Is Oral Sex to Blame for the Surge in Cancer of the Mouth and Throat?

It's the typical culprit, but other factors, including immune changes, damage from nicotine, and even a genetic disposition, could play a part.


Earlier this month, the American Cancer Society (ACS) released its annual Cancer Facts & Figures. The 2012 report includes some encouraging facts. Since 1990, the incidence of some common tumors including lung, colon, and prostate cancer has declined. Meanwhile, the rate of seven malignancies, like those of the lower mouth and throat linked to human papillomavirus (HPV), is increasing. The cause of this trend, which many assume is linked to people engaging in more oral sex, is not as straightforward as you might think.

Oropharyngeal cancers refer to tumors of the tonsils and rear tongue, back of the palate and posterior walls of the throat. Like their anatomical neighbors -- malignancies of the larynx, vocal cords, anterior and mid-tongue, other parts of the mouth and lips -- oropharyngeal cancers arise more often in people who drink and smoke heavily. These other head and neck cancers have waned in recent years, probably because North Americans are smoking fewer cigarettes and chewing less tobacco.

The ACS estimates there will be 13,500 new cases of oropharyngeal cancer in the U.S. this year. This includes both HPV positive and negative cases; nearly 11,000 men and over 2,500 women will be affected; some 2,300 will succumb to this condition. Between 1999 and 2008, the rate of HPV positive oropharyngeal cancers by rose 4.4 percent per year in white men and by 1.9 percent per year in white women. Changes among other racial and ethnic groups were not significant, according to the report. The biggest rise emerged in men between the ages of 55 and 64 years.

"At Georgetown, we have patients in their 80s with this kind of cancer. That raises questions about the sexual habits of Americans who are older, or about HPV."

"Like investigators elsewhere, we're seeing an increased incidence of oropharyngeal cancer," says Dr. John Deeken, a medical oncologist at Georgetown's Lombardi Cancer Center. Cancer-causing HPV strains tend to infect immune cells at the base of the tongue and tonsils, Deeken explains. "This may be why we're seeing the virus in tumors in those parts of the oropharynx, while the incidence of lip, larynx, and vocal cord cancers is not going up." If the cancer were simply caused by infection with HPV upon sexual transmission there would be more cases in women, he considers.

"The epidemiology is perplexing," he says. "The assumption, when we noticed the trend eight or nine years ago, was that this was a sexually transmitted disease due to more oral sex," he says. "But at least at Georgetown, we have patients in their 80s with this kind of cancer," he notes. "That raises questions about the sexual habits of Americans who are older, or about HPV."

The latency period between initial HPV infection and cancer can last decades, confirms Dr. Maura L. Gillison, an oncologist and professor at Ohio State who has published seminal findings on HPV and cancer. Her group carried out a case control study, reported in the New England Journal of Medicine, revealing that individuals who've had more vaginal and oral sex partners in their lifetime have a higher risk of developing oropharyngeal cancer, and that HPV-16 infection correlates with this cancer type.

Human papillomavirus was one of the first viruses identified in human cancers. Approximately 40 subtypes spread sexually. Two types, HPV-16 and HPV-18, account for most cases of cervical cancer in the U.S. Most women with HPV are asymptomatic and don't get cervical cancer; when and if malignancy develops, it's usually 20, 30 years or longer after initial infection. Most often, oropharyngeal cancers are caused by the HPV-16 subtype.

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Elaine Schattner is a physician and journalist based in New York City.

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