Oral carcinogenesis is a multifactorial process involving numerous genetic events that alter normal functions of oncogenes and tumour suppressor genes. This may increase the production of growth factors or the number of receptors on the cell surface, and/or increase transcription factors or intracellular signal messengers. Together with the loss of tumour suppressor activity, these changes lead to a cell phenotype that can increase cell proliferation, with loss of cell cohesion, and infiltration of adjacent tissue thus causing distant metastasis. Molecular pathology is responsible for defining the molecular mechanisms that underlie the onset of oral precancer and cancer. The aim of this review is to describe recent advances in our understanding of the molecular control of the innumerable pathways related to these processes. These may lead to short- or medium term improvements in the diagnosis and prognosis of oral precancerous and cancerous lesions and to the development of novel therapeutic approaches to this disease.