Avaliação morfométrica do colágeno total, tipo I e tipo III e análise da expressão in situ de citocinas em queloides

Abstract

Keloids are the result of physiological changes in the healing process. Characterized by growth beyond the borders of the initial lesion and by non-spontaneous regression. Its signs and symptoms include pain, itching, flushing and local stiffness and can cause psychological discomforts due to the aesthetic disfigurement very common in these lesions. It is characterized by the excessive deposition of collagen and several cytokines may be contributing to the pathophysiology. The objective of this study was to evaluate the collagen fibers, analyze in situ expression of cytokines in keloid lesions, and compare to the control group. 33 patients were followed up at the plastic surgery outpatient, treated with triamcinolone 20 mg/ml and referred for excision of the lesion. The fragments were stored in later RNA and buffered formalin. The control group consisted of 40 normal scar fragments taken from secondary or multiparous patients during cesarean section. The Leica Qwin Plus® and Image J® system were used for image capture and quantification of the collagen fibers. The results showed a predominance of women (60.60%), non-white (60.60) and direct black ancestry (66.66%). Keloid showed a significant increase in total and type III collagen (p <0.0001, p = 0.0001). Significantly, the expression of mRNA for TGF-β in keloid was increased, the expression of IFN-γ, IFN-γR1 and IL-10 were lower, and with no statistical difference for IFN-γR1 and TNF-α showed no statistical difference (p<0.001, p=0.009, p=0.246, p=0.037; p=0.911) compared to the control group. Correlations between collagen type III and TGF-β mRNA expression were positive and significant (p=0.001, z=3.210), and IFN-γ, IFN-γR1 and IL-10, were negative and significant (p=0.015, z=-2.425, p=0.021, z=-2.303, p=0.014, z=-2.445) and TNF-α with no statistical difference (p=0.555, z=0.590). Thus, with these results, it can be suggested that pro-inflammatory and anti-inflammatory cytokines may be directly assisting in the pathogenesis of the keloid mainly by inducing a more immature healing, with excessive collagen synthesis and with inefficient wound contraction. In addition, TGF-β appears to be the major induction factor for fibroblast activation and proliferation, and is an important target for studies to elucidate the keloid pathophysiology.