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Treatment of Periodontal Disease via Modulation of Innate Host Response- [electronic resource]
Treatment of Periodontal Disease via Modulation of Innate Host Response - [electronic reso...
Contents Info
Treatment of Periodontal Disease via Modulation of Innate Host Response- [electronic resource]
Material Type  
 학위논문
 
0016934454
Date and Time of Latest Transaction  
20240214101612
ISBN  
9798380481373
DDC  
600
Author  
Shehabeldin, Mostafa Salah.
Title/Author  
Treatment of Periodontal Disease via Modulation of Innate Host Response - [electronic resource]
Publish Info  
[S.l.] : University of Pittsburgh., 2021
Publish Info  
Ann Arbor : ProQuest Dissertations & Theses, 2021
Material Info  
1 online resource(139 p.)
General Note  
Source: Dissertations Abstracts International, Volume: 85-04, Section: B.
General Note  
Advisor: Sfeir, Charles.
학위논문주기  
Thesis (Ph.D.)--University of Pittsburgh, 2021.
Restrictions on Access Note  
This item must not be sold to any third party vendors.
Abstracts/Etc  
요약Periodontal disease (PD) is a chronic inflammatory disease characterized by progressive destruction of tooth supporting structures and microbial dysbiosis. The destructive inflammatory process underlying PD is mediated by components of both the innate and acquired immune systems including immune cells, cytokines, chemokines and lipid mediators. Macrophages and Thelper 17 (Th17) cells are key cellular mediators of the innate and acquired host responses in the periodontal environment, respectively. In many tissues including the periodontium, macrophages are the prototypic phagocytes of the innate immune response. These plastic cells can assume distinct phenotypic subsets to perform a wide array of functions ranging from host defense against invading pathogens to clearance of dead cells and promotion of tissue repair. Similarly, periodontal Th17 cells can exhibit both homeostatic and pathogenic subsets. Homeostatic Th17 cells are essential for immune surveillance and host defense by regulating neutrophils expansion and recruitment at oral barrier sites. Conversely, pathogenic Th17 cells arise in response to oral microbial challenge and drive inflammatory damage in PD via overproduction of their major cytokine IL-17A. In this study, we tested the therapeutic efficacy of modulating macrophages response or IL-17A activity in PD using two polymer based sustained delivery systems. To target macrophages, the chemokine CCL2 was encapsulated in PLGA microspheres and locally delivered at different stages of murine PD severity followed by analysis of bone levels, gene expression profile, osteoclastic activity, periodontal ligament organization and periodontal microbial load and composition. Using Sc-RNA sequencing technology, we also assessed murine periodontal macrophages gene expression profile and characterized their phenotypic subsets. We also tested the protective effect of local sustained delivery of IL-17A antibodies in murine periodontitis by assessing the changes in bone levels, osteoclastic activity and inflammatory markers. The overall aim of this study was to highlight the clinical translation potential of targeting cellular and noncellular components of the innate and acquired immune response to treat PD.
Subject Added Entry-Topical Term  
Infections.
Subject Added Entry-Topical Term  
Pathogens.
Subject Added Entry-Topical Term  
Chemokines.
Subject Added Entry-Topical Term  
Biofilms.
Subject Added Entry-Topical Term  
Periodontium.
Subject Added Entry-Topical Term  
Cytokines.
Subject Added Entry-Topical Term  
Inflammation.
Subject Added Entry-Topical Term  
Disease prevention.
Subject Added Entry-Topical Term  
Medical imaging.
Subject Added Entry-Topical Term  
Debridement.
Subject Added Entry-Topical Term  
Ligaments.
Subject Added Entry-Topical Term  
Homeostasis.
Subject Added Entry-Topical Term  
Fibroblasts.
Subject Added Entry-Topical Term  
Collagen.
Subject Added Entry-Topical Term  
Connective tissue.
Subject Added Entry-Topical Term  
Microbiota.
Subject Added Entry-Topical Term  
Gum disease.
Subject Added Entry-Topical Term  
Three dimensional imaging.
Subject Added Entry-Topical Term  
Statistical significance.
Subject Added Entry-Topical Term  
Pathogenesis.
Subject Added Entry-Topical Term  
Enzymes.
Subject Added Entry-Topical Term  
Dental plaque.
Subject Added Entry-Topical Term  
Cellular biology.
Subject Added Entry-Topical Term  
Dentistry.
Subject Added Entry-Topical Term  
Immunology.
Subject Added Entry-Topical Term  
Microbiology.
Subject Added Entry-Topical Term  
Pathology.
Subject Added Entry-Topical Term  
Physiology.
Subject Added Entry-Topical Term  
Surgery.
Added Entry-Corporate Name  
University of Pittsburgh.
Host Item Entry  
Dissertations Abstracts International. 85-04B.
Host Item Entry  
Dissertation Abstract International
Electronic Location and Access  
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소장사항  
202402 2024
Control Number  
joongbu:643325
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