Extensive burn injury causes bone collagen network alteration and growth delay related to RANK-L immunoexpression change.

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. 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. 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. 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. [ABSTRACT FROM AUTHOR]