Abstract
To assess the evolution profile of the immunohistochemical expression of stromal constituents over the time-course of wound healing in a murine model. Surgical wounds were performed in the back of 24 Wistar rats. After three, seven, 14 and 21 days, six rats were euthanized and the wounded histologically processed to assess the immunohistochemical expression of CD3, CD20, CD31, α-SMA and type-I collagen. Non-injured skin samples (NSS) were used as control. Data were subjected to statistical analysis using ANOVA and Tukey test. The mean of CD3 and CD20 positive cells in the wounds was significantly higher than in NSS at seven and 14 days (p<0.001). The blood vessels content was significantly lower than in NSS (p<0.05) at three days, but increased at seven and 14 days (p<0.01). The mean of α-SMA positive cells at seven, 14 and 21 days was higher than in NSS (p<0.05). The relative content of type I collagen increased from three to 21 days, but remained lower than in NSS (p<0.05). Lymphoid cells, myofibroblasts and microvessels contents varied over the time-course of wound healing, with peak at seven days and progressive reduction until 21 days. The type I collagen content increased over time.
Highlights
The major function of skin is to provide a protective barrier against the environment
Lymphoid cells, myofibroblasts and microvessels contents varied over the time-course of wound healing, with peak at seven days and progressive reduction until 21 days
Positivity for CD31 antigen was observed in the cytoplasm of spindle-shaped cells either forming small vascular spaces or proliferating in the connective tissue, which was compatible with endothelial cells (Figure 3a)
Summary
The major function of skin is to provide a protective barrier against the environment. It has been reported that partial thickness wounds are supposed to heal by mere epithelialization, whereas the healing of full thickness wound involves more complex wellregulated biological events, including the inflammatory response, granulation tissue formation, myofibroblastic differentiation and collagenization[2,3]. This process is directly or indirectly responsible or eliminating the bacterial load, removing necrotic debris, inducing wound contraction and stimulating the scar formation. There are only some few papers looking at the assessment and analysis of the histological features of stromal and inflammatory profile over the time-course of the spontaneous scar tissue formation[6]
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