TDA Meeting Preview

HPV and Oral Cancer: Fear, Facts, and the Future

Event: HPV and Oral Cancer in Young Patients: What Have We Learned?

Speaker: Thomas Schlieve, DDS, MD

Date: Friday, May 5

Time: 1:30 PM - 4:00 PM

Code: F26

Speaker

Thomas Schlieve, DDS, MD

UT Southwestern Medical Center

Texas Health- Dallas Presbyterian Medical Center, Parkland Memorial Hospital

Correspondence: Thomas Schlieve

6333 Forest Park Blvd, Dallas, TX 75390-9193

Thomas.Schlieve@utsouthwestern.edu

Ph: 214-645-3999 • Fax: 214-645-3989

Cell: 262-993-3432

The increasing rate of head and neck cancer is alarming. In 2005, approximately 29,000 oral cavity and pharyngeal cancers were documented in the United States. In 2015 that number rose to 48,000 and most recently it is estimated that there are 66,000 cases annually representing an increase of over 100% in just 15 years. These numbers are even more staggering when we consider the number of cases specific to the tongue and pharynx and when in comparison to other cancers, such as cervical cancer. It is estimated that there will be over 36,000 tongue and pharynx cancers this year, with over 26,000 of those cancers in males. Increases of 130% and 160% respectively. In contrast, cervical cancer has decreased from 9.7 cases per 100,000 people to 7.5 cases per 100,000 people during that same time period. Along with an overall increase in head and neck cancer, there has been a greater than 4-fold increase in oral squamous cell carcinoma in patients younger than 40 years of age (Figure 1,2). An investigation into the cause of this drastic increase in cancer incidence is of paramount importance.

The history of human papillomavirus (HPV) in the head and neck regions began in 1901 with the discovery of transmission of oral warts between individuals. Further research on HPV was driven by its infection of cervical tissues and the discovery of koilocytic atypia as a sign of HPV infection. It was not until 1989 that HPV16 DNA was noted in tonsillar squamous cell carcinoma, 2000 when the first causal associations of HPV and Head and Neck Cancer were reported, and 2010 when a survival advantage to HPV positive cancer was demonstrated. Since that time, our understanding of HPV infection, carcinogenesis, risk stratification, and treatment has evolved considerably.

In addition to the discovery of the connection between HPV and infection, the role of infection and inflammation in numerous cancer subtypes has been deciphered. In 1863, Rudolph Virchow first hypothesized that cancers could be driven by an inflammatory process and it is this observation that evolved into the current concept that the inflammatory microenvironment represents a risk factor for cancer development. It is accepted that infection with Hepatitis virus, Epstein-Barr virus, and Heliobacter Pylori bacteria can cause cancers of the liver, nasopharynx, and stomach respectively. Chronic inflammatory conditions such as Celiac disease, inflammatory bowel disease, chronic pancreatitis and gastric reflux can lead to cancers such as lymphoma, colon cancer, pancreatic cancer, and gastric cancer.

HPV is an epitheliotropic oncogenic double stranded circular deoxyribonucleic acid virus with over 120 different genotypes and only infecting humans. The larger group of papillomaviruses is one of the oldest known viruses with a history of some 330 million years. HPV causes both cutaneous and mucosal infection, with a specific subset of genetic types associated with the development of cancer (termed High Risk Subtypes). A much larger group of these viruses causes the “common” hand and foot warts that many people are familiar with or the oral papilloma that many dentists are accustomed to seeing (Figure 3). These visible lesions associated with HPV are not precursors to cancer or indicative of infection with one of the cancer-causing subtypes. It is important therefore to understand that there is no pre-malignant oral or throat lesion warning us to the presence of HPV infection and/or carcinogenesis in progress. Another important but often confusing feature of HPV-induced cancer is the very long latency period- the time from infection to cancer. Most individuals will contract HPV at a young age, becoming chronic carriers of the virus, and then develop their throat cancer some 30 years or more later. An HPV related cancer does not imply infidelity.

Cervical cancer, oropharyngeal cancer, penile cancer, anal cancer, vaginal cancer and vulvar cancer have all been associated with high-risk HPV infection and the percentage of these cancers attributable to HPV is on the rise as we develop improved methods of detection. If we know that PHV infection can lead to cancer, the medical miracle would be a medication, shot, IV infusion or other treatment that could prevent the infection and subsequent development of so many cancers. Fortunately, that medical miracle is already here in the form of the HPV vaccine.

The HPV vaccine has been in use since 2006. Systematic reviews of available data have demonstrated a high safety profile in over 60 million people. Vaccination has effectively decreased the rate of oral HPV infection, cervical HPV infection, and the precancerous changes associated with HPV infection.

TDA Council on Ethics and Judicial Affairs

This article is a reprint of a previously published article. For citation purposes, please use the original publication details; Nichols K; Pappas R. The #ethics behind social media influencers in dentistry. J. Am. Dent. Assoc. 2022; 153(10):1010-1011. https://doi.org/10.1016/j.adaj.2022.07.008.