Abstract. Inflammatory myofibroblastic tumor (IMT) is considered as a benign tumor with local aggressive course, consisting of myofibroblastic spindle cells with an inflammatory cells infiltration. IMTs are more usually found in the lung and very rarely in the mandible. We report an IMT of the mandible in a 54-year-old man. The patient complained of pain on the right side of mandible. Radiographically, the lesion was occupied in the right mandible with bone destruction. Although the initial diagnosis was an osteomyelitis, the histopathologic examination and immunohistochemistry revealed it to be an IMT. Histologically, the lesion was composed of inflammatory cells infiltration within a variably fibroblastic or myofibroblastic spindle cell background. Immunohistochemically, spindle cells stained with smooth muscle actin (SMA) and CD68 (KP1), but uniformly negative with desmin and cytokeratin.

Odontoblasts and/or dental pulp cells are responsible for tooth repair as well as dentin formation. Adhesion and migration are critical processes for tissue regeneration. This study was performed to clarify whether Pam3 modulates adhesion and migration of a murine odontoblast-like cell line, MDPC-23 cell and TLR2 signaling is engaged in this process. TLR2 expression in MDPC-23 cells was examined by RT-PCR. Adhesion assay was performed using type Ⅰ collagen-coated plates. Migration ability was determined by a commercial assay kit. Phosphorylation of IκB-α, JNK, p38, and ERK was examined by Western blot analysis. TLR2 was functionally expressed in MDPC-23 cells. Pam3CSK treatment enhanced adhesion and migration of MDPC-23 cells in a dose-dependent manner. Blockade of TLR2 using its antibody restored Pam3CSK-induced adhesion and migration of MDPC-23 cells. These findings indicate that Pam3CSK, an immune activator from gram negative bacteria, can promote adhesion and migration ability of MDPC-23 cells via TLR2.