“…In this descriptive study we investigated the pattern of vascularization in a physeal injury model in the context of post traumatic physeal bone bridge formation. Rats have been shown to form bone bridges in a predictable and reproducible manner in response to physeal injury (Garces et al 1994) which guided the decision to utilize this model for our study. However, the creation of a physeal defect, as in the model chosen for this study, is somewhat different to physeal damage occuring as a result of an injury.…”
Section: Discussionmentioning
confidence: 99%
“…The rarer injuries crossing all the zones of the physis (Salter-Harris type III and IV) are more frequently associated with bone bridge formation, thus the defect model is well established in the investigation of these injuries. In order to avoid complete physeal closure following the induced injury we chose a drill diameter of 1.2 mm based on the work of Garces et al (1994). Physiological closure of the tibial physis occurs in 10% of animals by the age of 3.9 months and in 90% by the age of 7.4 months (Martin et al 2003).…”
Injuries to growth plates may initiate the formation of reversible or irreversible bone-bridges, may leading to bone length discrepancy or axis deviation. As vascular invasion is essential for the formation of bone tissue, the aim of our study was to investigate the kinetic expression of Vascular Endothelial Growth Factor (VEGF) and its receptors R1 and R2 and the ingrowth of vessels in the formation of bone bridges in a rat physeal injury model. Quantitative Real-Time Polymerase Chain Reaction was performed for VEGF and its receptors. Samples from the proximal physis of the tibial bone were immunohistochemically evaluated for the expression of VEGF and its R1 and R2 receptors and Laminin. Morphologically, physeal bone bridge formation was validated by means of Magnetic Resonance Imaging. Kinetic expression of VEGF and VEGF-R1 mRNA documented a tendency towards an increase in expression on day 7. Histological analyses showed a hematoma containing bone debris on day 1 which was replaced with bony trabeculae by day 14, forming a bone bridge by day 28 which was preceded and accompanied by angiogenesis and consistent with MRI data. VEGF and VEGF-R2 was expressed on the debris within the hematoma and bone trabeculae from days 1 to 28. VEGF-R1 expression was only noted until day 14. The findings of our study suggest that physeal bone bridge formation is in part triggered by VEGF expression and associated with angiogenesis, which was shown to precede bone bridge formation and may be further stimulated through VEGF-positive bone debris.
“…In this descriptive study we investigated the pattern of vascularization in a physeal injury model in the context of post traumatic physeal bone bridge formation. Rats have been shown to form bone bridges in a predictable and reproducible manner in response to physeal injury (Garces et al 1994) which guided the decision to utilize this model for our study. However, the creation of a physeal defect, as in the model chosen for this study, is somewhat different to physeal damage occuring as a result of an injury.…”
Section: Discussionmentioning
confidence: 99%
“…The rarer injuries crossing all the zones of the physis (Salter-Harris type III and IV) are more frequently associated with bone bridge formation, thus the defect model is well established in the investigation of these injuries. In order to avoid complete physeal closure following the induced injury we chose a drill diameter of 1.2 mm based on the work of Garces et al (1994). Physiological closure of the tibial physis occurs in 10% of animals by the age of 3.9 months and in 90% by the age of 7.4 months (Martin et al 2003).…”
Injuries to growth plates may initiate the formation of reversible or irreversible bone-bridges, may leading to bone length discrepancy or axis deviation. As vascular invasion is essential for the formation of bone tissue, the aim of our study was to investigate the kinetic expression of Vascular Endothelial Growth Factor (VEGF) and its receptors R1 and R2 and the ingrowth of vessels in the formation of bone bridges in a rat physeal injury model. Quantitative Real-Time Polymerase Chain Reaction was performed for VEGF and its receptors. Samples from the proximal physis of the tibial bone were immunohistochemically evaluated for the expression of VEGF and its R1 and R2 receptors and Laminin. Morphologically, physeal bone bridge formation was validated by means of Magnetic Resonance Imaging. Kinetic expression of VEGF and VEGF-R1 mRNA documented a tendency towards an increase in expression on day 7. Histological analyses showed a hematoma containing bone debris on day 1 which was replaced with bony trabeculae by day 14, forming a bone bridge by day 28 which was preceded and accompanied by angiogenesis and consistent with MRI data. VEGF and VEGF-R2 was expressed on the debris within the hematoma and bone trabeculae from days 1 to 28. VEGF-R1 expression was only noted until day 14. The findings of our study suggest that physeal bone bridge formation is in part triggered by VEGF expression and associated with angiogenesis, which was shown to precede bone bridge formation and may be further stimulated through VEGF-positive bone debris.
“…Therefore, our study confirmed the rapid time course of bone bridge formation at the growth plate injury site, and was consistent with previous investigations that used a similar drill-hole injury model in rabbits, rats, and mice. These earlier studies reported either initial or full osseous bar formation at the injury site by 1-3 weeks post-surgery [5,9,13,15,16]. in a Salter type I fracture model of proximal tibia1 physis in young rats, bony bars were found at day 10 after fracture [20].…”
Salter's type I11 and type IV growth plate injuries often induce bone bridge formation at the injury site. To understand the cellular mechanisms, this study characterized proximal tibia1 transphyseal injury in rats. Histologically, bony bridge trabeculae appeared on day 7, increased on day 10, and became well-constructed on day 14 with marrow. Prior to and during bone bridging, there was no cartilage proteoglycan metachromatic staining and no collagen-)< immunostaining at the injury site, nor was there any up-regulation of BrdU-labelled chondrocyte proliferation at the adjacent physeal cartilage, suggesting no new cartilage formation at the injury site. However, infiltration of vimentin-immunopositive mesenchymal cells from metaphysis and epiphysis was apparent on day 3, with the mesenchymal population being prominent on days 7 and 10 and subsided on day 14. Among these infiltrates were osteoprogenitor precursors expressing osteoblast differentiation factor (cbf-al ) on day 3, along with some cbf-a1 osteoblast-like cells lining bone trabeculae on days 7 and 10. Some mesenchymal cells and trabecula-lining cells were also alkaline phosphataseimmunopositive, further suggesting their osteoblast differentiation. From day 7 onwards, some trabecula-lining cells became osteocalcin-producing mature osteoblasts. These results suggest that bone bridge formation after growth plate injury occurs directly via intramembranous ossification through recruitment of marrow-derived osteoprogenitor cells.Crown
“…Various animal experiments have been attempted to investigate the effect of drilling on the physeal plate, and the conclusion has been that drill injuries that destroy less than 8-9% of the physis and small central destructions would not alter overall bone growth (Garces et al 1994, Janarv et al 1998. There is some experimental and clinical evidence that temporary crossing of the physeal plate with K-wires for internal fixation of dislocated joint injuries does not lead to bone bridging or growth disturbance (Boelitz et al 1994, Yung et al 2004).…”
Section: Discussionmentioning
confidence: 99%
“…There is some experimental and clinical evidence that temporary crossing of the physeal plate with K-wires for internal fixation of dislocated joint injuries does not lead to bone bridging or growth disturbance (Boelitz et al 1994, Yung et al 2004). However, depending on the level of the surgeon's skill and experience, this technique may require one or more attempts-with potential damage to the physeal plate (Garces et al 1994). …”
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