| Objective To observe the effect of celluar prolification, apoptosis and apoptosis-related genes in hypertrophic scars with treatment of triamcinolone ,And to investigate the mechanism of steroid in treatment of abnormal scars. Methods Programmed cell death apoptosis was indentified by an in situ terminal deoxynucleotidyl transferas(TdT) -mediated dUTP-biotin nick and labelling staining (TUNEL) in 42 hypertrophic scars, 12 non-hypertrophic scars and 10 normal skins. Expression of proliferating cell neclear antigen(PCNA) and two protooncogenes, bcl-2 and bax, recently recognized to be involved in apoptosis, were detected by immunohistochemical technique. Results The densities of PCNA and bcl-2 staining were greater in hypertrophic scars than those in non-hypertrophic scars and normal skins(P<0.01),the proliferative index of hypertrophic scars in more than one year was higher than those in one year(P<0.01),whereas there was no obvious difference of apoptosis index (P>0.05).PCNA and bcl-2-positive cells decreased significantly in scars with treatment of triamcinolone in comparison with control group(P<0.01). Although the AI and PI of hypertrophic scars were more than those of NHS and NS,the AI/PI of HS was less than that of the latter(P<0.05). Weakly staining bax antigen was observed in all cases.Conclusion Intralesional injection of steroid has the effect of restraining the prolification of fibroblasts in hypertrophic scars by inhabiting PCNA gene expression in vivo.Intralesional injection steroid can inhibit bcl-2 gene expression of hypertrophic scars in vivo ,which induced apoptosis of cells. Excessive proliferation and lack of apoptosis of cells may cause the formation of hypertrophic scars, particularly the lack of apoptosis may delay the transition fromproliferative stage to muture stage.
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