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

نویسندگان

  • 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

کلمات کلیدی:

Cysts, COX-2, aggressive, inflammatory, prognosis

چکیده

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.

 

بیوگرافی نویسنده

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

مراجع

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.

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چاپ شده

2022-01-10

شماره

دوره 10 شماره 1 (2022)

نوع مقاله

Mechanisms of Oral Disease

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