Immunohistochemical expression of Cyclooxygenase 2 reflects the proliferative activity in the epithelium of odontogenic lesions

Authors

  • Vani Verma Former, Post graduate student Department of Oral Pathology and Microbiology Manipal College of Dental Sciences, Manipal Manipal Academy of Higher Education, Manipal 576104, Karnataka, India
  • Chetana Chandrashekar Associate Professor Department of Oral Pathology and Microbiology Manipal College of Dental Sciences, Manipal Manipal 576104, Karnataka, India
  • Raghu Radhakrishnan Professor Department of Oral Pathology and Microbiology Manipal College of Dental Sciences, Manipal Manipal 576104, Karnataka, India
  • Monica Charlotte Solomon Manipal College of Dental Sciences, Manipal Manipal University https://orcid.org/0000-0002-1836-887X

DOI:

https://doi.org/10.5195/d3000.2022.205

Keywords:

Cysts, COX-2, aggressive, inflammatory, prognosis

Abstract

Purpose:  Odontogenic cysts and tumors comprise a major component of lesions of the oral and maxillofacial region. The pathogenesis of these lesions involves the interaction between the odontogenic epithelium and the ectomesenchyme. However, the clinical behavior of these biological entities is unpredictable. The aim of this study was to evaluate the role of Cyclooxygenase 2 (COX-2) in the pathogenesis and prognostication of odontogenic lesions.

Material and method:  : In this study formalin-fixed paraffin-embedded tissue section of Odontogenic Keratocyst (n=10) Dentigerous cyst (n=10), Radicular cyst (n=10) and unicystic ameloblastoma (n=10) were immunohistochemically stained with COX-2 (NCL2-COX-2- 4H12) and with Ki 67 (Ki-67 GM001) using standard staining protocols. The cytoplasmic expression of COX-2 in all the lesions was semi-quantitatively assessed. The pattern of expression of COX-2 among the different odontogenic lesions was statistical analyzed using the ANOVA test and the chi-square test.

Results: All the 40 odontogenic lesions that were evaluated expressed COX-2 immunohistochemically. A high number of odontogenic epithelial cells expressed COX-2 in most of the odontogenic keratocyst, radicular cyst and unicystic ameloblastomas. The expression of COX-2 was significantly (p=0.036) higher in Unicystic Ameloblastomas and Radicular cyst compared to that of Odontogenic Keratocyst and the dentigerous cyst.

Conclusion: The recognition that expression of COX-2 by odontogenic epithelial cells may indeed shed a new light on the biological mechanisms involved in the development of these benign yet aggressive lesions of the jaws. An insight into the molecular interactions occurring in the odontogenic epithelium will aid in better management of these lesions.

 

Author Biography

Monica Charlotte Solomon, Manipal College of Dental Sciences, Manipal Manipal University

Professor

Department of Oral Pathology and Microbiology 

Manipal College of Dental Sciences, Manipal

Manipal 576104, Karnataka, India

References

Shear M, Speight P, Shear M. Cysts of the oral and maxillofacial regions. Oxford: Blackwell Pub.; 2007.

Koju S, Chaurasia NK, Marla V, Niroula D, Poudel P. Radicular cyst of the anterior maxilla: An insight into the most common inflammatory cyst of the jaws. J Dent Res Rev 2019; 6:26-9.

Kolokythas A, Karas M, Sarna T, Flick W, Miloro M. Does cytokine profiling of aspirate from jaw cysts and tumors have a role in diagnosis? J Oral Maxillofac Surg. 2012 70(5):1070-80.

Cysts of the orofacial region, Shafer’s textbook of oral pathology 9th Edition, Adaptive Editor Sivapathasundaram, Elsevier Page No 72-5.

Li TJ, Wu YT, Yu SF, Yu GY. Unicystic ameloblastoma: a clinicopathologic study of 33 Chinese patients. Am J Surg Pathol. 2000 Oct;24(10):1385-92.

Smith WL, Garavito RM, DEWitt DL. Prostaglandin endoperoxidase synthase (Cyclooxygenases)-1 and 2. J Biol Chem 1996; 271: 3157-60.

Chandrasekharan NV and Simmons DL The cyclooxygenases. Genome Biol 2004; 5:241

Wang D, Dubois RN. The role of COX-2 in intestinal inflammation and colorectal cancer. Oncogene 2010; 29: 781-9.

Van JR, Mitchell JA, Appelton I, Tomlinson A, Bishop -Bailey D, Croxtall X et al. Inducible isoforms of cyclooxygenase and nitric oxide synthase in inflammation. Proc Natl Acad Sci USA 1994; 91(16): 2046-50

Tsujii M, DuBois RN. Alteration in cellular adhesion and apoptosis in epithelial cells overexpressing prostaglandin endoperoxidase synthase 2. Cell 1995; 83 (3): 493-501,

Tsujii M Kawano S, Tuji S Sawaoka H, Hori M, DuBois RN. Cyclooxygenase regulates. angiogenesis induced by colon cancer cells. Cell 1998; 93 (5);705-16

Banerjee AG, Gopalkrishnan VK, Bhattacharya I, Vishwanatha JK. Deregulated Cyclooxygenase -2 expression in oral permalignant tissues. Mol Cancer Ther I 2002; 1265- 71.

Alsaegh MA, Miyashita H, Taniguchi T, Zhu SR. Odontogenic epithelial proliferation is correlated with COX-2 expression in dentigerous cyst and ameloblastoma. Experimental and therapeutic medicine 2017;13: 247-53

Mendes RA Carvalho JFC, Van der Waal I. A comparative immubohistochemical analysis of COX-2, p53, and Ki 67 expression in Keratocystic odontogenic tumors. Oral Surg Oral Med

Oral Path Oral Radiol Endod 2011; 111(3): 333-9.

Seyedmajidi M, Shafaee S, Siadati S, Moghaddam EA, Ghasemi N, Bijani A et al.Immunohistochemical analysis of COX-2 expression in dentigerous cyst, keratocystic odontogenic tumor and ameloblastoma: A comparative study. Dent Res J 2015;12(3):278 84.

Kaczmarzyk T, Kiselowski K, Koszowski R, Rynkiewicz M, Gawelek E, Babiuch K E, Bednarczyk A, Drozdzowska B. Investigationof clinicopathological parameters and

expression of COX-2, bcl-2, PCNA, and p53 in primary and recurrent sporadic odontogenic keratocyst. Clin Oral Invest 2018; 22: 3097-106.

Yoshikawa R, Sano H, Masuda C, Kawamura M, Tsubouchi Y, Chargui J et al Expression of cyclooxygenase-2 in prostate carcinoma. Cancer 2000;89(3):589-96.

Fujiwaki R, Iida K, Kanasaki H, Ozaki T, Hata K, Miyazaki K. Cyclooxygenase-2 expression in endometrial cancer: correlation with microvessel count and expression of vascular endothelial growth factor and thymidine phosphorylase. Human Pathology 2002; 33(2):213- 19.

Sheng H, Shao J, Morrow JD, Beauchamp RD, DuBois RN (1998) Modulation of apoptosis and Bcl-2 expression by prostaglandin E2 in human colon cancer cells. Cancer Res 1998;

(2):362-6.

Francon RN, Teofilo JM, satin RB and Lamano T. Prostaglandin and bone: potential risks and benefits related to the use of nonsteroidal anti-inflammatory drugs in clinical dentistry J oral

Sci 2008; 50:247-52.

Kumamoto H, Ohki K, Ooya. Expression of Sonic hedgehog (SHH) signaling molecules in ameloblastomas, J Oral Pathol Med 2004; 33: 185-90.

Han JA, Kim JL, Ongusaha PP, Hwang DH, Ballou LR, Mahale A et al. p53 mediated induction of COX-2 counteracts p53 or genotoxic stress induced apoptosis. EMBO J 2002; 21:5635- 44.

Tsai CH, Huang FM, Yang LC, Chou MY, Chang YC. Immunohistochemical localization of cyclooxygenase-2 in radicular cysts. Int Endod J. 2002 Oct;35(10):854-8.

Dubois RN, Abramson SB, Crofford L, Gupta RA, Simon LS, Van De Putte LB et al.Cyclooxygenase in biology and disease. FASEB J. 1998 Sep;12(12):1063-73.

Scully C, Beyli M, Ferreiro MC, Ficarra G, Gill Y, Griffiths M et al Holmstrup P, Mutlu S. Update on oral lichen planus: etiopathogenesis and management. Crit Rev Oral Biol Med 1998;9(1):86-122.

Ogata S, Kubota Y, Yamashiro T, Takeuchi H, Ninomiya T, Suyuma Y et al. Signaling pathways regulating IL-1 alpha induced COX-2 expression. J Dent Res 2007; 86: 186-91.

Prescott SM, Fitzpatrick FA, Cyclooxygenase 2 and carcinogenesis. Biochem Biophys Acta 2000; 1470:69-78.

Downloads

Published

2022-01-10

Issue

Vol. 10 No. 1 (2022)

Section

Mechanisms of Oral Disease

License

Authors who publish with this journal agree to the following terms:

  1. The Author retains copyright in the Work, where the term “Work” shall include all digital objects that may result in subsequent electronic publication or distribution.
  2. Upon acceptance of the Work, the author shall grant to the Publisher the right of first publication of the Work.
  3. The Author shall grant to the Publisher and its agents the nonexclusive perpetual right and license to publish, archive, and make accessible the Work in whole or in part in all forms of media now or hereafter known under a Creative Commons Attribution 4.0 International License or its equivalent, which, for the avoidance of doubt, allows others to copy, distribute, and transmit the Work under the following conditions:
    1. Attribution—other users must attribute the Work in the manner specified by the author as indicated on the journal Web site;
    with the understanding that the above condition can be waived with permission from the Author and that where the Work or any of its elements is in the public domain under applicable law, that status is in no way affected by the license.
  4. The Author is able to enter into separate, additional contractual arrangements for the nonexclusive distribution of the journal's published version of the Work (e.g., post it to an institutional repository or publish it in a book), as long as there is provided in the document an acknowledgement of its initial publication in this journal.
  5. Authors are permitted and encouraged to post online a prepublication manuscript (but not the Publisher’s final formatted PDF version of the Work) in institutional repositories or on their Websites prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work. Any such posting made before acceptance and publication of the Work shall be updated upon publication to include a reference to the Publisher-assigned DOI (Digital Object Identifier) and a link to the online abstract for the final published Work in the Journal.
  6. Upon Publisher’s request, the Author agrees to furnish promptly to Publisher, at the Author’s own expense, written evidence of the permissions, licenses, and consents for use of third-party material included within the Work, except as determined by Publisher to be covered by the principles of Fair Use.
  7. The Author represents and warrants that:
    1. the Work is the Author’s original work;
    2. the Author has not transferred, and will not transfer, exclusive rights in the Work to any third party;
    3. the Work is not pending review or under consideration by another publisher;
    4. the Work has not previously been published;
    5. the Work contains no misrepresentation or infringement of the Work or property of other authors or third parties; and
    6. the Work contains no libel, invasion of privacy, or other unlawful matter.
  8. The Author agrees to indemnify and hold Publisher harmless from Author’s breach of the representations and warranties contained in Paragraph 6 above, as well as any claim or proceeding relating to Publisher’s use and publication of any content contained in the Work, including third-party content.

Revised 7/16/2018. Revision Description: Removed outdated link.