Research has shown that people with certain risk factors are more likely than others to develop oral cancer. A risk factor is anything that increases your chance of developing a disease.
The following are risk factors for oral cancer:
Tobacco: Tobacco use accounts for most oral cancers. Smoking cigarettes, cigars, or pipes; using chewing tobacco; and dipping snuff are all linked to oral cancer. The use of other tobacco products (such as bidis and kreteks) may also increase the risk of oral cancer. Heavy smokers who use tobacco for a long time are most at risk. The risk is even higher for tobacco users who drink alcohol heavily. In fact, three out of four oral cancers occur in people who use alcohol, tobacco, or both alcohol and tobacco.
Alcohol: People who drink alcohol are more likely to develop oral cancer than people who don't drink. The risk increases with the amount of alcohol that a person consumes. The risk increases even more if the person both drinks alcohol and uses tobacco.
Sun: Cancer of the lip can be caused by exposure to the sun. Using a lotion or lip balm that has a sunscreen can reduce the risk. Wearing a hat with a brim can also block the sun's harmful rays. The risk of cancer of the lip increases if the person also smokes.
During the 88th General Session & Exhibition of the International Association for Dental Research, in Barcelona, Spain, author J. Meyle, Justus Liebig University, Giessen, Germany, presented an abstract titled "P. gingivalis Infection and Immune Evasion of Oral Carcinomas."
Meyle and his team are investigating the relationship of oral cancers and periodontal disease. They achieved results by infecting cell carcinoma cells SCC-25 with Porphyromonas gingivalis (P.g.) W83. After 48h the cells were stained with antibodies against human B7-H1, B7-DC and TLR4 and analysed by flow cytometry. RNA was extracted after 24h and gene expression of B7-H1, B7DC, TLR4, IFN-γ and IL-10 was quantified by real time PCR and analysed by the (2 triangles)CT method.
Up-regulation of B7-H1 in host cells may contribute to the chronicity of inflammatory disorders which frequently precede the development of human cancers. B7-H1 expression was detected in the majority of human cancers and leads to anergy and apoptosis of activated T cells, which might enable tumors to evade the immune response. TLR4 signalling has been shown to induce B7-H1 in bladder cancer cells.
P.g., a putative periodontal pathogen, is an etiologic agent of periodontitis and expresses a variety of virulence factors. In this study the expression of B7-H1 and B7-DC receptors and TLR4 on squamous cell carcinoma cells SCC-25 was analysed after infection with P.g. in vitro.
The research concludes that P.g. is able to induce the expression of the immune regulating receptors B7-H1 and B7-DC in squamous cell carcinoma which may facilitate immune evasion of oral cancers in patients with periodontal infections.
