Research Article Variation in Expression of Inflammation-Related Signaling Molecules with Profibrotic and Antifibrotic Effects in Cutaneous and Oral Mucosa Scars Mihai Bucur, 1,2 Octavian Dinca, 1,2 Cristian Vladan, 1,2 Cristiana Popp , 3 Luciana Nichita, 1,3 Mirela Cioplea , 3 Patricia Stînga, 3 Petronel Mustatea, 1,4 Sabina Zurac , 1,3 and Ecaterina Ionescu 1,5 1 “Carol Davila” University of Medicine and Pharmacy, 37 Dionisie Lupu, 020021 Bucharest, Romania 2 Department of OroMaxilloFacial Surgery, Clinical Hospital of OroMaxilloFacial Surgery Prof. Dr. Dan Theodorescu, 17 Calea Plevnei, 010221 Bucharest, Romania 3 Department of Pathology, Colentina University Hospital, 21 Stefan cel Mare, 020125 Bucharest, Romania 4 Department of Surgery, Clinical Hospital “Dr. Ion Cantacuzino”, 5 Ioan Movila, 020475 Bucharest, Romania 5 Ambulatory of Orthodontics, Clinical Hospital of OroMaxilloFacial Surgery Prof. Dr. Dan Theodorescu, 17 Calea Plevnei, 010221 Bucharest, Romania Correspondence should be addressed to Sabina Zurac; sabina_zurac@yahoo.com Received 2 May 2018; Revised 6 October 2018; Accepted 11 October 2018; Published 28 November 2018 Guest Editor: Iulia D. Popescu Copyright © 2018 Mihai Bucur et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Wound healing is a complex biologic process evolving in three phases: inflammation, proliferation, and tissue remodeling controlled by numerous growth factors and cytokines. Oral mucosa wounds heal with significantly less important scars with less numerous macrophages and mast cells and more numerous myofibroblasts than cutaneous counterparts. We analyzed 32 cutaneous and 32 oral mucosa scars for TGFbeta1, TGFbeta2, TGFbeta3, TNFalpha, PDGF BB and FGF1 expression in mesenchymal cells, endothelial cells, macrophages, and multinucleated giant cells. We identified differences in the expression of profibrotic and antifibrotic factors in oral mucosa and skin scars; TGFbeta2 was positive in cutaneous multinucleated giant cells, TNFalpha was positive in cutaneous macrophages, and both were negative in oral mucosa while TGFbeta3 was positive in oral macrophages and mostly negative in cutaneous ones. PDGF BB and FGF1 were positive in oral endothelial cells and oral macrophages and negative in macrophages with opposite positivity pattern in cutaneous scars. Based on these findings, macrophage seems to be the key player in modulating pro- and antifibrotic processes in wound regeneration. 1. Introduction Wound healing is a complex biologic process evolving in three phases: inflammation, proliferation, and tissue remod- eling [1]. These phases are controlled by myriad of growth factors and cytokines and, to some extent, overlap in time. Inflammation occurs almost immediately after wound formation—after the blood coagulation and lasts 2–4 days; several cells are chemotactically attracted to the wound site—neutrophils (they engulf bacteria and foreign bodies) and monocytes (they differentiate into macrophages that phagocyte necrotic debris, neutrophils, and foreign bodies); later on, macrophages secrete growth factors that stimulate the formation of granulation tissue [2–4]. Proliferation includes several processes such as angiogenesis and fibro- blasts proliferation and differentiation towards myofibro- blasts (formation of granulation tissue) and epithelial cells proliferation (reepithelization) [5–9]. Tissue remodeling (contraction phase, “maturation”) is the last and the longest phase of tissue healing; it consists of collagen synthesis and Hindawi Journal of Immunology Research Volume 2018, Article ID 5196023, 14 pages https://doi.org/10.1155/2018/5196023