Thesis (Ph. D.)--University of Alabama at Birmingham, 1997. / Includes bibliographical references.

Introduction. Osteoporosis is a chronic disease characterized by the loss of bone mass and the deterioration of bone micro-architecture leading to a subsequent increase in fracture risk. High-resolution peripheral quantitative computed tomography (HR-pQCT) provides non-invasive measures of bone micro-architecture and strength in live humans but its ability to monitor small skeletal changes is yet poorly understood. The objectives of this thesis were to 1) determine HR-pQCT precision for volumetric density, geometry, cortical and trabecular micro-architecture, as well as estimates of bone strength; 2) determine the monitoring time interval (MTI) and least significant change (LSC) metrics; and 3) to characterize annual changes in bone area, density, and micro-architecture at the distal radius and tibia using HR-pQCT in postmenopausal women. Methods. To determine precision error as well as monitoring and change metrics of the distal radius and tibia, 34 postmenopausal women (mean age 74, SD±7 years) from the Saskatoon cohort of the Canadian Multicentre Osteoporosis Study (CaMos) were measured using HR-pQCT. To characterize the annual change in bone outcomes of this same cohort, 51 women (mean age±SD: 77±7 years) were measuring at baseline and again 1 year later. Precision errors were calculated as coefficient of variation (CV% and CV%RMS). The LSC was determined from precision errors and then divided by the median annual percent changes to define MTIs for bone area, density, and micro-architecture. Repeated measures analysis of variance (ANOVA) with Bonferroni adjustment for multiple comparisons were used to characterize the mean annual change in total density, cortical perimeter, trabecular and cortical bone area, density, content, and micro-architecture. Significant changes were accepted at P<0.05. Results and Discussion. HR-pQCT precision errors were <10% for bone densitometric, geometric, and mechanical properties; while precision errors were <16% for cortical and trabecular micro-architectural outcomes. Further, the use of either automatic or modified contour methods for the dual-threshold technique for cortical micro-architectural analysis provided similar precision. Densitometric and geometric outcomes had longer monitoring times (>3 years), while micro-architecture had monitoring times of ~2 years. The observed annual changes were statistically significant for several outcomes; however, only cortical and trabecular area, as well as cortical density at the distal tibia changed beyond the LSC. Overall, thesis findings will assist design and interpretation of prospective HR-pQCT studies in postmenopausal women.

Chow, Dick Ho Kiu. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 93-103). / Abstracts in English and Chinese. / Abstract --- p.ii / Publications --- p.vii / Acknowledgement --- p.viii / Table of Contents --- p.x / List of Figures --- p.xiv / List of Tables --- p.xv / List of Abbreviations --- p.xvii / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Bone and its Cellular Components --- p.1 / Chapter 1.1.1 --- Cellular Components of Bone --- p.1 / Chapter 1.1.2 --- Macroscopic Structure --- p.4 / Chapter 1.1.3 --- Microscopic Structure --- p.4 / Chapter 1.2 --- Fracture Healing --- p.5 / Chapter 1.2.1 --- Inflammation --- p.6 / Chapter 1.2.2 --- Soft Callus Formation --- p.6 / Chapter 1.2.3 --- Hard Callus Formation --- p.7 / Chapter 1.2.4 --- Bone Remodeling --- p.7 / Chapter 1.3 --- Low Magnitude High Frequency Vibration (LMHFV) Stimulation --- p.7 / Chapter 1.3.1 --- Mechanical Stimulation --- p.10 / Chapter 1.3.2 --- Effect of LMHFV on Bone --- p.12 / Chapter 1.4 --- Osteoporosis and Osteoporotic Fractures --- p.16 / Chapter 1.4.1 --- Epidemiology of Osteoporotic Fracture --- p.17 / Chapter 1.4.2 --- Pathophysiology --- p.17 / Chapter 1.4.3 --- Osteoporotic Fracture Healing --- p.20 / Chapter 1.5 --- Bisphosphonate --- p.23 / Chapter 1.5.1 --- Background --- p.23 / Chapter 1.5.2 --- Mechanism of Action --- p.24 / Chapter 1.5.3 --- U sage of Bisphosphonate --- p.25 / Chapter 1.5.4 --- Bisphosphonate Effects on Fracture Healing --- p.27 / Chapter 1.6 --- Hypothesis --- p.27 / Chapter 1.7 --- Study Plan --- p.28 / Chapter 1.7.1 --- Objectives --- p.28 / Chapter 2 --- Method --- p.29 / Chapter 2.1 --- Ovariectomized Rat Femoral Fracture Model --- p.29 / Chapter 2.1.1 --- Ovariectomized Rat Model. --- p.29 / Chapter 2.1.2 --- Closed Femoral Fracture --- p.31 / Chapter 2.2 --- Study Design --- p.32 / Chapter 2.3 --- LMHFV Treatment Protocol --- p.32 / Chapter 2.4 --- Bisphosphonate Treatment Protocol --- p.35 / Chapter 2.4.1 --- Pharmacological Parameters --- p.35 / Chapter 2.4.2 --- Ibandronate Injection Solution Preparation --- p.37 / Chapter 2.4.3 --- Injection --- p.37 / Chapter 2.5 --- Fluorochrome Labeling --- p.38 / Chapter 2.5.1 --- Fluorochrome Preparation --- p.38 / Chapter 2.5.2 --- Injection --- p.38 / Chapter 2.6 --- Assessments --- p.39 / Chapter 2.6.1 --- Radiographic Analysis --- p.39 / Chapter 2.6.2 --- uCT Analysis --- p.40 / Chapter 2.6.3 --- Undecalcified Histology --- p.43 / Chapter 2.6.4 --- ELISA Analysis on Bone Markers --- p.47 / Chapter 2.7 --- Statistical Analysis --- p.50 / Chapter 3 --- Results --- p.51 / Chapter 3.1 --- Radiographic Analysis --- p.52 / Chapter 3.1.1 --- Callus Bridging Rate --- p.52 / Chapter 3.1.2 --- Callus Width and Area --- p.52 / Chapter 3.2 --- uCT Analysis --- p.55 / Chapter 3.3 --- Histomorphometric Analysis --- p.61 / Chapter 3.3.1 --- Bone Mineralization Rate --- p.61 / Chapter 3.4 --- Bone Markers Analysis --- p.64 / Chapter 3.4.1 --- Osteocalcin --- p.64 / Chapter 3.4.2 --- TRAP5b --- p.64 / Chapter 3.4.3 --- Summary --- p.67 / Chapter 4 --- Discussion --- p.69 / Chapter 4.1 --- LMHFV Enhanced Bone Remodeling --- p.69 / Chapter 4.1.1 --- LMHFV Reversed Bis Inhibition on Bone Remodeling --- p.70 / Chapter 4.1.2 --- LMHFV Effect on Osteoclastic Resorption During Bone Re-modeling --- p.71 / Chapter 4.2 --- Enhanced Fracture Healing by LMHFV --- p.72 / Chapter 4.2.1 --- Acceleration of Fracture Healing by LMHFV --- p.72 / Chapter 4.2.2 --- LMHFV Inhibits Osteoclast Activity in the Early Phase of Healing --- p.73 / Chapter 4.2.3 --- LMHFV Stimulates Osteoblast Activity in the Early Phase of Healing --- p.74 / Chapter 4.3 --- Bis Delays Fracture Healing --- p.75 / Chapter 4.4 --- Experimental Design --- p.78 / Chapter 4.4.1 --- Inhibition Study --- p.78 / Chapter 4.4.2 --- Bisphosphonate Injection Protocol --- p.79 / Chapter 4.4.3 --- Individual Analysis of Bone Formation and Resorption . --- p.81 / Chapter 4.5 --- Clinical Implications --- p.84 / Chapter 4.5.1 --- LMHFV Enhanced Remodeling --- p.84 / Chapter 4.5.2 --- Bisphosphonate Delayed Remodeling --- p.85 / Chapter 4.6 --- Limitations --- p.85 / Chapter 4.6.1 --- Measurement of Bone Resorption --- p.85 / Chapter 4.6.2 --- Osteoporotic Fracture Model --- p.86 / Chapter 4.6.3 --- Inhibition of Bone Remodeling --- p.87 / Chapter 4.7 --- Future Studies --- p.88 / Chapter 4.7.1 --- LMHFV Effect on Osteoclast in vitro --- p.88 / Chapter 4.7.2 --- Biomechanics of Fracture Callus --- p.89 / Chapter 4.7.3 --- LMHFV Effect on Leptin- Adrenergic Pathway --- p.89 / Chapter 5 --- Conclusion --- p.91 / Bibliography --- p.93

The present study was carried out to evaluate the osteoconductive nature of Bio-OssRTM (natural deproteinized bone mineral) when used as an onlay bone substitute in a Guided Bone Regeneration model. The lateral surface of the mandible was exposed bilaterally, in 8 rabbits. On one side of the mandible, two titanium chambers were filled with Bio-OssRTM material and the chambers were then firmly secured to the mandible using screws. The pores in the titanium chambers were covered with a layer of Bio-GideRTM material. On the opposite side of the mandible, chambers without Bio-OssRTM were placed on the lateral side of the mandible as a control. After a healing period of 3 months, histologic sections were obtained from each chamber. It was observed that new bone was generated in both test and control chambers to various degrees. In the test group, the newly generated bone was 18.41% and in the control group it was 5.31%. This difference was statistically significant. Thus, in this experiment, Bio-OssRTM was proven to be osteoconductive.

Bone remodelling is a complex process, which involves the coupling of bone formation to completed foci of bone resorption, the balance between these 2 processes determines if bone is lost or gained at a particular site. During bone resorption osteoclasts release growth factors sequestered in bone matrix, which are thought to initiate new bone formation. On the other hand, osteoblasts can regulate osteoclast activity through the expression of the counter-acting cytokines, RANKL and OPG. The aim of this project was to determine if factors released during bone resorption impact on the RANKL/OPG system or on osteoclasts directly to regulate bone remodelling. OPG secretion was characterized in a number of osteoblast-like cells and the osteosarcoma cell line MG-63 was chosen as a model for osteoblastic cell behaviour in vitro. EDTA bone extracts prepared from normal human cortical bone powder were used to treat MG-63 cells in vitro. The response to the extract was dependent on the purification procedure used. OPG production was inhibited by partially purified extracts prepared using hydrophobic interaction chromatography, C18 SPE. In comparison extracts prepared using size exclusion centrifugal filters stimulated OPG secretion in confluent MG-63 cells. Therefore bone matrix constituents were able to influence osteoclast activity directly and indirectly through the osteoblastic cells to produce the same response. The simplest mechanism for this co-ordinated response would be the presence of one factor in the extract that is able to influence both osteoblasts and osteoclasts. The identity of the factor responsible for the opposing effects seen in the bone matrix extracts is at the moment unknown. The work presented in this thesis clearly demonstrated that unknown growth factors present in bone matrix influence bone remodelling.

Thesis (Ph. D.)--School of Dentistry. University of Missouri--Kansas City, 2003. / "A dissertation in oral biology and molecular biology and biochemistry." Advisor: Jian Q. Feng. Typescript. Vita. Title from "catalog record" of the print edition Description based on contents viewed July 16, 2008. Includes bibliographical references (leaves 109-121). Online version of the print edition.

Akademisk avhandling--Universitetet i Göteborg. / Extra t.p., with thesis statement, inserted. Bibliography: p. 88-95.

Thesis (Ph. D.)--University of Lund, 1995. / Published dissertation.

Thesis (Ph. D.)--University of Lund, 1995. / Published dissertation.

Abstract A new animal model was developed to evaluate the effect of bovine native bone morphogenetic protein (BMP) on the healing of segmental, critical-sized bone defects. Laboratory-bred adult beagle dogs were used in the study. A 2 cm corticoperiosteal defect was created using an oscillating saw in mid-ulna, and the defect was treated with bone grafts and implants fixed by an intramedullary Kirschner wire through predrilled holes in the middle of the implant. Plate and screw fixation was also used in some groups. Coral, hydroxyapatite and demineralized xenograft bone were placed in the defects with or without BMP. Autografts and allografts were used as controls. The BMP was extracted from bovine diaphyseal bone. The follow-up period was 36 weeks. Radiographs were taken at regular intervals during the follow-up period, and bone formation and bone union were evaluated. The radiographs were digitized, and callus was measured and CT scans obtained to define bone density. At the end of the study, the bones were harvested and tested mechanically in a torsion machine until failure. After mechanical testing, the bones were reconstructed and histological sections were made. With autograft and allograft bone grafts, healing was nearly complete. Hydroxyapatite and demineralized xenograft bone did not result in healing of the bone defect, while coral enhanced bone formation, but the healing was not comparable to autografts or allografts. Hydroxyapatite implants did not resorb during the 36 weeks of follow-up to enhance bone healing, and there was a fibrous capsule around the hydroxyapatite implants in histology. Xenograft bone was resorbed, and very little bone formation and extensive fibrosis were seen at the implant site. Coral was resorbed and gradually replaced by new bone, but did not heal the defect completely. With every implant, added BMP had a positive effect on healing as evaluated either radiographically, mechanically or histologically. Coral was the most optimal carrier material for BMP among the materials tested in this study. The animal model seems to be suitable for studying the healing of bone defects, as all the animals were physically active from the first postoperative day and did not seem to have problems with motion during the follow-up period. Intramedullary fixation lacks rotational stability, which may have a negative effect on healing. The bones fixed with a plate and screws showed better scores in radiographs and were mechanically stronger, although the study groups were too small to allow definitive conclusions. As a conclusion, none of the transplants or implants were equally efficient as cortical autograft in healing segmental ulnar defects. BMP did not enhance the poor capacity of hydroxyapatite and xenograft bone to heal the bone defect. According to the present findings, the composite implant consisting of coral and BMP seemed to be the best of the composite implants tested.