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dc.contributor.authorKyritsis, Georgeen_US
dc.date.accessioned2019-12-16T15:55:07Z
dc.date.available2019-12-16T15:55:07Z
dc.date.issued1999
dc.date.submitted1999
dc.identifier.other(OCoLC)43728918
dc.identifier.otherb22703706
dc.identifier.urihttps://hdl.handle.net/2144/38940
dc.descriptionPLEASE NOTE: This work is protected by copyright. Downloading is restricted to the BU community: please click Download and log in with a valid BU account to access. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.en_US
dc.descriptionThesis (M.Sc.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 1999.en_US
dc.descriptionIncludes bibliographical references (leaves 41-59).en_US
dc.description.abstractTwenty wild type mice were given a local calvarial injection of 500 [mega]g of E. Coli LPS in 100[mega]l of 9% saline solution and were sacrificed at the following time intervals: day 2, day 5, day 9 and day 14. All the specimens were sectioned, stained, and analysed histomoaphometrically. Osteoclast index and osteoclast surface were the 2 parameters used to assess the amount of bone resorption. Our results show that a single dose of LPS can induce bone resorption by stimulating the production of osteoclasts. The 5 day time point was shown to be the optimum moment at which active murine bone resorption peaks following endotoxin stimulation. To assess the role that IL-1[Beta] plays in LPS induced bone resorption, I.C.E (Interleukin-1[Beta] converting enzyme) mutant mice and their respective wild type were injected with Porphyromonas gingivalis(P.g.) LPS. Two different concentrations of LPS were used: 500[mega]g and 100[mega]g. The mice were sacrificed 5 days following the injection of LPS and the osteoclast response was compared histopathologically between the 4 groups. Our results showed a significant decrease in osteoclast index and osteoclast surface in the IL-1[Beta] deficient mice (ICE (-/-)) compared to the wild type at the 500[mega]g LPS concentration group. (p [less than]0.01). The amount of bone resorption was inhibited by 37%. However, in the 100[mega]g LPS injected group there was no significant difference in bone resorption between ICE (-/-) mice and their wild type littermates. These results suggest that at high concentrations of endotoxin, IL-1[Beta] is a potent in-vivo mediator of the osteolytic properties of LPS. The decrease in bone resorption observed in the mutant mice is associated with a reduction in osteoclastogenesis. At lower doses of endotoxin, IL-1[Beta] activity in LPS induced bone resorption may not be as predominant as that of other mediators.en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.rightsThis work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.en_US
dc.subjectBone resorptionen_US
dc.subjectInterleukin-1.en_US
dc.subjectLipopolysaccharidesen_US
dc.titleIL-1B activity partially mediates LPS-induced calvarial bone resorptionen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameMaster of Science in Dentistryen_US
etd.degree.levelmastersen_US
etd.degree.disciplinePeriodontology and Oral Biologyen_US
etd.degree.grantorBoston Universityen_US


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