Thesis (Ph. D.)--University of Minnesota, 1970. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 159-170).

Thesis (doctoral)--University of Oslo, 1980. / Includes reprints of 7 papers by author.

Thesis (Ph. D.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on September 28, 2007) Vita. Includes bibliographical references.

Orientadores: Sérgio Roberto Peres Line, Alexandre Augusto Zaia / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba / Made available in DSpace on 2018-08-19T14:41:36Z (GMT). No. of bitstreams: 1 Frozoni_MarcosRobertodosSantos_D.pdf: 22284992 bytes, checksum: f3df32a5434f64642e63697df5e27202 (MD5) Previous issue date: 2011 / Resumo: Na polpa saudável, os odontoblastos pós-mitóticos responsáveis pela secreção de dentina primária e secundária sobrevivem durante a toda a vida do dente e são responsáveis pelas respostas às injúrias externas através da produção de dentina terciária focalmente abaixo do local da agressão. Os odontoblastos sobreviventes à injúria secretam uma matriz de dentina reacional, entretanto, os irreversivelmente danificados, são substituídos por uma segunda geração de células com as mesmas características morfofisiológicas. Estas células são derivadas do recrutamento, proliferação e diferenciação de células pulpares que possuam propriedades de células tronco, para formar uma nova matriz de dentina reparativa como parte do processo de reparo do complexo dentino pulpar. O mecanismo de reparo que segue após uma injúria dental é fundamental para a sobrevivência da polpa e envolve uma série de processos que precisam ser completamente esclarecidos mais precisamente a origem das células precursoras da nova geração de odontoblastos que irão secretar dentina reparativa. Embora evidências sugiram que esta nova geração de odontoblastos tenha origem de células do tecido conjuntivo pulpar, a exata origem destas células ainda não está completamente esclarecida. O objetivo deste estudo foi utilizar camundongos transgênicos que expressam green fluorecent protein (GFP) em todas as células do corpo, com exceção dos eritrócitos, e a técnica cirúrgica de parabiose para unir dois camundongos isogênicos, um GFP e outro não-GFP de maneira a formar um par parabiótico, que possa compartilhar a mesma circulação sanguínea cruzada (células marcadas do camundongo GFP passam para a corrente circulatória do camundongo não-GFP). Após a parabiose foi realizada uma exposição pulpar, devidamente capeada, nos molares dos camundongos não-GFP para estimular a produção de dentina terciária reparativa e conseqüentemente a diferenciação de novos odontoblastos. Os animais foram sacrificados e os molares dos camundongos não-GFP, processados para análise em microscopia de fluorescência. Foi observada a presença de células GFP (células verdes ao microscópio de fluorescência), originárias do sangue periférico (SP) de camundongos GFP, participando do processo de dentinogênese reparativa nos molares de camundongos não-GFP. Este estudo sugere a primeira evidência da participação de células troco mesenquimais do sangue periférico (CTM-SP) no processo de diferenciação de novos odontoblastos durante a dentinogênese reparativa / Abstract: In the healthy pulp, the post-mitotic odontoblasts responsible for secretion of primary and secondary dentin survives during the tooth life and are able to respond to injuries with the production of tertiary dentin focally beneath the site of the injury. If the odontoblast survives the injury it secrets a reactionary dentin matrix but if it is irreversibly damaged, it is replaced by a second generation of odontoblast-like cells, with the same morphophysiological profile. Those cells are derived from recruitment, proliferation, and differentiation of pulp cells, which can have stem cell properties to form a new reparative dentin matrix as part of repair process in the dentin-pulp organ. The repair mechanism that follows a tooth injury is critical to the pulp survival and involves a series of processes that need to be completely understood more precisely the origin of the odontoblast-like cells that will secrete reparative dentin. Although evidences suggesting that odontoblast-like cells originate from cells within dental pulp connective tissue the exact origin of these odontoblast-like cells is not clearly defined. The aim of this study was to use transgenic mice expressing green fluorescent protein (GFP) in all body cells except erythrocytes and parabiosis surgical technique for joining two inbred mice, a GFP and other non-GFP to form one parabiotic pair, who can share the same cross-circulation (labeled cells from GFP mice move into the bloodstream of non-GFP mice After parabiosis a pulp exposure, properly capped, was performed on the molar of the recipient non-GFP mice to stimulate the production of tertiary reparative dentin and hence differentiation of odontoblastlike cells. The animals were sacrificed and the molars of the non-GFP mice processed for fluorescence microscopy. It was observed the presence of GFP cells (green cells to the fluorescence microscope), originating from peripheral blood (PB) from GFP mice, participating in the reparative dentinogenesis process in the molars of non-GFP mice. This study suggests the first evidence of the participation of mesenchymal stem cells from PB (MSC-PB) in the differentiation process of odontoblast-like cells during reparative dentinogenesis / Doutorado / Endodontia / Doutor em Clínica Odontológica

This study evaluated the potential toxicity, genotoxicity, and cellular uptake of various sizes and concentrations of chitosan (CS) nanoparticles cultured with normal human dental pulp cells. Normal human dental pulp cells (hDPCs) were derived from human dental pulp tissues and cultured with (50–67) nm and (318–350) nm CS-nanoparticles in concentrations of 0.1 mg/mL, 0.5 mg/mL, 1 mg/mL, 2 mg/mL, and 4 mg/mL as study groups and 0 mg/mL as a control group for time intervals of 16 hours, 24 hours, 3 days, 7 days and 14 days. Attachment efficiency and proliferation rate were assessed by measuring the optical density of crystal violet-stained cells. Cell viability was determined by the activity of mitochondrial dehydrogenase enzymes. Genotoxicity was assessed using the cytokinesis-block micronucleus method and by measuring the fluorescent intensity of phosphorylated H2AX nuclear foci. Cellular uptake was determined by tagging chitosan nanoparticles with FITC stain and then measuring the fluorescence intensity of FITC-tagged chitosan nanoparticles using a spectrophotometer. Statistical analysis was performed using chi-square, one-way ANOVA, and post-hoc Tukey tests. All concentrations of the (50–67) nm group significantly reduced attachment efficiency in comparison with control (P< 0.01) and with (318–350) nm group (p<0.01). Proliferation rate and cell viability were significantly reduced in cells exposed to various concentrations of (50-67) nm chitosan when compared to (318-350) nm group (P<0.05) and control group (P<0.05). For both size groups, higher concentrations significantly showed lower proliferation rate and cell viability when compared to lower concentration (P< 0.01). CS-nanoparticles were able to internalize hDPCs and significantly induced micronuclei, nuclear buds, and pH2AX at concentrations of 0.5 mg/mL and 2 mg/mL as compared to 0.1 mg/mL (P<0.01) and control groups (P< 0.01). At both the 0.5 mg/mL and 2 mg/mL concentrations, (50–67) nm chitosan significantly induced higher proportions of micronuclei (P= 0.001), nuclear buds (P= 0.009), and pH2AX nuclear foci (P= 0.00004) compared to (318–350) nm chitosan. In conclusion, CS-nanoparticles at sizes (50–67) nm and (318–350) nm at a concentration of (0.5–4) mg/mL internalized hDPCs and exhibited cytotoxic and genotoxic effects in dose-dependent and size-associated manners.

Indiana University-Purdue University Indianapolis (IUPUI) / A modified double-blind method of investigation was used in which the pulps of 52 monkey teeth were surgically exposed and left open to the oral environment for a period of 24 hours. One-half of the exposed pulps were treated with an antibiotic preparation and one-half with a pure starch control. The antibiotic compound consisted of erythromycin estolate 10 percent, streptomycin sulfate 10 percent, and starch q. s. as the vehicle. The teeth were extracted at 30 and 90 day intervals after treatment and histologically evaluated. Inflammation of a varying degree was observed in all of the teeth treated with either the antibiotic preparation or the starch control. However, those teeth treated with the antibiotic capping material exhibited much less inflammation than did the great majority of teeth treated with the starch control, in which abscess formation and necrosis were frequently observed. The pulps of those teeth treated with the antibiotic capping material demonstrated a decidedly more favorable reaction than did those pulps treated with the starch capping material. Calcific repair at the exposure site was not observed to be complete in any instance. The histologic findings for the antibiotic treated teeth were encouraging and warrant additional investigations of longer duration.

Over 15 million root canal treatments (RCT) are performed yearly in the United States to treat deep caries and dental pulp infection. This procedure however, removes both the diseased and healthy pulp, leading to tooth devitalization. Furthermore, RCTs are associated with a high incidence of re-infection and dentin fracture, reduced sensitivity and eventual tooth loss. Thus there is an unmet clinical need for alternative endodontic therapies that can preserve tooth vitality and ensure long term dental health. The strategy of vital endodontic therapy explored in this thesis centers on the design of a bioactive scaffold that guides host cell homing while providing antibiotic release, in effect harnessing the intrinsic repair potential of the native pulp while simultaneously eliminating residual bacteria that can cause recurrent infection. Specifically, a bioactive polyethylene glycol fibrinogen (PEG-fibrinogen) hydrogel is optimized to support host cell infiltration, maintain dental pulp cell phenotype, and enable pulp regeneration. Ciprofloxacin, a clinically relevant antibiotic for RCT, is incorporated into PEG-fibrinogen to prevent infection. The scaffold and culturing parameters optimized in vitro using either explant or a tooth slice model includes fibrinogen, poly(ethylene glycol) diacrylate (PEGDA) and photoinitiator concentration, as well as cell source and density. In addition, dose-dependent antibiotic effects on both anaerobic bacteria isolated from deep caries and healthy pulp cells are evaluated. The collective findings of this thesis demonstrate that a cell-instructive hydrogel comprised of a fibrinogen backbone and cross-linked with difunctional poly(ethylene glycol) side chains supports pulp cell viability, phenotypic morphology, and host cell migration. Furthermore, increasing pulp cell density promotes cell biosynthesis and a higher fibrinogen concentration is found to enhance collagen deposition. Photoinitiator and PEGDA concentrations have been optimized to enhance hydrogel mechanical properties and gel degradation, while supporting pulp cell phenotype. An optimal antibiotic dosage in the hydrogel has been identified that significantly reduces bacteria count from infected dental pulp without harmful side effects on dental pulp cell phenotype and host cell migration. In summary, this thesis focuses on the design of a bioactive hydrogel-based scaffold with antibiotic release that can induce dental pulp regeneration without the addition of cells and stimuli such as growth factors and minimize post-therapy infection. The innovative scaffold design strategy presented here lays the foundation for the development of vital endodontic therapy that harnesses pulp self-repair and sustains long-term tooth function.

Thesis (M.S.)--West Virginia University, 2008. / Title from document title page. Document formatted into pages; contains vii, 45 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 32-37).

Thesis (M.S.)--University of Michigan, 1982.

Thesis (M.S.)--University of Michigan, 1968.