Objectives: In this study, we used a canine high-energy fracture model to examine the relationship between the early inflammatory reaction in adjacent tissues and the ability for osteophyte growth, aiming to identify causes that lead to atrophic nonunion inflammatory disease and to provide new strategies for prevention and treatment.
Materials and methods: Forty-eight models of canine femoral high energy fractures were prepared and randomly divided into groups A and B (n=24 in each group). Dogs in both groups underwent open reduction and 6-hole plate internal fixation. Group A models were re-opened, and muscle near the bone was scraped at 14 d after the operation. On days 3, 17, 28, and 42 after fracture, 6 experimental dogs were euthanized per group, and the fracture specimens were used to examine pathologic changes and the growth of callus in the fractured end and its adjacent tissues.
Results: At day 14, neutrophil infiltration, with no macrophage recruitment, no mesenchymal cell proliferation, and no fracture healing cascade were observed in the adjacent tissues of both groups. Immediately after the second injury was performed in group A, many macrophages were seen, and mesenchymal cells proliferated, which initiated vigorous osteophyte growth and led to osteophyte healing. Atrophic nonunion was observed in group B without secondary injury.
Conclusion: Macrophage recruitment deficiency in adjacent soft tissue in early surgery for high-energy fractures may be an important cause of atrophic nonunion. Secondary injury inflammation can effectively recruit mononuclear macrophages, generate osteoclasts, re-initiate the growth of osteophytes, and promote fracture healing.
Keywords: Canine femoral high energy fracture model; atrophic nonunion; macrophage; new callus; secondary injury.
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