A theoretical model of endochondral ossification and bone architectural construction in long bone ontogeny

1990 ◽  
Vol 181 (6) ◽  
Author(s):  
Marcy Wong ◽  
DennisR. Carter
Keyword(s):  
Theoretical Model ◽  
Endochondral Ossification ◽  
Long Bone

Computational model of endochondral ossification: simulating growth of a long bone

Bone ◽  
2021 ◽  
pp. 116132
Author(s):  
S. Mahsa Sadeghian ◽  
Frederic D. Shapiro ◽  
Sandra J. Shefelbine
Keyword(s):  
Computational Model ◽  
Endochondral Ossification ◽  
Long Bone

scholarly journals Exposure to the RXR Agonist SR11237 in Early Life Causes Disturbed Skeletal Morphogenesis in a Rat Model

2019 ◽  
Vol 20 (20) ◽  
pp. 5198
Author(s):  
Holly Dupuis ◽  
Michael Andrew Pest ◽  
Ermina Hadzic ◽  
Thin Xuan Vo ◽  
Daniel B. Hardy ◽  
...  
Keyword(s):  
Growth Plate ◽  
Endochondral Ossification ◽  
Bone Growth ◽  
Long Bone ◽  
Tunel Staining ◽  
Long Bones ◽  
Micro Computed Tomography ◽  
Calcified Tissue ◽  
Trap Staining ◽  
Stimulation Of

Longitudinal bone growth occurs through endochondral ossification (EO), controlled by various signaling molecules. Retinoid X Receptor (RXR) is a nuclear receptor with important roles in cell death, development, and metabolism. However, little is known about its role in EO. In this study, the agonist SR11237 was used to evaluate RXR activation in EO. Rats given SR11237 from post-natal day 5 to post-natal day 15 were harvested for micro-computed tomography (microCT) scanning and histology. In parallel, newborn CD1 mouse tibiae were cultured with increasing concentrations of SR11237 for histological and whole-mount evaluation. RXR agonist-treated rats had shorter long bones than the controls and developed dysmorphia of the growth plate. Cells invading the calcified and dysmorphic growth plate appeared pre-hypertrophic in size and shape, in correspondence with p57 immunostaining. Additionally, SOX9-positive cells were found surrounding the calcified tissue. The epiphysis of SR11237-treated bones showed increased TRAP staining and additional TUNEL staining at the osteo-chondral junction. MicroCT revealed morphological disorganization in the long bones of the treated animals. This study suggests that stimulation of RXR causes irregular ossification, premature closure of the growth plate, and disrupted long bone growth in rodent models

scholarly journals PH domain and leucine rich repeat phosphatase 1 (Phlpp1) suppresses parathyroid hormone receptor 1 (Pth1r) expression and signaling during bone growth

2020 ◽  
Author(s):  
Samantha R. Weaver ◽  
Earnest L. Taylor ◽  
Elizabeth L. Zars ◽  
Katherine M. Arnold ◽  
Elizabeth W. Bradley ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Growth Plate ◽  
Endochondral Ossification ◽  
Bone Growth ◽  
Long Bone ◽  
Leucine Rich Repeat ◽  
Ph Domain ◽  
Mineral Density ◽  
Longitudinal Bone Growth ◽  
Deficient Mice

ABSTRACTEndochondral ossification is tightly controlled by a coordinated network of signaling cascades including parathyroid hormone (PTH). PH domain and leucine rich repeat phosphatase (Phlpp1) affects endochondral ossification by suppressing chondrocyte proliferation in the growth plate, longitudinal bone growth, and bone mineralization. As such, Phlpp1−/− mice have shorter long bones, thicker growth plates, and proportionally larger growth plate proliferative zones. The goal of this study was to determine how Phlpp1 deficiency affects PTH signaling during bone growth. Transcriptomic analysis revealed greater Pth1r expression and H3K27ac enrichment at the Pth1r promoter in Phlpp1-deficient chondrocytes. PTH(1-34) enhanced and PTH(7-34) attenuated cell proliferation, cAMP signaling, CREB phosphorylation, and cell metabolic activity in Phlpp1-inhibited chondrocytes. To understand the role of Pth1r action in the endochondral phenotypes of Phlpp1-deficient mice, Phlpp1−/− mice were injected with Pth1r ligand PTH(7-34) daily for the first four weeks of life. PTH(7-34) reversed the abnormal growth plate and long bone growth phenotypes of Phlpp1−/− mice but did not rescue deficits in bone mineral density or trabecular number. These results demonstrate that elevated Pth1r expression and signaling contributes to increased proliferation in Phlpp1−/− chondrocytes and shorter bones in Phlpp1-deficient mice. Our data reveal a novel molecular relationship between Phlpp1 and Pth1r in chondrocytes during growth plate development and longitudinal bone growth.

scholarly journals Breeder age and bone development in broiler chicken embryos

2009 ◽  
Vol 61 (1) ◽  
pp. 219-226 ◽  
Author(s):  
K.A. Alfonso-Torres ◽  
L.H. Gargaglioni ◽  
J.M. Pizauro ◽  
D.E. Faria Filho ◽  
R.L. Furlan ◽  
...  
Keyword(s):  
Enzymatic Activity ◽  
Broiler Chicken ◽  
Endochondral Ossification ◽  
Bone Development ◽  
Long Bone ◽  
Alkaline Phosphatases ◽  
Morphometric Measurements ◽  
Absolute Weight ◽  
Chicken Embryos ◽  
Acid And Alkaline Phosphatases

The effect of breeder age on long bone development was studied in chicken embryos from 12 days of incubation until hatching. Fertile eggs were incubated and randomly assigned in a 2 x 6 factorial arrangement (two breeder ages - 38 and 60 weeks and six incubation days - 12, 14, 16, 18, 20, and 21). Enzymatic activity of acid and alkaline phosphatases in tibial epiphyses and weights as well as length and width in tibias and femurs of the embryos were determined. Tartrate-resistant acid and alkaline phosphatases activity in epiphyses was not affected by breeder age. Absolute weight and width of femur and tibia were larger in 60-week-old embryos compared to 38-week-old. Enzymatic activity and morphometric measurements increased with incubation day, independently of breeder age. The results showed that the process of endochondral ossification during the last two thirds of embryo development was not influenced by the age of the breeders. Although, in terms of absolute weight, the long bones of embryos from older breeders were heavier, which was associated with the larger width of the bones, but and not with their length.

scholarly journals Construction of developmentally inspired periosteum-like tissue for bone regeneration

Bone Research ◽  
2022 ◽  
Vol 10 (1) ◽  
Author(s):  
Kai Dai ◽  
Shunshu Deng ◽  
Yuanman Yu ◽  
Fuwei Zhu ◽  
Jing Wang ◽  
...  
Keyword(s):  
Endochondral Ossification ◽  
Bone Development ◽  
Autologous Transplantation ◽  
Tumor Resection ◽  
Bone Morphogenetic Protein 2 ◽  
Long Bone ◽  
Defect Repair ◽  
Novel Strategy ◽  
Bone Tumor Resection

AbstractThe periosteum, a highly vascularized thin tissue, has excellent osteogenic and bone regenerative abilities. The generation of periosteum-mimicking tissue has become a novel strategy for bone defect repair and regeneration, especially in critical-sized bone defects caused by trauma and bone tumor resection. Here, we utilized a bone morphogenetic protein-2 (BMP-2)-loaded scaffold to create periosteum-like tissue (PT) in vivo, mimicking the mesenchymal condensation during native long bone development. We found that BMP-2-induced endochondral ossification plays an indispensable role in the construction of PTs. Moreover, we confirmed that BMP-2-induced PTs exhibit a similar architecture to the periosteum and harbor abundant functional periosteum-like tissue-derived cells (PTDCs), blood vessels, and osteochondral progenitor cells. Interestingly, we found that the addition of chondroitin sulfate (CS), an essential component of the extracellular matrix (ECM), could further increase the abundance and enhance the function of recruited PTDCs from the PTs and finally increase the regenerative capacity of the PTs in autologous transplantation assays, even in old mice. This novel biomimetic strategy for generating PT through in vivo endochondral ossification deserves further clinical translation.

scholarly journals Functionalization of Electrospun Polycaprolactone Scaffolds with Matrix-Binding Osteocyte-Derived Extracellular Vesicles Promotes Osteoblastic Differentiation and Mineralization

2021 ◽  
Author(s):  
Mechiel Nieuwoudt ◽  
Ian Woods ◽  
Kian F. Eichholz ◽  
Carolina Martins ◽  
Kate McSweeney ◽  
...  
Keyword(s):  
Bone Tissue ◽  
Bone Repair ◽  
Endochondral Ossification ◽  
Polymeric Materials ◽  
Matrix Vesicles ◽  
Bone Tissue Regeneration ◽  
Long Bone ◽  
Great Promise ◽  
Material Surface ◽  
Matrix Mineralization

AbstractSynthetic polymeric materials have demonstrated great promise for bone tissue engineering based on their compatibility with a wide array of scaffold-manufacturing techniques, but are limited in terms of the bioactivity when compared to naturally occurring materials. To enhance the regenerative properties of these materials, they are commonly functionalised with bioactive factors to guide growth within the developing tissue. Extracellular matrix vesicles (EVs) play an important role in facilitating endochondral ossification during long bone development and have recently emerged as important mediators of cell-cell communication coordinating bone regeneration, and thus represent an ideal target to enhance the regenerative properties of synthetic scaffolds. Therefore, in this paper we developed tools and protocols to enable the attachment of MLO-Y4 osteocyte-derived EVs onto electrospun polycaprolactone (PCL) scaffolds for bone repair. Initially, we optimize a method for the functionalization of PCL materials with collagen type-1 and fibronectin, inspired by the behaviour of matrix vesicles during endochondral ossification, and demonstrate that this is an effective method for the adhesion of EVs to the material surface. We then used this functionalization process to attach osteogenic EVs, collected from mechanically stimulated MLO-Y4 osteocytes, to collagen-coated electrospun PCL scaffolds. The EV-functionalized scaffold promoted osteogenic differentiation (measured by increased ALP activity) and mineralization of the matrix. In particular, EV-functionalised scaffolds exhibited significant increases in matrix mineralization particularly at earlier time points compared to uncoated and collagen-coated controls. This approach to matrix-based adhesion of EVs provides a mechanism for incorporating vesicle signalling into polyester scaffolds and demonstrates the potential of osteocyte derived EVs to enhance the rate of bone tissue regeneration.

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