Published online Dec 10, 2015. doi: 10.5306/wjco.v6.i6.264
Peer-review started: April 11, 2015
First decision: June 4, 2015
Revised: August 4, 2015
Accepted: September 7, 2015
Article in press: September 8, 2015
Published online: December 10, 2015
Processing time: 243 Days and 15.8 Hours
Fibroblasts are the most abundant cellular components of connective tissue. They possess phenotypical heterogenicity and may be present in the form of smooth muscle cells or myofibroblasts (MFs). MFs are spindle-shaped cells with stress fibres and well-developed fibronexus, and they display α-smooth muscle actin immunohistochemically and smooth-muscle myofilaments ultrastructurally. MFs play a crucial role in physiological and pathological processes. Derived from various sources, they play pivotal roles not only by synthesizing and producing extracellular matrix components, such as other connective tissue cells, but also are involved in force production. In the tissue remodelling phase of wound closure, integrin-mediated interactions between MFs and type I collagen result in scar tissue formation. The tumour stroma in oral cancer actively recruits various cell types into the tumour mass, where they act as different sources of MFs. This article reviews the importance of MFs and its role in pathological processes such as wound healing, odontogenic cysts and tumours, salivary gland tumours, oral preneoplasia, and oral squamous cell carcinoma. Research oriented on blocking the transdifferentiation of fibroblasts into MFs can facilitate the development of noninvasive therapeutic strategies for the treatment of fibrosis and/or cancer.
Core tip: Myofibroblast (MFs) are spindle-shaped cells consisting α-smooth muscle actin myofilament. They have a multicellular origin. MFs of the oral cavity have more contractile ability than dermal fibroblasts in physiologic wound healing. Recently, carcinoma-associated fibroblasts (CAFs) have received considerable attention because of their role in carcinogenesis. Mainly, transforming growth factor-β released from oral cancer cells is responsible for transforming fibroblasts into CAFs, which leads to tumour progression. However, the role of MFs in oral leukoplakia and oral submucous fibrosis is not completely understood. Understanding the implications of therapeutic approaches for the transdifferentiation of fibroblasts into MFs at different stages of carcinogenesis will facilitate in developing a treatment plan.