As clinicians, we all know that oral cancer, when diagnosed in its later stages, can be disfiguring and deadly. We’ve also been trained to look at alcohol and tobacco use as two of the main factors, other than family history, that put patients in the high-risk category.
There is a relatively new risk factor that is rapidly overtaking smoking and drinking as the primary etiologic factor for newly-diagnosed cases of oral cancer: the oral human papillomavirus, or HPV. Of the 34,000 cases of oropharygeal cancers diagnosed each year, HPV is now found in up to 50 percent of them.1
So now we have a new causal suspect, and to make early diagnosis of cancerous lesions more challenging than ever, oral HPV-caused cancers generally occur in the back of the throat or base of the tongue, well beyond the view of a well-trained clinician’s naked eye—even when aided by an adjunctive screening technology such as VELscope. In other words, the tumor is below the horizon.
This may be the reason why a person like the actor Michael Douglas, who had access to the best medical care available, was diagnosed with oropharyngeal cancer at stage 4. Although Mr. Douglas’ cancer has not been officially attributed to oral HPV, the location of his tumor at the base of his tongue and beyond the clinician’s visual field fits the profile.
For every Michael Douglas, there are about 1,700 more people developing HPV-related oral cancers each year.1 The risk profile for oral HPV includes anyone over the age of 12 who is sexually active or who has had more than three sex partners.2
If you are a parent, you hate to think that your child can be infected with a sexually transmitted disease before they graduate from middle school, but this is the new reality, which is the result of a rampant misperception that oral sex is safe sex. This new reality is one of the drivers behind the evolution of dentistry to oral medicine and its paradigm shift from a disease model to a wellness model.
Another catalyst of this paradigm shift is salivary diagnostic testing. OralDNA Labs recently introduced the OraRisk HPV test, a noninvasive, easy-to-use screening tool for identifying the various types and levels of oral HPV infection, especially HPV-16 and HPV-18, which are the variants most commonly linked to oral cancer.3,4
The OraRisk HPV test is science made simple. It is a 30-second saline rinse & gargle, whereby the collected specimen is sent to the OralDNA laboratory in Brentwood, TN for advanced DNA analysis. Within 7 to 9 days, the dentist receives a report that indicates whether the patient is positive or negative for HPV.
Armed with this salivary diagnostic test, dentists are in a perfect position to diagnose oral HPV early, and have not only a positive impact on patient outcomes, but also the spread of HPV. For if patients are told they are infected with oral HPV, perhaps some of them will be responsible and practice safe sex.
Despite the potential for salivary diagnostic tests to help clinicians detect oral cancer earlier and also become stewards of public health in general, there are some naysayers who are recommending against incorporating this promising technology into everyday practice. Two of the most common reasons given are:
1. Oral HPV is frequently eradicated by the body’s own immune system.
2. When and how often should oral HPV retesting take place to determine the persistence of the infection?
OralDNA Labs recommends that the treating clinician follow standard follow-up protocols for patients who are determined to be at risk for oral cancer, regardless of whether the cause is tobacco, alcohol, or oral HPV.
In the case of a positive oral HPV diagnosis where there are no visible legions, this would result in a “watchful waiting” protocol, where the clinician keeps an eye on the infection and the possible development of lesions with periodic salivary tests and visual inspections. This is not unlike the watchful surveillance approach that urologists take with some patients diagnosed with prostate cancer.
Although it is true that the vast majority of patients who have oral HPV will not develop oral cancer, it is also true that many patients who are positive for oral HPV will develop oral cancer that is caused by oral HPV. Salivary diagnostic testing now makes it possible to look for the 1 person in 100 patients who may develop oral cancer after contracting an oral HPV infection. Extrapolate that number across the entire population who fit the at risk profile for oral HPV, and you’re talking about a lot of lives.
In my opinion, dismissing new screening tools and doing nothing is restricting our standard of care for oral cancer diagnosis, and presents the greatest risk to the very patients who put their health and, in some cases their lives, in our hands.
About the Author
Ron McGlennen, MD, is the Chief Medical Officer of OralDNA Labs Inc., a leading provider of salivary diagnostic tests to the dental profession, and a subsidiary of Quest Diagnostics Incorporated. Dr. McGlennen is board certified in Anatomic and Clinical Pathology, and also board certified by the American Board of Medical Genetics, with a specialty in Clinical Molecular Genetics. He is internationally recognized as an expert in Molecular Biology and Genetics.
References
1. Saraiya M, Kawaoka K. Incidence of human papillomavirus (HPV)-related head and neck cancers in the US from 1998-2003: Pre-HPV vaccine licensure. Proc Am Soc Clin Oncol. 2007;25:299s.
2. Heck JE, Berthiller J, Vaccarella S, Winn DM, Smith EM, Shan’gina O, Schwartz SM, Purdue MP, et. al. Sexual behaviours and the risk of head and neck cancers: a pooled analysis in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Int J Epidemiol. 2010 Feb;39(1):166-81. Epub 2009 Dec 18.
3. Herrero R, Castallsague X, Pawlita M, et al. Human papillomavirus and oral cancer: The International Agency for Research on Cancer multicenter study. J Natl Cancer Inst. 2003; 95:1772-1783.
4. Kreimer AR, Clifford GM, Boyle P. Human papillomavirus types in head and neck squamous cell carcinomas worldwide: a systematic review. Cancer Epidemiol Biomarkers Prev. 2005; 14:467-475.
