Spinal Hemiepiphysiodesis Decreases the Size of Vertebral Growth Plate Hypertrophic Zone and Cells

2009 ◽  
Vol 91 (3) ◽  
pp. 584-593 ◽  
Author(s):  
Donita I Bylski-Austrow ◽  
Eric J Wall ◽  
David L Glos ◽  
Edgar T Ballard ◽  
Andrea Montgomery ◽  
...  
Keyword(s):  
Growth Plate ◽  
Hypertrophic Zone ◽  
Vertebral Growth

scholarly journals Local Changes to the Distal Femoral Growth Plate Following Injury in Mice

2017 ◽  
Vol 139 (7) ◽  
Author(s):  
Lauren M. Mangano Drenkard ◽  
Meghan E. Kupratis ◽  
Katie Li ◽  
Louis C. Gerstenfeld ◽  
Elise F. Morgan
Keyword(s):  
Growth Plate ◽  
Skeletal Development ◽  
Global Changes ◽  
Mineral Density ◽  
Injury Site ◽  
Hypertrophic Zone ◽  
Proliferative Zone ◽  
Spatial Changes ◽  
Zonal Organization ◽  
Growth Plate Injury

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.

The fibroblast growth factor receptor, FGFR3, forms gradients of intact and degraded protein across the growth plate of developing bovine ribs

2002 ◽  
Vol 361 (2) ◽  
pp. 231-241 ◽  
Author(s):  
Sujata G. PANDIT ◽  
Prasanthi GOVINDRAJ ◽  
Joachim SASSE ◽  
Peter J. NEAME ◽  
John R. HASSELL
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Growth Plate ◽  
Point Mutations ◽  
Growth Factor Receptor ◽  
Fibroblast Growth ◽  
Fgf Receptor ◽  
Hypertrophic Zone ◽  
The Matrix ◽  
Maximum Expression

Point mutations in the human fibroblast growth factor (FGF) receptor 3 gene (Fgfr3) produce a constitutively active receptor, which disrupts chondrocyte differentiation in the growth plate and results in skeletal dysplasias with severe shortening of the limbs. Alternative splicing of the Fgfr3 transcript gives rise to two isoforms, IIIc and IIIb, which vary in their specificity for FGF ligands. We examined the expression of these FGFR3 isoforms in the bovine fetal rib growth plate to determine whether levels of FGFR3 expression are zone-related. Transcripts for both Fgfr3 isoforms are expressed in rib growth plate, with maximum expression in the hypertrophic region and the least expression in the reserve zone. Fgfr3 IIIc is the predominant isoform in the growth plate. Western-blot analysis revealed the presence of full-length FGFR3 (135kDa) for both isoforms in the reserve zone, a major 98kDa fragment in all zones and smaller fragments primarily in the hypertrophic zone. Immunostaining localized FGFR3 to the pericellular region of reserve chondrocytes and to the extracellular matrix in the hypertrophic zone. These results suggest that the transmembrane form of FGFR3 increasingly undergoes proteolytic cleavage towards the hypertrophic zone to produce an extracellular-domain fragment of FGFR3, which is present in large amounts in the matrix of hypertrophic cells. These findings suggest a proteolytic regulatory mechanism for FGFR3, whereby Fgfr3 fragments could control availability of FGF for the intact receptor, and by which proteolysis could inactivate the receptor.

P5. Experimental study on the expression of growth factors in the vertebral growth plate and pedicle in severe idiopathic scoliosis

2019 ◽  
Vol 19 (9) ◽  
pp. S160
Author(s):  
Tao Li ◽  
Yingsong Wang ◽  
Jing-Ming Xie ◽  
Zhiyue Shi ◽  
Quan Li ◽  
...  
Keyword(s):  
Experimental Study ◽  
Growth Factors ◽  
Idiopathic Scoliosis ◽  
Growth Plate ◽  
Vertebral Growth

Expression of Runx2 and Type X Collagen in Vertebral Growth Plate of Patients with Adolescent Idiopathic Scoliosis

2010 ◽  
Vol 51 (3) ◽  
pp. 188-196 ◽  
Author(s):  
Shoufeng Wang ◽  
Yong Qiu ◽  
Zhaolong Ma ◽  
Caiwei Xia ◽  
Feng Zhu ◽  
...  
Keyword(s):  
Adolescent Idiopathic Scoliosis ◽  
Idiopathic Scoliosis ◽  
Growth Plate ◽  
Type X Collagen ◽  
Vertebral Growth

scholarly journals The Somatostatin Analog Octreotide Inhibits GH-Stimulated, But Not IGF-I-Stimulated, Bone Growth in Hypophysectomized Rats

Endocrinology ◽  
2002 ◽  
Vol 143 (8) ◽  
pp. 2944-2952 ◽  
Author(s):  
Jürgen Zapf ◽  
Martina Gosteli-Peter ◽  
Gisbert Weckbecker ◽  
Ernst B. Hunziker ◽  
Manfred Reinecke
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Body Weight Gain ◽  
Somatostatin Analog ◽  
Hypertrophic Zone ◽  
Gh Secretion ◽  
Proliferative Zone ◽  
Igf I ◽  
Hypophysectomized Rats ◽  
Tibial Epiphyseal

Abstract IGF-I mediates growth-promoting actions of GH. In the present study we investigated whether the somatostatin analog octreotide blunts the stimulatory effects of GH and/or IGF-I on bone growth in hypophysectomized rats infused for 6 d with vehicle, GH, or IGF-I. We found that octreotide significantly suppressed the GH-induced rise in liver IGF-I mRNA (−27%) and peptide (−32%) and the serum IGF-I level (−26%) and concomitantly inhibited GH-stimulated, but not IGF-I-stimulated, body weight gain (−31%), tibial epiphyseal width (−14%), and bone growth rate (−24%). Furthermore, octreotide significantly reduced the GH-induced increase in the number of IGF-I immunoreactive chondrocytes in all layers (except in the upper hypertrophic zone) of the tibial growth plate cartilage (P < 0.0001 for stem cell and proliferative zone; P < 0.0005 for lower hypertrophic zone). These findings demonstrate that octreotide does not interfere with IGF-I action, but does interfere with local GH-stimulated IGF-I production in the growth plate. Thus, besides inhibiting pituitary GH secretion, octreotide exerts inhibitory peripheral effects on GH-stimulated longitudinal bone growth.

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