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Research: "Saliva - a pivotal player in the pathogenesis of oropharyngeal cancer. Reznick AZ, Hershkovich O, Nagler RM."
Br J Cancer. May 25th, 2004.
Cigarette smoke transforms healthy saliva into a deadly cocktail that can accelerate mouth cancer, according to research in the British Journal of Cancer.
Normally, saliva provides a protective buffer between toxins and the lining of the mouth because it contains important enzymes that fight and neutralise harmful substances.
But this research shows that the chemicals in tobacco smoke combine with saliva with devastating effect. They destroy the protective components of saliva, leaving a corrosive mix that damages cells in the mouth and can eventually turn them cancerous.
There are nearly 8,000 cases and 3,000 deaths from mouth cancer in the UK every year - the main cause being smoking. These figures refer to cancers of the head and neck, which include nose, mouth, lips, tongue, gums, tonsils, pharynx and larynx cancer.
The presumed connection between oropharyngeal cancer and cigarette smoke was based on the assumption that a constant direct attack of various carcinogens from cigarette smoke causes widespread accumulating cellular and DNA damage in the mucosal cells, in turn eventually resulting in malignancy. However, there is never a direct contact between cigarette smoke and the oral mucosa. Saliva covers the mucous membranes from the oral cavity to the larynx, and cigarette smoke must first interact with saliva before it reaches the mucosa.
The researchers in this study wanted to examine the role of saliva in the development of mouth cancer:
“A synergistic effect of Cigarette Smoke (CS) and saliva on oral cancer cells was demonstrated. This synergism is based on the reaction between redox active metals in saliva and low reactive free radicals in CS, which results in the production of highly active hydroxyl free radicals. Thus, when exposed to CS, salivary behavior is reversed and the saliva loses its antioxidant capacity and becomes a potent prooxidant milieu. The devastating role of CS-borne aldehydes was demonstrated as well.
“Based on these results and on our recent reports demonstrating that cigarette smoking destroys various salivary components, including protective ones such as peroxidase, the most important salivary antioxidant enzyme, a comprehensive view of the pivotal role of saliva in the pathogenesis of CS-induced oropharyngeal cancer is suggested.”
The research looked at the role of saliva in mouth cancer, but failed to take one important factor into account: salivary ABH secretor status.
Although salivary non-secretor status does not appear to be an associated risk marker for the development for oral cancer itself, being a non-secretor is a high risk factor for oral epithelial dysplasia.
Oral epithelial dysplasia is a disorder of differentiation of epithelial cells, and is likely to manifest as a solitary white patch. It is not possible to accurately predict the likely degree of dysplasia from the clinical features of such lesions, which may regress, remain stable, or progress to invasive carcinoma.
However there is also a strong link with non-secretor status and two other mouth conditions: chronic hyperplastic candidosis, where some degree of dysplasia may often be present, and also with potentially malignant oral lesions such as candidal leukoplakia, in which there is a risk of malignant change that may be greater than that of other leukoplakias.
It would perhaps be useful if future research into the role of cigarette smoking saliva and oropharyngeal cancer took secretor status into account.
The destruction of protective antioxidant substances in the saliva and the effect of other toxins in cigarette smoke are two more reasons to add to the many deterrents to smoking.
Tobacco addiction may be helped by the use of the herb Lobelia, which reduces cravings, but this should be taken under the supervision of a physician as it can be toxic in high doses. Eating oats regularly may also help, as they have sedative properties.
Vidas I, et. Al. Examining the secretor status in the saliva of patients with oral pre-cancerous lesions. J Oral Rehabil. 1999 Feb;26(2):177-82.
Lamey PJ, Douglas PS, Napier SS. Secretor status and oral cancer. Br J Oral Maxillofac Surg. 1994 Aug;32(4):214-7.
Lamey PJ, et. Al. Chronic hyperplastic candidosis and secretor status. J Oral Pathol Med. 1991 Feb;20(2):64-7.
Anand CL. Effect of Avena sativa on cigarette smoking. Nature. 1971 Oct 15;233(5320):496.
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