The role of MMP-2, MMP-9, and TIMP-1 in the pathogenesis of nasal polyps: Immunohistochemical assessment at eight different levels in the epithelial, subepithelial, and deep layers of the mucosa.

We conducted a prospective study to investigate the role of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) in the pathogenesis of nasal polyps. Our study group consisted of 24 patients-21 men and 3 women, aged 23 to 70 years (mean: 45.97 ± 11.60)-with nasal polyposis who underwent functional endoscopic sinus surgery. For comparison purposes, we assembled a control group of 11 patients-6 men and 5 women, aged 18 to 56 years (mean: 29.90 ± 14.22)-without nasal polyps who underwent septoplasty and/or rhinoplasty. We analyzed 36 polyp specimens obtained from the study group (10 from the nasal cavity, 10 from the maxillary sinus, and 16 from the ethmoid sinus) and 11 tissue specimens from the control group (each control provided 1 specimen from the inferior turbinate). We then calculated the mean number of these cells in the epithelium, subepithelial layer of the lamina propria, and the deep paraglandular layer of the mucosa. In general, we found that MMP-2, MMP-9, and TIMP-1 values were higher in the nasal polyp group. These differences became less so as patients' ages and the duration of polyps increased. We conclude that the most important role that MMP-2 plays in polyp growth may be in terms of perivascular localization and an increase in vascular permeability, which causes inflammatory cell migration and edema in the extracellular matrix. An increase in MMP-2 in glandular tissue may lead to hydrolysis of tissue matrix components. The degraded extracellular matrix may result in fibrosis of the polyps. An increase of MMP-9 in the apical part of the epithelium in the polypoid tissue of the nasal cavity, maxillary sinus, and ethmoid sinus may facilitate the epithelial and endothelial cell migration that is observed during polyp development and growth.