Decorin reduces hypertrophic scarring through inhibition of the TGF-β1/Smad signaling pathway in a rat osteomyelitis model.

Chronic osteomyelitis is a bone infection that results in hypertrophic scarring of the soft tissue surrounding the infected bone. This scarring can create functional problems and its treatment is challenging. The aim of the present study was to evaluate the efficacy of decorin in treating scar formation in osteomyelitis and the underlying mechanism of its action. A rat osteomyelitis model was used, and animals were divided into three groups, as follows: Group A (control), group B (osteomyelitis model) and group C (decorin-treated). X-ray scans, hematoxylin and eosin (H&E) staining and Masson's trichrome staining were performed to observe changes in femur and muscle tissue. In order to assess the role of the transforming growth factor β1 (TGF-β1)/Smad signaling pathway in scar formation in osteomyelitis, alterations in muscle tissue morphology and in the activation of key members of the TGF-β1/Smad signaling pathway were investigated in groups A and B. According to the results of H&E staining, evident fibrosis in muscle tissue were observed at days 14 and 28 in group B. Simultaneously, the expression levels of key members of the TGF-β1/Smad signaling pathway were increased. Subsequent to treatment with decorin in group C, scarring was reduced, and significant downregulation of collagen I, TGF-β1, phosphorylated (p)Smad2 and pSmad3 protein expression levels was observed at days 14 and 28 compared with the osteomyelitis group. In conclusion, these results suggest that activation of TGF-β1 may serve an important role in the formation of scars in osteomyelitis and that decorin can reduce scar formation in an osteomyelitis rat model through inhibition of the TGF-β1/Smad signaling pathway.