scholarly journals AB0087 DLX5 AND DLX6 PROMOTES THE COMMITMENT OF MSC TO OSTEOBLASTIC LINEAGE AND CORTICAL BONE FORMATION

2019 ◽  
Author(s):  
Camille Blandin ◽  
Morgane Bourmaud ◽  
Eris Hay ◽  
Giovanni Levi ◽  
Martine Cohen Solal
Keyword(s):  
Bone Formation ◽  
Cortical Bone ◽  
Osteoblastic Lineage

scholarly journals Osteopontin Deficiency Induces Parathyroid Hormone Enhancement of Cortical Bone Formation

Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 2132-2140 ◽  
Author(s):  
Keiichiro Kitahara ◽  
Muneaki Ishijima ◽  
Susan R. Rittling ◽  
Kunikazu Tsuji ◽  
Hisashi Kurosawa ◽  
...  
Keyword(s):  
Bone Mineral Density ◽  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Cancellous Bone ◽  
Wild Type ◽  
Mineral Density ◽  
Cortical Bone Mass ◽  
Intermittent Pth

Intermittent PTH treatment increases cancellous bone mass in osteoporosis patients; however, it reveals diverse effects on cortical bone mass. Underlying molecular mechanisms for anabolic PTH actions are largely unknown. Because PTH regulates expression of osteopontin (OPN) in osteoblasts, OPN could be one of the targets of PTH in bone. Therefore, we examined the role of OPN in the PTH actions in bone. Intermittent PTH treatment neither altered whole long-bone bone mineral density nor changed cortical bone mass in wild-type 129 mice, although it enhanced cancellous bone volume as reported previously. In contrast, OPN deficiency induced PTH enhancement of whole-bone bone mineral density as well as cortical bone mass. Strikingly, although PTH suppressed periosteal bone formation rate (BFR) and mineral apposition rate (MAR) in cortical bone in wild type, OPN deficiency induced PTH activation of periosteal BFR and MAR. In cancellous bone, OPN deficiency further enhanced PTH increase in BFR and MAR. Analysis on the cellular bases for these phenomena indicated that OPN deficiency augmented PTH enhancement in the increase in mineralized nodule formation in vitro. OPN deficiency did not alter the levels of PTH enhancement of the excretion of deoxypyridinoline in urine, the osteoclast number in vivo, and tartrate-resistant acid phosphatase-positive cell development in vitro. These observations indicated that OPN deficiency specifically induces PTH activation of periosteal bone formation in the cortical bone envelope.

Labeling studies on cortical bone formation in the antlers of red deer (Cervus elaphus)

Bone ◽  
2013 ◽  
Vol 52 (1) ◽  
pp. 506-515 ◽  
Author(s):  
S. Gomez ◽  
A.J. Garcia ◽  
S. Luna ◽  
U. Kierdorf ◽  
H. Kierdorf ◽  
...  
Keyword(s):  
Bone Formation ◽  
Cortical Bone ◽  
Cervus Elaphus ◽  
Red Deer

scholarly journals A New Synthetic Steroid, Osaterone Acetate (TZP-4238), Increases Cortical Bone Mass and Strength by Enhancing Bone Formation in Ovariectomized Rats

1997 ◽  
Vol 12 (4) ◽  
pp. 590-597 ◽  
Author(s):  
Hiroaki Fuse ◽  
Seiji Fukumoto ◽  
Hideyuki Sone ◽  
Yoshiko Miyata ◽  
Tomoyuki Saito ◽  
...  
Keyword(s):  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Ovariectomized Rats ◽  
Cortical Bone Mass

scholarly journals Modeling-based bone formation transforms trabeculae to cortical bone in the sclerotic areas in Buschke-Ollendorff syndrome. A case study of two females with LEMD3 variants

Bone ◽  
2020 ◽  
Vol 135 ◽  
pp. 115313
Author(s):  
M. Frost ◽  
E.T. Rahbek ◽  
C. Ejersted ◽  
P.F. Høilund-Carlsen ◽  
A. Bygum ◽  
...  
Keyword(s):  
Bone Formation ◽  
Cortical Bone

scholarly journals Cortical bone dynamics, strength, and densitometry after induction of emphysema in hamsters

2003 ◽  
Vol 95 (2) ◽  
pp. 631-634 ◽  
Author(s):  
Jill E. Shea ◽  
Scott C. Miller ◽  
David C. Poole ◽  
John P. Mattson
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Bone Formation ◽  
Cortical Bone ◽  
Pulmonary Disease ◽  
Bone Mineral ◽  
Bone Structure ◽  
Chronic Obstructive ◽  
Pathophysiological Mechanism ◽  
Mineral Density ◽  
Obstructive Pulmonary Disease

Recent evidence suggests that patients suffering from chronic obstructive pulmonary disease are also at an increased risk of developing osteoporosis. The pathophysiological mechanism(s) linking these progressive diseases is unknown. The goal of this investigation was to determine whether there were alterations in bone mineral density and content, cortical bone structure and strength, and indexes of bone formation and resorption in the elastase-induced emphysematous hamster. At 3 wk after induction of emphysema, the femoral bone mineral content was 8% less ( P = 0.026) and the femoral fracture strength was 6% less ( P = 0.032) in the emphysematous hamster than in controls. The cortical area was 8.4% less ( P = 0.013) and the periosteal mineral appositional rate was 27% less ( P = 0.05) than in controls. Additionally, the endocortical eroded surface in the emphysematous group was about twice that in the control group ( P = 0.003). Differences in some indexes of bone formation and resorption, paralleled by differences in bone structure and strength, were observed 3 wk after induction of emphysema. These differences in skeletal metabolism and strength may help explain some of the skeletal changes associated with chronic obstructive pulmonary disease in humans.

scholarly journals Cortical bone adaptation to a moderate level of mechanical loading in male Sost deficient mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Haisheng Yang ◽  
Alexander Büttner ◽  
Laia Albiol ◽  
Catherine Julien ◽  
Tobias Thiele ◽  
...  
Keyword(s):  
Physical Activity ◽  
Bone Formation ◽  
Bone Mass ◽  
Cortical Bone ◽  
Bone Adaptation ◽  
Moderate Level ◽  
Skeletal Maturation ◽  
Male Mice ◽  
Males And Females

AbstractLoss-of-function mutations in the Sost gene lead to high bone mass phenotypes. Pharmacological inhibition of Sost/sclerostin provides a new drug strategy for treating osteoporosis. Questions remain as to how physical activity may affect bone mass under sclerostin inhibition and if that effect differs between males and females. We previously observed in female Sost knockout (KO) mice an enhanced cortical bone formation response to a moderate level of applied loading (900 με at the tibial midshaft). The purpose of the present study was to examine cortical bone adaptation to the same strain level applied to male Sost KO mice. Strain-matched in vivo compressive loading was applied to the tibiae of 10-, 26- and 52-week-old male Sost KO and littermate control (LC) mice. The effect of tibial loading on bone (re)modeling was measured by microCT, 3D time-lapse in vivo morphometry, 2D histomorphometry and gene expression analyses. As expected, Sost deficiency led to high cortical bone mass in 10- and 26-week-old male mice as a result of increased bone formation. However, the enhanced bone formation associated with Sost deficiency did not appear to diminish with skeletal maturation. An increase in bone resorption was observed with skeletal maturation in male LC and Sost KO mice. Two weeks of in vivo loading (900 με at the tibial midshaft) induced only a mild anabolic response in 10- and 26-week-old male mice, independent of Sost deficiency. A decrease in the Wnt inhibitor Dkk1 expression was observed 3 h after loading in 52-week-old Sost KO and LC mice, and an increase in Lef1 expression was observed 8 h after loading in 10-week-old Sost KO mice. The current results suggest that long-term inhibition of sclerostin in male mice does not influence the adaptive response of cortical bone to moderate levels of loading. In contrast with our previous strain-matched study in females showing enhanced bone responses with Sost ablation, these results in males indicate that the influence of Sost deficiency on the cortical bone formation response to a moderate level of loading differs between males and females. Clinical studies examining antibodies to inhibit sclerostin may need to consider that the efficacy of additional physical activity regimens may be sex dependent.

scholarly journals High Bone Resorption in Adult Aging Transgenic Mice Overexpressing Cbfa1/Runx2 in Cells of the Osteoblastic Lineage

2002 ◽  
Vol 22 (17) ◽  
pp. 6222-6233 ◽  
Author(s):  
Valérie Geoffroy ◽  
Michaela Kneissel ◽  
Brigitte Fournier ◽  
Alan Boyde ◽  
Patrick Matthias
Keyword(s):  
Bone Marrow ◽  
Bone Resorption ◽  
Bone Formation ◽  
Transgenic Mice ◽  
Wild Type ◽  
Osteoblastic Lineage ◽  
High Bone ◽  
Transgenic Cells ◽  
Primary Osteoblasts ◽  
In Cells

ABSTRACT The runt family transcription factor core-binding factor α1 (Cbfa1) is essential for bone formation during development. Surprisingly, transgenic mice overexpressing Cbfa1 under the control of the 2.3-kb collagen type I promoter developed severe osteopenia that increased progressively with age and presented multiple fractures. Analysis of skeletally mature transgenic mice showed that osteoblast maturation was affected and that specifically in cortical bone, bone resorption as well as bone formation was increased, inducing high bone turnover rates and a decreased degree of mineralization. To understand the origin of the increased bone resorption, we developed bone marrow stromal cell cultures and reciprocal coculture of primary osteoblasts and spleen cells from wild-type or transgenic mice. We showed that transgenic cells of the osteoblastic lineage induced an increased number of tartrate-resistant acid phosphatase-positive multinucleated cells, suggesting that primary osteoblasts as well as bone marrow stromal cells from transgenic mice have stronger osteoclastogenic properties than cells derived from wild-type animals. We investigated the candidate genes whose altered expression could trigger this increase in bone resorption, and we found that the expression of receptor activator of NF-κB ligand (RANKL) and collagenase 3, two factors involved in bone formation-resorption coupling, was markedly increased in transgenic cells. Our data thus suggest that overexpression of Cbfa1 in cells of the osteoblastic lineage does not necessarily induce a substantial increase in bone formation in the adult skeleton but has a positive effect on osteoclast differentiation in vitro and can also dramatically enhance bone resorption in vivo, possibly through increased RANKL expression.

scholarly journals Porcupine inhibitors impair trabecular and cortical bone mass and strength in mice

2018 ◽  
Vol 238 (1) ◽  
pp. 13-23 ◽  
Author(s):  
Thomas Funck-Brentano ◽  
Karin H Nilsson ◽  
Robert Brommage ◽  
Petra Henning ◽  
Ulf H Lerner ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Bone Loss ◽  
Bone Formation ◽  
Bone Mass ◽  
Trabecular Bone ◽  
Cortical Bone ◽  
Bone Strength ◽  
Bending Test ◽  
Bone Homeostasis ◽  
Mineral Density

WNT signaling is involved in the tumorigenesis of various cancers and regulates bone homeostasis. Palmitoleoylation of WNTs by Porcupine is required for WNT activity. Porcupine inhibitors are under development for cancer therapy. As the possible side effects of Porcupine inhibitors on bone health are unknown, we determined their effects on bone mass and strength. Twelve-week-old C57BL/6N female mice were treated by the Porcupine inhibitors LGK974 (low dose = 3 mg/kg/day; high dose = 6 mg/kg/day) or Wnt-C59 (10 mg/kg/day) or vehicle for 3 weeks. Bone parameters were assessed by serum biomarkers, dual-energy X-ray absorptiometry, µCT and histomorphometry. Bone strength was measured by the 3-point bending test. The Porcupine inhibitors were well tolerated demonstrated by normal body weight. Both doses of LGK974 and Wnt-C59 reduced total body bone mineral density compared with vehicle treatment (P < 0.001). Cortical thickness of the femur shaft (P < 0.001) and trabecular bone volume fraction in the vertebral body (P < 0.001) were reduced by treatment with LGK974 or Wnt-C59. Porcupine inhibition reduced bone strength in the tibia (P < 0.05). The cortical bone loss was the result of impaired periosteal bone formation and increased endocortical bone resorption and the trabecular bone loss was caused by reduced trabecular bone formation and increased bone resorption. Porcupine inhibitors exert deleterious effects on bone mass and strength caused by a combination of reduced bone formation and increased bone resorption. We suggest that cancer targeted therapies using Porcupine inhibitors may increase the risk of fractures.

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