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Gingival Tissue Samples (gingival + tissue_sample)
Selected AbstractsMatrix metalloproteinase-7, -8, -9, -25, and -26 and CD43, -45, and -68 cell-markers in HIV-infected patients' saliva and gingival tissueJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 9 2006Liisa Mellanen Background:, Matrix metalloproteinases (MMPs) process the extracellular matrix and act in tissue remodelling in many physiological and pathological conditions. Certain MMPs can also exert protective anti-inflammatory properties. The levels and expression of MMPs and tissue inhibitors of MMPs (TIMPs) in saliva and gingival tissues of human immunodeficiency virus-seropositive (HIV+) patients are unclear. Methods:, Enzyme-linked immunosorbent assay methods and Western blots were used to study levels and molecular forms of MMP-7, -8, -9, -25, and -26 and TIMP-1 from salivary samples of HIV+ patients (n = 55) and healthy controls (n = 10). The expression of MMPs was also studied by immunohistochemical means in gingival tissue specimens (n = 11, HIV+ patients; n = 10, healthy controls). Results:, The HIV+ patients' MMP-8 levels in saliva were statistically significantly higher only in the acquired immunodeficiency syndrome (AIDS)-phase. MMP-9 levels in ASX- and AIDS-phases showed increased expression. TIMP-1 levels were significantly decreased in lymphadenopathy syndrome (LAS)- and AIDS-related complex (ARC)-phases, while MMP-8/TIMP-1 and MMP-9/TIMP-1 molar ratios were increased in all phases in comparison with controls. The molecular forms of MMP-7, -25, and -26 were different between patients and controls as assessed by Western blot. Immunohistochemical studies showed slightly enhanced MMP-7, -8, -9, -25, and -26 staining in HIV+ gingival tissue samples in comparison with controls. Conclusions:, This study confirmed and further demonstrated differences in salivary amounts and molecular forms of MMPs and TIMP-1 in HIV+ patients. The results may reflect alterations in host defence reactions associated with HIV infection. [source] In situ detection of matrix metalloproteinase-9 (MMP-9) in gingival epithelium in human periodontal diseaseJOURNAL OF PERIODONTAL RESEARCH, Issue 2 2004Patricio C. Smith Background and objective:, As the periodontal lesion develops, the junctional epithelium migrates apically in conjunction with the dissolution of the most coronal Sharpey's fibers. Because matrix metalloproteinase-9 (MMP-9) has been identified in migrating epithelial cells and invading tumors, we propose that this enzyme is produced by gingival keratinocytes in advanced periodontal lesions. Methods:, To test this idea, biopsies of inflamed gingival tissues were obtained from patients with advanced periodontitis. Healthy gingival tissue samples were utilized as controls. The presence and activity of MMP-9 was evaluated by combining indirect immunofluorescence of gingival tissue samples and gelatin zymography of gingival epithelium separated from connective tissue. Results and conclusions:, The staining pattern showed the presence of MMP-9 in junctional and pocket gingival epithelial cells, polymorphonuclear neutrophils (PMNs) and as a scattered deposit along connective tissues of periodontitis-affected gingival tissues. Gelatin zymography permitted the identification of pro-MMP-9 in surcular/pocket epithelium derived from inflamed gingival tissues. Lower levels of MMP-9 were detected in epithelium not exposed to inflammation. These observations suggest a role for MMP-9 in gingival epithelial response to periodontal infection. [source] Porphyromonas gingivalis lipids and diseased dental tissuesMOLECULAR ORAL MICROBIOLOGY, Issue 2 2006F. C. Nichols Background/aim:,Porphyromonas gingivalis synthesizes several classes of dihydroceramides and at least one of these lipid classes promotes proinflammatory secretory reactions in gingival fibroblasts as well as alters fibroblast morphology in culture. The purpose of this investigation was to determine whether the dihydroceramide lipids of P. gingivalis are recovered in lipid extracts of subgingival plaque, diseased teeth, and diseased gingival tissue samples. Methods:, Lipids were extracted from P. gingivalis, subgingival plaque, subgingival calculus, teeth laden with gross accumulations of subgingival calculus, and gingival tissue samples obtained from chronic severe periodontitis sites. Lipid samples were analyzed by gas chromatography-mass spectrometry as trimethylsilyl derivatives or by electrospray-mass spectrometry as underivatized products. High-performance liquid chromatography fractions of P. gingivalis lipids and gingival tissue lipids were also analyzed by electrospray-mass spectrometry analysis. Results:,P. gingivalis phosphorylated dihydroceramides were recovered in lipid extracts of subgingival plaque, subgingival calculus, calculus contaminated teeth, and diseased gingival tissue samples. However, the distribution of phosphorylated dihydroceramides varied between these samples. Conclusion:, Subgingival plaque, subgingival calculus, diseased teeth, and gingival tissue are contaminated with phosphorylated dihydroceramides produced by P. gingivalis. The previously reported biological activity of these substances together with the recovery of these lipids at periodontal disease sites argues strongly for their classification as virulence factors in promoting chronic inflammatory periodontal disease. [source] Herpesviruses in periodontal pocket and gingival tissue specimensMOLECULAR ORAL MICROBIOLOGY, Issue 1 2000A. Contreras Human cytomegalovirus (HCMV) and Epstein-Barr virus type 1 (EBV-1) are frequently detected in crevicular fluid of deep periodontal pockets, but little or no information is available on occurence of herpesviruses in gingival tissue. This investigation studied the presence of herpesviruses in periodontal pockets and the corresponding gingival tissues from 11 periodontally healthy and 14 periodontitis sites. A nested-polymerase chain reaction was employed to identify the presence of HCMV, EBV-1, EBV-2, herpes simplex virus, human herpesvirus (HHV)-6, HHV-7 and HHV-8 in each test sample. In healthy periodontal sites, HCMV was detected in 1 (9%) and EBV-1 in 2 (18%) pocket samples, and HCMV was detected in 2 (18%) and EBV-1 in 3 (27%) gingival tissue samples. In periodontitis lesions, HCMV was detected in 9 (64%) pocket samples and in 12 (86%) gingival tissue samples, and EBV-1 was detected in 6 (43%) pocket samples and in 11 (79%) gingival tissue samples. HHV-6 and HHV-8 were detected exclusively in gingival tissue samples. The present findings confirm the frequent presence of HCMV and EBV-1 in periodontitis lesions and suggest using gingival tissue specimens for detecting periodontal HHV-6, HHV-7 and HHV-8. [source] | ||||||||||