Oral lichen planus and the p53 family: what do we know?

J Oral Pathol Med. 2011 Apr;40(4):281-5. doi: 10.1111/j.1600-0714.2010.00979.x. Epub 2010 Dec 8.

Abstract

Oral lichen planus (OLP) is a relatively common chronic disease of the oral mucosa for which the aetiopathogenesis is not fully understood. It mainly affects middle aged and elderly. The finding of autoantibodies against p63, a member of the p53 family, is a strong indication of autoimmunity as a causative or contributing factor. The WHO classified OLP as a potentially malignant disorder, but still there is an ongoing debate in the literature on this subject. The TP53 gene encodes a tumour suppressor protein that is involved in induction of cell-cycle arrest or apoptosis of DNA-damaged cells. The p63 gene encodes six different proteins that are crucial for formation of the oral mucosa and skin. The coordinated stabilization of p53 and decreased expression of p63 seen in OLP cause induction of apoptosis enabling removal of DNA-damaged cells. In view of the complexity of cancerogenesis, no firm statement can at present be made about the relevance of the observed relationship between p53 and p63 and the possible malignant transformation of OLP.

Publication types

  • Review

MeSH terms

  • Apoptosis / genetics
  • Autoimmunity / genetics*
  • Cell Transformation, Neoplastic / genetics
  • DNA-Binding Proteins / genetics
  • Genes, p53*
  • Humans
  • Lichen Planus, Oral / genetics*
  • Lichen Planus, Oral / immunology
  • Membrane Proteins / genetics
  • Multigene Family
  • Nuclear Proteins / genetics
  • Protein Isoforms
  • Tumor Protein p73
  • Tumor Suppressor Proteins / genetics

Substances

  • CKAP4 protein, human
  • DNA-Binding Proteins
  • Membrane Proteins
  • Nuclear Proteins
  • Protein Isoforms
  • Tumor Protein p73
  • Tumor Suppressor Proteins