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https://www.readbyqxmd.com/read/28816826/tissue-engineered-bone-differentiated-from-human-adipose-derived-stem-cells-inhibit-posterolateral-fusion-in-an-athymic-rat-model
#1
Comron Saifi, Jonahtan Bernhard, Jamal N Shillingford, Petros Petridis, Samuel Robinson, X Edward Guo, Mark Weidenbaum, Ronald A Lehman, Howard S An, Lawrence G Lenke, Gordana Vunjak-Novakovic, Joseph L Laratta
STUDY DESIGN: Biological augmentation spinal arthrodesis trial in athymic rats OBJECTIVE.: To assess the efficacy of tissue-engineered bone to promote L4-L5 intertransverse process fusion in an athymic rat model. SUMMARY OF BACKGROUND DATA: Each year in the United States, over 400,000 spinal fusion surgeries are performed requiring bone graft. The current gold standard for posterolateral lumbar fusion is autogenous iliac crest bone graft (ICBG), but the harvesting of ICBG is associated with increased operative time and significant complications...
August 14, 2017: Spine
https://www.readbyqxmd.com/read/28816104/the-immune-response-to-allogeneic-differentiated-mesenchymal-stem-cells-in-the-context-of-bone-tissue-engineering
#2
Caoimhe H Kiernan, Eppo B Wolvius, Pieter A J Brama, Eric Farrell
The use of allogeneic differentiated mesenchymal stem cells (MSCs) to mediate bone formation may be a potential alternative to the current gold standards of bone repair. While it is known that undifferentiated MSCs are immunomodulatory and weakly immunogenic, the host immune reaction to differentiated MSCs is less known. Implantation of allogeneic osteogenic or chondrogenically differentiated MSC pellets may be promising routes to induce bone repair via the processes of intramembranous and endochondral ossification...
August 17, 2017: Tissue Engineering. Part B, Reviews
https://www.readbyqxmd.com/read/28802681/activated-fgfr3-promotes-bone-formation-via-accelerating-endochondral-ossification-in-mouse-model-of-distraction-osteogenesis
#3
Yusuke Osawa, Masaki Matsushita, Sachi Hasegawa, Ryusaku Esaki, Masahito Fujio, Bisei Ohgawara, Naoki Ishiguro, Kinji Ohno, Hiroshi Kitoh
Achondroplasia (ACH) is one of the most common short-limbed skeletal dysplasias caused by gain-of-function mutations in the fibroblast growth factor receptors 3 (FGFR3) gene. Distraction osteogenesis (DO) is a treatment option for short stature in ACH in some countries. Although the patients with ACH usually show faster healing in DO, details of the newly formed bone have not been examined. We have developed a mouse model of DO and analyzed new bone regenerates of the transgenic mice with ACH (Fgfr3(ach) mice) histologically and morphologically...
August 9, 2017: Bone
https://www.readbyqxmd.com/read/28798933/tumor-proteins-d52-and-d54-have-opposite-effects-on-the-terminal-differentiation-of-chondrocytes
#4
Chihiro Ito, Yoshiki Mukudai, Masakatsu Itose, Kosuke Kato, Hiromi Motohashi, Toshikazu Shimane, Seiji Kondo, Tatsuo Shirota
The tumor protein D (TPD) family consists of four members, TPD52, TPD53, TPD54, and TPD55. The physiological roles of these genes in normal tissues, including epidermal and mesenchymal tissues, have rarely been reported. Herein, we examined the expression of TPD52 and TPD54 genes in cartilage in vivo and in vitro and investigated their involvement in the proliferation and differentiation of chondrocytes in vitro. TPD52 and TPD54 were uniformly expressed in articular cartilage and trabecular bone and were scarcely expressed in the epiphyseal growth plate...
2017: BioMed Research International
https://www.readbyqxmd.com/read/28798204/imaging-igf-i-uptake-in-growth-plate-cartilage-using-in-vivo-multiphoton-microscopy
#5
Maria A Serrat, Gabriela Ion
Bones elongate through endochondral ossification in cartilaginous growth plates located at ends of primary long bones. Linear growth ensues from a cascade of biochemical signals initiated by actions of systemic and local regulators on growth plate chondrocytes. Although cellular processes are well defined, there is a fundamental gap in understanding how growth regulators are physically transported from surrounding blood vessels into and through dense, avascular cartilage matrix. Intravital imaging using in vivo multiphoton microscopy is one promising strategy to overcome this barrier by quantitatively tracking molecular delivery to cartilage from the vasculature in real time...
August 10, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28782836/histone-deacetylase-3-deletion-in-mesenchymal-progenitor-cells-hinders-long-bone-development
#6
Marina Feigenson, Lomeli Carpio Shull, Earnest L Taylor, Emily T Camilleri, Scott M Reister, Andre J van Wijnen, Elizabeth W Bradley, Jennifer J Westendorf
Long bone formation is a complex process that requires precise transcriptional control of gene expression programs in mesenchymal progenitor cells. Histone deacetylases (Hdacs) coordinate chromatin structure and gene expression by enzymatically removing acetyl groups from histones and other proteins. Hdac inhibitors are used clinically to manage mood disorders, cancers and other conditions, but are teratogenic to the developing skeleton and increase fracture risk in adults. In this study, the functions of Hdac3, one of the enzymes blocked by current Hdac inhibitor therapies, in skeletal mesenchymal progenitor cells were determined...
August 7, 2017: Journal of Bone and Mineral Research: the Official Journal of the American Society for Bone and Mineral Research
https://www.readbyqxmd.com/read/28758906/activin-a-enhances-mtor-signaling-to-promote-aberrant-chondrogenesis-in-fibrodysplasia-ossificans-progressiva
#7
Kyosuke Hino, Kazuhiko Horigome, Megumi Nishio, Shingo Komura, Sanae Nagata, Chengzhu Zhao, Yonghui Jin, Koichi Kawakami, Yasuhiro Yamada, Akira Ohta, Junya Toguchida, Makoto Ikeya
Fibrodysplasia ossificans progressiva (FOP) is a rare and intractable disease characterized by extraskeletal bone formation through endochondral ossification. Patients with FOP harbor point mutations in ACVR1, a type I receptor for BMPs. Although mutated ACVR1 (FOP-ACVR1) has been shown to render hyperactivity in BMP signaling, we and others have uncovered a mechanism by which FOP-ACVR1 mistransduces BMP signaling in response to Activin-A, a molecule that normally transduces TGF-β signaling. Although Activin-A evokes enhanced chondrogenesis in vitro and heterotopic ossification (HO) in vivo, the underlying mechanisms have yet to be revealed...
July 31, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28756737/mimicking-the-biochemical-and-mechanical-extracellular-environment-of-the-endochondral-ossification-process-to-enhance-the-in-vitro-mineralization-potential-of-human-mscs
#8
Fiona E Freeman, Jessica Schiavi, Meadhbh A Brennan, Peter Owens, Pierre Layrolle, Laoise McNamara
Chondrogenesis and mechanical stimulation of the cartilage template, are essential for bone formation via the endochondral ossification process in vivo. Recent studies have demonstrated that in vitro regeneration strategies that mimic these aspects separately, either chondrogenesis or mechanical stimulation, can promote mineralization to a certain extent both in vitro and in vivo. However, to date no study has sought to incorporate both the formation of the cartilage template and the application of mechanical stimulation simultaneously to induce osteogenesis...
July 29, 2017: Tissue Engineering. Part A
https://www.readbyqxmd.com/read/28740483/a-case-with-spondyloenchondrodysplasia-treated-with-growth-hormone
#9
Takanori Utsumi, Satoshi Okada, Kazushi Izawa, Yoshitaka Honda, Gen Nishimura, Ryuta Nishikomori, Rika Okano, Masao Kobayashi
Spondyloenchondrodysplasia (SPENCD) is an autosomal recessive skeletal dysplasia caused by loss of function mutations in acid phosphatase 5, tartrate resistant (ACP5). Hypomorphic ACP5 mutations impair endochondral bone growth and create an interferon (INF) signature, which lead to distinctive spondylar and metaphyseal dysplasias, and extraskeletal morbidity, such as neurological involvement and immune dysregulation, respectively. We report an affected boy with novel ACP5 mutations, a splice-site mutation (736-2 A>C) and a nonsense mutation (R176X)...
2017: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/28734986/exogenous-hedgehog-antagonist-delays-but-does-not-prevent-fracture-healing-in-young-mice
#10
Xiaochen Liu, Jennifer A McKenzie, Clayton W Maschhoff, Michael J Gardner, Matthew J Silva
Fracture healing recapitulates many aspects of developmental osteogenesis. The hedgehog (Hh) signaling pathway, essential to skeletal development, is upregulated during fracture healing, although its importance is unclear. Our goal was to assess the functional importance of Hh signaling in endochondral fracture healing. We created closed, transverse diaphyseal femur fractures in mice, stabilized with an intramedullary pin, and administered a systemic Hh inhibitor or vehicle. Because Hh pathway activation is mediated by the receptor Smoothened (Smo), we used the Smo antagonist GDC-0449 (GDC, 50mg/kg, twice daily) to target the pathway...
July 19, 2017: Bone
https://www.readbyqxmd.com/read/28687525/smd-kozlowski-type-caused-by-p-arg594his-substitution-in-trpv4-reveals-abnormal-ossification-and-notochordal-remnants-in-discs-and-vertebrae
#11
Tadeusz Bieganski, Peter Beighton, Maciej Lukaszewski, Krzysztof Bik, Lukasz Kuszel, Ewa Wasilewska, Kazimierz Kozlowski, Malwina Czarny-Ratajczak
Spondylometaphyseal dysplasia Kozlowski type (SMDK) is a monogenic disorder within the TRPV4 dysplasia spectrum and has characteristic spinal and metaphyseal changes. We report skeletal MR imaging in a two-year-old patient who manifested typical clinical and radiographic features of SMDK. The diagnosis was confirmed by molecular analysis which revealed a mutation NM_021625.4:c.1781G > A - p.(Arg594His) in exon 11 of the TRPV4 gene. We have documented abnormalities in endochondral formation of the long and short tubular bones as well as round bones of the wrists and feet...
July 4, 2017: European Journal of Medical Genetics
https://www.readbyqxmd.com/read/28681971/growth-plate-expression-profiling-large-and-small-breed-dogs-provide-new-insights-in-endochondral-bone-formation
#12
Michelle Teunissen, Frank M Riemers, Dik van Leenen, Marian J A Groot Koerkamp, Björn P Meij, Jacqueline Alblas, Louis C Penning, Alberto Miranda-Bedate, Marianna A Tryfonidou
The difference in the adult height of mammals, and hence in endochondral bone formation, is not yet fully understood and may serve to identify targets for bone and cartilage regeneration. In line with this hypothesis, the intra-species disparity between the adult height of Great Danes and Miniature Poodles was investigated at a transcriptional level. Microarray analysis of the growth plate of five Great Danes and five Miniature Poodles revealed 2,981 unique genes that were differentially expressed, including many genes with an unknown role in skeletal development...
July 6, 2017: Journal of Orthopaedic Research: Official Publication of the Orthopaedic Research Society
https://www.readbyqxmd.com/read/28675805/characterization-of-normal-murine-carpal-bone-development-prompts-re-evaluation-of-pathologic-osteolysis-as-the-cause-of-human-carpal-tarsal-osteolysis-disorders
#13
Syndia Lazarus, Hsu-Wen Tseng, Felicity Lawrence, Maria Ann Woodruff, Emma Letitia Duncan, Allison Robyn Pettit
Multicentric carpal-tarsal osteolysis; multicentric osteolysis, nodulosis, and arthropathy; and Winchester syndromes, skeletal dysplasias characterized by carpal/tarsal and epiphyseal abnormalities, are caused by mutations in v-maf musculoaponeurotic fibrosarcoma oncogene ortholog B (MAFB), matrix metalloproteinase 2 (MMP2), and MMP14, respectively; however, the underlying pathophysiology is unclear. Osteoclast-mediated osteolysis has been regarded as the main mechanism, but does not explain the skeletal distribution...
July 1, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/28668522/the-traumatic-bone-trauma-induced-heterotopic-ossification
#14
REVIEW
Devaveena Dey, Benjamin M Wheatley, David Cholok, Shailesh Agarwal, Paul B Yu, Benjamin Levi, Thomas A Davis
Heterotopic ossification (HO) is a common occurrence after multiple forms of extensive trauma. These include arthroplasties, traumatic brain and spinal cord injuries, extensive burns in the civilian setting, and combat-related extremity injuries in the battlefield. Irrespective of the form of trauma, heterotopic bone is typically endochondral in structure and is laid down via a cartilaginous matrix. Once formed, the heterotopic bone typically needs to be excised surgically, which may result in wound healing complications, in addition to a risk of recurrence...
June 15, 2017: Translational Research: the Journal of Laboratory and Clinical Medicine
https://www.readbyqxmd.com/read/28661587/endochondral-ossification-in-critical-sized-bone-defects-via-readily-implantable-scaffold-free-stem-cell-constructs
#15
Phuong N Dang, Samuel Herberg, Davood Varghai, Hooman Riazi, Daniel Varghai, Alexandra McMillan, Amad Awadallah, Lauren M Phillips, Oju Jeon, Minh K Nguyen, Neha Dwivedi, Xiaohua Yu, William L Murphy, Eben Alsberg
The growing socioeconomic burden of musculoskeletal injuries and limitations of current therapies have motivated tissue engineering approaches to generate functional tissues to aid in defect healing. A readily implantable scaffold-free system comprised of human bone marrow-derived mesenchymal stem cells embedded with bioactive microparticles capable of controlled delivery of transforming growth factor-beta 1 (TGF-β1) and bone morphogenetic protein-2 (BMP-2) was engineered to guide endochondral bone formation...
July 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28645539/gli1-labeled-adult-mesenchymal-stem-progenitor-cells-and-hedgehog-signaling-contribute-to-endochondral-heterotopic-ossification
#16
Chen Kan, Lijun Chen, Yangyang Hu, Na Ding, Yuyun Li, Tammy L McGuire, Haimei Lu, John A Kessler, Lixin Kan
Heterotopic ossification (HO), acquired or hereditary, endochondral or intramembranous, is the formation of true bone outside the normal skeleton. Since perivascular Gli1+ progenitors contribute to injury induced organ fibrosis, and CD133 is expressed by a variety of populations adult stem cells, this study utilized Cre-lox based genetic lineage tracing to test the contribution to endochondral HO of adult stem/progenitor cells that expressed either Gli1 or CD133. We found that both lineages contributed broadly to different normal tissues with distinct patterns, but that only Gli1-creERT labeled stem/progenitor cells contributed to all stages of endochondral HO in a BMP dependent, injury induced, transgenic mouse model...
June 20, 2017: Bone
https://www.readbyqxmd.com/read/28644737/circulatory-cnp-rescues-craniofacial-hypoplasia-in-achondroplasia
#17
S Yamanaka, Kazumasa Nakao, N Koyama, Y Isobe, Y Ueda, Y Kanai, E Kondo, T Fujii, M Miura, A Yasoda, Kazuwa Nakao, K Bessho
Achondroplasia is the most common genetic form of human dwarfism, characterized by midfacial hypoplasia resulting in occlusal abnormality and foramen magnum stenosis, leading to serious neurologic complications and hydrocephalus. Currently, surgery is the only way to manage jaw deformity, neurologic complications, and hydrocephalus in patients with achondroplasia. We previously showed that C-type natriuretic peptide (CNP) is a potent stimulator of endochondral bone growth of long bones and vertebrae and is also a potent stimulator in the craniofacial region, which is crucial for midfacial skeletogenesis...
June 1, 2017: Journal of Dental Research
https://www.readbyqxmd.com/read/28643905/diverse-contribution-of-col2a1-expressing-cells-to-the-craniofacial-skeletal-cell-lineages
#18
N Sakagami, W Ono, N Ono
OBJECTIVES: Craniofacial skeletal development requires deliberate coordination of two distinct mechanisms of endochondral and intramembranous ossification. Col2a1-expressing cells encompass growth-associated skeletal progenitors in endochondral bones of the limb. The objective of this study was to determine the contribution of Col2a1-expressing cells to the craniofacial skeletal cell lineages. We hypothesize that Col2a1-expressing progenitors significantly contribute to various modes of ossification associated with the craniofacial development...
June 2017: Orthodontics & Craniofacial Research
https://www.readbyqxmd.com/read/28643552/drug-induced-physeal-abnormalities-in-preclinical-toxicity-studies
#19
Kendall S Frazier
Most toxic physeal changes are characterized microscopically by altered chondrocyte development, proliferation, or maturation in the growth plate and eventually result in disordered appositional bone growth. Many therapeutic drugs directly or indirectly target proteins involved in chondrocytic differentiation and maturation pathways, so toxic physeal injury has become increasingly common in preclinical toxicologic pathology. While physeal dysplasia has been associated with several different drug classes including bisphosphonates, vascular endothelial growth factor receptor inhibitors, fibroblast growth factor receptor inhibitors, transforming growth factor beta receptor inhibitors, and vascular targeting agents, physeal changes often share similar morphologic features including thickening and disorganization of the hypertrophic layer, increased numbers of hypertrophic chondrocytes, altered mineralization of endochondral ossification, and/or increased thickness of subphyseal bone...
January 1, 2017: Toxicologic Pathology
https://www.readbyqxmd.com/read/28637283/an-essential-physiological-role-for-mct8-in-bone-in-male-mice
#20
Victoria D Leitch, Caterina Di Cosmo, Xiao-Hui Liao, Sam O'Boy, Thomas M Galliford, Holly Evans, Peter I Croucher, Alan Boyde, Alexandra Dumitrescu, Roy E Weiss, Samuel Refetoff, Graham R Williams, J H Duncan Bassett
T3 is an important regulator of skeletal development and adult bone maintenance. Thyroid hormone action requires efficient transport of T4 and T3 into target cells. We hypothesized that monocarboxylate transporter-8, encoded by Mct8 on the X-chromosome, is an essential thyroid hormone transporter in bone. To test this hypothesis, we determined the juvenile and adult skeletal phenotypes of male Mct8 knockout mice (Mct8KO) and Mct8D1D2KO compound mutants, which additionally lack the ability to convert the prohormone T4 to the active hormone T3...
June 15, 2017: Endocrinology
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