Tetracycline Double Labelling Tracing Investigation for In Vivo Osteogenetic Course of PDLLA/HA Composite

2011 ◽  
Vol 685 ◽  
pp. 394-398
Author(s):  
Xin Yu Wang ◽  
Xue Zhi Shan ◽  
Yin Chao Han ◽  
Shi Pu Li
Keyword(s):  
Bone Formation ◽  
Early Stage ◽  
Dynamic Balance ◽  
Formation Rate ◽  
Double Labelling ◽  
Image Analysis System ◽  
Bone Formation Rate ◽  
Calculation Results ◽  
Analysis System

The PDLLA(DL-Poly lactic acids)/HA(Hydroxyapatite) composite and pure PDLLA control were implanted in bone for test. Using fluorescent pictures of tetracycline double label and advanced image analysis system, the trend of bone-formation rate for the implanting region of PDLLA/HA composite was obtained via morphometry measurement of the slices labeled with tetracycline. The investigation and calculation results show that, the formation rate of new bone is stable and high (reaches 2.044μm/day) in the early stage of implantation for the PDLLA/HA composite, demonstrating the advantageous capability of bone formation for the composite. The formation rate of new bone seems to decrease continuously with time, and then the bone formation and bone decomposition tend towards equilibration. Namely, the dynamic balance of bony tissue’s metabolism is maintained.

IGF-binding protein-5 stimulates osteoblast activity and bone accretion in ovariectomized mice

2001 ◽  
Vol 281 (2) ◽  
pp. E283-E288 ◽  
Author(s):  
Dennis L. Andress
Keyword(s):  
Bone Formation ◽  
Binding Protein ◽  
Formation Rate ◽  
Bone Matrix ◽  
Secretory Protein ◽  
Mineral Density ◽  
Bone Formation Rate ◽  
Ovariectomized Mice ◽  
Osteoblast Activity

Insulin-like growth factor binding protein-5 (IGFBP-5) is an osteoblast secretory protein that becomes incorporated into the mineralized bone matrix. In osteoblast cultures, IGFBP-5 stimulates cell proliferation by an IGF-independent mechanism. To evaluate whether IGFBP-5 can stimulate osteoblast activity and enhance bone accretion in a mouse model of osteoblast insufficiency, daily subcutaneous injections of either intact [IGFBP-5 (intact)] or carboxy-truncated IGFBP-5 [IGFBP-5-(1–169)] were given to ovariectomized (OVX) mice for 8 wk. Femur and spine bone mineral density (BMD), measured every 2 wk, showed early and sustained increases in response to IGFBP-5. Bone histomorphometry of cancellous bone showed significant elevations in the bone formation rate in both the femur metaphysis [IGFBP-5- (1)] only) and spine compared with OVX controls. IGFBP-5 also stimulated osteoblast number in the femur IGFBP-5-(1–169) only) and spine. These data indicate that IGFBP-5 effectively enhances bone formation and bone accretion in OVX mice by stimulating osteoblast activity. The finding that IGFBP-5-(1–169) is bioactive in vivo indicates that the carboxy-terminal portion is not required for this bone anabolic effect.

1,25(OH)2D3 acts as a bone-forming agent in the hormone-independent senescence-accelerated mouse (SAM-P/6)

2005 ◽  
Vol 288 (4) ◽  
pp. E723-E730 ◽  
Author(s):  
Gustavo Duque ◽  
Michael Macoritto ◽  
Natalie Dion ◽  
Louis-Georges Ste-Marie ◽  
Richard Kremer
Keyword(s):  
Bone Formation ◽  
Bone Turnover ◽  
Bone Marrow Cells ◽  
Formation Rate ◽  
Mineral Density ◽  
Bone Formation Rate ◽  
Senile Osteoporosis ◽  
Dihydroxyvitamin D ◽  
Bone Formation Markers

Recent studies suggest that vitamin D signaling regulates bone formation. However, the overall effect of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] on bone turnover in vivo is still unclear. In this study, our aim was to examine the effect of 1,25(OH)2D3 on bone turnover in SAM-P/6, a hormone-independent mouse model of senile osteoporosis characterized by a decrease in bone formation. Male and female 4-mo-old SAM-P/6 mice were treated with 1,25(OH)2D3 (18 pmol/24 h) or vehicle for a period of 6 wk, and a group of age- and sex-matched nonosteoporotic animals was used as control. Bone mineral density (BMD) at the lumbar spine increased rapidly by >30 ± 5% ( P < 0.001) in 1,25(OH)2D3-treated SAM-P/6 animals, whereas BMD decreased significantly by 18 ± 2% ( P < 0.01) in vehicle-treated SAM-P/6 animals and remained stable in control animals during the same period. Static and dynamic bone histomorphometry indicated that 1,25(OH)2D3 significantly increased bone volume and other parameters of bone quality as well as subperiosteal bone formation rate compared with vehicle-treated SAM-P/6 mice. However, no effect on trabecular bone formation was observed. This was accompanied by a marked decrease in the number of osteoclasts and eroded surfaces. A significant increase in circulating bone formation markers and a decrease in bone resorption markers was also observed. Finally, bone marrow cells, obtained from 1,25(OH)2D3-treated animals and cultured in the absence of 1,25(OH)2D3, differentiated more intensely into osteoblasts compared with those derived from vehicle-treated mice cultured in the same conditions. Taken together, these findings demonstrate that 1,25(OH)2D3 acts simultaneously on bone formation and resorption to prevent the development of senile osteoporosis.

The anabolic effect of 17β-oestradiol on the trabecular bone of adult rats is suppressed by indomethacin

1992 ◽  
Vol 133 (2) ◽  
pp. 189-195 ◽  
Author(s):  
J. W. M. Chow ◽  
J. M. Lean ◽  
T. Abe ◽  
T. J. Chambers
Keyword(s):  
Bone Formation ◽  
Trabecular Bone ◽  
Bone Growth ◽  
Formation Rate ◽  
Bone Volume ◽  
Female Rats ◽  
Mineral Apposition Rate ◽  
Adult Rats ◽  
Bone Formation Rate

ABSTRACT We have previously demonstrated that administration of oestrogen, at doses sufficient to raise serum concentrations to those seen in late pregnancy, increases trabecular bone formation in the metaphysis of adult rats. To determine whether prostaglandins (PGs), which have been shown to induce osteogenesis in vivo, play a role in the induction of bone formation by oestrogen, 13-week-old female rats were given daily doses of 4 mg 17β-oestradiol (OE2)/kg for 17 days, alone or with indomethacin (1 mg/kg). The rats were also given double fluorochrome labels and at the end of the experiment tibias were subjected to histomorphometric assessment. Treatment with OE2 suppressed longitudinal bone growth and increased uterine wet weight, as expected, and neither response was affected by indomethacin. Oestrogen also induced a threefold increase in trabecular bone formation in the proximal tibial metaphysis, which resulted in a substantial increase in trabecular bone volume. As previously observed, the increase in bone formation was predominantly due to an increase in osteoblast recruitment (as judged by an increase in the percentage of bone surface showing double fluorochrome labels), with only a minor increase in the activity of mature osteoblasts (as judged by the mineral apposition rate). Indomethacin abolished the increase in osteoblastic recruitment, but the activity of mature osteoblastic cells remained high. The bone formation rate and bone volume remained similar to controls. The results suggest that PG production may be necessary for the increased osteoblastic recruitment induced by oestrogen, but not to mediate the effects of oestrogen on the activity of mature osteoblasts. Journal of Endocrinology (1992) 133, 189–195

scholarly journals CD13 is a Critical Regulator of Cell-cell Fusion in Osteoclastogenesis

2020 ◽  
Author(s):  
Mallika Ghosh ◽  
Ivo Kalajzic ◽  
Hector Leonardo Aguila ◽  
Linda H Shapiro
Keyword(s):  
Bone Marrow ◽  
Bone Formation ◽  
Progenitor Cells ◽  
Cell Fusion ◽  
Formation Rate ◽  
Giant Cells ◽  
Bone Formation Rate ◽  
Cell Cell

AbstractIn vertebrates, bone formation is dynamically controlled by the activity of two specialized cell types: the bone-generating osteoblasts and bone-degrading osteoclasts. Osteoblasts produce the soluble receptor activator of NFκB ligand (RANKL) that binds to its receptor RANK on the surface of osteoclast precursor cells to promote osteoclastogenesis, a process that involves cell-cell fusion and assembly of molecular machinery to ultimately degrade the bone. CD13 is a transmembrane aminopeptidase that is highly expressed in cells of myeloid lineage has been shown to regulate dynamin-dependent receptor endocytosis and recycling and is a necessary component of actin cytoskeletal organization. In the present study, we show that CD13-deficient mice display a normal distribution of osteoclast progenitor populations in the bone marrow, but present a low bone density phenotype. Further, the endosteal bone formation rate is similar between genotypes, indicating a defect in osteoclast-specific function in vivo. Loss of CD13 led to exaggerated in vitro osteoclastogenesis as indicated by significantly enhanced fusion of bone marrow-derived multinucleated osteoclasts in the presence of M-CSF and RANKL, resulting in abnormally large cells with remarkably high numbers of nuclei with a concomitant increase in bone resorption activity. Similarly, we also observed increased formation of multinucleated giant cells (MGC) in CD13KO bone marrow progenitor cells stimulated with IL-4 and IL-13, suggesting that CD13 may regulate cell-cell fusion events via a common pathway, independent of RANKL signaling. Mechanistically, while expression levels of the fusion-regulatory proteins dynamin and DC-STAMP are normally downregulated as fusion progresses in fusion-competent mononucleated progenitor cells, in the absence of CD13 they are uniformly sustained at high levels, even in mature multi-nucleated osteoclasts. Taken together, we conclude that CD13 may regulate cell-cell fusion by controlling expression and localization of key fusion proteins that are critical for both osteoclast and MGC fusion.

scholarly journals Combinatorial morphogenetic and mechanical cues to mimic bone development for defect repair

2019 ◽  
Vol 5 (8) ◽  
pp. eaax2476 ◽  
Author(s):  
S. Herberg ◽  
A. M. McDermott ◽  
P. N. Dang ◽  
D. S. Alt ◽  
R. Tang ◽  
...  
Keyword(s):  
Bone Formation ◽  
Transforming Growth Factor ◽  
Bone Development ◽  
Formation Rate ◽  
Natural Fracture ◽  
Bone Morphogenetic Protein 2 ◽  
Long Bone ◽  
Bone Formation Rate ◽  
Tgf Β1

Endochondral ossification during long bone development and natural fracture healing initiates by mesenchymal cell condensation, directed by local morphogen signals and mechanical cues. Here, we aimed to mimic development for regeneration of large bone defects. We hypothesized that engineered human mesenchymal condensations presenting transforming growth factor–β1 (TGF-β1) and/or bone morphogenetic protein-2 (BMP-2) from encapsulated microparticles promotes endochondral defect regeneration contingent on in vivo mechanical cues. Mesenchymal condensations induced bone formation dependent on morphogen presentation, with BMP-2 + TGF-β1 fully restoring mechanical function. Delayed in vivo ambulatory loading significantly enhanced the bone formation rate in the dual morphogen group. In vitro, BMP-2 or BMP-2 + TGF-β1 initiated robust endochondral lineage commitment. In vivo, however, extensive cartilage formation was evident predominantly in the BMP-2 + TGF-β1 group, enhanced by mechanical loading. Together, this study demonstrates a biomimetic template for recapitulating developmental morphogenic and mechanical cues in vivo for tissue engineering.

Increased bone formation in rat tibiae after a single short period of dynamic loading in vivo

1996 ◽  
Vol 270 (3) ◽  
pp. E419-E423 ◽  
Author(s):  
M. R. Forwood ◽  
I. Owan ◽  
Y. Takano ◽  
C. H. Turner
Keyword(s):  
Bone Formation ◽  
Formation Rate ◽  
Maximal Response ◽  
Response Relationship ◽  
Bone Formation Rate ◽  
Stimulus Response ◽  
Threshold Response ◽  
Short Period ◽  
Single Bout

Based on our quantum concept for mechanically adaptive bone formation, we hypothesized that a single bout of loading would increase bone formation at the endosteal surface in rat tibiae, with a maximal response 4-8 days after loading and a stimulus-response relationship for load magnitude. Bending loads were applied to right tibiae of rats at 31, 43, 53, or 65 N for a single bout of 36 or 360 cycles; bone formation was assessed 1-4, 5-8, or 9-12 days after loading. A single loading episode increased lamellar bone formation rate (BFR) in all groups (P<0.05) and was maximal 5-8 days after loading. A distinct dose-response relationship was not evident among all load magnitudes or for duration, but 65 N was significantly more osteogenic than loads of 31-53 N (P<0.05), consistent with a threshold response to loading. There was also evidence for a significant increase in BFR (P<0.05) and double-labeled surface (P<0.01) within 4 days of loading, suggesting that bone-lining cells were activated directly by the stimulus. Thus subtle changes in BFR may occur by modulating the activity of surface cells, but large modeling drifts and anabolic responses require recruitment and differentiation of osteoprogenitor cells near the bone surface.

scholarly journals Nck influences preosteoblastic/osteoblastic migration and bone mass

2015 ◽  
Vol 112 (50) ◽  
pp. 15432-15437 ◽  
Author(s):  
Smriti Aryal A.C ◽  
Kentaro Miyai ◽  
Yayoi Izu ◽  
Tadayoshi Hayata ◽  
Takuya Notomi ◽  
...  
Keyword(s):  
Cell Migration ◽  
Bone Formation ◽  
Bone Mass ◽  
Formation Rate ◽  
Osteoblastic Cell ◽  
Bone Formation Rate ◽  
Double Deletion ◽  
Osteoblastic Lineage ◽  
Bone Injury

Migration of the cells in osteoblastic lineage, including preosteoblasts and osteoblasts, has been postulated to influence bone formation. However, the molecular bases that link preosteoblastic/osteoblastic cell migration and bone formation are incompletely understood. Nck (noncatalytic region of tyrosine kinase; collectively referred to Nck1 and Nck2) is a member of the signaling adaptors that regulate cell migration and cytoskeletal structures, but its function in cells in the osteoblastic lineage is not known. Therefore, we examined the role of Nck in migration of these cells. Nck is expressed in preosteoblasts/osteoblasts, and its knockdown suppresses migration as well as cell spreading and attachment to substrates. In contrast, Nck1 overexpression enhances spreading and increases migration and attachment. As for signaling, Nck double knockdown suppresses migration toward IGF1 (insulin-like growth factor 1). In these cells, Nck1 binds to IRS-1 (insulin receptor substrate 1) based on immunoprecipitation experiments using anti-Nck and anti–IRS-1 antibodies. In vivo, Nck knockdown suppresses enlargement of the pellet of DiI-labeled preosteoblasts/osteoblasts placed in the calvarial defects. Genetic experiments indicate that conditional double deletion of both Nck1 and Nck2 specifically in osteoblasts causes osteopenia. In these mice, Nck double deficiency suppresses the levels of bone-formation parameters such as bone formation rate in vivo. Interestingly, bone-resorption parameters are not affected. Finally, Nck deficiency suppresses repair of bone injury after bone marrow ablation. These results reveal that Nck regulates preosteoblastic/osteoblastic migration and bone mass.

Human parathyroid hormone(1–34) increases bone formation and strength of cortical bone in aged rats

1994 ◽  
Vol 130 (2) ◽  
pp. 201-207 ◽  
Author(s):  
Charlotte Ejersted ◽  
Troels T Andreassen ◽  
Magnus HL Nilsson ◽  
Hans Oxlund
Keyword(s):  
Parathyroid Hormone ◽  
Bone Formation ◽  
Cortical Bone ◽  
Formation Rate ◽  
The Body ◽  
Male Rats ◽  
Double Labelling ◽  
Aged Rats ◽  
Human Parathyroid Hormone ◽  
Bone Formation Rate

Ejersted C, Andreassen TT, Nilsson MHL, Oxlund H. Human parathyroid hormone(1–34) increases bone formation and strength of cortical bone in aged rats. Eur J Endocrinol 1994;130:201–7. ISSN 0804–4643 The effect of parathyroid hormone (PTH(1–34)) on mid-diaphyseal femoral cortical bone was studied in 2-year-old male rats. The rats were treated with daily injections of 1 5 nmol/kg PTH(1–34) or vehicle for 56 days, and labelled with tetracycline and calcein on day 15 and day 40, respectively. The PTH(1–34) treatment did not affect the body weights or the lengths of the femora. Fluorescence microscopy showed large intracortical cavities in the old vehicle-treated rats. After PTH treatment, double labelling and new bone formation filling in these cavities were found. Furthermore, an increased bone formation rate was observed both at the periosteum and at the endosteum. This resulted in an increase in the cross-sectional area and a decrease in the medullary area. Three-point bending analysis revealed an increase in ultimate load, ultimate stiffness, energy absorption and ultimate stress after the PTH(1–34) treatment. No differences were found between the groups regarding the hydroxyproline concentration or apparent and real densities. The ash concentration was, however, slightly reduced after PTH(1–34) treatment. The PTH(1–34) treatment of old rats induced the formation of bone both from the periosteum and endosteum, with a pronounced filling in of intracortical cavities, and, furthermore, a marked increase in the biomechanical competence of the cortical bone. Charlotte Ejersted, Department of Connective Tissue Biology, Institute of Anatomy, University of Aarhus, DK-8000 Aarhus C. Denmark

scholarly journals May Autogenous Grafts Increase the Effectiveness of Hyalonect Membranes in Intraosseous Defects: An Experimental In Vivo Study

Medicina ◽  
2021 ◽  
Vol 57 (5) ◽  
pp. 430
Author(s):  
Caner Yilmaz ◽  
Selim Ersanli ◽  
Murat Karabagli ◽  
Vakur Olgac ◽  
Nilufer Bolukbasi Balcioglu
Keyword(s):  
Bone Formation ◽  
Formation Rate ◽  
Autogenous Bone ◽  
Control Group ◽  
Collagen Membrane ◽  
New Bone Formation ◽  
Bone Formation Rate ◽  
The Third ◽  
Autogenous Grafts

Background and Objectives: Guided bone regeneration (GBR) surgeries are used for dental implant placements with insufficient bone volume. Biomaterials used in GBR are expected to produce sufficient volume and quality of bone swiftly. This study aims to histologically evaluate the effectiveness of the use of Hyalonect membranes alone or with autogenous grafts in intraosseous defects. Materials and Methods: This study is an experimental study on sheep. Surgeries were performed under general anesthesia in accordance with ethical rules. Five 10 mm defects were surgically created in each ilium of six sheep. One defect was left empty in each ilium (group ED). The defects in the experimental group were covered with Hyalonect membrane while unfilled (group HY) or after being filled with autogenous bone grafts (ABG) (group G+HY). In the control group, the defects were either covered with collagen membrane while unfilled (group CM) or after being filled with the ABG group (G+CM). The sheep were histologically and histomorphometrically evaluated after being postoperatively sacrificed in the third and sixth week (three animals in each interval). Results: All animals completed the study without any complications. No difference was found between groups in the third and sixth weeks regarding the inflammation, necrosis, and fibrosis scores. The G+CM (52.83 ± 3.06) group was observed to have a significantly higher new bone formation rate than all the other groups in the third week, followed by the G+HY group (46.33 ± 2.25). Similar values were found for HY and CM groups (35.67 ± 4.55 ve 40.00 ± 3.41, respectively, p = 0.185), while the lowest values were observed to be in group ED (19.67 ± 2.73). The highest new bone formation was observed in group G+CM (82.33 ± 4.08) in the sixth week. There was no difference in new bone formation rates between groups G+CM, G+HY (77.17 ± 3.49, p = 0.206), and CM (76.50 ± 2.43, p = 0.118). The insignificant difference was found ED group and group HY (55.83 ± 4.92, 73.50 ± 3.27, respectively, p = 0.09). The residual graft amount in the G+CM group was found to be statistically significant at 3 weeks (p = 0.0001), compared to the G+HY group, and insignificantly higher at the 6th week (p = 0.4). Conclusions: In this study, close values were observed between G+HY and G+CM groups. Further experimental and clinical studies with different graft materials are required to evaluate the effectiveness of HY in GBR.

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