Harnessing Inflammatory Signaling to Promote Bone Regeneration and Mitigate Joint Damage

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dc.contributor.advisorMikos, Antonios G.
dc.creatorMountziaris, Paschalia Maria
dc.date.accessioned2013-03-08T00:36:57Z
dc.date.available2013-03-08T00:36:57Z
dc.date.issued2012
dc.descriptionOnly volume 2 has been digitized.en_US
dc.description.abstractInflammatory processes are infamous for their destructive effects on tissues and joints in a variety of diseases. Within the body, inflammation is a highly regulated biological response whose purpose is to promote tissue regeneration following injury. However, in certain settings, inflammation persists and leads to progressive tissue destruction. This thesis focused on modulating inflammatory signaling in both contexts. Part I investigated the effects of a model pro-inflammatory cytokine, tumor necrosis factor-alpha (TNF-α), on the in vitro osteogenic differentiation of mesenchymal stem cells (MSCs). In contrast, Part II describes the development and in vivo evaluation of the first intra-articular controlled release system for the temporomandibular joint (TMJ), which silences inflammatory signaling and thus mitigates the painful joint damage seen in inflammatory TMJ disease. The following specific aims were addressed: (1) to determine the concentration of TNF-α that enhances in vitro osteogenic differentiation of MSCs; (2) to determine the temporal pattern of TNF-α delivery that enhances in vitro osteogenic differentiation of MSCs; (3) to determine the impact of bone-like extracellular matrix (ECM) on the concentration and temporal pattern of TNF-α delivery that enhances in vitro osteogenic differentiation of MSCs; (4) to evaluate the biocompatibility of intra-articular microparticles in the rat TMJ; (5) to develop a microparticle-based formulation for sustained release of a model anti-inflammatory small interfering ribonucleic acid (siRNA); and (6) to evaluate the therapeutic efficacy of intra-articular microparticles delivering siRNA in an animal model of TMJ inflammation. These studies led to the development of powerful strategies to rationally control inflammation to promote bone regeneration and mitigate joint damage in the setting of disease, both of which will ultimately improve the quality and specificity of therapies available in modern medicine.
dc.format.extent155 p.en_US
dc.format.mimetypeapplication/pdf
dc.identifier.callnoTHESIS BIOENG. 2012 MOUNTZIARIS
dc.identifier.citationMountziaris, Paschalia Maria. "Harnessing Inflammatory Signaling to Promote Bone Regeneration and Mitigate Joint Damage." (2012) Diss., Rice University. <a href="https://hdl.handle.net/1911/70361">https://hdl.handle.net/1911/70361</a>.
dc.identifier.digitalMountziarisPen_US
dc.identifier.urihttps://hdl.handle.net/1911/70361
dc.language.isoeng
dc.rightsCopyright is held by the author, unless otherwise indicated. Permission to reuse, publish, or reproduce the work beyond the bounds of fair use or other exemptions to copyright law must be obtained from the copyright holder.
dc.subjectHealth sciences
dc.subjectEnvironmental science
dc.subjectApplied sciences
dc.subjectInflammatory signaling
dc.subjectBone regeneration
dc.subjectJoint damage
dc.subjectTMJ disorders
dc.subjectControlled release
dc.subjectBiomedical engineering
dc.subjectPharmacy sciences
dc.titleHarnessing Inflammatory Signaling to Promote Bone Regeneration and Mitigate Joint Damage
dc.typeThesis
dc.type.materialText
thesis.degree.departmentBioengineering
thesis.degree.disciplineEngineering
thesis.degree.grantorRice University
thesis.degree.levelDoctoral
thesis.degree.nameDoctor of Philosophy
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