Dynamic role of myofibroblasts in oral lesions

Figure 1 Origin of myofibroblasts-multicellular origin. Multicellular origin of myofibroblasts: Fibroblast, pericytes, endothelial cells, circulating hematopoietic precursor cells and fibrocytes can transform into myofibroblasts. E-MT: Epithelial-mesenchymal transition.

Figure 2 Differentiation of promyofibroblast to myofibroblast. By getting stimulus from various cytokines profibroblasts (promyofibroblasts) transforms into myofibroblasts by expressingα-smooth muscle actin. TGF-β1: Transforming growth factor-β1; ECM: Extracellular matrix; IL-1: Interleukin-1; KGF-1: Keratinocyte growth factor-1.

Figure 3 Transdifferentiation of fibroblasts into myofibroblasts. Major alkaloid of areca nuts, up-regulates keratinocyte αvß6 expression which induced transdifferentiation of oral fibroblasts into MF. OSMF: Oral submucous fibrosis.

Figure 4 Transdifferentiation of fibroblast into carcinoma associated fibroblast in oral squamous cell carcinoma. Mutual paracrine effect between oral cancer cells and normal fibroblasts is responsible for transdifferentiation of the latter into malignant fibroblasts. CAF: Carcinoma associated fibroblast; TGF-β: Transforming growth factor-β; B.V: Blood Vessels; E-M: Epithelial-mesenchymal.

Figure 5 Functional similarities and differences between wound healing and tumerogenesis. Wound healing and tumour progression phenomenon in relation with MF. TGF-β: Transforming growth factor-β; ECM: Extracellular matrix; CAF: Carcinoma-associated fibroblasts; OSMF: Oral submucous fibrosis; MMP: Matrix metalloproteinase; MF: Myofibroblast.