Cell cycle and programmed cell death are closely related to the development of oral diseases. Cyclins, cyclindependent kinase(CDK), and cyclin-dependent kinase inhibitor are the major important moleculars for the regulation of cell cycle. Cyclin-dependent kinase inhibitor protein(CIP) and kinase inhibited protein(KIP) are constituted by P21, P27, and P57, which are involved in regulating cell cycle, cell death programming, and inhibiting the activity of CDK. Most of the tissue destruction of oral disease is caused by pathogens that disturb host cell proliferation and programmed cell death. The reduced or absent expression of CIP and KIP leads to junctional epithelium thickening, leukoplakia with epithelial dysplasia, and uncontrolled proliferation of tumor cells. Therefore, CIP and KIP plays an irreplaceable role in the regulation of gingival epithelial cell proliferation, the maintenance of periodontal tissues, and the expression level and activity of their work as an important target of canceration of oral leukoplakia and the progression and prognosis of tumors. This article focuses on the composition and function of CIP and KIP and the relationship between CIP-KIP and oral disease.
