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Z. P. Pavelic - One of the best experts on this subject based on the ideXlab platform.

  • Prostaglandin H synthase isoenzyme distribution in the Gingival Tissue of patients with periodontitis: Pronounced expression adjacent to gram-positive bacteria
    InflammoPharmacology, 1997
    Co-Authors: J. S. Mcdonald, P. F. Cavanaugh, L. J. Pavelic, R. J. Limardi, J. L. Gluckman, Z. P. Pavelic
    Abstract:

    Prostaglandin (PGE_2) is an inflammatory mediator that plays a critical role in the pathogenesis of periodontal disease. Prostaglandin H synthase (PGHS) a rate-limiting enzyme in PGE_2 biosynthesis exists as two separate isoforms (PGHS-1 and PGHS-2). We have previously demonstrated that both isoforms are generally present in the Gingival Tissue of periodontitis patients. This study explores in greater detail the variable distribution of each isoenzyme in both inflamed and non-inflamed Gingival Tissues of patients with periodontitis, and the relationship to adjacent bacteria. Although the positive staining for PGHS-1 was never as intense as for PGHS-2 in the same Tissue specimen, either in inflamed or non-inflamed Tissues, there was strong staining for both isoenzymes in the epithelium. The keratin layer did not stain. Non-keratinizing crevicular and junctional epithelium contained both isoenzymes through their full thickness in both inflamed and non-inflamed Tissues. Pronounced staining of PGHS-2 was evident in the epithelia adjacent to Gram-positively stained organisms. In non-inflamed Tissue, PGHS-1 and PGHS-2 were particularly evident in the spinous cell layer; however, fewer of the fibroblasts, endothelial cells, and resident mononuclear inflammatory cells stained positively for PGHS-1 as compared to PGHS-2, but this was less apparent in the inflamed Tissues. The immunohistochemical staining patterns indicate that both crevicular and Gingival epithelium are important sources of prostaglandin production in the Gingival Tissue of patients with periodontitis and that bacteria entrapped near to these sites may be important in promoting expression of inducible PGHS-2.

  • Immunohistochemical localization of prostaglandin H synthase isoenzyme proteins in the Gingival Tissue of patients with periodontitis
    InflammoPharmacology, 1995
    Co-Authors: P. F. Cavanaugh, J. S. Mcdonald, L. J. Pavelic, R. J. Limardi, J. L. Gluckman, Z. P. Pavelic
    Abstract:

    Prostaglandins are inflammatory mediators that are believed to play an important role in the pathophysiology of periodontal disease. Prostaglandin H synthase (PGHS, EC 1.14.99.1) is the rate-limiting enzyme in prostaglandin biosynthesis. The enzyme exists as two separately encoded isoforms. PGHS-1 which is constitutively expressed and PGHS-2 which is induced by inflammatory stimuli. This is the first report describing the expression of the isoenzymes in Gingival Tissue from patients diagnosed with adult periodontitis. Tissue was fixed in an alcohol-based fixative and embedded in paraffin. Methods were developed using immunohistochemical controls, such that embedded sections could be processed and stained using isoform-specific antibodies and a peroxidase-antiperoxidase immunohistochemistry technique. Along with populations of mononuclear inflammatory cells, endothelial cells and fibroblasts, the Gingival epithelial cell layer appears to be a rich and important source of prostaglandin production within the periodontium of patients with periodontitis as detected by this newly developed immunohistochemical staining technique for PGHS-1 and PGHS-2.

Faming Chen - One of the best experts on this subject based on the ideXlab platform.

  • macrophage polarization in human Gingival Tissue in response to periodontal disease
    Oral Diseases, 2019
    Co-Authors: Lina Zhou, Chunsheng Bi, Ying An, Fang Chen, Faming Chen
    Abstract:

    OBJECTIVE: Although accumulating evidence indicates that macrophages are central players in the destructive and reparative phases of periodontal disease, their polarization states at different stages of periodontal inflammation remain unclear. METHODS: We collected Gingival biopsies from patients with chronic periodontitis (P group), gingivitis (G group), or periodontally healthy individuals (H group). Polarized macrophages were identified through immunofluorescence. M1- and M2-related cytokines were detected by immunohistochemistry. RESULTS: Compared with the H group, the P group had more M1 cells (higher M1/M2 ratio) and significantly higher TNF-α, IFN-γ, IL-6, and IL-12 levels. Although the G group also exhibited higher TNF-α and IL-12 levels than the H group, they had similar M1/M2 ratios. The M1/M2 ratio and IFN-γ and IL-6 levels were significantly higher in the P than the G group. Among M2-related cytokines, IL-4 levels were significantly higher in the G than the H group. The M1/M2 ratio was positively correlated with clinical probing depth (PD), and both were positively correlated with IFN-γ and IL-6. PD was negatively correlated with IL-4. CONCLUSION: Macrophage polarization in Gingival Tissue may be responsible for the development and progression of inflammation-induced Tissue destruction, and modulating macrophage function may be a potential strategy for periodontal disease management.

  • comparison of mesenchymal stem cells derived from Gingival Tissue and periodontal ligament in different incubation conditions
    Biomaterials, 2013
    Co-Authors: Hao Yang, Ying An, Chenghu Hu, Jun Zhou, Faming Chen
    Abstract:

    Gingival Tissue-derived mesenchymal stem cells (MSCs) were recently identified and characterized as having multipotential differentiation and immunomodulatory properties in vitro and in vivo, and they represent new postnatal stem cell types for cytotherapy and regenerative medicine. However, the utility of Gingival MSCs (GMSCs) as alternatives to periodontal ligament stem cells (PDLSCs), which have been demonstrated to be effective but with limited cell availability and reduced clinical feasibility, for periodontal regeneration in a previously diseased/inflamed environment remains obscure. In this study, patient-matched human GMSCs and PDLSCs were evaluated in terms of their colony-forming ability, proliferative capacity, cell surface epitopes, multi-lineage differentiation potentials, and related gene expression when incubated in different designed culture conditions, with or without the presence of inflammatory cytokines. An in vivo ectopic transplantation model using transplants from inflammatory cytokine-treated or untreated cells was applied to assess bone formation. We found that cells derived from both Tissues expressed MSC markers, including CD146, CD105, CD90, CD29, and STRO-1. Both cells successfully differentiated under osteogenic, adipogenic, and chondrogenic microenvironments; PDLSCs displayed a more effective differentiation potential in all of the incubation conditions compared to GMSCs (P < 0.01). Although inflammatory cytokine-treated GMSCs and PDLSCs are inferior to normally cultured, patient and Tissue-matched cells in terms of their osteogenic capacity and regenerative potential (P < 0.05), they retain the capacity for osteoblastic and adipose differentiation, as well as ectopic bone formation, similar to what has been demonstrated for other MSCs. Interestingly, GMSCs exhibited fewer inflammation-related changes in terms of osteogenic potential in vitro and bone formation in vivo compared to PDLSCs (P < 0.01). These results suggest that both gingiva and PDL Tissues are putative cell sources for future cytotherapeutic applications. Whether GMSCs act as an adjunctive or alternative cell source for cytotherapy of inflammatory periodontal disease warrants further investigation.

P. F. Cavanaugh - One of the best experts on this subject based on the ideXlab platform.

  • Prostaglandin H synthase isoenzyme distribution in the Gingival Tissue of patients with periodontitis: Pronounced expression adjacent to gram-positive bacteria
    InflammoPharmacology, 1997
    Co-Authors: J. S. Mcdonald, P. F. Cavanaugh, L. J. Pavelic, R. J. Limardi, J. L. Gluckman, Z. P. Pavelic
    Abstract:

    Prostaglandin (PGE_2) is an inflammatory mediator that plays a critical role in the pathogenesis of periodontal disease. Prostaglandin H synthase (PGHS) a rate-limiting enzyme in PGE_2 biosynthesis exists as two separate isoforms (PGHS-1 and PGHS-2). We have previously demonstrated that both isoforms are generally present in the Gingival Tissue of periodontitis patients. This study explores in greater detail the variable distribution of each isoenzyme in both inflamed and non-inflamed Gingival Tissues of patients with periodontitis, and the relationship to adjacent bacteria. Although the positive staining for PGHS-1 was never as intense as for PGHS-2 in the same Tissue specimen, either in inflamed or non-inflamed Tissues, there was strong staining for both isoenzymes in the epithelium. The keratin layer did not stain. Non-keratinizing crevicular and junctional epithelium contained both isoenzymes through their full thickness in both inflamed and non-inflamed Tissues. Pronounced staining of PGHS-2 was evident in the epithelia adjacent to Gram-positively stained organisms. In non-inflamed Tissue, PGHS-1 and PGHS-2 were particularly evident in the spinous cell layer; however, fewer of the fibroblasts, endothelial cells, and resident mononuclear inflammatory cells stained positively for PGHS-1 as compared to PGHS-2, but this was less apparent in the inflamed Tissues. The immunohistochemical staining patterns indicate that both crevicular and Gingival epithelium are important sources of prostaglandin production in the Gingival Tissue of patients with periodontitis and that bacteria entrapped near to these sites may be important in promoting expression of inducible PGHS-2.

  • Immunohistochemical localization of prostaglandin H synthase isoenzyme proteins in the Gingival Tissue of patients with periodontitis
    InflammoPharmacology, 1995
    Co-Authors: P. F. Cavanaugh, J. S. Mcdonald, L. J. Pavelic, R. J. Limardi, J. L. Gluckman, Z. P. Pavelic
    Abstract:

    Prostaglandins are inflammatory mediators that are believed to play an important role in the pathophysiology of periodontal disease. Prostaglandin H synthase (PGHS, EC 1.14.99.1) is the rate-limiting enzyme in prostaglandin biosynthesis. The enzyme exists as two separately encoded isoforms. PGHS-1 which is constitutively expressed and PGHS-2 which is induced by inflammatory stimuli. This is the first report describing the expression of the isoenzymes in Gingival Tissue from patients diagnosed with adult periodontitis. Tissue was fixed in an alcohol-based fixative and embedded in paraffin. Methods were developed using immunohistochemical controls, such that embedded sections could be processed and stained using isoform-specific antibodies and a peroxidase-antiperoxidase immunohistochemistry technique. Along with populations of mononuclear inflammatory cells, endothelial cells and fibroblasts, the Gingival epithelial cell layer appears to be a rich and important source of prostaglandin production within the periodontium of patients with periodontitis as detected by this newly developed immunohistochemical staining technique for PGHS-1 and PGHS-2.

J. S. Mcdonald - One of the best experts on this subject based on the ideXlab platform.

  • Prostaglandin H synthase isoenzyme distribution in the Gingival Tissue of patients with periodontitis: Pronounced expression adjacent to gram-positive bacteria
    InflammoPharmacology, 1997
    Co-Authors: J. S. Mcdonald, P. F. Cavanaugh, L. J. Pavelic, R. J. Limardi, J. L. Gluckman, Z. P. Pavelic
    Abstract:

    Prostaglandin (PGE_2) is an inflammatory mediator that plays a critical role in the pathogenesis of periodontal disease. Prostaglandin H synthase (PGHS) a rate-limiting enzyme in PGE_2 biosynthesis exists as two separate isoforms (PGHS-1 and PGHS-2). We have previously demonstrated that both isoforms are generally present in the Gingival Tissue of periodontitis patients. This study explores in greater detail the variable distribution of each isoenzyme in both inflamed and non-inflamed Gingival Tissues of patients with periodontitis, and the relationship to adjacent bacteria. Although the positive staining for PGHS-1 was never as intense as for PGHS-2 in the same Tissue specimen, either in inflamed or non-inflamed Tissues, there was strong staining for both isoenzymes in the epithelium. The keratin layer did not stain. Non-keratinizing crevicular and junctional epithelium contained both isoenzymes through their full thickness in both inflamed and non-inflamed Tissues. Pronounced staining of PGHS-2 was evident in the epithelia adjacent to Gram-positively stained organisms. In non-inflamed Tissue, PGHS-1 and PGHS-2 were particularly evident in the spinous cell layer; however, fewer of the fibroblasts, endothelial cells, and resident mononuclear inflammatory cells stained positively for PGHS-1 as compared to PGHS-2, but this was less apparent in the inflamed Tissues. The immunohistochemical staining patterns indicate that both crevicular and Gingival epithelium are important sources of prostaglandin production in the Gingival Tissue of patients with periodontitis and that bacteria entrapped near to these sites may be important in promoting expression of inducible PGHS-2.

  • Immunohistochemical localization of prostaglandin H synthase isoenzyme proteins in the Gingival Tissue of patients with periodontitis
    InflammoPharmacology, 1995
    Co-Authors: P. F. Cavanaugh, J. S. Mcdonald, L. J. Pavelic, R. J. Limardi, J. L. Gluckman, Z. P. Pavelic
    Abstract:

    Prostaglandins are inflammatory mediators that are believed to play an important role in the pathophysiology of periodontal disease. Prostaglandin H synthase (PGHS, EC 1.14.99.1) is the rate-limiting enzyme in prostaglandin biosynthesis. The enzyme exists as two separately encoded isoforms. PGHS-1 which is constitutively expressed and PGHS-2 which is induced by inflammatory stimuli. This is the first report describing the expression of the isoenzymes in Gingival Tissue from patients diagnosed with adult periodontitis. Tissue was fixed in an alcohol-based fixative and embedded in paraffin. Methods were developed using immunohistochemical controls, such that embedded sections could be processed and stained using isoform-specific antibodies and a peroxidase-antiperoxidase immunohistochemistry technique. Along with populations of mononuclear inflammatory cells, endothelial cells and fibroblasts, the Gingival epithelial cell layer appears to be a rich and important source of prostaglandin production within the periodontium of patients with periodontitis as detected by this newly developed immunohistochemical staining technique for PGHS-1 and PGHS-2.

L. J. Pavelic - One of the best experts on this subject based on the ideXlab platform.

  • Prostaglandin H synthase isoenzyme distribution in the Gingival Tissue of patients with periodontitis: Pronounced expression adjacent to gram-positive bacteria
    InflammoPharmacology, 1997
    Co-Authors: J. S. Mcdonald, P. F. Cavanaugh, L. J. Pavelic, R. J. Limardi, J. L. Gluckman, Z. P. Pavelic
    Abstract:

    Prostaglandin (PGE_2) is an inflammatory mediator that plays a critical role in the pathogenesis of periodontal disease. Prostaglandin H synthase (PGHS) a rate-limiting enzyme in PGE_2 biosynthesis exists as two separate isoforms (PGHS-1 and PGHS-2). We have previously demonstrated that both isoforms are generally present in the Gingival Tissue of periodontitis patients. This study explores in greater detail the variable distribution of each isoenzyme in both inflamed and non-inflamed Gingival Tissues of patients with periodontitis, and the relationship to adjacent bacteria. Although the positive staining for PGHS-1 was never as intense as for PGHS-2 in the same Tissue specimen, either in inflamed or non-inflamed Tissues, there was strong staining for both isoenzymes in the epithelium. The keratin layer did not stain. Non-keratinizing crevicular and junctional epithelium contained both isoenzymes through their full thickness in both inflamed and non-inflamed Tissues. Pronounced staining of PGHS-2 was evident in the epithelia adjacent to Gram-positively stained organisms. In non-inflamed Tissue, PGHS-1 and PGHS-2 were particularly evident in the spinous cell layer; however, fewer of the fibroblasts, endothelial cells, and resident mononuclear inflammatory cells stained positively for PGHS-1 as compared to PGHS-2, but this was less apparent in the inflamed Tissues. The immunohistochemical staining patterns indicate that both crevicular and Gingival epithelium are important sources of prostaglandin production in the Gingival Tissue of patients with periodontitis and that bacteria entrapped near to these sites may be important in promoting expression of inducible PGHS-2.

  • Immunohistochemical localization of prostaglandin H synthase isoenzyme proteins in the Gingival Tissue of patients with periodontitis
    InflammoPharmacology, 1995
    Co-Authors: P. F. Cavanaugh, J. S. Mcdonald, L. J. Pavelic, R. J. Limardi, J. L. Gluckman, Z. P. Pavelic
    Abstract:

    Prostaglandins are inflammatory mediators that are believed to play an important role in the pathophysiology of periodontal disease. Prostaglandin H synthase (PGHS, EC 1.14.99.1) is the rate-limiting enzyme in prostaglandin biosynthesis. The enzyme exists as two separately encoded isoforms. PGHS-1 which is constitutively expressed and PGHS-2 which is induced by inflammatory stimuli. This is the first report describing the expression of the isoenzymes in Gingival Tissue from patients diagnosed with adult periodontitis. Tissue was fixed in an alcohol-based fixative and embedded in paraffin. Methods were developed using immunohistochemical controls, such that embedded sections could be processed and stained using isoform-specific antibodies and a peroxidase-antiperoxidase immunohistochemistry technique. Along with populations of mononuclear inflammatory cells, endothelial cells and fibroblasts, the Gingival epithelial cell layer appears to be a rich and important source of prostaglandin production within the periodontium of patients with periodontitis as detected by this newly developed immunohistochemical staining technique for PGHS-1 and PGHS-2.