better define its biological behaviour.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Papilliferous keratoameloblastoma (PKA) is an exceptionally rare variant of conventional ameloblastoma, marked by papilliferous epithelial projections and prominent keratinization within an ameloblastomatous framework. Because of its rarity and overlap with other keratinizing odontogenic tumours, PKA is often overlooked and is not recognised in the current WHO classification. Limited awareness and inconsistent terminology contribute to diagnostic uncertainty and may affect clinical management.&lt;/p&gt;
&lt;h2&gt;Objectives&lt;/h2&gt;
&lt;p&gt;This review critically analysed all published PKA cases to describe their clinical, radiographic and histopathological features, evaluating whether PKA should be regarded as a distinct clinicopathological entity or a histological subtype of conventional ameloblastoma.&lt;/p&gt;
&lt;h2&gt;Materials and Methods&lt;/h2&gt;
&lt;p&gt;A comprehensive search of PubMed, Scopus, Web of Science, and Google Scholar was performed to identify all English-language reports of PKA. Extracted data included demographics, clinical presentation, radiographic findings, histopathology, treatment and outcomes. The information was synthesised and descriptively analysed.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Seven cases of PKA were included. Patients ranged from 18 to 76 years (mean age: 50.4 years), with a male predominance. All lesions involved the right mandible. Clinically, most patients presented with slow-growing mandibular swellings, occasionally accompanied by pain or mucosal changes. Radiographs most often show multilocular radiolucencies with buccolingual expansion or cortical perforation. Histopathology consistently reveals classic ameloblastomatous epithelium with squamous metaplasia, keratin pearl formation, and distinctive papilliferous projections lining cystic spaces.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;The uniform histopathological pattern observed across reported cases supports recognising PKA as a distinct histopathological subtype of conventional ameloblastoma. Its formal inclusion in odontogenic tumour classification appears justified, although further molecular and clinicopathological studies are needed to better define its biological behaviour.&lt;/p&gt;</content:encoded>
         <dc:creator>
Yet Ching Goh, 
Ronell Bologna‐Molina, 
Kelly Magliocca, 
Willie van Heerden, 
Liam Robinson, 
Elizabeth Ann Bilodeau, 
Haizal Mohd Hussaini, 
Merva Soluk‐Tekkesin, 
Madhu Shrestha, 
Marilena Vered, 
Akinyele Olumuyiwa Adisa, 
Jiang Li, 
Ricardo Santiago Gomez, 
Keith David Hunter, 
Wanninayake Mudiyanselage Tilakaratne
</dc:creator>
         <category>REVIEW</category>
         <dc:title>Papilliferous Keratoameloblastoma (PKA): Is It a Different Clinicopathological Entity or Histological Subtype of Conventional Ameloblastoma?</dc:title>
         <dc:identifier>10.1111/jop.70115</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70115</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70115?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70116?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70116</guid>
         <title>Assessment of Organ‐Specific Fibrotic Biomarkers in Patients With Oral Submucous Fibrosis</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 601-604, May 2026. </description>
         <dc:description>
ABSTRACT

Background
Oral submucous fibrosis is a potentially malignant disorder with a high malignant transformation rate. Areca nut, being the chief etiologic factor, when chewed, is known to be swallowed and absorbed into circulation resulting in several systemic effects. This is the first kind of report presenting serum organ‐specific fibrosis biomarkers suggestive of functional and fibrotic changes in the visceral organs.


Methods
Various fibrotic biomarkers such as kidney injury molecule‐1 (KIM‐1), alanine aminotransferace (ALT), aspartate aminotransferase (AST), and its ratio to platelet index (APRI), suppression of tumorigenicity‐2 (ST2), Krebs von den Lungen‐6 (KL‐6) and von Willebrand factor (vWF) were analyzed.


Results
The present study evaluated potential systemic fibrotic involvement, modest elevations in ST2 and KL‐6 levels in advanced OSF compared to early cases; however, all values remained within normal physiological limits. No significant differences were found between the OSF and healthy groups across all biomarkers. There was no renal involvement, no significant association between liver fibrosis and its systemic biomarkers, and there was minimal vascular involvement. Collectively, these findings support the hypothesis that OSF may be a localized fibrotic disorder with no detectable systemic biomarker alterations in its early to moderate stages.


Conclusions
This study provides an important step in bridging localized oral pathology and systemic disease monitoring. No significant systemic fibrosis was observed but methodology, findings, and recommendations offer a strong basis for future research. Despite the presence of evidence that favors a localized disease model for OSF in its early and advanced stages, systemic monitoring in future clinical paradigms is acknowledged.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Oral submucous fibrosis is a potentially malignant disorder with a high malignant transformation rate. Areca nut, being the chief etiologic factor, when chewed, is known to be swallowed and absorbed into circulation resulting in several systemic effects. This is the first kind of report presenting serum organ-specific fibrosis biomarkers suggestive of functional and fibrotic changes in the visceral organs.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Various fibrotic biomarkers such as kidney injury molecule-1 (KIM-1), alanine aminotransferace (ALT), aspartate aminotransferase (AST), and its ratio to platelet index (APRI), suppression of tumorigenicity-2 (ST2), Krebs von den Lungen-6 (KL-6) and von Willebrand factor (vWF) were analyzed.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The present study evaluated potential systemic fibrotic involvement, modest elevations in ST2 and KL-6 levels in advanced OSF compared to early cases; however, all values remained within normal physiological limits. No significant differences were found between the OSF and healthy groups across all biomarkers. There was no renal involvement, no significant association between liver fibrosis and its systemic biomarkers, and there was minimal vascular involvement. Collectively, these findings support the hypothesis that OSF may be a localized fibrotic disorder with no detectable systemic biomarker alterations in its early to moderate stages.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;This study provides an important step in bridging localized oral pathology and systemic disease monitoring. No significant systemic fibrosis was observed but methodology, findings, and recommendations offer a strong basis for future research. Despite the presence of evidence that favors a localized disease model for OSF in its early and advanced stages, systemic monitoring in future clinical paradigms is acknowledged.&lt;/p&gt;</content:encoded>
         <dc:creator>
Nikita Baheti, 
Gargi Sarode, 
Abhirami Premarajan, 
Sachin Sarode
</dc:creator>
         <category>BRIEF REPORT</category>
         <dc:title>Assessment of Organ‐Specific Fibrotic Biomarkers in Patients With Oral Submucous Fibrosis</dc:title>
         <dc:identifier>10.1111/jop.70116</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70116</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70116?af=R</prism:url>
         <prism:section>BRIEF REPORT</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70117?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70117</guid>
         <title>Duplicated, Translocated Upper Lip and Maxilla: An Extremely Rare Congenital Craniofacial Anomaly With Novel Genetic Findings</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 605-610, May 2026. </description>
         <dc:description>
ABSTRACT

Importance
Diprosopus is an exceedingly rare craniomaxillofacial dysmorphosis that is considered a subgroup of conjoined twins. This phenotype encompasses a broad spectrum of duplications ranging from partial structures to complete dicephalus. The embryogenesis and mechanism of disease are not well understood. The objective of this investigation was to describe a case of partial dentofacial duplication and to discuss the possible etiology with novel genetic insights thereof.


Observations
A newborn Kazakh boy was referred to the First Affiliated Hospital of Xinjiang Medical University because of a maxillary mass detected on prenatal imaging. Physical examination revealed a unilateral cleft lip and a soft lump around 2.5 cm in diameter with the appearance of an accessory upper lip. He underwent two surgical procedures at 11 months and 4 years of age for definitive treatment. He demonstrated favorable recovery outcomes, maintaining normal speech and oral intake capabilities during long‐term follow‐up.


Conclusions and Relevance
Our preliminary findings and comprehensive literature review suggest that mutations in the 
PAX7
 gene could contribute to the pathogenesis of craniofacial duplication. This hypothesis establishes a previously unrecognized association between specific genetic alterations and the clinical manifestations of this condition, potentially offering a molecular foundation for prenatal diagnostic approaches. The present case provides more profound insights into the disease mechanisms compared to prior reports. Further validation through basic scientific investigations and clinical studies, incorporating comprehensive genetic analyses, will be essential to substantiate this proposed mechanism.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Importance&lt;/h2&gt;
&lt;p&gt;Diprosopus is an exceedingly rare craniomaxillofacial dysmorphosis that is considered a subgroup of conjoined twins. This phenotype encompasses a broad spectrum of duplications ranging from partial structures to complete dicephalus. The embryogenesis and mechanism of disease are not well understood. The objective of this investigation was to describe a case of partial dentofacial duplication and to discuss the possible etiology with novel genetic insights thereof.&lt;/p&gt;
&lt;h2&gt;Observations&lt;/h2&gt;
&lt;p&gt;A newborn Kazakh boy was referred to the First Affiliated Hospital of Xinjiang Medical University because of a maxillary mass detected on prenatal imaging. Physical examination revealed a unilateral cleft lip and a soft lump around 2.5 cm in diameter with the appearance of an accessory upper lip. He underwent two surgical procedures at 11 months and 4 years of age for definitive treatment. He demonstrated favorable recovery outcomes, maintaining normal speech and oral intake capabilities during long-term follow-up.&lt;/p&gt;
&lt;h2&gt;Conclusions and Relevance&lt;/h2&gt;
&lt;p&gt;Our preliminary findings and comprehensive literature review suggest that mutations in the 
&lt;i&gt;PAX7&lt;/i&gt;
 gene could contribute to the pathogenesis of craniofacial duplication. This hypothesis establishes a previously unrecognized association between specific genetic alterations and the clinical manifestations of this condition, potentially offering a molecular foundation for prenatal diagnostic approaches. The present case provides more profound insights into the disease mechanisms compared to prior reports. Further validation through basic scientific investigations and clinical studies, incorporating comprehensive genetic analyses, will be essential to substantiate this proposed mechanism.&lt;/p&gt;</content:encoded>
         <dc:creator>
Chen‐Xi Li, 
Di‐Shu Huang, 
Zhong‐Cheng Gong
</dc:creator>
         <category>BRIEF REPORT</category>
         <dc:title>Duplicated, Translocated Upper Lip and Maxilla: An Extremely Rare Congenital Craniofacial Anomaly With Novel Genetic Findings</dc:title>
         <dc:identifier>10.1111/jop.70117</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70117</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70117?af=R</prism:url>
         <prism:section>BRIEF REPORT</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70120?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70120</guid>
         <title>No Evidence of Microsatellite Instability in Head and Neck Squamous Cell Carcinoma of Non‐Smokers and Non‐Drinkers</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 611-615, May 2026. </description>
         <dc:description>
ABSTRACT

Introduction
While the prevalence of microsatellite instability (MSI) is low in the whole head and neck squamous cell carcinoma (HNSCC) population, it has been suggested to be more prominent in tumors of non‐smokers. Therefore, the goal of this study was to determine the presence of MSI in a cohort of well‐defined HNSCC of non‐smokers and non‐drinkers (NSND).


Methods
Clinical characteristics and tumor tissue of 119 NSND with HNSCC were retrospectively collected and analyzed for MLH1, PMS2, MSH2, and MSH6 protein expression on tissue microarrays (TMA). In case of negative staining for one of these mismatch repair proteins in the TMA cores, immunohistochemistry (IHC) was repeated on a whole slide section and additional molecular analyses were performed using polymerase chain reaction (PCR) and quantitative PCR (qPCR).


Results
Two cases showed dubious loss of MSH2 expression, one of these with concurrent dubious loss of MSH6 on the TMA. However, MSH2 and MSH6 expression was retained on whole slide sections and PCR and qPCR analyses did not show any mutations, compatible with a microsatellite stable result.


Conclusion
This study shows no single case with MSI in the NSND subgroup of HNSCC. Although a deficient DNA mismatch repair system is a predictive biomarker for response to immune checkpoint inhibitors, we found no evidence to support routine analysis of MSI in HNSCC, also not in the subgroup of NSND.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Introduction&lt;/h2&gt;
&lt;p&gt;While the prevalence of microsatellite instability (MSI) is low in the whole head and neck squamous cell carcinoma (HNSCC) population, it has been suggested to be more prominent in tumors of non-smokers. Therefore, the goal of this study was to determine the presence of MSI in a cohort of well-defined HNSCC of non-smokers and non-drinkers (NSND).&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Clinical characteristics and tumor tissue of 119 NSND with HNSCC were retrospectively collected and analyzed for MLH1, PMS2, MSH2, and MSH6 protein expression on tissue microarrays (TMA). In case of negative staining for one of these mismatch repair proteins in the TMA cores, immunohistochemistry (IHC) was repeated on a whole slide section and additional molecular analyses were performed using polymerase chain reaction (PCR) and quantitative PCR (qPCR).&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Two cases showed dubious loss of MSH2 expression, one of these with concurrent dubious loss of MSH6 on the TMA. However, MSH2 and MSH6 expression was retained on whole slide sections and PCR and qPCR analyses did not show any mutations, compatible with a microsatellite stable result.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This study shows no single case with MSI in the NSND subgroup of HNSCC. Although a deficient DNA mismatch repair system is a predictive biomarker for response to immune checkpoint inhibitors, we found no evidence to support routine analysis of MSI in HNSCC, also not in the subgroup of NSND.&lt;/p&gt;</content:encoded>
         <dc:creator>
F. J. Mulder, 
T. F. B. Gielgens, 
E. J. de Ruiter, 
R. de Bree, 
M. F. C. M. van den Hout, 
B. Kremer, 
S. M. Willems, 
E. J. M. Speel
</dc:creator>
         <category>BRIEF REPORT</category>
         <dc:title>No Evidence of Microsatellite Instability in Head and Neck Squamous Cell Carcinoma of Non‐Smokers and Non‐Drinkers</dc:title>
         <dc:identifier>10.1111/jop.70120</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70120</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70120?af=R</prism:url>
         <prism:section>BRIEF REPORT</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70112?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70112</guid>
         <title>Molecular Insights Into Epithelial Detachment in Odontogenic Keratocyst: The Role of Matrix Metalloproteinases and Effects of Marsupialization</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 532-538, May 2026. </description>
         <dc:description>
ABSTRACT

Introduction
Odontogenic keratocyst (OKC) is a developmental odontogenic cyst characterized by a fragile epithelial lining attachment to the capsula and high recurrence rates. Matrix metalloproteinases (MMPs) and adhesion‐related proteins (TLN1, FBLN1) may contribute to epithelial detachment, which could facilitate lesion recurrence. This study investigated the mRNA expression of MMP2, MMP9, TLN1, and FBLN1 in OKCs and their association with epithelial detachment, including the impact of marsupialization.


Methods
Gene expression was analyzed by RT‐qPCR in samples from OKCs (n = 10), marsupialized OKCs (n = 5), and oral mucosa controls (n = 4). Gelatinase activity was assessed by gelatin zymography in fresh samples (OKCs n = 7; oral mucosa n = 4). Histological sections were digitally measured to quantify areas of epithelial detachment. Correlation analyses were performed between mRNA expression levels and epithelial separation.


Results

MMP2 and MMP9 mRNA levels were significantly higher in OKCs compared to oral mucosa (p &lt; 0.05), with decreased mRNA levels after marsupialization. Gelatin zymography confirmed elevated gelatinase activity, particularly for MMP9, in OKC tissues. TLN1 and FBLN1 mRNA expressions were also elevated in OKCs, consistent with previous proteomic data, though not statistically significant. A significant correlation was observed between MMP9 mRNA expression and the total area of detached epithelium.


Conclusion

MMP9 may play a critical role in epithelial detachment in OKCs and could serve as a therapeutic target or prognostic marker. Marsupialization appears to modulate matrix metalloproteinases expression, suggesting a molecular mechanism for its clinical benefits.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Introduction&lt;/h2&gt;
&lt;p&gt;Odontogenic keratocyst (OKC) is a developmental odontogenic cyst characterized by a fragile epithelial lining attachment to the capsula and high recurrence rates. Matrix metalloproteinases (MMPs) and adhesion-related proteins (TLN1, FBLN1) may contribute to epithelial detachment, which could facilitate lesion recurrence. This study investigated the mRNA expression of &lt;i&gt;MMP2&lt;/i&gt;, &lt;i&gt;MMP9, TLN1&lt;/i&gt;, and &lt;i&gt;FBLN1&lt;/i&gt; in OKCs and their association with epithelial detachment, including the impact of marsupialization.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Gene expression was analyzed by RT-qPCR in samples from OKCs (&lt;i&gt;n&lt;/i&gt; = 10), marsupialized OKCs (&lt;i&gt;n&lt;/i&gt; = 5), and oral mucosa controls (&lt;i&gt;n&lt;/i&gt; = 4). Gelatinase activity was assessed by gelatin zymography in fresh samples (OKCs &lt;i&gt;n&lt;/i&gt; = 7; oral mucosa &lt;i&gt;n&lt;/i&gt; = 4). Histological sections were digitally measured to quantify areas of epithelial detachment. Correlation analyses were performed between mRNA expression levels and epithelial separation.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;
&lt;i&gt;MMP2&lt;/i&gt; and &lt;i&gt;MMP9&lt;/i&gt; mRNA levels were significantly higher in OKCs compared to oral mucosa (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.05), with decreased mRNA levels after marsupialization. Gelatin zymography confirmed elevated gelatinase activity, particularly for MMP9, in OKC tissues. &lt;i&gt;TLN1&lt;/i&gt; and &lt;i&gt;FBLN1&lt;/i&gt; mRNA expressions were also elevated in OKCs, consistent with previous proteomic data, though not statistically significant. A significant correlation was observed between &lt;i&gt;MMP9&lt;/i&gt; mRNA expression and the total area of detached epithelium.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;
&lt;i&gt;MMP9&lt;/i&gt; may play a critical role in epithelial detachment in OKCs and could serve as a therapeutic target or prognostic marker. Marsupialization appears to modulate matrix metalloproteinases expression, suggesting a molecular mechanism for its clinical benefits.&lt;/p&gt;</content:encoded>
         <dc:creator>
Arthur Henrique Soares Pacheco, 
Marina Rocha Fonseca Souza, 
Alline Teixeira Valeriano,  Savio Almeida Botrel, 
Laís Santos Câmara, 
Amanda Gabrielle De Sousa, 
Carolina Cavalieri Gomes, 
Vanessa de Fátima Bernardes, 
Ricardo Santiago Gomez, 
Marina Gonçalves Diniz
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Molecular Insights Into Epithelial Detachment in Odontogenic Keratocyst: The Role of Matrix Metalloproteinases and Effects of Marsupialization</dc:title>
         <dc:identifier>10.1111/jop.70112</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70112</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70112?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70114?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70114</guid>
         <title>High Expression of CHD1L, a Potent Oncogene Is Associated With Aggressive Head and Neck Cancer and Poor Survival Outcome</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 546-554, May 2026. </description>
         <dc:description>
ABSTRACT

Objective
Head and Neck Squamous Cell Carcinoma (HNSCC) is one of the most common cancers worldwide and has a significant impact on the lives of patients. This study aimed to examine the role and significance of Chromodomain Helicase/ATPase DNA Binding protein 1‐Like (CHD1L) in HNSCC.


Methods
CHD1L expression was analyzed using the Cancer Genome Atlas (TCGA‐HNSCC) dataset, along with the clinical and clinicopathological features of HNSCC. Additionally, CHD1L mRNA expression was quantified using real‐time quantitative PCR (RT‐qPCR). The survival rate of patients with HNSCC was assessed using Kaplan–Meier analysis. Furthermore, in silico tools were employed to investigate CHD1L protein networks and functional pathways involved in HNSCC development.


Results
mRNA and protein expression studies, along with in vitro and in silico analyses, confirmed that CHD1L expression was significantly higher in HNSCC tissues than in normal tissues. Clinicopathological analysis revealed associations between CHD1L expression and HPV status, nodal metastasis, disease stage, and tumor grade. Elevated CHD1L levels are also associated with poor patient survival. Functional enrichment analysis showed that CHD1L was associated with HNSCC progression.


Conclusion
CHD1L is significantly upregulated in HNSCC and associated with poor survival outcomes. This suggests that CHD1L may serve as a potential therapeutic target and prognostic marker for HNSCC. Further research is necessary to explore the functional role of CHD1L in the development and progression of HNSCC.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;Head and Neck Squamous Cell Carcinoma (HNSCC) is one of the most common cancers worldwide and has a significant impact on the lives of patients. This study aimed to examine the role and significance of Chromodomain Helicase/ATPase DNA Binding protein 1-Like (CHD1L) in HNSCC.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;CHD1L expression was analyzed using the Cancer Genome Atlas (TCGA-HNSCC) dataset, along with the clinical and clinicopathological features of HNSCC. Additionally, &lt;i&gt;CHD1L&lt;/i&gt; mRNA expression was quantified using real-time quantitative PCR (RT-qPCR). The survival rate of patients with HNSCC was assessed using Kaplan–Meier analysis. Furthermore, in silico tools were employed to investigate CHD1L protein networks and functional pathways involved in HNSCC development.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;mRNA and protein expression studies, along with in vitro and in silico analyses, confirmed that CHD1L expression was significantly higher in HNSCC tissues than in normal tissues. Clinicopathological analysis revealed associations between CHD1L expression and HPV status, nodal metastasis, disease stage, and tumor grade. Elevated CHD1L levels are also associated with poor patient survival. Functional enrichment analysis showed that CHD1L was associated with HNSCC progression.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;CHD1L is significantly upregulated in HNSCC and associated with poor survival outcomes. This suggests that CHD1L may serve as a potential therapeutic target and prognostic marker for HNSCC. Further research is necessary to explore the functional role of CHD1L in the development and progression of HNSCC.&lt;/p&gt;</content:encoded>
         <dc:creator>
Aishvarya Rukmani Panayappan, 
Chandra Pandi, 
Vijayashree Priyadharshini Jayaseelan, 
Paramasivam Arumugam
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>High Expression of CHD1L, a Potent Oncogene Is Associated With Aggressive Head and Neck Cancer and Poor Survival Outcome</dc:title>
         <dc:identifier>10.1111/jop.70114</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70114</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70114?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70118?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70118</guid>
         <title>Prevalence and Molecular Insights of Human Papillomavirus in Dentigerous Cysts and Odontogenic Keratocysts: A Comparative Study</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 567-573, May 2026. </description>
         <dc:description>
ABSTRACT

Background
No studies to date have examined human papillomavirus (HPV) positivity in both odontogenic keratocysts (OKCs) and dentigerous cysts (DCs) or performed HPV genotyping in these lesions. This research aims to compare HPV expression rates in DCs and OKCs to provide insight into the molecular behavior of OKCs.


Methods
Forty DC and forty OKC cases were randomly selected and analyzed for HPV‐DNA expression. Positive cases underwent HPV genotyping. Additionally an immunohistochemical staining for p16 was performed for each case.


Results
Due to epithelial integrity loss or inflammation, 18 samples were excluded, leaving 32 DCs and 30 OKCs for evaluation. HPV was detected in five DC cases but absent in all OKC samples. The difference between DC and OKC groups was not statistically significant (p = 0.053). Genotyping identified HPV‐16 in four cases and HPV‐66 in one.


Discussion
Despite OKCs' aggressive behavior, this study found no significant association between HPV and their pathogenesis. These findings suggest HPV is unlikely to contribute to OKC proliferation or recurrence, underscoring the need for larger studies to clarify its role in odontogenic cysts.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;No studies to date have examined human papillomavirus (HPV) positivity in both odontogenic keratocysts (OKCs) and dentigerous cysts (DCs) or performed HPV genotyping in these lesions. This research aims to compare HPV expression rates in DCs and OKCs to provide insight into the molecular behavior of OKCs.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Forty DC and forty OKC cases were randomly selected and analyzed for HPV-DNA expression. Positive cases underwent HPV genotyping. Additionally an immunohistochemical staining for p16 was performed for each case.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Due to epithelial integrity loss or inflammation, 18 samples were excluded, leaving 32 DCs and 30 OKCs for evaluation. HPV was detected in five DC cases but absent in all OKC samples. The difference between DC and OKC groups was not statistically significant (&lt;i&gt;p&lt;/i&gt; = 0.053). Genotyping identified HPV-16 in four cases and HPV-66 in one.&lt;/p&gt;
&lt;h2&gt;Discussion&lt;/h2&gt;
&lt;p&gt;Despite OKCs' aggressive behavior, this study found no significant association between HPV and their pathogenesis. These findings suggest HPV is unlikely to contribute to OKC proliferation or recurrence, underscoring the need for larger studies to clarify its role in odontogenic cysts.&lt;/p&gt;</content:encoded>
         <dc:creator>
Nelli Agbulut, 
Mualla Özcan
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Prevalence and Molecular Insights of Human Papillomavirus in Dentigerous Cysts and Odontogenic Keratocysts: A Comparative Study</dc:title>
         <dc:identifier>10.1111/jop.70118</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70118</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70118?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70123?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70123</guid>
         <title>Sjögren's Disease and Cancer: Key Predictors From the Spanish Multicenter SjögrenSER‐TRANS Cohort</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 583-590, May 2026. </description>
         <dc:description>
ABSTRACT

Objective
To identify key clinical and therapeutic predictors of malignancy in a well‐characterized, multicenter Spanish cohort of patients with Sjögren's disease (SjD).


Methods
A retrospective, cross‐sectional study was conducted using data from the SjögrenSER‐TRANS registry, a national cohort of 437 SjD patients from 33 Spanish hospitals who fulfilled the 2002 AECG classification criteria. Clinical, serological, and treatment‐related variables were systematically collected. Descriptive statistics were used to summarize demographic and clinical characteristics. Bivariate analysis (chi‐squared for categorical variables and t‐tests for continuous variables) was performed to identify associations with malignancy (p &lt; 0.05), followed by multivariate logistic regression to determine independent predictors.


Results
Malignancy was identified in 30 patients (6.86%), with gynecological cancers (30%) and lymphomas (23.3%) being the most common types. Independent predictors of malignancy included older age (OR 1.042, 95% CI 1.007–1.079), glandular inflammation (OR 2.888, 95% CI 1.281–6.512), and rituximab use (OR 3.959, 95% CI 1.461–10.730).


Conclusion
This study underscores the role of older age, glandular inflammation, and rituximab use as key risk factors for malignancy in SjD. However, the association with rituximab should be interpreted with caution, as indication bias cannot be ruled out. These findings emphasize the need for improved risk stratification and targeted surveillance strategies to facilitate early detection and enhance malignancy management in clinical practice. Prospective studies are warranted to refine monitoring protocols and optimize patient outcomes.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;To identify key clinical and therapeutic predictors of malignancy in a well-characterized, multicenter Spanish cohort of patients with Sjögren's disease (SjD).&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A retrospective, cross-sectional study was conducted using data from the SjögrenSER-TRANS registry, a national cohort of 437 SjD patients from 33 Spanish hospitals who fulfilled the 2002 AECG classification criteria. Clinical, serological, and treatment-related variables were systematically collected. Descriptive statistics were used to summarize demographic and clinical characteristics. Bivariate analysis (chi-squared for categorical variables and &lt;i&gt;t&lt;/i&gt;-tests for continuous variables) was performed to identify associations with malignancy (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.05), followed by multivariate logistic regression to determine independent predictors.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Malignancy was identified in 30 patients (6.86%), with gynecological cancers (30%) and lymphomas (23.3%) being the most common types. Independent predictors of malignancy included older age (OR 1.042, 95% CI 1.007–1.079), glandular inflammation (OR 2.888, 95% CI 1.281–6.512), and rituximab use (OR 3.959, 95% CI 1.461–10.730).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This study underscores the role of older age, glandular inflammation, and rituximab use as key risk factors for malignancy in SjD. However, the association with rituximab should be interpreted with caution, as indication bias cannot be ruled out. These findings emphasize the need for improved risk stratification and targeted surveillance strategies to facilitate early detection and enhance malignancy management in clinical practice. Prospective studies are warranted to refine monitoring protocols and optimize patient outcomes.&lt;/p&gt;</content:encoded>
         <dc:creator>
Olga Rusinovich‐Lovgach, 
Zulema Plaza, 
Mónica Fernández Castro, 
Carlos Sánchez‐Piedra, 
José Rosas, 
Victor Martínez‐Taboada, 
Alejandro Olivé, 
Raul Menor Almagro, 
Beatriz Rodrígez‐Lozano, 
Angel Garcia‐Aparicio, 
Francisco Javier Lopez Longo, 
Sara Manrique‐Arija, 
Jesús Alberto Garcia‐Vadillo, 
Susana Gil Barato, 
Ruth Lopez‐Gonzalez, 
Javier Narvaez García, 
Carlos Galisteo Lencastre, 
Jorge Gonzalez‐Martin, 
Fernando Alonso, 
Jose Luis Andreu,  on behalf of SJÖGRENSER Group, part of the Spanish Society of Rheumatology Systemic Autoimmune Diseases Study Group (EASSER)
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Sjögren's Disease and Cancer: Key Predictors From the Spanish Multicenter SjögrenSER‐TRANS Cohort</dc:title>
         <dc:identifier>10.1111/jop.70123</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70123</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70123?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70100?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70100</guid>
         <title>The Putative Role of Mast Cells in Oral Leukoplakia—A Systematic Review and Meta‐Analysis</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 555-566, May 2026. </description>
         <dc:description>
ABSTRACT

Background
Mast cells are believed to contribute to inflammation‐associated carcinogenesis, but their specific role in the development of oral leukoplakia (OLK) and its progression to oral squamous cell carcinoma (OSCC) remains uncertain. This systematic review and meta‐analysis aimed to determine whether mast cell density differs among normal oral mucosa (NOM), OLK, and OSCC.


Methods
A comprehensive literature search was conducted in PubMed, Scopus, Web of Science and Embase along with Google Scholar for studies that reported mast cell counts in OLK, OSCC, and NOM published up to September 30, 2025. Data were extracted, and the mean difference was calculated. Risk of bias was assessed using the JBI critical appraisal tool, and meta‐analysis was performed using MetaAnalysisOnline.com.


Results
Thirty‐four studies were included for qualitative and 26 contributed to quantitative data synthesis. The studies opined that mast cells were highest in OSCC, followed by OLK and NOM. Mast cell density was higher in OSCC than in OLK; however, the difference was not significant. A random‐effects model revealed a significant increase in mast cell density in OLK than NOM (p &lt; 0.0001) and OSCC than NOM (p = 0.0055); however, when OLK was compared with OSCC, the difference was not significant (p = 0.2865).


Conclusion
The existing data validate that mast cells were increased in oral leukoplakia, indicating their potential involvement in early oral carcinogenesis; however, future studies focusing on the prognostic value of mast cells in oral leukoplakia are warranted.Trial Registration: PROSPERO number: CRD42024533723

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Mast cells are believed to contribute to inflammation-associated carcinogenesis, but their specific role in the development of oral leukoplakia (OLK) and its progression to oral squamous cell carcinoma (OSCC) remains uncertain. This systematic review and meta-analysis aimed to determine whether mast cell density differs among normal oral mucosa (NOM), OLK, and OSCC.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A comprehensive literature search was conducted in PubMed, Scopus, Web of Science and Embase along with Google Scholar for studies that reported mast cell counts in OLK, OSCC, and NOM published up to September 30, 2025. Data were extracted, and the mean difference was calculated. Risk of bias was assessed using the JBI critical appraisal tool, and meta-analysis was performed using &lt;a target="_blank"
   title="Link to external resource"
   href="http://metaanalysisonline.com"&gt;MetaAnalysisOnline.com&lt;/a&gt;.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Thirty-four studies were included for qualitative and 26 contributed to quantitative data synthesis. The studies opined that mast cells were highest in OSCC, followed by OLK and NOM. Mast cell density was higher in OSCC than in OLK; however, the difference was not significant. A random-effects model revealed a significant increase in mast cell density in OLK than NOM (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.0001) and OSCC than NOM (&lt;i&gt;p&lt;/i&gt; = 0.0055); however, when OLK was compared with OSCC, the difference was not significant (&lt;i&gt;p&lt;/i&gt; = 0.2865).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;The existing data validate that mast cells were increased in oral leukoplakia, indicating their potential involvement in early oral carcinogenesis; however, future studies focusing on the prognostic value of mast cells in oral leukoplakia are warranted.&lt;b&gt;Trial Registration:&lt;/b&gt; PROSPERO number: CRD42024533723&lt;/p&gt;</content:encoded>
         <dc:creator>
Nikita Kashyap, 
Achla Bharti, 
Mala Kamboj, 
Anjali Narwal, 
Anju Devi, 
Adarsh Kumar, 
Gitika Sharma
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>The Putative Role of Mast Cells in Oral Leukoplakia—A Systematic Review and Meta‐Analysis</dc:title>
         <dc:identifier>10.1111/jop.70100</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70100</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70100?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70105?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70105</guid>
         <title>The Risk of Cardiometabolic Conditions Among Patients With Oral Candidiasis: A Global Large‐Scale Population‐Based Study</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 539-545, May 2026. </description>
         <dc:description>
ABSTRACT

Background
The cardiometabolic burden of oral candidiasis (OC) is yet to be thoroughly elucidated.


Objective
To assess the risk of long‐term cardiovascular and metabolic outcomes in patients with OC relative to those with two other common oral conditions: herpes simplex virus (HSV) infections and recurrent aphthous stomatitis (RAS).


Methods
A global retrospective cohort study comprised two analyses comparing patients with OC to those with HSV and RAS. The study groups were compared regarding the risk of 11 different cardiovascular and four metabolic outcomes. Propensity score matching was performed to optimize inter‐group comparability.


Results
Relative to those with HSV infections, patients with OC were found to experience a higher risk of stroke (HR, 1.78; 95% CI, 1.65–1.92), sudden cardiac death (HR, 2.46; 95% CI, 2.14–2.82), congestive heart failure (CHF; HR, 1.92; 95% CI, 1.80–2.06), hypertension (HR, 1.56; 95% CI, 1.50–1.62), hyperlipidemia (HR, 1.18; 95% CI, 1.13–1.24), type‐2 diabetes mellitus (DM; HR, 1.72; 95% CI, 1.63–1.81), and obesity (HR, 1.32; 95% CI, 1.27–1.38). Compared to RAS, OC demonstrated an elevated risk of myocardial infarction (HR, 1.47; 95% CI, 1.40–1.54), stroke (HR, 1.30; 95% CI, 1.25–1.36), pulmonary embolism (HR, 2.23; 95% CI, 2.11–2.35), peripheral vascular disease (HR, 1.35; 95% CI, 1.29–1.41), atrial fibrillation (HR, 1.61; 95% CI, 1.55–1.68), CHF (HR, 1.79; 95% CI, 1.73–1.86), hyperlipidemia (HR, 1.36; 95% CI, 1.33–1.40), DM (HR, 1.44; 95% CI, 1.40–1.48), and obesity (HR, 1.30; 95% CI,1.27–1.34).


Conclusion
OC is associated with an elevated risk of cardiometabolic outcomes. Physicians managing patients with OC should be aware of these associations.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;The cardiometabolic burden of oral candidiasis (OC) is yet to be thoroughly elucidated.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;To assess the risk of long-term cardiovascular and metabolic outcomes in patients with OC relative to those with two other common oral conditions: herpes simplex virus (HSV) infections and recurrent aphthous stomatitis (RAS).&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A global retrospective cohort study comprised two analyses comparing patients with OC to those with HSV and RAS. The study groups were compared regarding the risk of 11 different cardiovascular and four metabolic outcomes. Propensity score matching was performed to optimize inter-group comparability.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Relative to those with HSV infections, patients with OC were found to experience a higher risk of stroke (HR, 1.78; 95% CI, 1.65–1.92), sudden cardiac death (HR, 2.46; 95% CI, 2.14–2.82), congestive heart failure (CHF; HR, 1.92; 95% CI, 1.80–2.06), hypertension (HR, 1.56; 95% CI, 1.50–1.62), hyperlipidemia (HR, 1.18; 95% CI, 1.13–1.24), type-2 diabetes mellitus (DM; HR, 1.72; 95% CI, 1.63–1.81), and obesity (HR, 1.32; 95% CI, 1.27–1.38). Compared to RAS, OC demonstrated an elevated risk of myocardial infarction (HR, 1.47; 95% CI, 1.40–1.54), stroke (HR, 1.30; 95% CI, 1.25–1.36), pulmonary embolism (HR, 2.23; 95% CI, 2.11–2.35), peripheral vascular disease (HR, 1.35; 95% CI, 1.29–1.41), atrial fibrillation (HR, 1.61; 95% CI, 1.55–1.68), CHF (HR, 1.79; 95% CI, 1.73–1.86), hyperlipidemia (HR, 1.36; 95% CI, 1.33–1.40), DM (HR, 1.44; 95% CI, 1.40–1.48), and obesity (HR, 1.30; 95% CI,1.27–1.34).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;OC is associated with an elevated risk of cardiometabolic outcomes. Physicians managing patients with OC should be aware of these associations.&lt;/p&gt;</content:encoded>
         <dc:creator>
Samer Kridin, 
Hala Karayanni Matanis, 
Idan Redenski, 
Mariam Abdelghaffar, 
Samer Srouji, 
Khalaf Kridin
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>The Risk of Cardiometabolic Conditions Among Patients With Oral Candidiasis: A Global Large‐Scale Population‐Based Study</dc:title>
         <dc:identifier>10.1111/jop.70105</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70105</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70105?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70119?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70119</guid>
         <title>Association of 
p16

INK4A

 Methylation With Oral Squamous Cell Carcinoma and Oral Potentially Malignant Disorders: A Systematic Review and Meta‐Analysis</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 591-600, May 2026. </description>
         <dc:description>
ABSTRACT

Introduction
Methylation of tumor‐suppressor gene promoters, particularly p16

INK4A
, is implicated in oral carcinogenesis. Although associations with oral squamous cell carcinoma (OSCC) and oral potentially malignant disorders (OPMD) have been reported, no systematic review has examined these conditions while assessing evidence certainty. This review evaluated whether p16

INK4A
 promoter methylation is associated with OSCC and OPMD.


Materials and Methods
PubMed, Embase, Web of Science, Scopus, Livivo, and Google Scholar were searched. Studies were selected by title/abstract and then full‐text review. Eligible studies investigated p16

INK4A
 methylation in OSCC or OPMD with comparator groups. Data were meta‐analyzed using random‐effects models to obtain pooled odds ratios (OR). Heterogeneity, publication bias, sensitivity analyses, and prediction intervals were assessed. Evidence certainty was rated using GRADE.


Results
Twenty‐four studies were included, comprising 1330 OSCC patients, 606 OPMD patients, and 681 healthy controls. Meta‐analyses demonstrated a strong association between p16

INK4A
 methylation and OSCC when compared with healthy controls (OR = 11.59; 95% CI = 6.01–22.37; p &lt; 0.0001), with surgical margins (OR = 3.24; 95% CI = 1.86–5.65; p &lt; 0.0001) and with OPMD (OR = 3.72; 95% CI = 2.47–5.59; p &lt; 0.0001). OPMD also showed increased methylation versus healthy controls (OR = 24.8; 95% CI = 7.4–83.14; p &lt; 0.0001).


Conclusions

p16

INK4A
 methylation is strongly associated with OSCC and OPMD; however, due to heterogeneity and low certainty of evidence, these findings should be interpreted cautiously. Further standardized, well‐designed studies are needed to clarify the role of p16

INK4A
 methylation in oral carcinogenesis.

Trial Registration: International Prospective Register of Systematic Reviews (PROSPERO): CRD42023410477

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Introduction&lt;/h2&gt;
&lt;p&gt;Methylation of tumor-suppressor gene promoters, particularly &lt;i&gt;p16&lt;/i&gt;
&lt;sup&gt;
   &lt;i&gt;INK4A&lt;/i&gt;
&lt;/sup&gt;, is implicated in oral carcinogenesis. Although associations with oral squamous cell carcinoma (OSCC) and oral potentially malignant disorders (OPMD) have been reported, no systematic review has examined these conditions while assessing evidence certainty. This review evaluated whether &lt;i&gt;p16&lt;/i&gt;
&lt;sup&gt;
   &lt;i&gt;INK4A&lt;/i&gt;
&lt;/sup&gt; promoter methylation is associated with OSCC and OPMD.&lt;/p&gt;
&lt;h2&gt;Materials and Methods&lt;/h2&gt;
&lt;p&gt;PubMed, Embase, Web of Science, Scopus, Livivo, and Google Scholar were searched. Studies were selected by title/abstract and then full-text review. Eligible studies investigated &lt;i&gt;p16&lt;/i&gt;
&lt;sup&gt;
   &lt;i&gt;INK4A&lt;/i&gt;
&lt;/sup&gt; methylation in OSCC or OPMD with comparator groups. Data were meta-analyzed using random-effects models to obtain pooled odds ratios (OR). Heterogeneity, publication bias, sensitivity analyses, and prediction intervals were assessed. Evidence certainty was rated using GRADE.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Twenty-four studies were included, comprising 1330 OSCC patients, 606 OPMD patients, and 681 healthy controls. Meta-analyses demonstrated a strong association between &lt;i&gt;p16&lt;/i&gt;
&lt;sup&gt;
   &lt;i&gt;INK4A&lt;/i&gt;
&lt;/sup&gt; methylation and OSCC when compared with healthy controls (OR = 11.59; 95% CI = 6.01–22.37; &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.0001), with surgical margins (OR = 3.24; 95% CI = 1.86–5.65; &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.0001) and with OPMD (OR = 3.72; 95% CI = 2.47–5.59; &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.0001). OPMD also showed increased methylation versus healthy controls (OR = 24.8; 95% CI = 7.4–83.14; &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.0001).&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;
&lt;i&gt;p16&lt;/i&gt;
&lt;sup&gt;
   &lt;i&gt;INK4A&lt;/i&gt;
&lt;/sup&gt; methylation is strongly associated with OSCC and OPMD; however, due to heterogeneity and low certainty of evidence, these findings should be interpreted cautiously. Further standardized, well-designed studies are needed to clarify the role of &lt;i&gt;p16&lt;/i&gt;
&lt;sup&gt;
   &lt;i&gt;INK4A&lt;/i&gt;
&lt;/sup&gt; methylation in oral carcinogenesis.&lt;/p&gt;
&lt;p&gt;
&lt;b&gt;Trial Registration:&lt;/b&gt; International Prospective Register of Systematic Reviews (PROSPERO): CRD42023410477&lt;/p&gt;</content:encoded>
         <dc:creator>
Rairam Fernandes de Aguiar, 
Denis Francisco Gonçalves de Oliveira, 
Lucas Moreira de Araújo, 
Khalil Fernandes Viana, 
Douglas Matheus Lima Farias, 
Joyce Magalhães de Barros, 
Filipe Nobre Chaves, 
Alexia Nathália Brígido Assef, 
Thâmara Manoela Marinho Bezerra, 
Sthefane Gomes Feitosa, 
Karuza Maria Alves Pereira
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Association of 
p16

INK4A

 Methylation With Oral Squamous Cell Carcinoma and Oral Potentially Malignant Disorders: A Systematic Review and Meta‐Analysis</dc:title>
         <dc:identifier>10.1111/jop.70119</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70119</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70119?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70113?af=R</link>
         <pubDate>Wed, 06 May 2026 20:42:17 -0700</pubDate>
         <dc:date>2026-05-06T08:42:17-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDate>
         <prism:coverDisplayDate>Fri, 01 May 2026 00:00:00 -0700</prism:coverDisplayDate>
         <guid isPermaLink="false">10.1111/jop.70113</guid>
         <title>Machine Learning for Predicting Malignant Transformation in Actinic Cheilitis: A Prognostic Support System Based on Demographic and Clinical Descriptors</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, Volume 55, Issue 5, Page 574-582, May 2026. </description>
         <dc:description>
ABSTRACT

Objective
This study aimed to develop and evaluate Machine Learning models to predict the malignant transformation (MT) in patients with actinic cheilitis (AC).


Methods
Three hundred forty patients diagnosed with AC (322 in the no MT group, and 18 in the MT group) were carefully documented. The study used the Adaptive Synthetic Sampling to adaptively balance the dataset (322 in the no MT group and 319 in the MT group). Four supervised Machine Learning classifiers (Random Forest, Xtreme Gradient Boosting, Multilayer Perceptron, and Support Vector Machine) were trained and tested using 5‐fold cross‐validation to correlate inputs (clinical descriptors and demographic data) to outputs (MT). SHAP values were used to identify the most influential predictors of MT.


Results
The Xtreme Gradient Boosting model stood out, achieving 96.72% accuracy, 96.87% sensitivity, 96.57% specificity, 96.61% precision, 96.73% of F1‐Score, and 0.9498 AUC. Multilayer Perceptron showed the best sensitivity (98.44%), and Random Forest presented comparable results. In contrast, Support Vector Machine underperformed, with higher values of false negatives and false positives. Across models, ulceration, multifocality, and long‐standing lesions were the strongest predictors of MT, while small, asymptomatic, or solitary lesions were associated with lower risk.


Conclusion
The results revealed promising performance metrics for Xtreme Gradient Boosting and Multilayer Perceptron suggesting their potential value as tools in a support system for monitoring AC. Additionally, synthetic data proved constructive in training, enhancing the models' robustness and predictive capabilities.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;This study aimed to develop and evaluate Machine Learning models to predict the malignant transformation (MT) in patients with actinic cheilitis (AC).&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Three hundred forty patients diagnosed with AC (322 in the no MT group, and 18 in the MT group) were carefully documented. The study used the Adaptive Synthetic Sampling to adaptively balance the dataset (322 in the no MT group and 319 in the MT group). Four supervised Machine Learning classifiers (Random Forest, Xtreme Gradient Boosting, Multilayer Perceptron, and Support Vector Machine) were trained and tested using 5-fold cross-validation to correlate inputs (clinical descriptors and demographic data) to outputs (MT). SHAP values were used to identify the most influential predictors of MT.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The Xtreme Gradient Boosting model stood out, achieving 96.72% accuracy, 96.87% sensitivity, 96.57% specificity, 96.61% precision, 96.73% of F1-Score, and 0.9498 AUC. Multilayer Perceptron showed the best sensitivity (98.44%), and Random Forest presented comparable results. In contrast, Support Vector Machine underperformed, with higher values of false negatives and false positives. Across models, ulceration, multifocality, and long-standing lesions were the strongest predictors of MT, while small, asymptomatic, or solitary lesions were associated with lower risk.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;The results revealed promising performance metrics for Xtreme Gradient Boosting and Multilayer Perceptron suggesting their potential value as tools in a support system for monitoring AC. Additionally, synthetic data proved constructive in training, enhancing the models' robustness and predictive capabilities.&lt;/p&gt;</content:encoded>
         <dc:creator>
Ivan José Correia‐Neto, 
Alex Franco da Costa, 
Anna Luíza Damaceno Araújo, 
Cristina Saldivia‐Siracusa, 
Raísa Sales de Sá, 
Thiago Martini Pereira, 
Pablo Agustin Vargas, 
Alan Roger Santos‐Silva, 
Luiz Paulo Kowalski, 
Matheus Cardoso Moraes, 
Marcio Ajudarte Lopes
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Machine Learning for Predicting Malignant Transformation in Actinic Cheilitis: A Prognostic Support System Based on Demographic and Clinical Descriptors</dc:title>
         <dc:identifier>10.1111/jop.70113</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70113</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70113?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
         <prism:volume>55</prism:volume>
         <prism:number>5</prism:number>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70148?af=R</link>
         <pubDate>Thu, 30 Apr 2026 00:14:47 -0700</pubDate>
         <dc:date>2026-04-30T12:14:47-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70148</guid>
         <title>Lymphatic Vessel Density or Area Are Not Reliable Prognostic Factors in Oral Cancer</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Oral tongue squamous cell carcinomas (OTSCC) frequently metastasise via lymphatic vessels, thus lymphangiogenesis may enhance tumour cell dissemination by increasing tumour‐lymphatic interactions. The prognostic significance of lymphatic vessel density (LVD) and lymphatic vessel area (LVA) in OTSCC remains inconclusive. This study aimed to evaluate the association of tumour‐associated LVD and LVA with clinical outcomes and pathological characteristics in a homogenous OTSCC cohort.


Methods
We analysed tumour samples from 121 OTSCC patients using D2‐40 immunohistochemical staining to visualise lymphatic vessels. We calculated mean LVD and LVA from five peritumoural hotspots per tumour and examined their relationships to clinical‐pathological data including 5‐year disease‐specific survival (DSS) using cross‐tabulation, Kaplan–Meier, and Cox regression analyses.


Results
High LVD was more prevalent in well/moderately differentiated compared to poorly differentiated tumours (78.1% and 45.5%, respectively, p = 0.017). No significant associations were found between LVD or LVA and other clinical‐pathological variables. Neither low LVD nor LVA significantly impacted 5‐year DSS in univariate (HR = 0.65 CI: 0.32, 1.31; HR = 0.69, 95% CI: 0.34, 1.40, respectively) or multivariate analyses (HR = 0.75, 95% CI: 0.32, 1.76; HR = 0.54, 95% CI: 0.23, 1.25, respectively).


Conclusions
LVD and LVA did not predict prognosis in this OTSCC cohort. Further standardised studies investigating lymphatic vessels within the tumour microenvironment are necessary to better understand their role and potential prognostic significance.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Oral tongue squamous cell carcinomas (OTSCC) frequently metastasise via lymphatic vessels, thus lymphangiogenesis may enhance tumour cell dissemination by increasing tumour-lymphatic interactions. The prognostic significance of lymphatic vessel density (LVD) and lymphatic vessel area (LVA) in OTSCC remains inconclusive. This study aimed to evaluate the association of tumour-associated LVD and LVA with clinical outcomes and pathological characteristics in a homogenous OTSCC cohort.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;We analysed tumour samples from 121 OTSCC patients using D2-40 immunohistochemical staining to visualise lymphatic vessels. We calculated mean LVD and LVA from five peritumoural hotspots per tumour and examined their relationships to clinical-pathological data including 5-year disease-specific survival (DSS) using cross-tabulation, Kaplan–Meier, and Cox regression analyses.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;High LVD was more prevalent in well/moderately differentiated compared to poorly differentiated tumours (78.1% and 45.5%, respectively, &lt;i&gt;p&lt;/i&gt; = 0.017). No significant associations were found between LVD or LVA and other clinical-pathological variables. Neither low LVD nor LVA significantly impacted 5-year DSS in univariate (HR = 0.65 CI: 0.32, 1.31; HR = 0.69, 95% CI: 0.34, 1.40, respectively) or multivariate analyses (HR = 0.75, 95% CI: 0.32, 1.76; HR = 0.54, 95% CI: 0.23, 1.25, respectively).&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;LVD and LVA did not predict prognosis in this OTSCC cohort. Further standardised studies investigating lymphatic vessels within the tumour microenvironment are necessary to better understand their role and potential prognostic significance.&lt;/p&gt;</content:encoded>
         <dc:creator>
Ida Andersson Cronblad, 
Cathrine Elise Warvik, 
Inger‐Heidi Bjerkli, 
Sonja Eriksson Steigen, 
Lars Uhlin‐Hansen, 
Synnøve Norvoll Magnussen, 
Elin Hadler‐Olsen, 
Anna Maria Wirsing
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Lymphatic Vessel Density or Area Are Not Reliable Prognostic Factors in Oral Cancer</dc:title>
         <dc:identifier>10.1111/jop.70148</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70148</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70148?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70146?af=R</link>
         <pubDate>Tue, 28 Apr 2026 00:34:39 -0700</pubDate>
         <dc:date>2026-04-28T12:34:39-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70146</guid>
         <title>Global Prevalence of Oral Potentially Malignant Disorders: An Updated Systematic Review and Meta‐Analysis</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Oral potentially malignant disorders (OPMDs) represent a diverse group of mucosal disorders with varying risks of progression to oral cancer.


Objective
This updated systematic review (SR) and meta‐analysis (MA) estimated the global prevalence of histopathologically confirmed OPMDs, excluding oral lichen planus and lichenoid lesions.


Methods
A comprehensive literature search was conducted using predefined eligibility criteria. A total of 108 studies were included, comprising 86 additional studies and 22 from a previous SR.


Results
The overall pooled prevalence of OPMDs was 4.67% (95% CI: 3.62–5.84). Prevalence of OPMDs was as follows: Asia (5.44%), followed by South America/Caribbean (5.21%), and Europe (4.89%). Considering OPMD cases, the proportion was higher among males (62.87%) and individuals aged ≥ 50 years (68.1%). Histopathological evidence of epithelial dysplasia was present in 46.21% of cases. Oral leukoplakia (OL), oral submucous fibrosis (OSMF), and actinic cheilitis (AC) emerged as the most prevalent lesions, with relevant differences considering the geographic regions. OL and OSMF were the most common OPMDs in Asia, while OL and AC predominated in South America/Caribbean, and in Europe OL remains the most frequently encountered OPMD.


Conclusions
The global prevalence of OPMDs, estimated at approximately 5%, should be interpreted as a broad summary measure, given the substantial heterogeneity driven by regional variations possibly related to behavioral, biological, and/or environmental risk factors. Future preventive efforts should focus on the type of OPMD prevalent in the region/country. The heterogeneity across studies highlights the need for standardized, population‐based studies using WHO nomenclature to better define the global burden.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Oral potentially malignant disorders (OPMDs) represent a diverse group of mucosal disorders with varying risks of progression to oral cancer.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;This updated systematic review (SR) and meta-analysis (MA) estimated the global prevalence of histopathologically confirmed OPMDs, excluding oral lichen planus and lichenoid lesions.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A comprehensive literature search was conducted using predefined eligibility criteria. A total of 108 studies were included, comprising 86 additional studies and 22 from a previous SR.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The overall pooled prevalence of OPMDs was 4.67% (95% CI: 3.62–5.84). Prevalence of OPMDs was as follows: Asia (5.44%), followed by South America/Caribbean (5.21%), and Europe (4.89%). Considering OPMD cases, the proportion was higher among males (62.87%) and individuals aged ≥ 50 years (68.1%). Histopathological evidence of epithelial dysplasia was present in 46.21% of cases. Oral leukoplakia (OL), oral submucous fibrosis (OSMF), and actinic cheilitis (AC) emerged as the most prevalent lesions, with relevant differences considering the geographic regions. OL and OSMF were the most common OPMDs in Asia, while OL and AC predominated in South America/Caribbean, and in Europe OL remains the most frequently encountered OPMD.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;The global prevalence of OPMDs, estimated at approximately 5%, should be interpreted as a broad summary measure, given the substantial heterogeneity driven by regional variations possibly related to behavioral, biological, and/or environmental risk factors. Future preventive efforts should focus on the type of OPMD prevalent in the region/country. The heterogeneity across studies highlights the need for standardized, population-based studies using WHO nomenclature to better define the global burden.&lt;/p&gt;</content:encoded>
         <dc:creator>
Nicole Lonni, 
Tulio Silva Rosa, 
Camilla Kammer Pereira, 
Gilberto Melo, 
Saman Warnakulasuriya, 
Eliete Neves Silva Guerra, 
Elena Riet Correa Rivero
</dc:creator>
         <category>REVIEW</category>
         <dc:title>Global Prevalence of Oral Potentially Malignant Disorders: An Updated Systematic Review and Meta‐Analysis</dc:title>
         <dc:identifier>10.1111/jop.70146</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70146</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70146?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70145?af=R</link>
         <pubDate>Tue, 21 Apr 2026 00:36:45 -0700</pubDate>
         <dc:date>2026-04-21T12:36:45-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70145</guid>
         <title>Hemidesmosomal Proteins in Oral Cancer Progression: An Immunohistochemical Study of Human and Mouse</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Hemidesmosomal subunits have gained attention for their potential role in the progression of oral squamous cell carcinoma (OSCC). However, formal analysis of quantitative expression patterns correlating with OSCC disease pathogenesis remains limited. This study evaluated the expression of key yet overlooked hemidesmosomal subunits, plectin isoform Ia (PIa), dystonin, and CD151 antigen, from normal tissue as well as tissue from hyperplasia, dysplasia, and OSCC in the human and murine oral cavity.


Methods
Immunohistochemistry was performed on custom‐built human tissue microarrays and 4‐Nitroquinoline 1‐oxide (4‐NQO)‐induced murine OSCC covering the spectrum of histological changes from normal to cancer. Quantitative image analysis of subunit expression was conducted using QuPath, with distinct analytical approaches applied to human tissues, including a refined method focusing on the basement membrane zone (BMZ) and adjacent basal epithelial layers, key sites of hemidesmosomal protein localization.


Results
A significant increase in expression of all three proteins was observed comparing normal tissue with hyperplasia, dysplasia, and OSCC in murine tissues, but not in humans. The expression of hemidesmosomal proteins increased across this spectrum, suggesting their potential as progression biomarkers in mice. A focused analysis of the basement membrane zone and adjacent basal epithelial layers in human tissues revealed a sustained baseline expression and a significant reduction in CD151 antigen in OSCC compared with control and high‐grade dysplasia groups, as well as a significant reduction in dystonin expression in OSCC compared to high‐grade dysplasia.


Conclusion
Our findings highlight the importance of biologically targeted region‐of‐interest selection when assessing hemidesmosomal protein expression in OSCC while demonstrating that BMZ‐focused digital analysis provides a more informative approach for exploratory evaluation of heterogeneous human tissues alongside progression‐associated patterns observed in a murine model.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Hemidesmosomal subunits have gained attention for their potential role in the progression of oral squamous cell carcinoma (OSCC). However, formal analysis of quantitative expression patterns correlating with OSCC disease pathogenesis remains limited. This study evaluated the expression of key yet overlooked hemidesmosomal subunits, plectin isoform Ia (PIa), dystonin, and CD151 antigen, from normal tissue as well as tissue from hyperplasia, dysplasia, and OSCC in the human and murine oral cavity.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Immunohistochemistry was performed on custom-built human tissue microarrays and 4-Nitroquinoline 1-oxide (4-NQO)-induced murine OSCC covering the spectrum of histological changes from normal to cancer. Quantitative image analysis of subunit expression was conducted using QuPath, with distinct analytical approaches applied to human tissues, including a refined method focusing on the basement membrane zone (BMZ) and adjacent basal epithelial layers, key sites of hemidesmosomal protein localization.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;A significant increase in expression of all three proteins was observed comparing normal tissue with hyperplasia, dysplasia, and OSCC in murine tissues, but not in humans. The expression of hemidesmosomal proteins increased across this spectrum, suggesting their potential as progression biomarkers in mice. A focused analysis of the basement membrane zone and adjacent basal epithelial layers in human tissues revealed a sustained baseline expression and a significant reduction in CD151 antigen in OSCC compared with control and high-grade dysplasia groups, as well as a significant reduction in dystonin expression in OSCC compared to high-grade dysplasia.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Our findings highlight the importance of biologically targeted region-of-interest selection when assessing hemidesmosomal protein expression in OSCC while demonstrating that BMZ-focused digital analysis provides a more informative approach for exploratory evaluation of heterogeneous human tissues alongside progression-associated patterns observed in a murine model.&lt;/p&gt;</content:encoded>
         <dc:creator>
Nikhil Mongia, 
Ali Ibrahim Mohammed, 
Michael McCullough, 
Rita Paolini, 
James A. Rickard, 
Massimo Mascolo, 
Silvia Varricchio, 
Lorraine A. O'Reilly, 
John Silke, 
Nicola Cirillo, 
Antonio Celentano
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Hemidesmosomal Proteins in Oral Cancer Progression: An Immunohistochemical Study of Human and Mouse</dc:title>
         <dc:identifier>10.1111/jop.70145</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70145</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70145?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70142?af=R</link>
         <pubDate>Mon, 20 Apr 2026 22:02:14 -0700</pubDate>
         <dc:date>2026-04-20T10:02:14-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70142</guid>
         <title>Prognostic Significance of CD105‐Assessed Angiogenesis in Relation to Survival and Clinicopathological Features of Oral Squamous Cell Carcinoma</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Objective
The aim of this study was to determine the clinical significance of mean vascular density (MVD) using the expression of CD105 (endoglein) to predict the 3‐ and 5‐year survival rates of oral squamous cell carcinoma (OSCC), as well as assess its value for predicting clinical outcomes of OSCC.


Methods
A total of 217 OSCC patients treated surgically between 2010 and 2015 were included. Immuno‐histochemistry for CD105 was performed, and MVD was quantified. The correlations of MVD with histopathological (HSPL) grade, the clinical Tumor Node Metastasis (TNM) stage, nodal status and survival were analyzed. Multivariate Cox proportional hazards regression analysis was also performed.


Results
The MVD significantly increased with increasing HSPL grade from well‐differentiated OSCC to poorly‐differentiated OSCC (p &lt; 0.001). MVD was significantly increased for advanced‐stage TNM cases (III/IV) and metastatic cases when compared to early‐stage and non‐metastatic tumors (p &lt; 0.001). Survival analysis revealed an inverse relationship between MVD and both three‐ and five‐year disease‐free survival. Patients with low MVD had the highest disease‐free survival (3 years: 96.2%, 5 years: 92.7%), whereas those with high MVD had poor survival (3 years: 34.0%, 5 years: 27.9%). Multivariate Cox regression analysis confirmed MVD and HSPL grade as independent prognostic factors for overall survival.


Conclusion
An elevated MVD by CD105 expression is strongly correlated with aggressive HSPL features, stage, nodal metastasis, and poor prognosis in OSCC. In addition to prognostic information, CD105 has the potential to be a target for anti‐angiogenic strategies in OSCC indicating its potential use in clinical risk stratification and planning.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;The aim of this study was to determine the clinical significance of mean vascular density (MVD) using the expression of CD105 (endoglein) to predict the 3- and 5-year survival rates of oral squamous cell carcinoma (OSCC), as well as assess its value for predicting clinical outcomes of OSCC.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A total of 217 OSCC patients treated surgically between 2010 and 2015 were included. Immuno-histochemistry for CD105 was performed, and MVD was quantified. The correlations of MVD with histopathological (HSPL) grade, the clinical Tumor Node Metastasis (TNM) stage, nodal status and survival were analyzed. Multivariate Cox proportional hazards regression analysis was also performed.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The MVD significantly increased with increasing HSPL grade from well-differentiated OSCC to poorly-differentiated OSCC (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001). MVD was significantly increased for advanced-stage TNM cases (III/IV) and metastatic cases when compared to early-stage and non-metastatic tumors (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001). Survival analysis revealed an inverse relationship between MVD and both three- and five-year disease-free survival. Patients with low MVD had the highest disease-free survival (3 years: 96.2%, 5 years: 92.7%), whereas those with high MVD had poor survival (3 years: 34.0%, 5 years: 27.9%). Multivariate Cox regression analysis confirmed MVD and HSPL grade as independent prognostic factors for overall survival.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;An elevated MVD by CD105 expression is strongly correlated with aggressive HSPL features, stage, nodal metastasis, and poor prognosis in OSCC. In addition to prognostic information, CD105 has the potential to be a target for anti-angiogenic strategies in OSCC indicating its potential use in clinical risk stratification and planning.&lt;/p&gt;</content:encoded>
         <dc:creator>
Amol Ramchandra Gadbail, 
Minal Chaudhary, 
Satyajit Ashok Tekade, 
Alka Hande, 
Monal Yuwanati, 
Pranali Nimonkar, 
Shailesh M. Gondivkar, 
Sachin Sarode
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Prognostic Significance of CD105‐Assessed Angiogenesis in Relation to Survival and Clinicopathological Features of Oral Squamous Cell Carcinoma</dc:title>
         <dc:identifier>10.1111/jop.70142</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70142</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70142?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70143?af=R</link>
         <pubDate>Mon, 20 Apr 2026 21:30:09 -0700</pubDate>
         <dc:date>2026-04-20T09:30:09-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70143</guid>
         <title>Transcriptome Analysis and Histological Validation Identified the HO‐1‐u‐1 Cell Line as a Model for Perineural Invasion in Oral Squamous Cell Carcinoma</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Perineural invasion (PNI) is a pathological feature of oral squamous cell carcinoma (OSCC) that is associated with a poor prognosis. However, the molecular mechanisms remain poorly understood. The aim of this study was to establish an in vivo model to explore PNI in OSCC.


Methods
We performed an integrated analysis of The Cancer Genome Atlas transcriptome data from tongue squamous cell carcinoma (TSCC) and floor of the mouth squamous cell carcinoma (FOMSCC) by the presence of PNI and identified differentially expressed genes (DEGs). We also performed xenografts of five OSCC cell lines (OSC19, OSC20, HSC2, KOSC2, and HO‐1‐u‐1) into nude mouse tongues and assessed PNI histology. Furthermore, transcriptome profiles of the cell lines were analyzed to identify cell line‐specific genes associated with PNI.


Results
Among OSCCs, PNI cases were more prevalent in TSCC and FOMSCC. Expression analysis detected 103 DEGs in TSCC and 401 in FOMSCC. In TSCC, 42.2% of the DEGs were non‐coding RNAs, whereas DEGs in FOMSCC were predominantly protein‐coding genes enriched in pathways related to muscle contraction and fibrosis. Xenograft analysis revealed that HO‐1‐u‐1 uniquely exhibited a nerve‐directed invasion phenotype. Transcriptome analysis of OSCC cell lines demonstrated that HO‐1‐u‐1 was enriched in neural‐ and glial‐related pathways, consistent with its neurotropic behavior in vivo.


Conclusions
Our transcriptome analysis suggested that different pathways might drive PNI in TSCC and FOMSCC, depending on their origin. We also demonstrated that HO‐1‐u‐1 is a unique OSCC cell line with strong neurotropic properties and a valuable xenograft model for OSCC PNI.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Perineural invasion (PNI) is a pathological feature of oral squamous cell carcinoma (OSCC) that is associated with a poor prognosis. However, the molecular mechanisms remain poorly understood. The aim of this study was to establish an in vivo model to explore PNI in OSCC.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;We performed an integrated analysis of The Cancer Genome Atlas transcriptome data from tongue squamous cell carcinoma (TSCC) and floor of the mouth squamous cell carcinoma (FOMSCC) by the presence of PNI and identified differentially expressed genes (DEGs). We also performed xenografts of five OSCC cell lines (OSC19, OSC20, HSC2, KOSC2, and HO-1-u-1) into nude mouse tongues and assessed PNI histology. Furthermore, transcriptome profiles of the cell lines were analyzed to identify cell line-specific genes associated with PNI.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Among OSCCs, PNI cases were more prevalent in TSCC and FOMSCC. Expression analysis detected 103 DEGs in TSCC and 401 in FOMSCC. In TSCC, 42.2% of the DEGs were non-coding RNAs, whereas DEGs in FOMSCC were predominantly protein-coding genes enriched in pathways related to muscle contraction and fibrosis. Xenograft analysis revealed that HO-1-u-1 uniquely exhibited a nerve-directed invasion phenotype. Transcriptome analysis of OSCC cell lines demonstrated that HO-1-u-1 was enriched in neural- and glial-related pathways, consistent with its neurotropic behavior in vivo.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;Our transcriptome analysis suggested that different pathways might drive PNI in TSCC and FOMSCC, depending on their origin. We also demonstrated that HO-1-u-1 is a unique OSCC cell line with strong neurotropic properties and a valuable xenograft model for OSCC PNI.&lt;/p&gt;</content:encoded>
         <dc:creator>
Taisuke Hani, 
Tomoo Kudo, 
Toshiki Nishimura, 
Yuuichi Soeno
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Transcriptome Analysis and Histological Validation Identified the HO‐1‐u‐1 Cell Line as a Model for Perineural Invasion in Oral Squamous Cell Carcinoma</dc:title>
         <dc:identifier>10.1111/jop.70143</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70143</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70143?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70138?af=R</link>
         <pubDate>Thu, 16 Apr 2026 21:31:33 -0700</pubDate>
         <dc:date>2026-04-16T09:31:33-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70138</guid>
         <title>Effect of miR‐214‐3p on Cisplatin Resistance in Oral Squamous Cell Carcinoma by Regulating Ferroptosis Through Targeting GPX4</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Introduction
Emerging evidence underscores the potential of ferroptosis as a promising therapeutic target in cancer. However, the role of microRNAs (miRNAs) in modulating ferroptosis sensitivity remains largely unexplored, particularly in the context of oral squamous cell carcinoma (OSCC) chemoresistance. This study was designed to investigate the role of miR‐214‐3p in regulating ferroptosis by targeting glutathione peroxidase 4 (GPX4) and its influence on cisplatin (DDP) resistance in OSCC.


Methods
Patients diagnosed with OSCC and receiving DDP‐based chemotherapy between February 2022 and February 2024 at our institution were included in this study. Expression levels of miR‐214‐3p and GPX4 were quantitatively assessed in DDP‐sensitive versus DDP‐resistant OSCC tissues and cell lines using qRT‐PCR and Western blot. Cell viability, IC50 values, and apoptosis were evaluated using the CCK‐8 assay and flow cytometry. Intracellular reactive oxygen species (ROS) and Fe2+ levels were measured to determine the status of ferroptosis. Bioinformatics prediction and dual‐luciferase reporter assays confirmed the interaction between miR‐214‐3p and GPX4. In vivo xenograft models were utilized to investigate the impact of miR‐214‐3p on OSCC tumor growth.


Results
As an initial assessment of clinical relevance, miR‐214‐3p was significantly downregulated in DDP‐resistant OSCC tissues and cells, whereas GPX4 expression was markedly upregulated. Overexpression of miR‐214‐3p substantially decreased cell viability, reduced the IC50 values of DDP, and promoted apoptosis in resistant cells. In comparison to parental cells, resistant cells demonstrated lower levels of ROS and Fe2+. Overexpression of miR‐214‐3p or treatment with a ferroptosis inducer (Erastin) increased ROS and Fe2+ levels, an effect that was effectively reversed by a ferroptosis inhibitor (Ferrostatin‐1). Bioinformatics analysis combined with luciferase reporter assays confirmed the direct binding of miR‐214‐3p to the 3′ untranslated region (UTR) of GPX4. The overexpression of miR‐214‐3p resulted in the downregulation of GPX4, whereas overexpression of GPX4 reversed the effects mediated by miR‐214‐3p. Additionally, the overexpression of miR‐214‐3p in xenograft models inhibited tumor growth, which was correlated with decreased GPX4 expression and increased sensitivity to DDP.


Conclusion
Our findings reveal a novel miR‐214‐3p/GPX4/ferroptosis axis in OSCC DDP resistance. miR‐214‐3p suppresses GPX4 to promote ferroptosis, thereby reversing DDP resistance. This study identifies miR‐214‐3p as a potential therapeutic target for overcoming chemoresistance in OSCC by modulating ferroptosis.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Introduction&lt;/h2&gt;
&lt;p&gt;Emerging evidence underscores the potential of ferroptosis as a promising therapeutic target in cancer. However, the role of microRNAs (miRNAs) in modulating ferroptosis sensitivity remains largely unexplored, particularly in the context of oral squamous cell carcinoma (OSCC) chemoresistance. This study was designed to investigate the role of miR-214-3p in regulating ferroptosis by targeting glutathione peroxidase 4 (GPX4) and its influence on cisplatin (DDP) resistance in OSCC.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Patients diagnosed with OSCC and receiving DDP-based chemotherapy between February 2022 and February 2024 at our institution were included in this study. Expression levels of miR-214-3p and GPX4 were quantitatively assessed in DDP-sensitive versus DDP-resistant OSCC tissues and cell lines using qRT-PCR and Western blot. Cell viability, IC50 values, and apoptosis were evaluated using the CCK-8 assay and flow cytometry. Intracellular reactive oxygen species (ROS) and Fe&lt;sup&gt;2+&lt;/sup&gt; levels were measured to determine the status of ferroptosis. Bioinformatics prediction and dual-luciferase reporter assays confirmed the interaction between miR-214-3p and GPX4. In vivo xenograft models were utilized to investigate the impact of miR-214-3p on OSCC tumor growth.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;As an initial assessment of clinical relevance, miR-214-3p was significantly downregulated in DDP-resistant OSCC tissues and cells, whereas GPX4 expression was markedly upregulated. Overexpression of miR-214-3p substantially decreased cell viability, reduced the IC&lt;sub&gt;50&lt;/sub&gt; values of DDP, and promoted apoptosis in resistant cells. In comparison to parental cells, resistant cells demonstrated lower levels of ROS and Fe&lt;sup&gt;2+&lt;/sup&gt;. Overexpression of miR-214-3p or treatment with a ferroptosis inducer (Erastin) increased ROS and Fe&lt;sup&gt;2+&lt;/sup&gt; levels, an effect that was effectively reversed by a ferroptosis inhibitor (Ferrostatin-1). Bioinformatics analysis combined with luciferase reporter assays confirmed the direct binding of miR-214-3p to the 3′ untranslated region (UTR) of GPX4. The overexpression of miR-214-3p resulted in the downregulation of GPX4, whereas overexpression of GPX4 reversed the effects mediated by miR-214-3p. Additionally, the overexpression of miR-214-3p in xenograft models inhibited tumor growth, which was correlated with decreased GPX4 expression and increased sensitivity to DDP.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Our findings reveal a novel miR-214-3p/GPX4/ferroptosis axis in OSCC DDP resistance. miR-214-3p suppresses GPX4 to promote ferroptosis, thereby reversing DDP resistance. This study identifies miR-214-3p as a potential therapeutic target for overcoming chemoresistance in OSCC by modulating ferroptosis.&lt;/p&gt;</content:encoded>
         <dc:creator>
Rongxia Zhang, 
Jing Zhang, 
Yongle Qiu, 
Alin Tian, 
Weiwei Yin, 
Nan Zhang, 
Yang Liu, 
Yunfang Bai
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Effect of miR‐214‐3p on Cisplatin Resistance in Oral Squamous Cell Carcinoma by Regulating Ferroptosis Through Targeting GPX4</dc:title>
         <dc:identifier>10.1111/jop.70138</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70138</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70138?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70141?af=R</link>
         <pubDate>Wed, 15 Apr 2026 02:52:24 -0700</pubDate>
         <dc:date>2026-04-15T02:52:24-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70141</guid>
         <title>Fragmented Thresholds, Unified Vision: Advancing Salivary Diagnostics for OSCC and OPMD</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT
Salivary diagnostics for oral squamous cell carcinoma (OSCC) and oral potentially malignant disorders (OPMD) have advanced significantly, yet clinical translation remains limited. A key barrier is the lack of harmonized thresholds for candidate biomarkers, ranging from cytokines to genetic and epigenetic markers, across studies. This variability undermines biosensor calibration, impedes algorithmic integration, and restricts the scalability of AI and eHealth tools. Paradoxically, saliva is well‐established in systemic disease diagnostics but remains undervalued in oral oncology. Recent initiatives, such as COST Action CA21140—INTERCEPTOR, are working to intercept oral carcinogenesis through collaborative innovation in molecular diagnostics and surveillance technologies. This letter calls for standardized protocols, multicenter validation, and digital integration to unlock saliva's full potential as a frontline diagnostic fluid. By addressing biomarker variability and embracing cross‐sector collaboration, the field can move toward clinically actionable, digitally enabled solutions for early detection and monitoring of OSCC and OPMD.
</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;Salivary diagnostics for oral squamous cell carcinoma (OSCC) and oral potentially malignant disorders (OPMD) have advanced significantly, yet clinical translation remains limited. A key barrier is the lack of harmonized thresholds for candidate biomarkers, ranging from cytokines to genetic and epigenetic markers, across studies. This variability undermines biosensor calibration, impedes algorithmic integration, and restricts the scalability of AI and eHealth tools. Paradoxically, saliva is well-established in systemic disease diagnostics but remains undervalued in oral oncology. Recent initiatives, such as COST Action CA21140—INTERCEPTOR, are working to intercept oral carcinogenesis through collaborative innovation in molecular diagnostics and surveillance technologies. This letter calls for standardized protocols, multicenter validation, and digital integration to unlock saliva's full potential as a frontline diagnostic fluid. By addressing biomarker variability and embracing cross-sector collaboration, the field can move toward clinically actionable, digitally enabled solutions for early detection and monitoring of OSCC and OPMD.&lt;/p&gt;</content:encoded>
         <dc:creator>
Hichem Moulahoum, 
Faezeh Ghorbanizamani
</dc:creator>
         <category>LETTER TO THE EDITOR</category>
         <dc:title>Fragmented Thresholds, Unified Vision: Advancing Salivary Diagnostics for OSCC and OPMD</dc:title>
         <dc:identifier>10.1111/jop.70141</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70141</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70141?af=R</prism:url>
         <prism:section>LETTER TO THE EDITOR</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70139?af=R</link>
         <pubDate>Tue, 14 Apr 2026 23:39:31 -0700</pubDate>
         <dc:date>2026-04-14T11:39:31-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70139</guid>
         <title>Risk of Malignant Transformation in Patients With Oral Lichen Planus or Lichenoid Lesions: A Retrospective Study of 323 Patients With a Minimum of 5‐Year Follow‐Up</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Objective
To estimate the risk for oral squamous cell carcinoma (OSCC) among patients with oral lichen planus (OLP) or lichenoid lesions (OLL) and the possible risk factors.


Material and Methods
Two hundred thirty‐nine OLP and 84 OLL patients diagnosed between years 1982 and 2017 were followed up to December 2023, diagnosis of an OSCC, or death. Potential demographic and clinical risk factors were compared, and a Cox proportional‐hazards model was used to investigate associations between time to OSCC onset and variables of interest.


Results
Six OLP patients (2.5%; three females), in a mean follow‐up of 17.5 years, and six OLL patients (7.1%; three females), in a mean follow‐up of 13.8 years, developed OSCC. The annual MT rate was 0.14% for OLP and 0.5% for OLL. The mean time for OSCC development from OLP diagnosis was 11.4 years and from OLL diagnosis 12 years. Four OLP patients (67%; two females) developed OSCC in the mobile tongue, while in OLL patients OSCCs occurred at various sites. A potential association was observed between floor‐of‐mouth lesions in OLP and gingival or extraoral LP involvement in OLL and increased OSCC risk.


Conclusion
This study confirms that both OLP and OLL patients are at a long‐term risk of OSCC, and the risk is higher for OLL patients. Site‐specific lesions in OLP and OLL were linked to increased OSCC risk, warranting confirmation in larger studies.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;To estimate the risk for oral squamous cell carcinoma (OSCC) among patients with oral lichen planus (OLP) or lichenoid lesions (OLL) and the possible risk factors.&lt;/p&gt;
&lt;h2&gt;Material and Methods&lt;/h2&gt;
&lt;p&gt;Two hundred thirty-nine OLP and 84 OLL patients diagnosed between years 1982 and 2017 were followed up to December 2023, diagnosis of an OSCC, or death. Potential demographic and clinical risk factors were compared, and a Cox proportional-hazards model was used to investigate associations between time to OSCC onset and variables of interest.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Six OLP patients (2.5%; three females), in a mean follow-up of 17.5 years, and six OLL patients (7.1%; three females), in a mean follow-up of 13.8 years, developed OSCC. The annual MT rate was 0.14% for OLP and 0.5% for OLL. The mean time for OSCC development from OLP diagnosis was 11.4 years and from OLL diagnosis 12 years. Four OLP patients (67%; two females) developed OSCC in the mobile tongue, while in OLL patients OSCCs occurred at various sites. A potential association was observed between floor-of-mouth lesions in OLP and gingival or extraoral LP involvement in OLL and increased OSCC risk.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This study confirms that both OLP and OLL patients are at a long-term risk of OSCC, and the risk is higher for OLL patients. Site-specific lesions in OLP and OLL were linked to increased OSCC risk, warranting confirmation in larger studies.&lt;/p&gt;</content:encoded>
         <dc:creator>
Mari Vehviläinen, 
Tuomas Selander, 
Tuula Salo, 
Maria Siponen
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Risk of Malignant Transformation in Patients With Oral Lichen Planus or Lichenoid Lesions: A Retrospective Study of 323 Patients With a Minimum of 5‐Year Follow‐Up</dc:title>
         <dc:identifier>10.1111/jop.70139</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70139</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70139?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70140?af=R</link>
         <pubDate>Sun, 12 Apr 2026 17:05:38 -0700</pubDate>
         <dc:date>2026-04-12T05:05:38-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70140</guid>
         <title>Evaluation of GPT‐5, a Large Language Model, in Replicating German Clinical Practice Guideline Recommendations in Oral Oncology: A Cross‐Sectional Concordance Study</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Artificial intelligence (AI) technologies, particularly large language models (LLMs) such as ChatGPT, are increasingly utilised in medical education and clinical information retrieval. Nevertheless, their capacity to accurately reproduce recommendations from established clinical practice guidelines (CPGs) has not been thoroughly examined. The present study evaluated the concordance between responses generated by GPT‐5 and recommendations contained in German CPGs addressing oral potentially malignant disorders (OPMDs) and oral carcinomas (OCs).


Methods
A cross‐sectional analytical comparison was performed between GPT‐5 outputs and German CPG recommendations available as of October 2025. Individual guideline statements were entered verbatim into GPT‐5, which was asked to confirm or reject the statements. To assess methodological robustness, inverted versions of the same statements were additionally tested. GPT‐5 was accessed through the free version without internet connectivity to ensure that responses originated solely from the model's internal training data. Accuracy was defined as the proportion of correctly classified statements. Concordance between guideline content and model responses was quantified using Cohen's 𝝹.


Results
Two German CPGs comprising 111 recommendations were included: the S2k guideline for OPMDs (15 recommendations) and the S3 guideline for OCs (96 recommendations). GPT‐5 correctly affirmed all authentic recommendations and rejected all inverted statements. Agreement between guideline statements and GPT‐5 responses was perfect when the original recommendations were analysed (𝝹 = 1.0) and remained very high when both original and inverted statements were evaluated jointly (𝝹 = 0.96). The majority of references cited within the guidelines were published in English (&gt; 93%) and originated from outside Germany (&gt; 77%).


Conclusion
When guideline recommendations were presented verbatim, GPT‐5 demonstrated complete concordance with German oral oncology CPGs. These findings indicate that the model is capable of recognising and retrieving established guideline information. However, this experimental design evaluates recognition of existing statements rather than autonomous clinical reasoning. At present, LLMs should therefore be regarded primarily as educational and informational tools rather than a replacement for expert clinical judgement in oral oncology.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Artificial intelligence (AI) technologies, particularly large language models (LLMs) such as ChatGPT, are increasingly utilised in medical education and clinical information retrieval. Nevertheless, their capacity to accurately reproduce recommendations from established clinical practice guidelines (CPGs) has not been thoroughly examined. The present study evaluated the concordance between responses generated by GPT-5 and recommendations contained in German CPGs addressing oral potentially malignant disorders (OPMDs) and oral carcinomas (OCs).&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A cross-sectional analytical comparison was performed between GPT-5 outputs and German CPG recommendations available as of October 2025. Individual guideline statements were entered verbatim into GPT-5, which was asked to confirm or reject the statements. To assess methodological robustness, inverted versions of the same statements were additionally tested. GPT-5 was accessed through the free version without internet connectivity to ensure that responses originated solely from the model's internal training data. Accuracy was defined as the proportion of correctly classified statements. Concordance between guideline content and model responses was quantified using Cohen's 𝝹.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Two German CPGs comprising 111 recommendations were included: the S2k guideline for OPMDs (15 recommendations) and the S3 guideline for OCs (96 recommendations). GPT-5 correctly affirmed all authentic recommendations and rejected all inverted statements. Agreement between guideline statements and GPT-5 responses was perfect when the original recommendations were analysed (𝝹 = 1.0) and remained very high when both original and inverted statements were evaluated jointly (𝝹 = 0.96). The majority of references cited within the guidelines were published in English (&amp;gt; 93%) and originated from outside Germany (&amp;gt; 77%).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;When guideline recommendations were presented verbatim, GPT-5 demonstrated complete concordance with German oral oncology CPGs. These findings indicate that the model is capable of recognising and retrieving established guideline information. However, this experimental design evaluates recognition of existing statements rather than autonomous clinical reasoning. At present, LLMs should therefore be regarded primarily as educational and informational tools rather than a replacement for expert clinical judgement in oral oncology.&lt;/p&gt;</content:encoded>
         <dc:creator>
Julius Hirsch, 
Keskanya Subbalekha, 
Chatpong Tangmanee, 
Christian Stoll, 
Poramate Pitak‐Arnnop
</dc:creator>
         <category>BRIEF REPORT</category>
         <dc:title>Evaluation of GPT‐5, a Large Language Model, in Replicating German Clinical Practice Guideline Recommendations in Oral Oncology: A Cross‐Sectional Concordance Study</dc:title>
         <dc:identifier>10.1111/jop.70140</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70140</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70140?af=R</prism:url>
         <prism:section>BRIEF REPORT</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70136?af=R</link>
         <pubDate>Wed, 08 Apr 2026 03:30:16 -0700</pubDate>
         <dc:date>2026-04-08T03:30:16-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70136</guid>
         <title>Dual‐Wavelength PDT With Chlorin‐Based Photosensitizers for Oral Wounds Healing: Study of Proliferative Activity and Angiogenesis</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
The aim of the study is the comparative analysis of the effectiveness of photodynamic therapy in the management of the wound surface of the oral mucosa of rats using combined dual‐wavelength photodynamic therapy (PDT).


Methods
The study was performed on 36 females outbred Wistar stock rats. The animals were divided into control (n = 18) and PDT (n = 18) groups. Wound surfaces were modeled on the cheek mucosa. Dual‐wave photodynamic therapy was performed on the 1st postoperative day in the PDT group. An immunohistochemical study with Ki67 and CD31 markers was performed on days 3, 7, and 14 to determine the proliferative activity and assess the state of the microvascular bed.


Results
Macroscopic examination of the tissues of the wound surface after a single photodynamic exposure revealed the acceleration of healing processes and the reduction in the time of tissue reorganization compared to the control group. The stratum corneum of the epithelium, which serves as one of the main protective mechanisms, was completely restored on day 7. The peak of proliferative activity occurred on day 3, which indicated the earlier activation of regenerative processes after photodynamic exposure. The highest expression rates of the CD31 endothelial marker in the early phase of the wound process in the PDT group indicate the active formation of the microvascular bed.


Conclusion
The use of photodynamic therapy is an effective way to activate and intensify regenerative processes in tissues due to timely restoration of trophism and provision of oxygen to tissues.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;The aim of the study is the comparative analysis of the effectiveness of photodynamic therapy in the management of the wound surface of the oral mucosa of rats using combined dual-wavelength photodynamic therapy (PDT).&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;The study was performed on 36 females outbred Wistar stock rats. The animals were divided into control (&lt;i&gt;n&lt;/i&gt; = 18) and PDT (&lt;i&gt;n&lt;/i&gt; = 18) groups. Wound surfaces were modeled on the cheek mucosa. Dual-wave photodynamic therapy was performed on the 1st postoperative day in the PDT group. An immunohistochemical study with Ki67 and CD31 markers was performed on days 3, 7, and 14 to determine the proliferative activity and assess the state of the microvascular bed.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Macroscopic examination of the tissues of the wound surface after a single photodynamic exposure revealed the acceleration of healing processes and the reduction in the time of tissue reorganization compared to the control group. The stratum corneum of the epithelium, which serves as one of the main protective mechanisms, was completely restored on day 7. The peak of proliferative activity occurred on day 3, which indicated the earlier activation of regenerative processes after photodynamic exposure. The highest expression rates of the CD31 endothelial marker in the early phase of the wound process in the PDT group indicate the active formation of the microvascular bed.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;The use of photodynamic therapy is an effective way to activate and intensify regenerative processes in tissues due to timely restoration of trophism and provision of oxygen to tissues.&lt;/p&gt;</content:encoded>
         <dc:creator>
M. A. Shakhova, 
E. A. Durnovo, 
N. Yu. Orlinskaya, 
V. A. Tarakanova, 
V. V. Antoshina, 
K. A. Bylinskaya, 
M. Yu. Kirillin
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Dual‐Wavelength PDT With Chlorin‐Based Photosensitizers for Oral Wounds Healing: Study of Proliferative Activity and Angiogenesis</dc:title>
         <dc:identifier>10.1111/jop.70136</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70136</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70136?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70135?af=R</link>
         <pubDate>Tue, 07 Apr 2026 01:40:05 -0700</pubDate>
         <dc:date>2026-04-07T01:40:05-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70135</guid>
         <title>Dual Beneficial Effects of Topical l‐Glutamine on Oral Mucositis in 5‐Fluorouracil‐Treated Mice</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Oral mucositis is a severe health and economic problem that occurs in about 40%–90% of patients undergoing cancer treatments. Systemic or topical application of l‐glutamine has been shown to improve mucosal healing and ameliorate oral mucositis (OM) symptoms according to clinical score systems. To further establish the beneficial effects of this amino acid, our study examined the actions of topical application of l‐glutamine on inflammation and mucosal healing markers in tongue lesions in mice treated with 5‐Fluorouracil.


Methods
The animals received 3 doses of the chemotherapeutic agent (non‐consecutive days) at concentrations of 60, 40, and 40 mg/kg, respectively. Tongue lesions were made by acetic acid (bolus injection) on the ventral face. Ten mg/50 μL of l‐glutamine were applied at the site of the lesion in the treated group (n = 15) twice a day for 5 days; the control group (n = 15) received filtered water. On day 6, the animals were euthanized, the tongues removed, and processed for inflammatory and fibrogenic markers.


Results
The treatment decreased myeloperoxidase (MPO) and N‐acetyl‐β‐glucosaminidase (NAG) activities, tumor necrosis factor alpha levels (TNF‐α), and mast cell numbers at the site of the lesions. The amino acid was able to decrease the number of Ki‐67 positive cells in the treated group. There was increased mucosal remodeling through collagen deposition in the treated group.


Conclusion
Topical application of l‐glutamine acted on multiple axes of OM, modulating inflammation and tissue remodeling in immunosuppressed mice.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Oral mucositis is a severe health and economic problem that occurs in about 40%–90% of patients undergoing cancer treatments. Systemic or topical application of &lt;span class="smallCaps"&gt;l&lt;/span&gt;-glutamine has been shown to improve mucosal healing and ameliorate oral mucositis (OM) symptoms according to clinical score systems. To further establish the beneficial effects of this amino acid, our study examined the actions of topical application of &lt;span class="smallCaps"&gt;l&lt;/span&gt;-glutamine on inflammation and mucosal healing markers in tongue lesions in mice treated with 5-Fluorouracil.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;The animals received 3 doses of the chemotherapeutic agent (non-consecutive days) at concentrations of 60, 40, and 40 mg/kg, respectively. Tongue lesions were made by acetic acid (bolus injection) on the ventral face. Ten mg/50 μL of &lt;span class="smallCaps"&gt;l&lt;/span&gt;-glutamine were applied at the site of the lesion in the treated group (&lt;i&gt;n&lt;/i&gt; = 15) twice a day for 5 days; the control group (&lt;i&gt;n&lt;/i&gt; = 15) received filtered water. On day 6, the animals were euthanized, the tongues removed, and processed for inflammatory and fibrogenic markers.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The treatment decreased myeloperoxidase (MPO) and &lt;i&gt;N&lt;/i&gt;-acetyl-&lt;i&gt;β&lt;/i&gt;-glucosaminidase (NAG) activities, tumor necrosis factor alpha levels (TNF-α), and mast cell numbers at the site of the lesions. The amino acid was able to decrease the number of Ki-67 positive cells in the treated group. There was increased mucosal remodeling through collagen deposition in the treated group.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Topical application of &lt;span class="smallCaps"&gt;l&lt;/span&gt;-glutamine acted on multiple axes of OM, modulating inflammation and tissue remodeling in immunosuppressed mice.&lt;/p&gt;</content:encoded>
         <dc:creator>
Juliana Francisca Grossi Heleno, 
Igor de Campos Fontes, 
Leticia Cristine Cardoso dos Santos, 
Victor Prokop Gonçalves Campos, 
Iury Berckmann Freitas Gomes, 
Derek William Gilroy, 
Silvia Passos Andrade, 
Paula Peixoto Campos
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Dual Beneficial Effects of Topical l‐Glutamine on Oral Mucositis in 5‐Fluorouracil‐Treated Mice</dc:title>
         <dc:identifier>10.1111/jop.70135</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70135</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70135?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70133?af=R</link>
         <pubDate>Sun, 29 Mar 2026 17:54:30 -0700</pubDate>
         <dc:date>2026-03-29T05:54:30-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70133</guid>
         <title>Multifocal Perineural Invasion Predicts Poor Disease‐Free Survival in Early‐Stage Tongue Squamous Cell Carcinoma Exhibiting WPOI‐4</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Objectives
Perineural invasion (PNI) is a pathological hallmark associated with tumor spread. Evidence suggested that PNI location (extratumoural vs. intratumoural) held prognostic significance in early‐stage oral squamous cell carcinoma (OSCC), whereas the prognostic impact of PNI extent (unifocal versus multifocal) remained to be elucidated. The primary aim of this study was to evaluate the prognostic relevance of PNI extent in early‐stage tongue squamous cell carcinoma (TSCC) characterized by worst pattern of invasion 4 (WPOI‐4).


Materials and Methods
A total of 130 patients with pT1/T2 pN0/Nx TSCC were included in this retrospective study, of whom 104 did not receive postoperative radiotherapy (PORT), while the remaining 26 underwent PORT. Based on the Yamauchi–Kuratomi (YK) classification, WPOI‐4 cases were further stratified into 4C/4D and non‐4C/4D subtypes. Depth of invasion (DOI) was dichotomized using a 4 mm threshold.


Results
Multivariate analysis revealed that both multifocal and unifocal PNI were significantly associated with disease‐free survival (DFS), whereas no meaningful association was observed with overall survival (OS). Compared to unifocal PNI (odds ratio [OR] = 5.504; 95% confidence interval (CI) = 1.994–15.188; p &lt; 0.001), multifocal PNI conferred an approximately fivefold increased risk of disease progression (OR = 27.009; 95% CI = 8.695–83.900; p &lt; 0.001). In addition, multifocal PNI showed a notable correlation with DOI &gt; 4 mm and 4C/4D histology. Elective neck dissection (END) combined with postoperative radiotherapy (PORT) significantly reduced disease progression in PNI‐positive patients, particularly those with multifocal PNI (OR = 0.01; 95% CI = 0.002–0.051; p &lt; 0.001). Among patients who did not receive PORT, END showed limited benefit in multivariate analysis. However, after excluding cases with isolated local recurrence, END was associated with improved DFS in patients with cervical lymph node metastasis (CLNM) (p = 0.017).


Conclusion
These findings support incorporating the extent of PNI into routine pathology reporting and suggest that END and PORT may be considered, particularly in cases of multifocal PNI.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Objectives&lt;/h2&gt;
&lt;p&gt;Perineural invasion (PNI) is a pathological hallmark associated with tumor spread. Evidence suggested that PNI location (extratumoural vs. intratumoural) held prognostic significance in early-stage oral squamous cell carcinoma (OSCC), whereas the prognostic impact of PNI extent (unifocal versus multifocal) remained to be elucidated. The primary aim of this study was to evaluate the prognostic relevance of PNI extent in early-stage tongue squamous cell carcinoma (TSCC) characterized by worst pattern of invasion 4 (WPOI-4).&lt;/p&gt;
&lt;h2&gt;Materials and Methods&lt;/h2&gt;
&lt;p&gt;A total of 130 patients with pT1/T2 pN0/Nx TSCC were included in this retrospective study, of whom 104 did not receive postoperative radiotherapy (PORT), while the remaining 26 underwent PORT. Based on the Yamauchi–Kuratomi (YK) classification, WPOI-4 cases were further stratified into 4C/4D and non-4C/4D subtypes. Depth of invasion (DOI) was dichotomized using a 4 mm threshold.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Multivariate analysis revealed that both multifocal and unifocal PNI were significantly associated with disease-free survival (DFS), whereas no meaningful association was observed with overall survival (OS). Compared to unifocal PNI (odds ratio [OR] = 5.504; 95% confidence interval (CI) = 1.994–15.188; &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001), multifocal PNI conferred an approximately fivefold increased risk of disease progression (OR = 27.009; 95% CI = 8.695–83.900; &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001). In addition, multifocal PNI showed a notable correlation with DOI &amp;gt; 4 mm and 4C/4D histology. Elective neck dissection (END) combined with postoperative radiotherapy (PORT) significantly reduced disease progression in PNI-positive patients, particularly those with multifocal PNI (OR = 0.01; 95% CI = 0.002–0.051; &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001). Among patients who did not receive PORT, END showed limited benefit in multivariate analysis. However, after excluding cases with isolated local recurrence, END was associated with improved DFS in patients with cervical lymph node metastasis (CLNM) (&lt;i&gt;p&lt;/i&gt; = 0.017).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;These findings support incorporating the extent of PNI into routine pathology reporting and suggest that END and PORT may be considered, particularly in cases of multifocal PNI.&lt;/p&gt;</content:encoded>
         <dc:creator>
Xiaoli Jia, 
Ting Gu, 
Jiang Li
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Multifocal Perineural Invasion Predicts Poor Disease‐Free Survival in Early‐Stage Tongue Squamous Cell Carcinoma Exhibiting WPOI‐4</dc:title>
         <dc:identifier>10.1111/jop.70133</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70133</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70133?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70134?af=R</link>
         <pubDate>Mon, 23 Mar 2026 17:39:31 -0700</pubDate>
         <dc:date>2026-03-23T05:39:31-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70134</guid>
         <title>Interpreting Machine Learning in Rare Outcomes</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description/>
         <content:encoded/>
         <dc:creator>
Carlos M. Ardila, 
Anny Marcela Vivares‐Builes, 
Eliana Pineda‐Vélez
</dc:creator>
         <category>LETTER TO THE EDITOR</category>
         <dc:title>Interpreting Machine Learning in Rare Outcomes</dc:title>
         <dc:identifier>10.1111/jop.70134</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70134</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70134?af=R</prism:url>
         <prism:section>LETTER TO THE EDITOR</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70130?af=R</link>
         <pubDate>Sun, 15 Mar 2026 00:00:00 -0700</pubDate>
         <dc:date>2026-03-15T12:00:00-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70130</guid>
         <title>Early‐Onset Oral Squamous Cell Carcinoma: Emerging Biological Insights, Risk Factors and Clinical Implications</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Early‐onset oral squamous cell carcinoma (EO‐OSCC), commonly defined as occurring in individuals under 50 years of age, is increasingly recognized as a potentially distinct clinical subset with differences in exposure patterns and tumor biology compared with conventional oral squamous cell carcinoma (OSCC). Unlike typical OSCC, which is strongly associated with tobacco and alcohol, EO‐OSCC more frequently affects never‐smokers/never‐drinkers, posing challenges for early recognition, risk stratification, and management.


Objective
This review integrates evidence mapping with narrative synthesis to summarize current knowledge on EO‐OSCC, focusing on epidemiology, emerging risk factors, molecular alterations, tumor microenvironment characteristics, and clinical implications.


Methods
Literature was searched across PubMed, Scopus, Embase, Web of Science, and the Cochrane Library up to August 2025, complemented by global cancer databases (GLOBOCAN/Cancer Tomorrow) and international trial registries.


Results
Available data suggest distinct biological features, including relatively low tumor mutational burden, recurrent alterations in CDKN2A, TP53, NOTCH1, and EGFR, epigenetic dysregulation, and a checkpoint‐dominant immunosuppressive tumor microenvironment. Alongside traditional carcinogens, modifiable determinants such as sugar‐sweetened beverages, electronic cigarette use, and oral microbial dysbiosis have emerged as plausible contributors, although evidence remains heterogeneous. Despite frequently aggressive histopathologic features, younger patients may tolerate intensive multimodal therapies better and achieve favorable outcomes.


Conclusion
These findings highlight the urgent need for age‐specific prognostic tools, biomarker‐guided therapies, and early detection protocols. International collaboration will be key to improving survival and long‐term quality of life in this growing patient population.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Early-onset oral squamous cell carcinoma (EO-OSCC), commonly defined as occurring in individuals under 50 years of age, is increasingly recognized as a potentially distinct clinical subset with differences in exposure patterns and tumor biology compared with conventional oral squamous cell carcinoma (OSCC). Unlike typical OSCC, which is strongly associated with tobacco and alcohol, EO-OSCC more frequently affects never-smokers/never-drinkers, posing challenges for early recognition, risk stratification, and management.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;This review integrates evidence mapping with narrative synthesis to summarize current knowledge on EO-OSCC, focusing on epidemiology, emerging risk factors, molecular alterations, tumor microenvironment characteristics, and clinical implications.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Literature was searched across PubMed, Scopus, Embase, Web of Science, and the Cochrane Library up to August 2025, complemented by global cancer databases (GLOBOCAN/Cancer Tomorrow) and international trial registries.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Available data suggest distinct biological features, including relatively low tumor mutational burden, recurrent alterations in CDKN2A, TP53, NOTCH1, and EGFR, epigenetic dysregulation, and a checkpoint-dominant immunosuppressive tumor microenvironment. Alongside traditional carcinogens, modifiable determinants such as sugar-sweetened beverages, electronic cigarette use, and oral microbial dysbiosis have emerged as plausible contributors, although evidence remains heterogeneous. Despite frequently aggressive histopathologic features, younger patients may tolerate intensive multimodal therapies better and achieve favorable outcomes.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;These findings highlight the urgent need for age-specific prognostic tools, biomarker-guided therapies, and early detection protocols. International collaboration will be key to improving survival and long-term quality of life in this growing patient population.&lt;/p&gt;</content:encoded>
         <dc:creator>
Gennaro Musella, 
Cristina D'Antonio, 
Federica Canfora, 
Michele D. Mignogna, 
Valentino Vellone, 
Vito Carlo Alberto Caponio, 
Amerigo Giudice, 
Alessandro Villa, 
Daniela Adamo
</dc:creator>
         <category>REVIEW</category>
         <dc:title>Early‐Onset Oral Squamous Cell Carcinoma: Emerging Biological Insights, Risk Factors and Clinical Implications</dc:title>
         <dc:identifier>10.1111/jop.70130</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70130</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70130?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70131?af=R</link>
         <pubDate>Tue, 10 Mar 2026 20:08:53 -0700</pubDate>
         <dc:date>2026-03-10T08:08:53-07:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70131</guid>
         <title>Immunological Biomarkers in Oral Leukoplakia According to Oral Intraepithelial Neoplasia (OIN) Classification: A Comparative Analysis of Salivary and Plasma Cytokines</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Oral leukoplakia (OL) is the most common oral potentially malignant disorder, defined as a white patch or plaque not attributable to other causes. While OL carries an inherent risk of malignant transformation, the underlying immunological changes remain poorly characterized. This study aimed to profile a broad panel of cytokines in saliva and plasma of OL patients in comparison to healthy controls, in order to elucidate local and systemic immunoinflammatory alterations associated with OL.


Methods
Thirty patients with clinically and histopathologically confirmed OL and 30 age‐ and gender‐matched healthy controls were enrolled. Detailed clinical examinations were performed, including lesion characterization and psychosocial assessments. Unstimulated whole saliva and peripheral blood samples were collected, and concentrations of 13 cytokines/chemokines (IL‐1β, IL‐6, IL‐8/CXCL8, IL‐10, IL‐12p70, IL‐17A, IL‐18, IL‐23, IL‐33, TNF‐α, IFN‐γ, IFN‐α2, and MCP‐1/CCL2) were measured using a multiplex bead‐based immunoassay. Group comparisons were performed using appropriate statistical tests (χ2/Fisher's exact test for categorical variables and t‐test or Mann–Whitney U test for continuous variables), with statistical significance set at p &lt; 0.05.


Results
OL patients (mean age 52.4 ± 10.7 years) and controls (59.9 ± 12.8 years) showed no significant differences in gender, socioeconomic status, or psychological scores. Salivary levels of IL‐1β, TNF‐α, MCP‐1, IL‐8, and IL‐18 were significantly lower in OL patients compared to controls (p &lt; 0.01 for all), whereas other salivary cytokines (IFN‐α2, IFN‐γ, IL‐6, IL‐10, IL‐12p70, IL‐17A, IL‐23, IL‐33) showed no significant differences. In contrast, plasma levels of IFN‐α2, IL‐6, IL‐12p70, IL‐17A, IL‐18, and IL‐33 were significantly higher in OL patients than in controls (p &lt; 0.05), indicating systemic inflammation, while plasma IL‐1β, IFN‐γ, TNF‐α, MCP‐1, IL‐8, IL‐10, and IL‐23 did not differ. No significant differences in salivary cortisol, liver enzymes, or hepatitis viral markers were observed between groups. Across histopathological subgroups, cytokine concentrations did not significantly differ between lesions graded as hyperkeratosis, OIN1, OIN2, or OIN3, although a trend toward higher plasma IL‐6, IL‐17A, and IL‐18 levels was observed in cases with higher OIN grades.


Conclusion
These findings shed light on the inflammatory profile of OL. The decrease in salivary IL‐1β, IL‐8, TNF‐α, and MCP‐1 may indicate a more suppressed local immune response, whereas the higher plasma levels of IL‐6, IL‐17A, IL‐18, and IL‐33 tend to be seen in lesions showing greater degrees of dysplasia. In particular, patients with higher OIN grades often display this systemic inflammatory shift, which may signal an increased risk of progression.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Oral leukoplakia (OL) is the most common oral potentially malignant disorder, defined as a white patch or plaque not attributable to other causes. While OL carries an inherent risk of malignant transformation, the underlying immunological changes remain poorly characterized. This study aimed to profile a broad panel of cytokines in saliva and plasma of OL patients in comparison to healthy controls, in order to elucidate local and systemic immunoinflammatory alterations associated with OL.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Thirty patients with clinically and histopathologically confirmed OL and 30 age- and gender-matched healthy controls were enrolled. Detailed clinical examinations were performed, including lesion characterization and psychosocial assessments. Unstimulated whole saliva and peripheral blood samples were collected, and concentrations of 13 cytokines/chemokines (IL-1β, IL-6, IL-8/CXCL8, IL-10, IL-12p70, IL-17A, IL-18, IL-23, IL-33, TNF-α, IFN-γ, IFN-α2, and MCP-1/CCL2) were measured using a multiplex bead-based immunoassay. Group comparisons were performed using appropriate statistical tests (&lt;i&gt;χ&lt;/i&gt;
&lt;sup&gt;2&lt;/sup&gt;/Fisher's exact test for categorical variables and &lt;i&gt;t&lt;/i&gt;-test or Mann–Whitney &lt;i&gt;U&lt;/i&gt; test for continuous variables), with statistical significance set at &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.05.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;OL patients (mean age 52.4 ± 10.7 years) and controls (59.9 ± 12.8 years) showed no significant differences in gender, socioeconomic status, or psychological scores. Salivary levels of IL-1β, TNF-α, MCP-1, IL-8, and IL-18 were significantly lower in OL patients compared to controls (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.01 for all), whereas other salivary cytokines (IFN-α2, IFN-γ, IL-6, IL-10, IL-12p70, IL-17A, IL-23, IL-33) showed no significant differences. In contrast, plasma levels of IFN-α2, IL-6, IL-12p70, IL-17A, IL-18, and IL-33 were significantly higher in OL patients than in controls (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.05), indicating systemic inflammation, while plasma IL-1β, IFN-γ, TNF-α, MCP-1, IL-8, IL-10, and IL-23 did not differ. No significant differences in salivary cortisol, liver enzymes, or hepatitis viral markers were observed between groups. Across histopathological subgroups, cytokine concentrations did not significantly differ between lesions graded as hyperkeratosis, OIN1, OIN2, or OIN3, although a trend toward higher plasma IL-6, IL-17A, and IL-18 levels was observed in cases with higher OIN grades.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;These findings shed light on the inflammatory profile of OL. The decrease in salivary IL-1β, IL-8, TNF-α, and MCP-1 may indicate a more suppressed local immune response, whereas the higher plasma levels of IL-6, IL-17A, IL-18, and IL-33 tend to be seen in lesions showing greater degrees of dysplasia. In particular, patients with higher OIN grades often display this systemic inflammatory shift, which may signal an increased risk of progression.&lt;/p&gt;</content:encoded>
         <dc:creator>
Hakan Yülek, 
Gaye Keser, 
Başak Aru, 
Filiz Namdar Pekiner, 
Gülderen Yanıkkaya Demirel
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Immunological Biomarkers in Oral Leukoplakia According to Oral Intraepithelial Neoplasia (OIN) Classification: A Comparative Analysis of Salivary and Plasma Cytokines</dc:title>
         <dc:identifier>10.1111/jop.70131</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70131</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70131?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70129?af=R</link>
         <pubDate>Wed, 18 Feb 2026 00:17:06 -0800</pubDate>
         <dc:date>2026-02-18T12:17:06-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70129</guid>
         <title>Mucosal Melanoma of Head and Neck: A Rare and Aggressive Disease—A Register‐Based Cohort Study</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Mucosal melanomas of the head and neck are rare and often diagnosed in the advanced stage. This study examines the incidence, survival and histology of mucosal melanoma compared to its cutaneous counterpart.


Methods
This register‐based cohort study reviews head and neck melanomas at Helsinki University Hospital, Finland, from 2002 to 2023.


Results
A total of 56 patients with mucosal and 714 with cutaneous melanoma were reviewed. The incidence of head and neck mucosal melanoma in the region was 1.55/million/year. The most common sites for mucosal melanomas were the nose and paranasal sinuses. Mucosal melanoma was more common in women, whereas cutaneous melanoma was more common in men (p &gt; 0.05). A significant difference emerged in mortality between mucosal and cutaneous melanoma, as 5‐year survival was only 12.0% in the mucosal melanoma group compared with 60.3% in the cutaneous melanoma group.


Conclusions
Mucosal melanoma is a highly aggressive malignancy with poor survival; thus, prompt diagnosis is essential.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Mucosal melanomas of the head and neck are rare and often diagnosed in the advanced stage. This study examines the incidence, survival and histology of mucosal melanoma compared to its cutaneous counterpart.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;This register-based cohort study reviews head and neck melanomas at Helsinki University Hospital, Finland, from 2002 to 2023.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;A total of 56 patients with mucosal and 714 with cutaneous melanoma were reviewed. The incidence of head and neck mucosal melanoma in the region was 1.55/million/year. The most common sites for mucosal melanomas were the nose and paranasal sinuses. Mucosal melanoma was more common in women, whereas cutaneous melanoma was more common in men (&lt;i&gt;p&lt;/i&gt; &amp;gt; 0.05). A significant difference emerged in mortality between mucosal and cutaneous melanoma, as 5-year survival was only 12.0% in the mucosal melanoma group compared with 60.3% in the cutaneous melanoma group.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;Mucosal melanoma is a highly aggressive malignancy with poor survival; thus, prompt diagnosis is essential.&lt;/p&gt;</content:encoded>
         <dc:creator>
Sara C. Degerholm, 
Tuula A. Salo, 
Matti O. Mauramo
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Mucosal Melanoma of Head and Neck: A Rare and Aggressive Disease—A Register‐Based Cohort Study</dc:title>
         <dc:identifier>10.1111/jop.70129</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70129</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70129?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70125?af=R</link>
         <pubDate>Wed, 18 Feb 2026 00:00:00 -0800</pubDate>
         <dc:date>2026-02-18T12:00:00-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70125</guid>
         <title>Sclerosing Odontogenic Carcinoma: A Review of a Challenging Entity in Malignant Odontogenic Classification With a Focus on Perineural Invasion and Cellular Proliferation</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Sclerosing odontogenic carcinoma (SOC) is a rare intraosseous neoplasm defined by the World Health Organization as a locally aggressive tumor with “no metastatic potential”.


Objective
This review provides a critical evaluation of the biological behavior, clinicopathologic features, and clinical management of SOC cases, with a particular focus on neural invasion and cellular proliferation scores.


Methods
A comprehensive literature was performed using the Pubmed and Scopus databases to identify all published English‐language reports of SOC.


Results
The analysis of 22 reported cases revealed that SOC predominantly affects the mandible in middle‐aged adults, typically presenting as a radiolucent lesion associated with cortical resorption. Histopathologically, perineural invasion was identified in 77.3% of cases and revealed a wide range of Ki‐67 expression (1%–%30).


Conclusion
This challenging entity exhibits a spectrum of malignant potential, and the current classification standard of “no metastatic potential” requires revision. In cases exhibiting diverse biological behaviors, the Ki‐67 proliferation score can be used an ancillary marker for risk stratification; higher rates (e.g., &gt; 10%–15%) may be associated with aggressive local invasion and metastatic events. Further molecular studies on aggressive “metastatic” cases are imperative to allow for identification of definitive markers that can establish SOC as a distinct entity and provide a rational basis for risk assessment and treatment.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Sclerosing odontogenic carcinoma (SOC) is a rare intraosseous neoplasm defined by the World Health Organization as a locally aggressive tumor with “no metastatic potential”.&lt;/p&gt;
&lt;h2&gt;Objective&lt;/h2&gt;
&lt;p&gt;This review provides a critical evaluation of the biological behavior, clinicopathologic features, and clinical management of SOC cases, with a particular focus on neural invasion and cellular proliferation scores.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A comprehensive literature was performed using the Pubmed and Scopus databases to identify all published English-language reports of SOC.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;The analysis of 22 reported cases revealed that SOC predominantly affects the mandible in middle-aged adults, typically presenting as a radiolucent lesion associated with cortical resorption. Histopathologically, perineural invasion was identified in 77.3% of cases and revealed a wide range of Ki-67 expression (1%–%30).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;This challenging entity exhibits a spectrum of malignant potential, and the current classification standard of “no metastatic potential” requires revision. In cases exhibiting diverse biological behaviors, the Ki-67 proliferation score can be used an ancillary marker for risk stratification; higher rates (e.g., &amp;gt; 10%–15%) may be associated with aggressive local invasion and metastatic events. Further molecular studies on aggressive “metastatic” cases are imperative to allow for identification of definitive markers that can establish SOC as a distinct entity and provide a rational basis for risk assessment and treatment.&lt;/p&gt;</content:encoded>
         <dc:creator>
Merva Soluk‐Tekkesin, 
Keith David Hunter, 
Ronell Bologna‐Molina, 
Kelly Magliocca, 
Liam Robinson, 
Akinyele Olumuyiwa Adisa, 
Jiang Li, 
Elizabeth Ann Bilodeau, 
Haizal Mohd Hussaini, 
Madhu Shrestha, 
Ricardo Santiago Gomez, 
Willie van Heerden, 
Wanninayake Mudiyanselage Tilakaratne
</dc:creator>
         <category>REVIEW</category>
         <dc:title>Sclerosing Odontogenic Carcinoma: A Review of a Challenging Entity in Malignant Odontogenic Classification With a Focus on Perineural Invasion and Cellular Proliferation</dc:title>
         <dc:identifier>10.1111/jop.70125</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70125</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70125?af=R</prism:url>
         <prism:section>REVIEW</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70128?af=R</link>
         <pubDate>Tue, 17 Feb 2026 05:21:32 -0800</pubDate>
         <dc:date>2026-02-17T05:21:32-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70128</guid>
         <title>p16 and MGMT Methylation in Chronic Traumatic Ulcers: A Plausible Link Between Chronic Mechanical Irritation and Oral Carcinogenesis?</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Chronic mechanical irritation (CMI) has been proposed as a risk factor for oral cancer. Epigenetic alterations, particularly methylation, are early events in carcinogenesis, and it has been proposed that they can be prompted by CMI. Thus, the aim of this study was to describe p16 and MGMT methylation in chronic traumatic ulcer (CTU).


Methods
A case–control split‐mouth study was performed. Two samples per individual (N = 27) were taken using exfoliative cytology using a split‐mouth design, one from the CTU and the other from a contralateral site of clinically normal mucosa. DNA was extracted and bisulfite‐treated, and specific sites at the promoter region of p16 and MGMT genes were amplified by qPCR using validated primers. Then, the PCR product was sequenced. The statistical analysis was performed by McNemar and the Chi‐square test.


Results
Patients had a mean age of 59.1 years. CTU showed higher methylation than control sites for both p16 (85% vs. 20%, p &lt; 0.0001) and MGMT (80% vs. 24%, p &lt; 0.0005).


Conclusion
Oral mucosa subjected to continuous exposure to CMI is associated with increased methylation of p16 and MGMT. Proper management of mechanical injury factors could be an important measure for OSCC prevention. In CMI, exfoliative cytology and the split‐mouth design could be useful tools to study biomarkers. However, the role of CMI in oral carcinogenesis needs more evidence focusing on the biological phenomenon.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Chronic mechanical irritation (CMI) has been proposed as a risk factor for oral cancer. Epigenetic alterations, particularly methylation, are early events in carcinogenesis, and it has been proposed that they can be prompted by CMI. Thus, the aim of this study was to describe p16 and MGMT methylation in chronic traumatic ulcer (CTU).&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;A case–control split-mouth study was performed. Two samples per individual (&lt;i&gt;N&lt;/i&gt; = 27) were taken using exfoliative cytology using a split-mouth design, one from the CTU and the other from a contralateral site of clinically normal mucosa. DNA was extracted and bisulfite-treated, and specific sites at the promoter region of p16 and MGMT genes were amplified by qPCR using validated primers. Then, the PCR product was sequenced. The statistical analysis was performed by McNemar and the Chi-square test.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Patients had a mean age of 59.1 years. CTU showed higher methylation than control sites for both p16 (85% vs. 20%, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.0001) and MGMT (80% vs. 24%, &lt;i&gt;p&lt;/i&gt; &amp;lt; 0.0005).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;Oral mucosa subjected to continuous exposure to CMI is associated with increased methylation of p16 and MGMT. Proper management of mechanical injury factors could be an important measure for OSCC prevention. In CMI, exfoliative cytology and the split-mouth design could be useful tools to study biomarkers. However, the role of CMI in oral carcinogenesis needs more evidence focusing on the biological phenomenon.&lt;/p&gt;</content:encoded>
         <dc:creator>
Jeronimo Pablo Lazos, 
Marcela Hernandez Rios, 
Jessica Astorga, 
Rene Luis Panico, 
Eduardo David Piemonte, 
Ana María Zárate
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>p16 and MGMT Methylation in Chronic Traumatic Ulcers: A Plausible Link Between Chronic Mechanical Irritation and Oral Carcinogenesis?</dc:title>
         <dc:identifier>10.1111/jop.70128</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70128</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70128?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70126?af=R</link>
         <pubDate>Thu, 12 Feb 2026 18:49:00 -0800</pubDate>
         <dc:date>2026-02-12T06:49:00-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70126</guid>
         <title>Epithelial‐Mesenchymal Transition, Immune Response, and Extracellular Matrix Remodelling in Oral Cancer</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Aim
This retrospective study investigates the interplay between epithelial‐mesenchymal transition (EMT) and immune response within the tumor microenvironment (TME) of oral squamous cell carcinoma (OSCC).


Methodology
Immunohistochemistry was conducted on OSCC specimens to evaluate the expression of podoplanin (PDP), E‐cadherin (CDH1), vimentin (VIM), fibronectin (FN), tenascin‐C (TNC), and vascular endothelial growth factor (VEGF). Cancer‐associated fibroblasts (CAFs) were identified by alpha‐smooth muscle actin (α‐SMA), and immune cells were quantified using CD66b for neutrophils and CD8 for T lymphocytes.


Results
Higher α‐SMA and moderate‐to‐strong VEGF expression were associated with reduced CDH1 and increased VIM and PDP expression (p &lt; 0.05), indicating an EMT‐like phenotype. Cases with elevated PDP—also linked to high α‐SMA—showed increased CD66b+ cell density (p = 0.072). VEGF expression additionally correlated with greater tumor thickness and depth of invasion (p = 0.059). Strong TNC expression was associated with reduced CD8+ T‐cell infiltration in the tumor centre and increased CD66b+ neutrophils (p &lt; 0.046). Strong FN expression was linked to a higher neutrophil‐to‐lymphocyte ratio (p = 0.031). Elevated CD66b+ cell counts and a higher neutrophil‐to‐lymphocyte ratio were both significantly associated with poorer overall survival (p &lt; 0.015).


Conclusion
These exploratory findings suggest that CAFs serve not only as a marker of stromal activation but may also contribute to immunomodulation and invasive tumor phenotype.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Aim&lt;/h2&gt;
&lt;p&gt;This retrospective study investigates the interplay between epithelial-mesenchymal transition (EMT) and immune response within the tumor microenvironment (TME) of oral squamous cell carcinoma (OSCC).&lt;/p&gt;
&lt;h2&gt;Methodology&lt;/h2&gt;
&lt;p&gt;Immunohistochemistry was conducted on OSCC specimens to evaluate the expression of podoplanin (PDP), E-cadherin (CDH1), vimentin (VIM), fibronectin (FN), tenascin-C (TNC), and vascular endothelial growth factor (VEGF). Cancer-associated fibroblasts (CAFs) were identified by alpha-smooth muscle actin (α-SMA), and immune cells were quantified using CD66b for neutrophils and CD8 for T lymphocytes.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;Higher α-SMA and moderate-to-strong VEGF expression were associated with reduced CDH1 and increased VIM and PDP expression (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.05), indicating an EMT-like phenotype. Cases with elevated PDP—also linked to high α-SMA—showed increased CD66b&lt;sup&gt;+&lt;/sup&gt; cell density (&lt;i&gt;p&lt;/i&gt; = 0.072). VEGF expression additionally correlated with greater tumor thickness and depth of invasion (&lt;i&gt;p&lt;/i&gt; = 0.059). Strong TNC expression was associated with reduced CD8&lt;sup&gt;+&lt;/sup&gt; T-cell infiltration in the tumor centre and increased CD66b&lt;sup&gt;+&lt;/sup&gt; neutrophils (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.046). Strong FN expression was linked to a higher neutrophil-to-lymphocyte ratio (&lt;i&gt;p&lt;/i&gt; = 0.031). Elevated CD66b&lt;sup&gt;+&lt;/sup&gt; cell counts and a higher neutrophil-to-lymphocyte ratio were both significantly associated with poorer overall survival (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.015).&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;These exploratory findings suggest that CAFs serve not only as a marker of stromal activation but may also contribute to immunomodulation and invasive tumor phenotype.&lt;/p&gt;</content:encoded>
         <dc:creator>
Nicole Lonni, 
Camilla Kammer Pereira, 
Amanda Maciel Costa, 
Aline Hsiao Bona, 
Andressa Fernanda Paza Miguel, 
Elis Ângela Batistella, 
Daniella Serafin Couto Vieira, 
Elena Riet Correa Rivero
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Epithelial‐Mesenchymal Transition, Immune Response, and Extracellular Matrix Remodelling in Oral Cancer</dc:title>
         <dc:identifier>10.1111/jop.70126</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70126</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70126?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70127?af=R</link>
         <pubDate>Wed, 11 Feb 2026 17:55:35 -0800</pubDate>
         <dc:date>2026-02-11T05:55:35-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70127</guid>
         <title>Vitamin D Modulates Doxorubicin‐Induced ACE2 Expression and Pro‐Inflammatory Cytokines in the Rat Tongue</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Purpose
Doxorubicin (DOX) is a widely used chemotherapy drug, but its severe toxic effects, including inflammation and taste disturbances, limit its clinical use. This study examined the protective effects of vitamin D on DOX‐induced changes in tongue tissue and systemic inflammation in rats.


Methods
Twenty‐eight adult male Wistar Albino rats (10–12 weeks old) were divided into four groups: Control, DOX, Vitamin D 5000 + DOX, and Vitamin D 60 000 + DOX. Vitamin D3 was administered intraperitoneally either daily (5000 IU/kg) or 3 days a week (60 000 IU/kg) for 21 days. DOX (18 mg/kg, intraperitoneally) was administered on days 19–21. Tongue tissues were analyzed for angiotensin‐converting enzyme 2 (ACE2) expression via immunohistochemistry, and serum cytokine levels (TNF‐α, IL‐1β, and IL‐6) were measured using enzyme‐linked immunosorbent assay (ELISA).


Results
DOX treatment significantly increased ACE2 expression in tongue tissue compared with controls (p &lt; 0.001), accompanied by elevated serum inflammatory cytokine levels and reduced body weight. Vitamin D supplementation significantly attenuated DOX‐induced ACE2 upregulation and inflammatory cytokine elevations (p &lt; 0.05). However, no clear dose‐dependent difference was observed between the two vitamin D regimens, as ACE2 expression did not differ significantly between the 5000 IU/kg and 60 000 IU/kg groups.


Conclusion
DOX administration is associated with increased ACE2 expression in tongue tissue and systemic inflammation in a rat model. Vitamin D supplementation mitigates these DOX‐induced alterations; however, within the tested dose range, no additional benefit of the higher vitamin D dose was demonstrated. These findings suggest a potential modulatory role of vitamin D on chemotherapy‐associated inflammatory and molecular changes, while highlighting the need for further mechanistic and functional studies.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Purpose&lt;/h2&gt;
&lt;p&gt;Doxorubicin (DOX) is a widely used chemotherapy drug, but its severe toxic effects, including inflammation and taste disturbances, limit its clinical use. This study examined the protective effects of vitamin D on DOX-induced changes in tongue tissue and systemic inflammation in rats.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Twenty-eight adult male Wistar Albino rats (10–12 weeks old) were divided into four groups: Control, DOX, Vitamin D 5000 + DOX, and Vitamin D 60 000 + DOX. Vitamin D3 was administered intraperitoneally either daily (5000 IU/kg) or 3 days a week (60 000 IU/kg) for 21 days. DOX (18 mg/kg, intraperitoneally) was administered on days 19–21. Tongue tissues were analyzed for angiotensin-converting enzyme 2 (ACE2) expression via immunohistochemistry, and serum cytokine levels (TNF-α, IL-1β, and IL-6) were measured using enzyme-linked immunosorbent assay (ELISA).&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;DOX treatment significantly increased ACE2 expression in tongue tissue compared with controls (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.001), accompanied by elevated serum inflammatory cytokine levels and reduced body weight. Vitamin D supplementation significantly attenuated DOX-induced ACE2 upregulation and inflammatory cytokine elevations (&lt;i&gt;p&lt;/i&gt; &amp;lt; 0.05). However, no clear dose-dependent difference was observed between the two vitamin D regimens, as ACE2 expression did not differ significantly between the 5000 IU/kg and 60 000 IU/kg groups.&lt;/p&gt;
&lt;h2&gt;Conclusion&lt;/h2&gt;
&lt;p&gt;DOX administration is associated with increased ACE2 expression in tongue tissue and systemic inflammation in a rat model. Vitamin D supplementation mitigates these DOX-induced alterations; however, within the tested dose range, no additional benefit of the higher vitamin D dose was demonstrated. These findings suggest a potential modulatory role of vitamin D on chemotherapy-associated inflammatory and molecular changes, while highlighting the need for further mechanistic and functional studies.&lt;/p&gt;</content:encoded>
         <dc:creator>
Mustafa Sami Demirsoy, 
Aras Erdil, 
Sefa Çolak, 
Ali Tuğrul Akin, 
Necla Değer, 
Derya Karabulut, 
Fadime Demir, 
Hatice Aygün
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>Vitamin D Modulates Doxorubicin‐Induced ACE2 Expression and Pro‐Inflammatory Cytokines in the Rat Tongue</dc:title>
         <dc:identifier>10.1111/jop.70127</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70127</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70127?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
      <item>
         <link>https://onlinelibrary.wiley.com/doi/10.1111/jop.70122?af=R</link>
         <pubDate>Tue, 03 Feb 2026 21:16:16 -0800</pubDate>
         <dc:date>2026-02-03T09:16:16-08:00</dc:date>
         <source url="https://onlinelibrary.wiley.com/journal/16000714?af=R">Wiley-Online-Library: Journal of Oral Pathology &amp; Medicine: Table of Contents</source>
         <prism:coverDate/>
         <prism:coverDisplayDate/>
         <guid isPermaLink="false">10.1111/jop.70122</guid>
         <title>The Expression and Potential Role of MicroRNAs in Oral Lichen Planus</title>
         <description>Journal of Oral Pathology &amp;amp;Medicine, EarlyView. </description>
         <dc:description>
ABSTRACT

Background
Oral lichen planus (OLP) is a chronic T‐cell‐mediated immune disease of unknown aetiology. MicroRNA (miRNAs) are short non‐coding RNAs capable of regulating mRNA and may have roles in T‐cell‐related diseases. The aim of this study was to investigate the profile of miRNAs in OLP patients and its interaction with potential target genes.


Methods
Total RNA was extracted from fresh frozen biopsies from 24 patients with OLP and 8 control patients. The NanoString Counter Analysis System was used to analyse total RNA samples for differential miRNA expression. NanoString expression was confirmed by RT‐qPCR analysis. Genes potentially targeted by upregulated and downregulated miRNAs were identified, and RT‐qPCR was employed to investigate the expression of target genes in OLP and controls. Probability values &lt; 0.05 were considered statistically significant.


Results
NanoString analysis showed that eight miRNAs, miR‐155, miR‐146a, miR‐3195, miR‐342, miR‐4516, miR‐21, miR‐29a and miR‐193 were upregulated in OLP tissues. Contrarily, the other eight miRNAs, miR‐221, miR‐200b, miR‐149, miR‐205, miR‐27b, miR‐95, miR‐127b, miR‐95, miR‐206 were downregulated in OLP tissues. NanoString findings have been confirmed by RT‐qPCR results for four upregulated miRNAs, miR‐155, miR‐146a, miR‐29a and miR‐342, and one downregulated miRNA, namely miR‐205. The expression of two target genes, namely MYC for miR‐29a and interleukin‐24 (IL‐24) for miR‐205, was found to negatively correlate with the respective miRNA. This suggests that MYC and IL‐24 could be regulated by the above miRNAs in OLP.


Conclusions
The work presented in this study suggests that miRNAs could be involved in both the immunopathogenesis and malignant transformation of OLP.

</dc:description>
         <content:encoded>
&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;h2&gt;Background&lt;/h2&gt;
&lt;p&gt;Oral lichen planus (OLP) is a chronic T-cell-mediated immune disease of unknown aetiology. MicroRNA (miRNAs) are short non-coding RNAs capable of regulating mRNA and may have roles in T-cell-related diseases. The aim of this study was to investigate the profile of miRNAs in OLP patients and its interaction with potential target genes.&lt;/p&gt;
&lt;h2&gt;Methods&lt;/h2&gt;
&lt;p&gt;Total RNA was extracted from fresh frozen biopsies from 24 patients with OLP and 8 control patients. The NanoString Counter Analysis System was used to analyse total RNA samples for differential miRNA expression. NanoString expression was confirmed by RT-qPCR analysis. Genes potentially targeted by upregulated and downregulated miRNAs were identified, and RT-qPCR was employed to investigate the expression of target genes in OLP and controls. Probability values &amp;lt; 0.05 were considered statistically significant.&lt;/p&gt;
&lt;h2&gt;Results&lt;/h2&gt;
&lt;p&gt;NanoString analysis showed that eight miRNAs, miR-155, miR-146a, miR-3195, miR-342, miR-4516, miR-21, miR-29a and miR-193 were upregulated in OLP tissues. Contrarily, the other eight miRNAs, miR-221, miR-200b, miR-149, miR-205, miR-27b, miR-95, miR-127b, miR-95, miR-206 were downregulated in OLP tissues. NanoString findings have been confirmed by RT-qPCR results for four upregulated miRNAs, miR-155, miR-146a, miR-29a and miR-342, and one downregulated miRNA, namely miR-205. The expression of two target genes, namely MYC for miR-29a and interleukin-24 (IL-24) for miR-205, was found to negatively correlate with the respective miRNA. This suggests that MYC and IL-24 could be regulated by the above miRNAs in OLP.&lt;/p&gt;
&lt;h2&gt;Conclusions&lt;/h2&gt;
&lt;p&gt;The work presented in this study suggests that miRNAs could be involved in both the immunopathogenesis and malignant transformation of OLP.&lt;/p&gt;</content:encoded>
         <dc:creator>
Mousa Ali Heba, 
Resteu Anastasia, 
Werner Andreas, 
Carrozzo Marco
</dc:creator>
         <category>ORIGINAL ARTICLE</category>
         <dc:title>The Expression and Potential Role of MicroRNAs in Oral Lichen Planus</dc:title>
         <dc:identifier>10.1111/jop.70122</dc:identifier>
         <prism:publicationName>Journal of Oral Pathology &amp; Medicine</prism:publicationName>
         <prism:doi>10.1111/jop.70122</prism:doi>
         <prism:url>https://onlinelibrary.wiley.com/doi/10.1111/jop.70122?af=R</prism:url>
         <prism:section>ORIGINAL ARTICLE</prism:section>
      </item>
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