Most oral cancer are cell cancers.
USMLE® Step 1 style questions USMLE
USMLE® Step 2 style questions USMLE
A 55-year-old woman comes to the clinic for a physical examination required for her new job. Inspection of her oral cavity reveals the image shown below. The lesion is tender rather than painful, but she says that she has had recurrent painful canker sores before. Which of the following is the most appropriate next step in management?
Content Reviewers:Rishi Desai, MD, MPH
Oral cancer describes cancers that originate in the oral cavity.
The oral cavity includes the lips, the gingiva, or gums, the floor of the mouth, the buccal mucosa which is the soft lining of the inner lips and cheeks, the anterior or front two-thirds of the tongue, the hard palate which is the tough front part of the roof of the mouth, and the retromolar trigone which is the mucosa right behind the last molars on the bottom row of teeth.
Behind the oral cavity is the oropharynx.
The oropharynx includes the soft palate which is the soft part of the roof of the mouth right behind the hard palate, the tonsils, the walls of the throat, and the posterior or back one-third of the tongue.
The oral cavity and oropharynx are lined by epithelium - and there are a few different types.
The first type of epithelium is called keratinized stratified squamous epithelium.
These epithelial cells produce keratin, a protein that makes the layer tough, and protects against normal wear and tear from food and drinks.
Beneath the epithelium, there’s another layer called the basement membrane made of tough connective tissue, and below that is the lamina propria which yet more connective tissue that houses blood vessels, lymphatics, nerves, and immune cells.
The oral surfaces covered in keratinized epithelium include the hard palate, the dorsal surface, or top, of the tongue, and the gingiva.
A second type of epithelium is non-keratinized stratified squamous epithelium, and it contains cells that don’t produce much keratin, making this layer less tough.
The oral surfaces covered by non-keratinized stratified squamous epithelium include the buccal mucosa, the floor of the mouth, the lateral and ventral, or bottom, surfaces of the tongue, the soft palate, and the retromolar trigone.
Now the mucosal tissue in the oral cavity can undergo several premalignant pathological changes.
The first one of these is leukoplakia, where leuko- means white and -plakia means a flat, raised patch or plaque.
And leukoplakia specifically relates to a white plaque with no clear underlying cause.
These leukoplakias are usually painless but can’t be easily scraped away.
Now, the exact cause for leukoplakia is unknown, but a known risk factor is tobacco use.
Early on, these lesions are usually pretty thin, so it’s called thin leukoplakia.
These can either go away on their own, remain unchanged, or grow and become thicker, at which point it’s called thick leukoplakia.
If it becomes bumpy it’s called nodular leukoplakia, and if it becomes wart-like it’s called verrucous leukoplakia.
Now a more serious form of leukoplakia is called proliferative verrucous leukoplakia, which usually affects women, with no risk factors and it has a predilection for gingiva and causes multiple rough white lesions that grow and spread, and in most cases, eventually develop into squamous cell carcinoma.
At the cellular level, leukoplakia typically shows a thickened keratin layer.
Since keratin absorbs water, a thick keratin layer looks white when it’s wet.
At a cellular level, leukoplakia may show cells that have undergone some degree of dysplasia, meaning they look abnormal in some way, but are not cancerous, or malignant, yet.
However, leukoplakia is considered a precancerous condition, meaning that compared to normal tissue, it’s more likely to develop into a cancer in the future.
And that change could happen at the microscopic level, meaning that the lesion might look the same on the outside, even though the cells have become cancerous.
Generally speaking, the transition from dysplastic cells to malignant cells occurs gradually.
And as cells become more and more dysplastic the lesions sometimes develop red spots, and at that point it’s called erythroleukoplakia.
Cells in these red areas have suffered serious damage to their DNA and don’t mature normally and therefore can’t produce keratin.
And as they become more and more atypical, the more immature becomes the epithelium and it will start becoming thinner or atrophic and allow more of the underlying blood vessels to be seen through the mucosa.
At that point the lesion will be completely red and will be called erythoplakia.
Erythroplakias are more serious than leukoplakia because almost always when they are removed and examined under the microscope they will show severe dysplasia, or early cancer.
Now, a lesion that looks like leukoplakia, but isn’t, is an area of frictional keratosis.
That’s where there’s repeated physical trauma like rubbing of the tooth surface against the mucosa of the cheeks.
For example, after a dental procedure that leaves a rough tooth surface, or a broken tooth rubbing against the mucosa.
It’s a normal hyperplastic response, meaning the epithelial cells in the area divide more than usual and build up a protective layer of keratin.
It’s a bit like developing a callus on your hands after spending the weekend raking leaves.
An area of frictional keratosis is not a precancerous lesion and usually fades away once the irritation stops.