{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T23:51:43Z","timestamp":1785887503910,"version":"3.56.0"},"reference-count":22,"publisher":"Georg Thieme Verlag KG","license":[{"start":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T00:00:00Z","timestamp":1785801600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Dent"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The nuclear protein Ki-67 and caspase-3 regulate cell proliferation and apoptosis as well as the preservation of tissue homeostasis in response to genetic and inflammatory signals that have a role in the pathogenesis of different conditions such as gingival overgrowth. Yet, the distinct pathogenesis of these lesions could be determined by variations in cellular homeostasis mechanisms. The aim of this study was to assess and compare the immunohistochemical expression of Ki-67 and caspase-3 in hereditary gingival fibromatosis (HGF) and inflammatory gingival hyperplasia (IGH), measure quantitative histopathological parameters, and investigate their association with the balance of proliferation and apoptosis underlying these different gingival overgrowth forms.<\/jats:p>\n                  <jats:p>An observational cross-sectional study involved 31 gingival biopsies collected from subjects with a history of recurrent gingival enlargement, 15 subjects (9 females and 6 males, 11\u201346 years) with moderate\/severe IGH and 16 subjects with HGF (12 females and 4 males, 16\u201359 years) during gingivectomy and flap procedures. Anti-caspase-3 antibody and anti-Ki-67 antibody were utilized for immunohistochemistry staining. Imaging was performed at 400\u00d7 magnification using a light microscope (Olympus BX51 model) equipped with an Olympus XC10-IR color camera; digital images were taken and saved in Joint Photographic Experts Group (JPEG) format. Computer-assisted image analysis was conducted using Q Path software version 0.5.1, an open-source software for digital pathology, to quantify marker expression in tissue sections.<\/jats:p>\n                  <jats:p>Mann\u2013Whitney U-test evaluated expression levels; Spearman's correlation assessed biomarker association. Significance was set at p &lt;0.05.<\/jats:p>\n                  <jats:p>The present finding revealed that the percentage of caspase-3\u2013positive cells was higher in HGF (mean rank: 21.44) compared with IGH (mean rank: 10.20), with a statistically significant difference (U\u2009=\u200933.000, p\u2009&lt;\u20090.001). Similarly, the H-score for caspase-3 expression was markedly elevated in HGF (mean rank: 21.25) compared with IGH (mean rank: 10.40), with a statistically significant difference (U\u2009=\u200936.000, p\u2009&lt;\u20090.001). However, the proportion of Ki-67\u2013positive cells was significantly greater in HGF (mean rank: 21.31) than in IGH (mean rank: 10.33), with a statistically significant difference (U\u2009=\u200935.000, p\u2009&lt;\u20090.001). In contrast, the evaluation of optical density revealed higher values in IGH (mean rank: 20.07) compared with HGF (mean rank: 12.19); this difference was statistically significant (U\u2009=\u200959.000, p\u2009=\u20090.016).<\/jats:p>\n                  <jats:p>The findings of this study indicate that both groups reflect divergent pathobiological mechanisms. Specifically, HGF appears to involve genetically mediated tissue remodeling accompanied by compensatory apoptotic activity, while IGH is correlated with inflammation-driven, focally increased proliferation. Our results suggest that HGF and IGH should be regarded as biologically distinct entities.<\/jats:p>","DOI":"10.1055\/s-0046-1825553","type":"journal-article","created":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T23:30:45Z","timestamp":1785886245000},"source":"Crossref","is-referenced-by-count":0,"title":["Differential Expression of Caspase-3 and Ki-67 in Hereditary Gingival Fibromatosis and Inflammatory Gingival Hyperplasia"],"prefix":"10.1055","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9418-2877","authenticated-orcid":false,"given":"Zinah A.","family":"Hamdala","sequence":"additional","affiliation":[{"name":"Department of Oral Pathology, College of Dentistry, Mustansiriyah University, Baghdad, Iraq"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hussein A.","family":"Mousa","sequence":"additional","affiliation":[{"name":"Department of Periodontics, College of Dentistry, Mustansiriyah University, Baghdad, Iraq"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-8083-7204","authenticated-orcid":false,"given":"Wael Abdulazeez","family":"Kzar","sequence":"additional","affiliation":[{"name":"Department of Periodontology, Ministry of Health, Baghdad, Iraq"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3095-7092","authenticated-orcid":false,"given":"Athraa Ali","family":"Mahmood","sequence":"additional","affiliation":[{"name":"Department of Periodontics, College of Dentistry, Mustansiriyah University, Baghdad, Iraq"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"194","published-online":{"date-parts":[[2026,8,4]]},"reference":[{"key":"ref1","doi-asserted-by":"crossref","first-page":"9","DOI":"10.1186\/s13023-016-0395-1","article-title":"Gingival fibromatosis: clinical, molecular and therapeutic issues","volume":"11","author":"K Gawron","year":"2016","journal-title":"Orphanet J Rare Dis"},{"issue":"01","key":"ref2","doi-asserted-by":"crossref","first-page":"46","DOI":"10.1038\/s41368-023-00244-1","article-title":"Double heterozygous pathogenic mutations in KIF3C and ZNF513 cause hereditary gingival fibromatosis","volume":"15","author":"J Chen","year":"2023","journal-title":"Int J Oral Sci"},{"issue":"01","key":"ref3","doi-asserted-by":"crossref","first-page":"492","DOI":"10.1186\/s13023-021-02104-9","article-title":"Clinics and genetic background of hereditary gingival fibromatosis","volume":"16","author":"K Strzelec","year":"2021","journal-title":"Orphanet J Rare Dis"},{"issue":"01","key":"ref4","doi-asserted-by":"crossref","first-page":"25","DOI":"10.1177\/154405910708600104","article-title":"Hereditary gingival fibromatosis: characteristics and novel putative pathogenic mechanisms","volume":"86","author":"L H\u00e4kkinen","year":"2007","journal-title":"J Dent 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destruction","volume":"79","author":"D Graves","year":"2008","journal-title":"J Periodontol"},{"issue":"01","key":"ref20","doi-asserted-by":"crossref","first-page":"89","DOI":"10.32828\/mdj.v16i1.1028","article-title":"The immunohistochemical expression Ki-67 in polymorphous low-grade adenocarcinoma of the salivary glands","volume":"16","author":"M M Abdulhussain","year":"2019","journal-title":"Mustansiria Dent J."},{"issue":"03","key":"ref21","first-page":"1","article-title":"Assessment of immunoexpression of Ki-67 and CD105 in oral pyogenic granuloma","author":"A S Salman","year":"2023","journal-title":"J Emerg Med Trauma Acute Care"},{"issue":"01","key":"ref22","first-page":"FTTL2717","article-title":"Immunohistochemicalstudy of IL-6 and IL-10 expression in breast cancer: correlationswith ER, PR, Her-2, Ki-67, and clinicopathological features in Iraqiwomen","volume":"08","author":"S AR Al-Gharrawi","year":"2025","journal-title":"Israa Univ J Appl Sci"}],"container-title":["European Journal of Dentistry"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/www.thieme-connect.de\/products\/ejournals\/pdf\/10.1055\/s-0046-1825553.pdf","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,8,4]],"date-time":"2026-08-04T23:30:57Z","timestamp":1785886257000},"score":1,"resource":{"primary":{"URL":"http:\/\/www.thieme-connect.de\/DOI\/DOI?10.1055\/s-0046-1825553"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,8,4]]},"references-count":22,"URL":"https:\/\/doi.org\/10.1055\/s-0046-1825553","archive":["Portico","CLOCKSS"],"relation":{},"ISSN":["1305-7456","1305-7464"],"issn-type":[{"value":"1305-7456","type":"print"},{"value":"1305-7464","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,8,4]]}}}