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Öğe A case of cheilitis glandularis superimposed on oral lichen planus: successful palliative treatment with topical tacrolimus and pimecrolimus(Blackwell Publishing, 2007) Erkek, E.; Sahin, S.; Kilic, R.; Erdogan, S.…Öğe Expressions of MMP2, MMP9, and TIMP-1 in the inflammatory cells of nasal polyps: granulocytes, monocytes, and mast cells(Verduci Publisher, 2023) Muluk, N. Bayar; Arikan, O. K.; Atasoy, P.; Kilic, R.; Yalcinozan, E. TunaOBJECTIVE: We investigated the role of matrix metalloproteinase-2 (MMP-2) and MMP-9 in nasal polyp (NP) pathogenesis. PATIENTS AND METHODS: In group 1 (n = 24), polyp specimens were obtained from maxillary sinus, ethmoid sinus, and nasal cavity. In group 2 without NP (control) (n = 11), inferior turbinate samples were taken. Inflammatory cell count and MMP2, MMP9 and tissue inhibitor of metalloproteinase-1 ( TIMP-1), positivity indexes (PIs) were evaluated. RESULTS: Granulocyte and mast cell-MMP2 and MMP9-PI were higher than the rate of monocyte-MMP2-PI and monocyte-MMP9-PI, respectively, in the ethmoid sinus, maxillary sinus, and nasal cavity. Mast Cell-TIMP1-PI was higher than the rates of granulocyte-TIMP1-PI and monocyte-TIMP1-PI in the maxillary sinus and was higher than the rate of monocyte-TIMP1-PI in the ethmoid sinus. CONCLUSIONS: Excessive MMP2 and MMP9, compared to TIMP1, are present in granulocytes and mast cells, respectively. With matrix MMPs, the extracellular matrix is destroyed, leading inflammatory cells to pass through, causing polypoid degeneration.Öğe Inducible nitric oxide synthase (iNOS) in sinonasal polyp pathogenesis(Royal Belgian Soc Ear, Nose, Throat, Head & Neck Surgery, 2013) Muluk, N. Bayar; Arikan, O. K.; Atasoy, P.; Kilic, R.; Yalcinozan, E. TunaObjectives: We investigated the role of inducible nitric oxide synthase (iNOS) in the pathogenesis of sinonasal polyps. Methods: Adult patients (21 men, 3 women) with nasal polyposis underwent functional endoscopic sinus surgery. Nine adults without polyps (6 men) who underwent septoplasty and/or rhinoplasty served as controls. Polyp specimens came from three regions: the maxillary sinus (10), ethmoid sinus (14), and nasal cavity (10). Control group samples (9) came from the inferior turbinate. Specimens were evaluated in eight mucosal layers for count and distribution of inflammatory cells and iNOS expression. An iNOS positivity index (PI) was determined for the epithelium (E), subepithelial layer of the lamina propria (SE), and deep paraglandular layer of the mucosa (D). Results: Polymorphonuclear cell (PMNC) % values of the ethmoid and maxillary sinus and overall ethmoid sinus PI were significantly higher in the polyp group. Patients with longer polyp duration, D-perivascular (D-pv), and a higher Brinkmann index had decreased ethmoid sinus D Pis. However, in older patients and patients with longer polyp duration, perivascular PIs increased in maxillary sinus SE and D, respectively. Furthermore, as PMNC % and iNOS-PMNC PI increased, SE_glandular and epithelial_apical iNOS values decreased. In the ethmoid and maxillary sinuses, iNOS_D_endothelial values increased but decreased in the nasal cavity. Conclusions: iNOS may play a role in sinonasal polyp pathogenesis, especially in mucosal SE and D layers. Increased vascular permeability, stromal edema, inflammatory cell migration into the stroma of the mucosa, and increased mucosal gland secretion may result in polyp formation.
