Oral Lichen Planus as a Preneoplastic Inflammatory Model

Figure 1

The current hypothesis on the development of dysplasia and cancer in OLP suggests that changes in epithelial cells (keratinocytes) is a result of detuning in cellular replication, DNA damage and disorganization of epithelial integrity, secondary to oxidative stress, cytokine, and transcription factor signals originating from the inflammatory infiltrate.