Differential Expression of E‐Cadherin and Cytokeratin 19 and Net Proliferative Rate of Gingival Keratinocytes in Oral Epithelium in Periodontal Health and Disease

Nagarakanti, Sandhya; Ramya, S; Babu, P. Suresh; Arun, KV; Sudarsan, Sabitha

doi:10.1902/jop.2007.070070

Cited by 31 publications

(30 citation statements)

References 27 publications

(61 reference statements)

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“…Similar to the present study, Nagarakanti et al 52 found a significant increase in the proliferative marker (Ki‐67) in periodontitis tissue samples versus healthy gingiva. They reported that the oral gingival epithelium should be the main source of this proliferation and differentiation; moreover, the proliferation did not seem to be inhibited by tissue destruction.…”

Section: Discussionsupporting

confidence: 90%

Immunoexpression of Angiogenesis, Nitric Oxide Synthase, and Proliferation Markers in Gingival Samples of Patients With Aggressive and Chronic Periodontitis

Artese¹,

Piattelli²,

Cardoso³

et al. 2010

Journal of Periodontology

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Section: Discussionsupporting

confidence: 90%

Immunoexpression of Angiogenesis, Nitric Oxide Synthase, and Proliferation Markers in Gingival Samples of Patients With Aggressive and Chronic Periodontitis

Artese¹,

Piattelli²,

Cardoso³

et al. 2010

Journal of Periodontology

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“…C). CK19 expression was increased in inflamed gingival epithelium from patients with chronic periodontitis . The physiological means of increase or decrease of CK19 expressions are not clear; therefore, further study is necessary to dissolve these discrepancies.…”

Section: Discussionmentioning

confidence: 97%

Transcriptional regulation of human amelotin gene by interleukin‐1β

et al. 2018

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One of the major causes of tooth loss is chronic inflammation of the periodontium, the tissues surrounding the tooth. Amelotin ( AMTN ) is a tooth enamel protein which is expressed in maturation‐stage ameloblasts and also in the internal basal lamina of junctional epithelium, a unique epithelial structure attached to the tooth surface which protects against the constant microbiological challenge to the periodontium. Localization of AMTN suggests that its function could be involved in the dentogingival attachment. The purpose of this study was to investigate the effect of interleukin‐1β ( IL ‐1β) on AMTN gene transcription in human gingival epithelial Ca9‐22 cells. IL ‐1β increased AMTN mRNA and protein levels at 3 h, and the levels reached maximum at 6 and 12 h. IL ‐1β induced luciferase activities of human AMTN gene promoter constructs (−211, −353, −501, −769, and −950AMTN), but these activities were partially inhibited in −353AMTN constructs that included 3‐bp mutations in CCAAT /enhancer binding protein 1 (C/ EBP 1), C/ EBP 2, and Ying Yang 1 ( YY 1) elements. Transcriptional activities induced by IL ‐1β were abrogated by protein kinase A ( PKA ), tyrosine kinase, mitogen‐activated protein kinase kinase ( MEK 1/2), and phosphatidylinositol 3‐kinase ( PI 3K) inhibitors. Gel shift and ChIP assays showed that IL ‐1β increased C/ EBP β binding to C/ EBP 1 and C/ EBP 2, and YY 1 binding to YY 1 elements after 3 h, and that these DNA –protein interactions were inhibited by PKA , tyrosine kinase, MEK 1/2, and PI 3K inhibitors. These results demonstrated that IL ‐1β increases AMTN gene transcription in human gingival epithelial cells mediated through C/ EBP 1, C/ EBP 2, and YY 1 elements in the human AMTN gene promoter.

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“…It can be a result of the worsening of gingivitis [9]. The periodontium, the gums and bones that support the teeth, are destroyed, leading to eventual loss of teeth as well as a possible increased risk of heart attacks and stroke [10,11].…”

Section: Introductionmentioning

confidence: 99%

“…It is found in the infected gum tissue of gingivitis and periodontitis patients and therefore COX-2 inhibitors improve the symptoms of periodontitis by reducing the swelling and pain [15]. In addition, studies have shown that the expression of E-Cadherin is uniformly present in healthy gums, but decreased expression of the protein were found in the basal areas of the oral gingival epithelium in diseased samples [9]. This suggests that E-Cadherin expression plays a role in the progression of chronic periodontitis.…”

Section: Introductionmentioning

confidence: 99%

Epigenetic change in e-cardherin and COX-2 to predict chronic periodontitis

Loo

Cheung³

et al. 2010

J Transl Med

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BackgroundDNA methylation of certain genes frequently occurs in neoplastic cells. Although the cause remains unknown, many genes have been identified with such atypical methylation in neoplastic cells. The hypermethylation of E-Cadherin and Cyclooxygenase 2 (COX-2) in chronic inflammation such as chronic periodontitis may demonstrate mild lesion/mutation epigenetic level. This study compares the hypermethylation status of E-Cadherin and COX-2 genes which are often found in breast cancer patients with that in chronic periodontitis.MethodsTotal DNA was extracted from the blood samples of 108 systemically healthy non-periodontitis subjects, and the gingival tissues and blood samples of 110 chronic periodontitis patient as well as neoplastic tissues of 106 breast cancer patients. Methylation-specific PCR for E-Cadherin and COX-2 was performed on these samples and the PCR products were analyzed on 2% agarose gel.ResultsHypermethylation of E-Cadherin and COX-2 was observed in 38% and 35% of the breast cancer samples, respectively. In chronic periodontitis patients the detection rate was 25% and 19% respectively, and none was found in the systemically healthy non-periodontitis control subjects. The hypermethylation status was shown to be correlated among the three groups with statistical significance (p < 0.0001). The methylation of CpG islands in E-Cadherin and COX-2 genes in periodontitis patients occurs more frequently in periodontitis patients than in the control subjects, but occurs less frequently than in the breast cancer patients.ConclusionsThis set of data shows that the epigenetic change in E-Cadherin and Cyclooxygenase-2 is associated with chronic periodontitis. The epigenetic changes presented in chronic inflammation patients might demonstrate an irreversible destruction in the tissues or organs similar to the effects of cancer. Chronic periodontitis to some extent might be associated with DNA hypermethylation which is related to cancer risk factors.

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Differential Expression of E‐Cadherin and Cytokeratin 19 and Net Proliferative Rate of Gingival Keratinocytes in Oral Epithelium in Periodontal Health and Disease

Abstract: OGE appears to undergo significant changes in proliferation and differentiation during pocket formation that do not seem to be restricted to proteolytic destruction by the invading microorganisms.

Cited by 31 publications

References 27 publications

Immunoexpression of Angiogenesis, Nitric Oxide Synthase, and Proliferation Markers in Gingival Samples of Patients With Aggressive and Chronic Periodontitis

Immunoexpression of Angiogenesis, Nitric Oxide Synthase, and Proliferation Markers in Gingival Samples of Patients With Aggressive and Chronic Periodontitis

Transcriptional regulation of human amelotin gene by interleukin‐1β

Epigenetic change in e-cardherin and COX-2 to predict chronic periodontitis

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