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Severe Burn Injury in a Swine Model for Clinical Dressing Assessment
Published on: November 6, 2018
Extensive burn injury causes bone collagen network alteration and growth delay related to RANK-L immunoexpression
Tabata De Carvalho Tomé1, Hananiah Tardivo Quintana1, Jeferson André Bortolin1
1Departamento de Biociências, Universidade Federal de São Paulo, Campus Baixada Santista , SP, Brazil.
Insights
Extensive burn injury in young rats delayed bone growth and altered collagen structure. Increased RANK-L expression suggests enhanced bone resorption, contributing to growth impairment.
Area of Science:
- Biomedical research
- Skeletal biology
- Burn injury consequences
Background:
- Extensive burn injuries in children can cause hypermetabolism and growth delay.
- Understanding the bone development impact is crucial for pediatric burn care.
Purpose of the Study:
- To investigate bone histopathology and morphometrics in an experimental burn model.
- To analyze collagen fiber networks and bone development markers post-burn.
Main Methods:
- Wistar rats were divided into control and scald burn injury (SBI) groups.
- Femur epiphyses were analyzed histologically, morphometrically, and for RUNX-2 and RANK-L expression.
- Samples were collected 4 and 14 days post-injury.
Main Results:
- SBI delayed secondary ossification center appearance and reduced epiphyseal plate thickness.
- Collagen networks in articular cartilage were altered in SBI groups.
- RANK-L expression was significantly higher in SBI rats compared to controls.
Conclusions:
- Extensive burn injury leads to delayed bone growth and structural changes.
- Altered collagen and increased RANK-L contribute to enhanced osteoclastogenesis and impaired bone development.
Purpose:
Extensive burn injury mainly affects children, and hypermetabolic state can lead to growth delay. This study aimed to investigate bone histopathological and morphometric aspects, collagen fibers network and the immunoexpression of biological markers related to bone development in a young experimental model for extensive burn.
Materials And Methods:
A total of 28 male Wistar rats were distributed into Control (C) and subjected to scald burn injury (SBI) groups. Sham or injured animals were euthanized 4 or 14 days post-lesion and proximal epiphyses of the femur were submitted to histological, morphometric (thickness epiphyseal plate), and RUNX-2 and receptor activator of nuclear factor kappa- β ligand (RANK-L) immunoexpression methods.
Results:
Histopathological femoral findings showed delayed appearance of the secondary ossification center in SBI, 14 days post-injury. Collagen fibers 4 days after injury were observed in articular cartilage as a pantographic network with a transversally oriented lozenge-shaped mesh, but this network was thinner in SBI. Fourteen days after the injury, the pantographic network of collagen presented square-shaped mesh in C, but this aspect was changed to a wider mesh in SBI. Morphometric analysis of epiphyseal plate revealed that the SBI group had less thickness than the respective controls (p<0.05). RUNX-2 showed no difference between groups, but RANK-L score was higher in all SBI groups.
Conclusions:
Extensive burn injury causes delayed bone growth and morphological changes. Alterations in collagen network and enhancement in immunoreactivity of RANK-L result in increased osteoclastogenesis.
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