Structural and molecular analyses of bone bridge formation within the growth plate injury site and cartilage degeneration at the adjacent uninjured area

Bone ◽  
2011 ◽  
Vol 49 (4) ◽  
pp. 904-912 ◽  
Author(s):  
C.E. Macsai ◽  
B. Hopwood ◽  
R. Chung ◽  
B.K. Foster ◽  
C.J. Xian
Keyword(s):  
Growth Plate ◽  
Cartilage Degeneration ◽  
Injury Site ◽  
Molecular Analyses ◽  
Bone Bridge ◽  
Bridge Formation ◽  
Growth Plate Injury ◽  
And Cartilage

scholarly journals Adipose-derived stromal vascular fraction prevent bone bridge formation on growth plate injury in rat (in vivo studies) an experimental research

2020 ◽  
Vol 60 ◽  
pp. 211-217
Author(s):  
Panji Sananta ◽  
Rahaditya I Gede Made Oka ◽  
Prof Respati Suryanto Dradjat ◽  
Heri Suroto ◽  
Edi Mustamsir ◽  
...  
Keyword(s):  
Growth Plate ◽  
Experimental Research ◽  
Stromal Vascular Fraction ◽  
In Vivo Studies ◽  
Bone Bridge ◽  
Bridge Formation ◽  
Growth Plate Injury

The spatial and temporal expression of VEGF and its receptors 1 and 2 in post-traumatic bone bridge formation of the growth plate

2011 ◽  
Vol 42 (6) ◽  
pp. 513-522 ◽  
Author(s):  
Eva Fischerauer ◽  
Nima Heidari ◽  
Bernhard Neumayer ◽  
Alexander Deutsch ◽  
Annelie M. Weinberg
Keyword(s):  
Growth Plate ◽  
Temporal Expression ◽  
Bone Bridge ◽  
Bridge Formation ◽  
Post Traumatic

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.

scholarly journals Application of Autologous Bone Marrow Derived Mesenchymal Stem Cells to an Ovine Model of Growth Plate Cartilage Injury

2010 ◽  
Vol 4 (1) ◽  
pp. 204-210 ◽  
Author(s):  
Rosa C McCarty ◽  
Cory J Xian ◽  
Stan Gronthos ◽  
Andrew C.W Zannettino ◽  
Bruce K Foster
Keyword(s):  
Bone Marrow ◽  
Animal Model ◽  
Growth Plate ◽  
Autologous Bone Marrow ◽  
Gelatin Sponge ◽  
Large Animal ◽  
Bone Bridge ◽  
Bridge Formation ◽  
Growth Plate Cartilage ◽  
Autologous Bone

Injury to growth plate cartilage in children can lead to bone bridge formation and result in bone growth deformities, a significant clinical problem currently lacking biological treatment. Mesenchymal stem/stromal cells (MSC) offer a promising therapeutic option for regeneration of damaged cartilage, due to their self renewing and multi-lineage differentiation attributes. Although some small animal model studies highlight the therapeutic potential of MSC for growth plate repair, translational research in large animal models, which more closely resemble the human condition, are lacking. Our laboratory has recently characterised MSCs derived from ovine bone marrow, and demonstrated these cells form cartilage-like tissue when transplanted within the gelatin sponge, Gelfoam,in vivo. In the current study, autologous bone marrow MSC were seeded into Gelfoam scaffold containing TGF-β1, and transplanted into a surgically created defect of the proximal ovine tibial growth plate. Examination of implants at 5 week post-operatively revealed transplanted autologous MSC failed to form new cartilage structure at the defect site, but contributed to an increase in formation of a dense fibrous tissue. Importantly, the extent of osteogenesis was diminished, and bone bridge formation was not accelerated due to transplantation of MSCs or the gelatin scaffold. The current study represents the first work that has utilised this ovine large animal model to investigate whether autologous bone marrow derived MSC can be used to initiate regeneration at the injured growth plate.

Towards a better understanding of bone bridge formation in the growth plate – an immunohistochemical approach

2013 ◽  
Vol 54 (6) ◽  
pp. 408-415 ◽  
Author(s):  
Karin Pichler ◽  
Giuseppe Musumeci ◽  
Ines Vielgut ◽  
Elisabeth Martinelli ◽  
Patrick Sadoghi ◽  
...  
Keyword(s):  
Growth Plate ◽  
Bone Bridge ◽  
Bridge Formation

scholarly journals The potential role of VEGF-induced vascularisation in the bony repair of injured growth plate cartilage

2014 ◽  
Vol 221 (1) ◽  
pp. 63-75 ◽  
Author(s):  
Rosa Chung ◽  
Bruce K Foster ◽  
Cory J Xian
Keyword(s):  
Blood Vessel ◽  
Growth Plate ◽  
Bone Growth ◽  
Fracture Repair ◽  
Bone Lengthening ◽  
Bony Tissue ◽  
Injury Site ◽  
Repair Tissue ◽  
Anti Vegf ◽  
Growth Plate Injury

Growth plate injuries often result in undesirable bony repair causing bone growth defects, for which the underlying mechanisms are unclear. Whilst the key importance of pro-angiogenic vascular endothelial growth factor (VEGF) is well-known in bone development and fracture repair, its role during growth plate bony repair remains unexplored. Using a rat tibial growth plate injury repair model with anti-VEGF antibody, Bevacizumab, as a single i.p. injection (2.5 mg/kg) after injury, this study examined the roles of VEGF-driven angiogenesis during growth plate bony repair. Histology analyses observed isolectin-B4-positive endothelial cells and blood vessel-like structures within the injury site on days 6 and 14, with anti-VEGF treatment significantly decreasing blood-vessel-like structures within the injury site (P<0.05). Compared with untreated controls, anti-VEGF treatment resulted in an increase in undifferentiated mesenchymal repair tissue, but decreased bony tissue at the injury site at day 14 (P<0.01). Consistently, microcomputed tomography analysis of the injury site showed significantly decreased bony repair tissue after treatment (P<0.01). RT-PCR analyses revealed a significant decrease in osteocalcin (P<0.01) and a decreasing trend in Runx2 expression at the injury site following treatment. Furthermore, growth plate injury-induced reduced tibial lengthening was more pronounced in anti-VEGF-treated injured rats on day 60, consistent with the observation of a significantly increased height of the hypertrophic zone adjacent to the growth plate injury site (P<0.05). These results indicate that VEGF is important for angiogenesis and formation of bony repair tissue at the growth plate injury site as well as for endochondral bone lengthening function of the uninjured growth plate.

In vivo protective effects of upper zone of growth plate and cartilage matrix associated protein against cartilage degeneration in a monosodium iodoacetate induced osteoarthritis model

2020 ◽  
Vol 98 (11) ◽  
pp. 763-770
Author(s):  
Hamza Malik Okuyan ◽  
Menderes Yusuf Terzi ◽  
İhsan Karaboğa ◽  
Serdar Doğan ◽  
Aydıner Kalacı
Keyword(s):  
Growth Plate ◽  
Matrix Protein ◽  
Critical Role ◽  
Cartilage Degeneration ◽  
Cartilage Matrix ◽  
Bone Morphogenetic Protein 2 ◽  
Monosodium Iodoacetate ◽  
And Cartilage

Osteoarthritis (OA) is a degenerative disease affecting the majority of over 65 year old people and characterized by cartilage degeneration, subchondral abnormal changes, and inflammation. Despite the enormous socioeconomic burden caused by OA, currently, there is no effective therapy against it. Upper zone of growth plate and cartilage matrix associated protein (UCMA) is a vitamin K dependent protein and has a critical role in pathophysiological conditions associated with bone and cartilage. However, there is no research on the protective role of intra-articular UCMA treatment in OA pathogenesis. Therefore, we aimed to investigate the potential therapeutic role of UCMA in an in vivo model of OA. We report for the first time that intra-articular UCMA injection ameliorated cartilage degeneration in a monosodium iodoacetate induced OA rat model. Furthermore, the OA-induced activation of nuclear factor kappa B and bone morphogenetic protein 2 signals was attenuated by UCMA. Our results indicated that UCMA decreased cartilage oligomeric matrix protein levels but did not affect interleukin 6, total antioxidant status, and total oxidant status levels in the serum. In conclusion, UCMA exhibited a therapeutic potential in the treatment of OA. This protective effect of UCMA is possibly achieved by reducing the aggrecanase activity and the production of inflammatory cytokines.

scholarly journals Post-Traumatic Caspase-3 Expression in the Adjacent Areas of Growth Plate Injury Site: A Morphological Study

2013 ◽  
Vol 14 (8) ◽  
pp. 15767-15784 ◽  
Author(s):  
Giuseppe Musumeci ◽  
Paola Castrogiovanni ◽  
Carla Loreto ◽  
Sergio Castorina ◽  
Karin Pichler ◽  
...  
Keyword(s):  
Growth Plate ◽  
Morphological Study ◽  
Caspase 3 ◽  
Injury Site ◽  
Post Traumatic ◽  
Growth Plate Injury

scholarly journals Prevention of Bone Bridge Formation Using Transplantation of the Autogenous Mesenchymal Stem Cells to Physeal Defects: An Experimental Study in Rabbits

2007 ◽  
Vol 76 (2) ◽  
pp. 253-263 ◽  
Author(s):  
L. Plánka ◽  
A. Nečas ◽  
P. Gál ◽  
H. Kecová ◽  
E. Filová ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Growth Plate ◽  
Valgus Deformity ◽  
Type I ◽  
Repair Capacity ◽  
Left Femur ◽  
Bone Bridge ◽  
Bridge Formation ◽  
The Right

Physeal cartilage is known to have poor self-repair capacity after injury. Evaluation of the ability of cultured mesenchymal stem cells to repair damaged physis is the topic of current research. In 10 immature New Zealand white rabbits autogenous mesenchymal stem cells were transplanted into a iatrogenic physeal defect in a lateral portion of the distal growth plate of the right femur. The same defect without stem cells transplantation in the left femoral distal physis served as a control. In our study, we used our own technique of implantation of MSCs with a newly modified gel scaffold (New Composite Hyaluronate/Collagen Type I/Fibrin Scaffold). The rabbits were euthanized 4 months after transplantation. Bone length discrepancy and valgus deformity were measured from femoral radiographs. Healing of the defect was investigated histologically. The ability of mesenchymal stem cells to survive and promote cartilage healing in the physeal defect was assessed by immunofluorescence. Average difference in femur length measured from surgery to euthanasia (4 months) was 0.61 ± 0.19 cm after preventive transplantation of MSCs in the right femur, but only 0.11 ± 0.07 cm in the left femur. Average angular (valgus) deformity of the right femur with MSCs preventively transplanted to iatrogenically damaged distal femoral physis was 1.2 ± 0.72 °. Valgus deformity in the left femur was 5.4 ± 2.5 °. Prophylactic transplantation of autogenous mesenchymal stem cells to iatrogenically damaged distal growth plate of the rabbit femur prevented a bone bridge formation and resulted in healing of the physeal defect with hyaline cartilage. Immunofluorescence examination showed that the chondrocytes newly formed in growth zone are the result of implanted MSCs differentiation. Femur growth in traumatized physis was maintained even after transplantation of autogenous MSCs. As compared with the opposite femur (with physeal defect but without transplanted MSCs), the bone showed no significant shortening or valgus deformity (p = 0.018).

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