Jack: Hi everyone.
In this lecture, we'll be discussing epidemiology
of cancers of the oral cavity.
Our goals for this lecture
are to review the anatomy and function of the oral cavity,
to summarize the global pattern
of deaths from oral cavity cancer,
as well as the incidence.
We'll describe high-risk populations
and review key studies of tobacco, alcohol,
and oral cavity cancer.
We'll also describe tobacco and alcohol carcinogenesis
and review studies of HPV and oral cavity cancer.
Finally, we're going to describe
other risk factors for oral cavity cancer.
So first, to give a brief overview
of the anatomy of the oral cavity,
it's also known as the mouth.
It's the initial portion of the alimentary canal.
The digestive process begins when food enters
the oral cavity and is mechanically masticated
or mechanically digested by chewing.
It is moistened by saliva and undergoes reactions
with salivary enzymes to initiate chemical digestion.
Anatomic structures of the oral cavity include the lips,
teeth, hard and soft palate,
upper and lower gingiva or gums,
the tongue, the uvula, tonsils, and pharynx.
The pharynx is a channel situated behind the oral cavity
and beneath the nasal cavity
that extends to the level of the larynx.
The oropharynx is continuous,
with the back of the oral cavity
extending from the soft palette to the epiglottis.
A closely related structure is the nasopharynx,
which is a channel that connects the nasal cavity
and paranasal sinuses
to the upper portion of the oropharynx.
The laryngopharynx is the portion of the pharynx
between the oropharynx and larynx.
Finally, the oral cavity and pharynx are lined
by stratified squamous epithelium,
which is important when we discuss
the various types of cancers
that can occur in the oral cavity.
So we see that there's a number of benign
or non-cancerous tumors of the oral cavity and oropharynx.
Most tumors of the oral cavity are benign,
but some are pre-malignant.
For example, leukoplakia
and erythroplakia are pre-malignant lesions
and should be removed.
Without treatment, these two kinds of tumors
may transform into invasive squamous cell
carcinoma of the oral mucosa,
though this transformation is estimated
to take 5 to 10 years.
When we think about the histology of oral cavity cancer,
more than 90% of malignant tumors of the oral cavity
and related structures are squamous cell carcinomas,
which arise from the mucosal lining of the oral cavity.
5% are a dental carcinomas
arising from the salivary glands within the mouth.
Late-stage diagnosis is common,
and survival rate for oral cancer
has not changed over the past three decades.
When we turn to look at the incidence rates
for cancer of the lip and oral cavity,
we see the malignancies of the oral cavity and lip
caused 145,328 deaths in 2012.
And there were significantly more deaths
in men than in women.
In the same year, in 2012,
300,373 new cases of oral cavity
and lip cancer were diagnosed
with approximately 200,000 being diagnosed in men
and approximately 100,000 being diagnosed in women.
This represents an overall increase of 14.1%
from 2008 to 2012.
Cancers of the lip and oral cavity
constitute approximately 2.1% of all malignant neoplasms
and account for about 1.8% of cancer deaths
in the human population.
Rates of oral cavity cancer are highest
in populations with high rates of tobacco and alcohol use.
So rates are very high in populations
where individuals commonly chew, (indistinct),
or practice reverse smoking.
And rates of lip cancer are high
in Australia and New Zealand
due to the high levels of solar radiation there.
When we turn to look at mortality,
we see mortality rates
that track closely with incidence rates.
So a high mortality rates in areas exposed
or in communities exposed to risk factors for oral cancer.
When we look at 2020 data in the United States,
we see that the overall incidence
was 4.1 per 100,000 people,
with a rate in men almost three times that of women.
When we look at mortality,
overall, there was 1.9 deaths per 100,000 people,
and 2.8 deaths per 100,000 men,
while only 1 death per 100,000 women.
In the US, cancers of the oral cavity
and oropharynx represent approximately 3%
of all malignancies in men
and 2% of all malignancies in women.
When we look at some of the risk factors
for oral cavity cancer, we see that tobacco use
is responsible for more than 90% of tumors
of the oral cavity among men and 60% among women.
Tobacco use is responsible for 90%
of oral cancer deaths in males.
All forms of tobacco, cigarettes, pipes, cigars,
and snuff have been implicated
in the development of oral cancers,
and while tobacco confers the highest rate of cancer
of the floor of the mouth, it's associated
with an increased risk for all sites of oral cancer.
We also see that alcohol use
is an independent major risk factor
for the development of oral cancer,
and there's a suggestion that beer and hard liquor
confer a greater risk than wine.
We also see that the risk of oral cancer increases
with the number of cigarettes smoked per day,
as well as the number of alcoholic drinks consumed per day
in a dose-dependent fashion.
The combined use of alcohol and tobacco
increases the risk for oral cancer
far greater than either independently,
as we can tell from this figure.
We also see that tobacco and alcohol use
have been associated with the development of leukoplakia
or erythroplakia which can progress to cancer.
When we look at the etiology and biology of oral cancer,
we see that there's a number of risk factors.
There appears to be an association
between human papillomavirus or HPV and oral cancer,
and in particular, HPV type 16.
Multiple case control studies have shown this association.
Independently, the Association of HPV infection
with oral cancer is much lower than tobacco or alcohol,
although it can modify the effect of these two substances.
We also see that there's relationships
between other viral infections and oral cancer in humans,
and those would be human immunodeficiency virus, or HIV,
and Epstein-Barr Virus, or EBV.
Oral cancer is also known to exhibit field cancerization,
resulting in development of second primary tumors.
Studies utilizing a variety
of chemo preventive interventions
have demonstrated promising results
for induction of apoptosis in oral malignant
and pre-malignant cells.
In HPV-16 related disease,
chronic exposure to tobacco and alcohol may be absent.
The age of diagnosis is much earlier, 20 to 50 years.
The male to female ratio is closest to one to one
and tumors develop on the tonsils and base of the tongue.
HPV-16 and 18 are the same viruses responsible
for the vast majority of cervical cancers,
and HPV is the most common sexually transmitted infection
in the US and elsewhere.
Though, as we've discussed before,
infection by these high-risk HPV strains
is preventable by vaccination.
The Plummer-Vinson Syndrome,
which is characterized by iron deficiency, dysphagia,
and atrophy of the oral cavity mucosa
is associated with predisposition to oral cavity cancer.
Other conditions, which associated
with oral cavity neoplasms include sprue,
which is the malabsorption of wheat germ,
and scurvy, or deficiency in vitamin C.
Pipe smoking and cigar smoking,
sunburn, and other excessive exposures
to UV radiation are noted risk factors
for development of squamous cell carcinomas of the lip.
We also see that rare malignant neoplasms
of the oral cavity include cancers of the salivary glands,
including the parotid glands and submandibular glands.
These are typically glandular carcinomas
with mixed histologic features.
The risk of salivary gland cancer is increased
by ionizing radiation like that which occurs
in atomic bomb survivors and after radiotherapy.
We also see that malignant melanomas
can present initially in the oral cavity.
Certain genetic syndromes predisposed
to oral cavity malignant melanomas
including Peutz-Jeghers syndrome and Addison's disease,
both of which lead to melanotic pigmentation
of the oral cavity mucosa.
Finally, to briefly discuss the etiology
and biology of oral cancer,
we see that the cessation of cigarette smoking
is associated with a 50% reduction
of risk of developing oral cancer
within three to five years, and a return to normal level
of risk for development of oral cancer within 10 years.
Because of this, dentists
and other health professionals can play an integral role
in smoking cessation advice and encouragement.
Dentists can also participate
in the full scope of pharmacological
and behavioral interventions for smoking cessation.
However, only 25% of tobacco users
report receiving advice to quit tobacco use
from their dentist, a proportion that is less
than that is received from their physician.
Because alcohol is associated with oral cancer
in a dose-dependent fashion,
cessation or avoidance of alcohol
would result in lower incidence of oral cancer.
The evidence is inadequate, however, of reduced oral cancer
among people who have stopped consuming alcohol.
Several studies also have shown an inverse association
of fruit intake and the development of oral cancer,
particularly in those who use tobacco.
Fiber in the form of vegetable intake
has similarly been shown to be associated
with a decreased risk of oral cancer.
It's estimated that intake of fruits
and vegetables may lower the development
of oral cancer by 30% to 50%.
The evidence is inadequate, however, of reduced oral cancer
among people who have made changes in their diet.
Considering all of these various preventive measures
and risk factors, it's clear that both doctors
and dentists and nutritionists can all play important roles
in oral and lip cancer prevention campaigns.