Cyclooxygenase-2 expression in maxillary sinus lesions

Abstract

Cyclooxygenases (COXs) are rate-limiting enzymes that initiate the conversion of arachidonic acid to prostanoids. COXs are classified into two isoforms: COX-1 and COX-2. COX-2 is an inducible isoform upregulated by proinflammatory cytokines. Recently, prominent COX-2 expression has been reported in several human cancers, including carcinoma of the colon, breast, lung, head and neck, and gallbladder. Overexpression of COX-2, which is involved in cell proliferation via prostaglandin E₂ (PGE2) synthesis, may play a role in tumor progression. In this study, we immunohistochemically characterized COX-2 expression in various diseases of the maxillary sinus, including 5 cases of postoperative maxillary cyst, 5 of maxillary sinusitis, 5 of inverted papilloma, and 5 of maxillary sinus carcinoma. In addition, secretory phospholipase A₂-V, CD3, CD20, and CD68 expression in these lesions was also examined to clarify the relation to COX-2 upregulation. COX-2 was not expressed in the ciliated columnar epithelium in sinusitis, but was expressed in squamous cell metaplasia in maxillary cyst and inverted papilloma. In carcinoma of the maxillary sinus, COX-2 was overexpressed in numerous cancer cells. The proportions of CD3 and CD68 positive cells in carcinoma were clearly lower than those in sinusitis. These results indicated that COX-2 expression correlates with squamous cell metaplasia and epithelial cell proliferation. The end product of the arachidonic acid cascade, PGE₂, may be involved in downregulation of CD3 and CD68 and the proliferation of maxillary sinus carcinoma. Further studies of COX-2 inhibitors as potential antitumor agents in maxillary sinus carcinoma are warranted.