Oral lichen planus (OLP) is a chronic inflammatory disease characterized by T-cell infiltration immediately under the basement membrane (BM), hyperkeratosis, BM damage, and basal cell liquefaction. As to the etiology of OLP, cellular immunity abnormality is believed to play some role. BM damage, basal cell liquefaction and tissue remodeling associated with OLP require degradation of surrounding exracellular matrix (ECM).

Objective: In order to clarify molecular mechanism of OLP related inflammatory change, we immunohistochemically examined urokinase-type plasminogen activator (uPA), uPA receptor (uPAR) and matrix metalloprotenase (MMP)-2, 3, 9 expression in OLP.

Materials and Methods: Subject comprised 15 patients diagnosed with OLP and treated at the Department of Dentistry, Oral and Maxillofacial Surgery, Jichi Mecical University Hospital. Immunohistochemical staining was performed using biopsy samples. The primary antibodies used were anti-human uPA monoclonal antibody, anti-human uPAR monoclonal antibody (American Diagnostica USA), anti-human MMP-2, 3, 9 nomoclonal antibodies (Fine Technology Japan). Microdissection-based RT-PCR was used to confirm mRNA expression.

Results: uPA protein was mostly localized from the spinous cell layer to the BM, and uPAR protein was seen in macrophages and some cellular membranes from the spinous cell layer to the BM in OLP. Expression of uPA and uPAR was localized to areas of cell proliferation. MMP-2 and MMP-3 proteins were localized from the spinous cell layer to the BM, and MMP-9 protein was mostly seen in areas with BM and epithelium degeneration showing marked inflammatory changes. Microdissection-based RT-PCR confirmed mRNA expression of uPA in the spinous cell layer to the BM of OLP lesion. Conclusion: These results suggest that not only MMP-2, 3, 9 but also uPA and uPAR play an important role in BM degeneration, basal cell liquefaction and tissue remodeling of OLP lesion.

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