High Grade Squamous Dysplasia of the Esophagus: Understanding Your Pathology Report

by Jason Wasserman MD PhD FRCPC
July 29, 2026

High grade squamous dysplasia of the esophagus is a precancerous change in the cells lining the esophagus, the muscular tube that carries food and liquid from the mouth to the stomach. The inner surface of the esophagus is covered by squamous epithelium, a layered sheet of flat protective cells. New cells are made at the bottom of this layer and mature steadily as they move toward the surface.

In high grade squamous dysplasia, that maturation fails across most or all of the layer. The squamous cells look markedly abnormal from the bottom of the layer all the way up toward the surface. The abnormal cells have not, however, broken through into the tissue underneath, which is what separates dysplasia from cancer.

High grade squamous dysplasia is not cancer. It is the last recognized step before squamous cell carcinoma of the esophagus develops, and without treatment a substantial proportion of cases progress. It is also highly treatable at this stage, because the abnormal cells are confined to the surface lining and cannot have spread anywhere. This article will help you understand the findings in your pathology report, what each term means, and why it matters for your care.

What causes high grade squamous dysplasia of the esophagus?

High grade squamous dysplasia of the esophagus develops after years of repeated injury to the squamous lining. It shares its causes with squamous cell carcinoma of the esophagus, the cancer it can lead to, and these differ from the causes of Barrett esophagus and the gland-forming cancers that arise from it.

The two most important causes are tobacco use and heavy alcohol consumption. Each damages the lining on its own, and together they raise the risk far more than either alone, because alcohol makes the lining more permeable to the cancer-causing chemicals in tobacco smoke. Other contributors include:

Very hot beverages — Drinking tea, coffee, or maté at high temperatures over many years repeatedly scalds the lining. The temperature is what matters, not the type of drink.
Diet low in fruits and vegetables — Associated with higher risk in every population studied.
Poor oral health — One of the stronger associations in recent studies.
Achalasia — A condition in which the esophagus does not empty properly, so its contents sit against the lining.
Scarring from a caustic injury — Such as after swallowing lye or another corrosive substance, often decades earlier.
Previous radiation therapy to the chest or neck.
A previous squamous cell carcinoma of the mouth, throat, or voice box — The same exposures affect the entire lining of the upper airway and digestive tract, so abnormal areas can appear in more than one place at once.
Tylosis — A rare inherited condition causing thickened skin on the palms and soles, along with a substantially increased lifetime risk of esophageal squamous cell carcinoma.

Two things sometimes listed as causes are worth correcting. Chronic acid reflux is not a cause of squamous dysplasia; reflux injures the lower esophagus in a different way, producing reflux esophagitis and, over time, Barrett esophagus, which is a change to gland-forming cells. Reflux matters here only because the inflammation it causes can make squamous cells look abnormal in ways that resemble dysplasia. And while human papillomavirus (HPV) has been studied as a possible contributor in some parts of the world, the evidence is conflicting, and unlike in cancers of the throat and cervix, HPV is not an established cause of esophageal squamous disease.

What are the symptoms of high grade squamous dysplasia of the esophagus?

High grade squamous dysplasia of the esophagus causes no symptoms of its own. The change is microscopic and involves only the thin surface lining, so it does not narrow the esophagus, bleed, or cause pain.

Most people learn of it after an upper endoscopy performed for another reason: investigation of swallowing difficulty, follow-up after a previous head or neck cancer, or screening in someone with several risk factors. When symptoms such as difficulty swallowing, pain on swallowing, or a sensation of food sticking are present, they usually come from whatever prompted the endoscopy rather than from the dysplasia itself. Symptoms of that kind should always be taken seriously, because they can also signal an invasive cancer elsewhere in the esophagus. Because the dysplasia itself is silent, how a person feels is not a way to judge whether it is stable or progressing.

How is the diagnosis made?

High grade squamous dysplasia of the esophagus is diagnosed only after a tissue sample from the esophagus is examined under a microscope by a pathologist. The sample is obtained during an upper endoscopy, in which a thin flexible tube with a camera is passed through the mouth into the esophagus, and a biopsy is taken from any abnormal area.

Squamous dysplasia can be hard to see, because the affected lining often looks close to normal. To find it, the endoscopist may spray the esophagus with Lugol’s iodine, a brown dye that stains healthy squamous cells because they are rich in glycogen, a stored sugar. Dysplastic cells contain little glycogen and stay pale, appearing as unstained patches against a brown background. Special light settings that highlight the surface blood vessels are used for the same purpose.

Under the microscope, the pathologist assesses two things. The first is how the individual cells look, described as cytologic atypia: in high grade dysplasia the nuclei, the compartments holding each cell’s genetic material, are enlarged, dark, and irregular in size and shape; the cells are crowded and overlapping; and dividing cells, called mitoses, are numerous and found high in the layer where they do not belong. The second is how the tissue as a whole is organized: instead of maturing and flattening as they rise toward the surface, the cells stay immature all the way up, and the layer may be thickened and disordered.

The diagnosis of high grade dysplasia is made when these abnormalities involve more than half the thickness of the squamous epithelium, or when the cell changes are severe enough to warrant the label even if less of the thickness is affected. When abnormal cells replace the full thickness of the lining, the change may also be called squamous cell carcinoma in situ, which is managed in the same way. Crucially, the pathologist also confirms that no cells have broken through the base of the epithelium into the tissue beneath, since that would be invasive cancer rather than dysplasia.

One limitation of a biopsy is worth understanding. A biopsy samples only a small piece of the abnormal area, and in a minority of cases an invasive cancer is present nearby but was not captured. This is a central reason that removing the whole lesion in one piece, rather than simply destroying it, is generally favored: it lets the pathologist examine the entire abnormality and confirm that nothing invasive is hidden within it. Because grading squamous dysplasia is also a subjective judgment on which pathologists do not always agree, a diagnosis of high grade dysplasia is commonly reviewed by a second pathologist before treatment is planned.

Grading of squamous dysplasia

Squamous dysplasia of the esophagus is graded by how far the abnormal cells extend upward through the layered squamous lining. The current system used in most pathology reports has two levels:

Low grade squamous dysplasia — Abnormal cells occupy roughly the lower half of the epithelium, and cells nearer the surface still mature and flatten normally.
High grade squamous dysplasia — Abnormal cells extend into the upper half of the epithelium and normal surface maturation is lost. This is the diagnosis described in this article, and it carries a much higher risk of progressing to cancer.

Your report may use different wording for the same finding. Some pathologists use the term intraepithelial neoplasia, so high grade squamous dysplasia may appear as high grade squamous intraepithelial neoplasia. Older reports, and some centers still, use a three-level system of mild, moderate, and severe dysplasia; severe dysplasia corresponds to high grade. Squamous cell carcinoma in situ describes full-thickness involvement and sits at the same end of the scale. All of these terms describe a lesion that has not invaded and that is managed the same way, so a change in wording between reports does not mean the diagnosis has changed.

What is the risk that high grade squamous dysplasia will become cancer?

High grade squamous dysplasia of the esophagus carries the highest risk of progression of any precancerous change in the esophageal squamous lining, which is why treatment rather than watching is the usual course. Unlike low grade dysplasia, it rarely regresses on its own.

In large screening programs in northern China, where esophageal squamous cell carcinoma is common, people with severe dysplasia or carcinoma in situ developed invasive cancer at a rate of roughly 1.8% per year, with a cumulative risk of about 15% over eight years of follow-up without treatment. Compared with a normal esophageal lining, the risk is increased roughly twenty-eight fold. Put the other way, most people with this diagnosis had not developed invasive cancer eight years later, but the proportion who do is high enough that treatment is offered rather than surveillance alone.

Circumstances that raise the risk further include:

Continued smoking and drinking — The strongest factor that can actually be changed.
A larger or more extensive abnormal area — Particularly a large unstained area on Lugol’s iodine staining.
Dysplasia found at more than one site — Suggesting the whole lining has been affected.
A visible nodule, thickening, or depression — These features raise the possibility that invasive cancer is already present within the lesion.
A previous squamous cell carcinoma of the head, neck, or esophagus.
Older age and male sex — Both associated with higher progression rates in screening studies.

Because the abnormal cells are still confined to the surface lining, high grade squamous dysplasia found and treated at this stage cannot have spread to lymph nodes or to other organs. Treatment at this point is done with the intent to cure.

What happens after this diagnosis?

Once high grade squamous dysplasia of the esophagus is confirmed, the usual approach is to remove or destroy the abnormal lining rather than to monitor it, because the risk of progression is high and the abnormal area is still confined to the surface. The case is generally reviewed by a team that includes gastroenterology and, where relevant, thoracic surgery, and referral to a center with particular expertise in early esophageal disease is common.

Endoscopic treatment is the standard approach, and the options the team considers include:

Endoscopic submucosal dissection (ESD) — The abnormal area is dissected away in a single piece through the endoscope. Removing the lesion whole is favored for larger or nodular lesions because it gives the pathologist the entire abnormality to examine, confirming both that the margins are clear and that no invasive cancer was hidden inside.
Endoscopic mucosal resection (EMR) — The abnormal area is lifted and removed through the endoscope. This is a reasonable option for smaller lesions, generally under about 15 mm, where the whole lesion can still be taken in one piece.
Ablation, using radiofrequency energy or cryotherapy — Heat or extreme cold destroys the abnormal lining so healthy squamous lining can grow back. Because ablation destroys the tissue rather than retrieving it, nothing is left for the pathologist to examine, so it is generally reserved for flat lesions where invasive cancer has already been reasonably excluded, or used to treat remaining abnormal lining after a lesion has been resected.
Esophagectomy — Surgical removal of part of the esophagus. This is now rarely needed for dysplasia alone and is considered only in unusual situations, such as very extensive disease or when endoscopic treatment has not succeeded.

Which of these is appropriate depends on the size, number, and appearance of the abnormal areas, on whether anything suggests invasion, on other health conditions, and on the person’s own priorities. This is a decision made together with the treatment team.

Alongside treatment, reducing the exposures that caused the change has a large effect. Stopping smoking and reducing or stopping alcohol lower the chance that new abnormal areas will develop, both in the esophagus and in the mouth, throat, and voice box, where the same exposures act. Support for both is available through the care team.

Follow-up endoscopy with biopsies continues at intervals for years after successful treatment, because new areas of dysplasia can appear elsewhere in a lining that has been damaged throughout. Examination of the mouth, throat, and voice box is often included for the same reason.

Questions to ask your doctor

Did my report use the words severe dysplasia or carcinoma in situ, and does that change anything about my treatment?
Is there any sign that invasive cancer may already be present?
How large was the abnormal area, and was it found in more than one place?
Was Lugol’s iodine or another dye used during my endoscopy to map the abnormal areas?
Which endoscopic treatment is most appropriate for my lesion, and why?
Will the removed tissue be examined to confirm the margins are clear and that no cancer was present?
What are the risks of the procedure, including narrowing of the esophagus afterward?
Should I be referred to a center that specializes in early esophageal disease?
What is my risk of developing esophageal cancer if the dysplasia is treated successfully?
How often will I need follow-up endoscopy and biopsies, and for how long?
What help is available to stop smoking and reduce alcohol, and how much difference would that make for me?
Should I also be examined for abnormal areas in my mouth, throat, or voice box?
What symptoms should prompt me to contact you before my next scheduled endoscopy?