Growth plate injury of the long bones in treated ?-thalassemia

1992 ◽  
Vol 21 (1) ◽  
Author(s):  
Carlo Orzincolo ◽  
PierNuccio Scutellari ◽  
Giuseppe Castaldi
2017 ◽  
Vol 139 (7) ◽  
Author(s):  
Lauren M. Mangano Drenkard ◽  
Meghan E. Kupratis ◽  
Katie Li ◽  
Louis C. Gerstenfeld ◽  
Elise F. Morgan

Injury to the growth plate is associated with growth disturbances, most notably premature cessation of growth. The goal of this study was to identify spatial changes in the structure and composition of the growth plate in response to injury to provide a foundation for developing therapies that minimize the consequences for skeletal development. We used contrast-enhanced microcomputed tomography (CECT) and histological analyses of a murine model of growth plate injury to quantify changes in the cartilaginous and osseous tissue of the growth plate. To distinguish between local and global changes, the growth plate was divided into regions of interest near to and far from the injury site. We noted increased thickness and CECT attenuation (a measure correlated with glycosaminoglycan (GAG) content) near the injury, and increased tissue mineral density (TMD) of bone bridges within the injury site, compared to outside the injury site and contralateral growth plates. Furthermore, we noted disruption of the normal zonal organization of the physis. The height of the hypertrophic zone was increased at the injury site, and the relative height of the proliferative zone was decreased across the entire injured growth plate. These results indicate that growth plate injury leads to localized disruption of cellular activity and of endochondral ossification. These local changes in tissue structure and composition may contribute to the observed retardation in femur growth. In particular, the changes in proliferative and hypertrophic zone heights seen following injury may impact growth and could be targeted when developing therapies for growth plate injury.


2019 ◽  
Author(s):  
Holly Dupuis ◽  
Michael Andrew Pest ◽  
Ermina Hadzic ◽  
Thin Xuan Vo ◽  
Daniel B. Hardy ◽  
...  

AbstractLongitudinal 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 on EO.Rats given SR11237 from post-natal day 5 to 15 were harvested for micro-computed tomography 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 were smaller than controls, and developed dysmorphia of the growth plate. Cells invading the calcified and dysmorphic growth plate appeared pre-hypertrophic in size and shape corresponding 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 treated animals. Isolated mouse long bones treated with SR11237 grew significantly less than their DMSO controls.This study demonstrates that stimulation of the RXR receptor causes irregular ossification, premature closure of the growth plate, and disrupted long bone growth in rodent models.


2020 ◽  
Vol 60 ◽  
pp. 211-217
Author(s):  
Panji Sananta ◽  
Rahaditya I Gede Made Oka ◽  
Prof Respati Suryanto Dradjat ◽  
Heri Suroto ◽  
Edi Mustamsir ◽  
...  

2016 ◽  
Vol 24 (4) ◽  
pp. 204-207 ◽  
Author(s):  
María Roxana Viamont Guerra ◽  
Jose Renato Depari Estelles ◽  
Yussef Ali Abdouni ◽  
Diego Figueira Falcochio ◽  
Joao Roberto Polydoro Rosa ◽  
...  

1990 ◽  
Vol 19 (7) ◽  
Author(s):  
Mark Arvin ◽  
SusanJ. White ◽  
EthanM. Braunstein

2009 ◽  
Vol 7 (2) ◽  
pp. 161
Author(s):  
E. Topkan ◽  
A.A. Yavuz ◽  
R. Erdem ◽  
D. Bacanli ◽  
C. Onal ◽  
...  

Author(s):  
Christopher B. Erickson ◽  
Nichole Shaw ◽  
Nancy Hadley-Miller ◽  
Michael S. Riederer ◽  
Melissa D. Krebs ◽  
...  

2014 ◽  
Vol 53 (1) ◽  
pp. T45-T61 ◽  
Author(s):  
Rosa Chung ◽  
Cory J Xian

Injuries to the growth plate cartilage often lead to bony repair, resulting in bone growth defects such as limb length discrepancy and angulation deformity in children. Currently utilised corrective surgeries are highly invasive and limited in their effectiveness, and there are no known biological therapies to induce cartilage regeneration and prevent the undesirable bony repair. In the last 2 decades, studies have investigated the cellular and molecular events that lead to bony repair at the injured growth plate including the identification of the four phases of injury repair responses (inflammatory, fibrogenic, osteogenic and remodelling), the important role of inflammatory cytokine tumour necrosis factor alpha in regulating downstream repair responses, the role of chemotactic and mitogenic platelet-derived growth factor in the fibrogenic response, the involvement and roles of bone morphogenic protein and Wnt/B-catenin signalling pathways, as well as vascular endothelial growth factor-based angiogenesis during the osteogenic response. These new findings could potentially lead to identification of new targets for developing a future biological therapy. In addition, recent advances in cartilage tissue engineering highlight the promising potential for utilising multipotent mesenchymal stem cells (MSCs) for inducing regeneration of injured growth plate cartilage. This review aims to summarise current understanding of the mechanisms for growth plate injury repair and discuss some progress, potential and challenges of MSC-based therapies to induce growth plate cartilage regeneration in combination with chemotactic and chondrogenic growth factors and supporting scaffolds.


2012 ◽  
Vol 36 (9) ◽  
pp. 1961-1966 ◽  
Author(s):  
Karin Pichler ◽  
Barbara Schmidt ◽  
Eva E. Fischerauer ◽  
Beate Rinner ◽  
Gottfried Dohr ◽  
...  

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