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dc.contributor.authorTsatsas, Dmitris V.en_US
dc.date.accessioned2020-03-04T17:22:42Z
dc.date.available2020-03-04T17:22:42Z
dc.date.issued2006
dc.date.submitted2006
dc.identifier.other(OCoLC)70657935
dc.identifier.otherb26819843
dc.identifier.urihttps://hdl.handle.net/2144/39764
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 Goldman School of Dental Medicine, 2006 (Oral Biology)en_US
dc.descriptionIncludes bibliographic references : (leaves 56-69).en_US
dc.description.abstractIt is well known that patients with diabetes type I exhibit significant problems with fracture healing due to delayed or inadequate bone formation. We tested the hypothesis that diabetes impairs the healing process by delaying or inhibiting chondrocyte apoptosis, thereby interfering with the conversion of cartilage to bone in the fracture callus. Chondrocyte apoptosis was examined in two groups of CD1 mice; the experimental group was rendered diabetic by multiple low dose strepozotocin treatment, which induces diabetes via an autoimmune response in the pancreas, and the control group was treated with vehicle alone, citrate buffer. A previously validated method was used to produce standardized tibial fractures and mice were sacrificed at 12, 16 and 22 days post-fracture. Samples were prepared for histomorphometric analysis. New bone, cartilage and chondroclast formation were determined using Van Gieson, Saffranin-O and TRAP staining, respectively. The TUNEL assay together with Saffranin-O staining was used to detect apoptotic chondrocytes, which were normalized per cartilage area. The center of the fracture callus was determined with the use of H&E stain and radiographically, and all measurements were made for the center of the fracture. There was 10-fold lower new bone formation in the diabetic group on day 12 compared to non-diabetic controls (p[less than]0.05). Although not as marked, less new bone formation was also found in the diabetic group on day 22 (p[less than]0.05). In contrast, on day 12 cartilage formation was similar between the two groups (p[more than]0.05), whereas on day 16 the diabetic group demonstrated about 50% less cartilage and this difference was significant (p[less than]0.05). Chondroclast number on day 12 was about 2.5-fold greater in the diabetic group (p[less than]0.05), possibly explaining the decreased amount of cartilage on day 16. Most interestingly, the number of apoptotic chondrocytes was 4-fold lower (p[less than]0.05) in the diabetic group for both days 12 and 16. These results indicate that diabetes may affect fracture healing by increased formation of chondroclasts and diminished apoptosis of chondrocytes, consistent with delayed and diminished conversion of cartilage to bone.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.subjectDiabetes mellitus, type 1en_US
dc.subjectFracture healingen_US
dc.subjectOsteoclastsen_US
dc.titleImpaired fracture healing in diabetes may be due to increased osteoclast activityen_US
dc.typeThesis/Dissertationen_US
etd.degree.nameMaster of Science in Dentistryen_US
etd.degree.levelmastersen_US
etd.degree.disciplineOral Biologyen_US
etd.degree.grantorBoston Universityen_US


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