Immunohistochemical analysis of myofibroblasts, TGF‐β1, and IFN‐γ in epithelial odontogenic lesions

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In the group of odontogenic lesions, ameloblastomas (AMBs) and keratocystic odontogenic tumors (KCOTs) are particularly important because of their intriguing biological behavior. Although benign, AMBs, and KCOTs show a locally aggressive behavior and tendency to recur 1. In contrast, adenomatoid odontogenic tumors (AOTs) exhibit slow growth and an indolent biological behavior, although they also originate from the odontogenic epithelium 3.
Myofibroblasts (MFBs) are connective tissue cells that exhibit features of both fibroblasts and smooth muscle cells 4. This cell can be identified based on certain characteristics of its cytoskeleton, particularly the expression of α‐smooth muscle actin (α‐SMA). Myofibroblasts play an important role in physiological processes such as wound healing and fibrotic diseases 5. Studies suggest that MFBs are the main producer of extracellular matrix (ECM) in some pathological conditions and an increase in the density of MFBs has been demonstrated in different lesions, including malignant neoplasms 6.
Certain growth factors have been shown to induce the transdifferentiation of fibroblasts, epithelial, and endothelial cells via epithelial (EMT), endothelial‐to‐mesenchymal transition (EndoMT), smooth muscle cells (SMCs), resident mesenchymal progenitor cells (MSCs), adipose cells, bone‐marrow‐derived circulating fibrocytes and MSCs into MFBs and the role of transforming growth factor β1 (TGF‐β1) as the main stimulator of this transdifferentiation has been demonstrated 7. In contrast, interferon gamma (IFN‐γ) inhibits this transdifferentiation and its antagonistic action to TGF‐β1 reduces the number of MFBs 8.
In view of the multifunctional role of MFBs in both physiological and pathological mechanisms and of the strong correlation between the density of MFBs and tumor aggressiveness 11, the objective of the present study was to quantify MFBs in selected epithelial odontogenic lesions by analyzing their immunohistochemical expression of α‐SMA and to evaluate the expression of TGF‐β1 and IFN‐γ as a stimulator and inhibitor of MFBs, respectively, during the transdifferentiation of these cells.

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