Abstract

Skeletal changes occuring secondary to burn injuries were studied in an experimental animal model for thermal injury. One hindlimb of female Sprague-Dawley rats (200–250g) was subjected to a standardized thermal injury; the other hindlimb was left untreated. Control animals received no experimental treatment. Effects on skeletal architecture were studied at the proximal tibial metaphysis and tibial diaphysis using static histomorphometry. Bone formation dynamics were studied from a series of bone fluorochrome labels administered before the experiment began, early (days 8, 9) postburn treatment (PBT) and late PBT (days 17, 18). Animals were sacrificed on day 21 PBT. In proximal tibial metaphyses of burn-treated limbs, trabecular bone area (TBA) and trabecular number in all regions except the primary spongiosa, were significantly reduced. TBA was also decreased, but not significantly in nontreated limbs. Longitudinal growth rate, growth plate thickness and growth cartilage cell production rate are greater in burn-treated than in nonburned and control bones. Burn-treated diaphyses showed extensive woven bone formation at periosteal surfaces, and corresponding increases of bone areas and periosteal perimeters. Endocortical surfaces showed only typical occasional resorption areas. No intracortical changes were observed. Mineral appositional rate (MAR) and bone formation rate (BFR) at endocortical surfaces were markedly depressed after thermal injury, significant changes were noted in both limbs of treated animals. Among burned limbs, the early PBT label was absent from all specimens, indicating a virtual shutdown of osteoblast activity and recruitment. Similarly in nonburned limb bone, the label was absent from 50% of the specimens; in those bones in which the label was present, label lengths, appositional and bone formation rates were significantly reduced relative to the control specimens. Comparison of average bone formation dynamics for the total PBT interval indicates that MAR and BFR in burned treated tibiae were reduced to approximately 25% of control values. MAR and BFR from the nonburned side of treated animals were significantly reduced as well, to about 55% of control values. These data indicate that the principal metaphyseal effects of thermal injury are stimulation of growth cartilage proliferation, and depression of ossification and osteoblast activity. In diaphyses, thermal injury causes extensive local periosteal woven bone proliferation and a dramatic depression of endosteal bone formation. The latter effect, while more severe locally, is also evident systemically.

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