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The Effects of Selective COX‐2 Inhibitor/Celecoxib and Omega‐3 Fatty Acid on Matrix Metalloproteinases, TIMP‐1, and Laminin‐5γ2‐Chain Immunolocalization in Experimental Periodontitis
Author(s) -
VardarSengul Saynur,
Buduneli Eralp,
Turkoglu Oya,
Buduneli Nurcan,
Atilla Gül,
Wahlgren Jaana,
Sorsa Timo,
Baylas Haluk
Publication year - 2008
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2008.080001
Subject(s) - matrix metalloproteinase , laminin , celecoxib , periodontitis , chemistry , omega 3 fatty acid , omega , cox 2 inhibitor , matrix metalloproteinase inhibitor , matrix (chemical analysis) , pharmacology , fatty acid , extracellular matrix , biochemistry , medicine , enzyme , cyclooxygenase , docosahexaenoic acid , polyunsaturated fatty acid , physics , chromatography , quantum mechanics
Background: Matrix metalloproteinases (MMPs) play important roles in tissue‐destruction mechanisms–associated periodontitis. MMP‐8 and −13 are the predominant collagenases that are important in the extracellular matrix degradation in periodontal tissues. MMP‐14 is a membrane‐type MMP, whereas laminin‐5 indicates basal membrane modification and epithelial induction. The purpose of the present study was to evaluate the effects of celecoxib and omega‐3 fatty acid administration on the gingival tissue expression of MMP‐8, −13, and −14, tissue inhibitor of MMP (TIMP)‐1, and laminin (Ln)‐5γ2‐chain in rat experimental periodontitis induced by Escherichia coli endotoxin (lipopolysaccharide [LPS]). Methods: Experimental periodontitis was induced in rats by repeated LPS injection. Fifty‐one adult male Sprague‐Dawley rats were divided into six study groups: saline control, LPS, LPS + celecoxib, LPS + therapeutic omega‐3 (TO3), prophylactic omega‐3 + LPS + omega‐3 (P+TO3), and LPS + celecoxib + omega‐3 fatty acid. Celecoxib and omega‐3 fatty acid were given as a single agent or as combination therapy for 14 days. On day 15, all rats were sacrificed, and gingival tissues were analyzed immunohistochemically for the expression of MMP‐8, −13, and −14, TIMP‐1, and Ln‐5γ2‐chain. Alveolar bone loss was evaluated morphometrically under a stereomicroscope. Data were tested statistically by Kruskal‐Wallis and Mann‐Whitney tests and Spearman correlation analysis. Results: Alveolar bone loss was significantly higher in all study groups compared to the saline control group (all P <0.01). MMP‐8 expression was significantly higher in the LPS group than in the saline group ( P = 0.001). Very low expression of MMP‐8 was found in the celecoxib, P+TO3, and combination groups. TO3 increased TIMP‐1 expression significantly compared to the LPS group ( P <0.05). Individual celecoxib and P+TO3 administration increased MMP‐14 significantly compared to saline control and LPS groups ( P <0.05). No significant differences were found among the study groups with regard to Ln‐5γ2‐chain and MMP‐13 expressions ( P >0.05). Conclusions: Selective cyclooxygenase‐2 inhibitor, prophylactic omega‐3 fatty acid, and a combination of these two agents can inhibit gingival tissue MMP‐8 expression. Moreover, the individual administration of therapeutic omega‐3 may increase gingival TIMP‐1 expression in contrast to no effect on MMP‐8, −13, and −14 expressions in experimental periodontitis. These experimental findings in a rat model of LPS‐induced periodontitis need to be verified by clinical human studies.