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dc.contributor.authorKuo, David Da-Weien_US
dc.date.accessioned2019-12-16T15:54:56Z
dc.date.available2019-12-16T15:54:56Z
dc.date.issued2005
dc.date.submitted2005
dc.identifier.other(OCoLC)63200122
dc.identifier.otherb26130865
dc.identifier.urihttps://hdl.handle.net/2144/38938
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 (MSD)--Boston University, Henry M. Goldman School of Dental Medicine, 2005 (Periodontics).en_US
dc.descriptionIncludes bibliographical references: leaves 55-74.en_US
dc.description.abstractOral microorganisms plays a significant role in the initiation and progression of periodontal disease, which is characterized by gingival inflammation, alveolar bone destruction and eventual tooth loss. A mouse calvaria model was used to study bone changes in vivo due to infection with P. gingivalis, one of the most common bacteria associated with chronic periodontitis. This study examined the effect of sequential infection with P. gingivalis on osteoclast activity. Mice were separated into different groups and then injected with P. gingivalis into the scalp area at two time points (day 0 and day 5) to mimic sequential infection. All animals were sacrificed at day 8 and calvaria bone was examined histologically. We found that the animals with two bacterial injections had a significant decrease in osteoclast number compared to the animals with only a single injection. New bone formation measured at day 8 showed a similar result, with less new bone formation in the animals with the double injection. The results indicate that the second dose of bacteria dampens the ongoing osteoclast activity and new bone formation. It seems likely that the repeat infectious challenge recapitulates the early inflammation phase of wound healing, and turns off/down the later repair signals. These results have impact on understanding the complex interplay between microbial pathogens and host responses in periodontal disease. Moreover, our model system, although simple, allowed us to test the notion that the continuous presence of bacterial pathogen within periodontal pockets leads to superimposed acute and chronic immune responses.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.subjectWound healingen_US
dc.subjectPorphyromonas gingivalisen_US
dc.titleReinfection of mouse calvaria with porphyromonas gingivalis during the proliferative phase of would healing dampens repair processes in boneen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameMaster of Science in Dentistryen_US
etd.degree.levelmastersen_US
etd.degree.disciplinePeriodonticsen_US
etd.degree.grantorBoston Universityen_US


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