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Strive-The Student View
January, 2010 edition  

Can Oral Sex Be as Dangerous as Smoking?


By Sigrid Goberville

Oral Cancer: An Introduction

Approximately 35,000 people in the U.S. will be newly diagnosed with oral cancer in 2010.[1] Worldwide, the problem is far greater, with new cases annually exceeding 481,000.[1] This is the third year in a row in which there has been an increase in the rate of occurrence of oral cancers; in 2009, there was a major jump of over 11 percent in that single year.[1] One person dies each hour due to complications associated with oral cancer.[1]

Most oral cancers are asymptomatic and diagnosed during the late stage of the disease.[2] When found early, oral cancers have an 80 percent to 90 percent survival rate.[2] Unfortunately, at this time, the majority are found as late-stage cancers, and this accounts for the very high death rate of about 45 percent at five years following diagnosis, as well as high treatment-related morbidity in survivors.[2] Late-stage diagnosis occurs not because these cancers are hard to discover, but because of a lack of public awareness coupled with the lack of a national program for opportunistic screenings that would yield early discovery by medical and dental professionals.[2]

Oral cancer has many symptoms such as sores or lesions in the mouth that do not heal within two weeks; a lump or thickening in the cheek; a white or red patch on the gums, tongue, tonsil or lining of the mouth; a sore throat that does not resolve in one to two weeks, even with antibiotics, or a feeling that something is caught in the throat; difficulty chewing or swallowing; difficulty moving the jaw or tongue; numbness of the tongue or other area of the mouth; coughing up blood; neck pain; and swelling of the jaw that causes dentures to fit poorly or become uncomfortable.[3]

 

Oral Cancer Risk Factors, Changing Demographics and the Human Papillomavirus

There are two distinct pathways by which most people develop oral cancer. The long-recognized one is through the use of tobacco and alcohol. The second is through exposure to the human papillomavirus (HPV), particularly HPV 16, a newly identified etiology, and the same one responsible for the vast majority of cervical cancers in women. Older patients who smoked and drank alcohol used to be the main high-risk group for oral cancer; however, younger patients who may or may not smoke or drink are increasingly affected by the disease.[2] This has been confirmed in younger age groups, including those who have never used tobacco products.[2]

Biological factors associated with oral cancers include viruses and fungi.[4] HPV 16 has been definitively implicated in oral cancers, particularly those that occur in the back of the mouth (oropharynx, base of tongue, tonsillar pillars and crypt, as well as the tonsils themselves).[4]

HPV is a double-stranded DNA virus that infects the epithelial cells of skin and mucosa. It is a common virus, infecting about 40 million Americans today. There are over 120 strains of HPV, most thought to be harmless. Alarmingly, one percent of those infected have the HPV 16 strain, which is a primary causative agent in cervical, anal and penile cancers, and now is a known cause of oral cancer as well.[4] According to the American Cancer Society, 39 percent of oral cancers are related to HPV.[2]

HPV, particularly HPV 16, has now been shown to be sexually transmitted between partners and is conclusively implicated in the increasing incidence of young, non-smoking oral cancer patients.[4] The latest studies show that 46,000 cases of oral cancers are due to sexual activity.[2] In a study conducted at Johns Hopkins Oncology Center, 25 percent of the tumors in 253 patients with head and neck cancer tested positive for HPV.[5] It is believed that in people under the age of 50, HPV may even be replacing tobacco as the primary causative agent in the initiation of the disease process.[6]

The anatomical malignancy sites associated with each pathway (use of tobacco and alcohol and HPV) appear to differ. In the broadest terms, HPV-related lesions appear on the tonsillar area, the base of the tongue and the oropharynx, while the non-HPV-positive tumors tend to involve the anterior tongue, the floor of the mouth, the mucosa that covers the inside of the cheeks and the alveolar ridges.

Researchers are increasingly addressing these two distinct etiologies and discovering additional distinctions. In general, it appears that HPV-positive tumors occur most frequently in a younger group of individuals than tobacco-related malignancies, which occur most frequently in the fifth through the seventh decade of life.[1] HPV-related tumors also occur more in white males and in nonsmokers. The HPV-positive group is the fastest-growing segment of the oral cancer population.

 

HPV, Dysplasia and Oral Cancer

The most dangerous HPVs, 16 and 18, are commonly transmitted through sexual contact.[4] These HPVs can produce two kinds of abnormal tissues: condyloma tissue and dysplasia tissue. Condyloma tissues are wart-like growths that, while usually painless, can cause some irritation, itching or burning. This tissue appears like a small, cauliflower-like growth on the skin. It is nonmalignant and can be treated whenever it flares up. Dysplastic tissue is the presence of abnormal cells on the surface of the skin. Dysplasia is not cancer, but it is a precursor tissue change prior to malignancy.[6] On the female cervix, dysplasia can be detected through a Pap smear test (and the following lab histopathology process), or visually observed with a magnifying glass called a colposcope.[7]

Both HPV16 and HPV 18 express E6 and E7 proteins, which play important roles in the virus’ life cycle and bind to tumor suppressor proteins, inhibiting their suppressive ability.[7] These proteins’ very strong binding capabilities allow HPV16 and HPV18 to reproduce quickly and in great numbers, leading to uncontrolled reproduction of viral cells and eventually cancer.[8]

A study conducted by No-Hee Park, DMD, PhD, showed that the mouth was, at the cellular level, structurally very similar to the vagina and cervix.[9] Both organs have the same type of epithelial cells that are the target of HPV 16. The majority of oral cancers are cancers of epithelial cells, primarily squamous cell carcinomas, and these are not unlike the cancer that affects the cervix. Recognizing the similarities between these tissues and the way that disease that affects them led to the research linking oral cancers to HPV.[10]

 

HPV Transmission, Risk Factors and Prevention

HPV is transmitted only through direct contact, and oral sex is the primary method of transmission.[1] The major risk factor for HPV-related oral cancers is a high number of sexual partners,[11] especially in teenagers.[2] Many teens assume that oral sex is safe and ignore the use of protective measures.[2] It is likely that the changes in sexual behaviors of young adults over the last few decades, and those continuing today, are increasing the spread of HPV and the oncogenic versions of it.

HPV attaches to moist epithelial surfaces (squamous cells), which include all areas covered by skin and/or mucosa such as the mouth, throat, tongue, tonsils, vagina, penis and anus. Transmission occurs when these areas come into contact with the virus, allowing it to transfer between the epithelial cells of the infected person with that of the newly infected person.[11] While it is established now that sexual contacts, both genital and oral, are means of transferring HPV, other transfer pathways are not fully understood. It is not known why certain HPV types target skin on the hands or feet, for example, while others attack the cells lining the mouth, and still others the genitalia of both males and females.[11]

Park’s study of mouth tissue also showed that smoking and drinking alcohol help promote HPV invasion.[12] Alcoholic beverages contain ethanol alcohol, and ethanol is known to inhibit the production of the p53 protein. The carcinogens in tobacco have been shown to damage cell DNA, the precursor event to malignancy.[12] More recent work seems to indicate that the relationship among tobacco, alcohol and HPV is compounding in its effect as opposed to synergistic. This means that one factor alone (tobacco or HPV) can be enough to begin the cascade of cellular events that culminate in a cancerous cell.[12]

 

Role of the Oral Health Care Provider

HPV-related oral cancer is rapidly increasing.[13] Early detection is the key to survival, and oral health care providers can help by communicating with physicians. HPV questions on medical history forms, annual screening for all patients (not only high-risk patients), and an examination in the dental office that includes a thorough extra-/intraoral cancer screening using the toluidine blue dye and fluorescence visualization are tools that facilitate early detection.

Any suspicious lesions should be sent for biopsy or referred for further evaluation. Tumors should be surgically removed, followed by radiation therapy, chemotherapy and continuing education. Prior to the commencement of curative treatment, it is likely that other oral health needs will be addressed to decrease the likelihood of developing post-therapeutic complications.[2]

Teeth with poor prognosis from periodontal problems, caries, etc., may be extracted. This avoidance of post-radiotherapy surgery is important, as surgery can sometimes induce osteonecrosis, a condition that can develop when tissue damaged by radiation exposes the underlying bone. The bone, which, as a result of the radiation exposure, has lost its ability to efficiently repair itself due to reduced blood supply, yields a chronic and difficult-to-treat situation.[1] A thorough prophylaxis is indicated as well.

 

Conclusion: Can Oral Sex Be as Dangerous as Smoking?

Oral sex is not as dangerous as smoking, but it is still dangerous, and precautions are warranted. Oral sex has been identified as the number one mode of HPV transmission to the oral cavity.[1] More and more studies are showing that, with the increase in warnings and information about sexually transmitted diseases, more people, adolescents especially, are looking at oral sex as the safe alternative.[2] However, oral sex is not a safe alternative.[2] We need to inform teenagers and parents about the link between HPV and oral cancer. We need to stress precautionary measures including abstinence, monogamy, use of condoms and dental dams and the HPV vaccine (for women under the age of 26). Nor should we neglect to continue educating patients about traditional risk factors such as tobacco use, alcohol consumption, traumatic lesions and sun exposure; as well as encourage them to visit their oral health care provider regularly.

References

  1. The Oral Cancer Foundation Web site. Available at www.oralcancerfoundation.com. Accessed Dec. 9, 2009.
  2. American Cancer Society Web site. Available at www.cancer.org. Accessed Dec. 9, 2009.
  3. The Oral Cancer Foundation Web site: diagnosis. Available at www.oralcancerfoundation.com/diagnosis. Accessed Dec. 9, 2009.
  4. The Oral Cancer Foundation Web site: oral cancer facts. http://www.oralcancerfoundation.org/facts/index.htm. Accessed Dec. 9, 2009.
  5. Vizilite Web site. Available at www.vizilite.com.
  6. HPV: cervical dysplasia questions and answers. American Social Health Association Web site. Available at http://www.ashastd.org/learn/learn_hpv_dysplasia.cfm. Accessed Dec. 9, 2009.
  7. Oh ST, Longworth MS, Laimins LA. Roles of the E6 and E7 proteins in the life cycle of low-risk human papillomavirus type 11. J Virology 2004; 78(5): 2620-6. Available at http://jvi.asm.org/cgi/content/full/78/5/2620. Accessed Dec. 9, 2009.
  8. American Society for Microbiology Web site. Available at www.asm.org
  9. RDH magazine. Everyone is at risk for oral cancer. Available at www.rdhmag.com/display_article/343446/54/none/none/IndNw/Everyone-is-at-risk-for-oral-cancer. Accessed Dec. 9, 2009.
  10. The National Cancer Institute Web site. Available at http://www.nci.nih.gov/. Accessed Dec. 9, 2009.
  11. Dental health and sex. Available at www.dentalgentlecare.com/dental_health_and_sex.htm. Accessed Dec. 9, 2009.
  12. Patient’s guide: human papillomavirus. Available at www.mouthcancerfoundation.org. Accessed Dec. 9, 2009.
  13. Web MD. Available at www.webMD.com. Accessed Dec. 9, 2009.

Sigrid Goberville is a dental hygiene student at Palm Beach State College. She resides in Parkland, Fla., with her husband and three children.

The faculty mentor for this edition of Strive was Judy McCauley, RDH, MA.


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