Tobacco smoking or chewing is the most common causative factor, with more than 80% of persons with leukoplakia having a positive smoking history. Smokers are much more likely to suffer from leukoplakia than non-smokers. The size and number of leukoplakia lesions in an individual is also correlated with the level of smoking and how long the habit has lasted for. Other sources argue that there is no evidence for a direct causative link between smoking and oral leukoplakia. Cigarette smoking may produce a diffuse leukoplakia of the buccal mucosa, lips, tongue and rarely the floor of mouth. Reverse smoking, where the lit end of the cigarette is held in the mouth is also associated with mucosal changes. Tobacco chewing, e.g. betel leaf and areca nut, called paan, tends to produce a distinctive white patch in a buccal sulcus termed "tobacco pouch keratosis". In the majority of persons, cessation triggers shrinkage or disappearance of the lesion, usually within the first year after stopping.

Although the synergistic effect of alcohol with smoking in the development of oral cancer is beyond doubt, there is no clear evidence that alcohol is involved in the development of leukoplakia, but it does appear to have some influence. Excessive use of a high alcohol containing mouth wash (> 25%) may cause a grey plaque to form on the buccal mucosa, but these lesions are not considered true leukoplakia.

About 6 to 14 percent of patients who receive a routine barium swallow test of the esophagus are found to have a Schatzki ring.

Gastroesophageal reflux disease (GERD) affects approximately 40% of adults. Strictures occur in 7 to 23% of patients with GERD who are untreated.

They are mainly observed in the Plummer–Vinson syndrome, which is associated with chronic iron deficiency anemia. One in 10 patients with Plummer-Vinson syndrome will eventually develop squamous cell carcinoma of the esophagus, but it is unclear if esophageal webs in and of themselves are a risk factor.

Esophageal webs are associated with bullous diseases (such as epidermolysis bullosa, pemphigus, and bullous pemphigoid), with graft versus host disease involving the esophagus, and with celiac disease.

Esophageal webs are more common in white individuals and in women (with a ratio 2:1). The literature describes relations between these webs and Plummer-Vinson Syndrome, bullous dermatologic disorders, inlet patch, graft-versus-host disease and celiac disease. The postulated mechanisms are sideropenic anemia (mechanism unknown) or some interference of the immune system.

Esophageal webs can be ruptured during upper endoscopy.

Barrett's esophagus is a premalignant condition. Its malignant sequela, oesophagogastric junctional adenocarcinoma, has a mortality rate of over 85%. The risk of developing esophageal adenocarcinoma in people who have Barrett's esophagus has been estimated to be 6–7 per 1000 person-years, however a cohort study of 11,028 patients from Denmark published in 2011 showed an incidence of only 1.2 per 1000 person-years (5.1 per 1000 person-years in patients with dysplasia, 1.0 per 1000 person-years in patients without dysplasia). The relative risk of esophageal adenocarcinoma is approximately 10 in those with Barret's esophagus, compared to the general population. Most patients with esophageal carcinoma survive less than one year.

Esophageal webs and rings can be treated with endoscopic dilation.

Esophageal diseases can derive from congenital conditions, or they can be acquired later in life.

Many people experience a burning sensation in their chest occasionally, caused by stomach acids refluxing into the esophagus, normally called heartburn. Extended exposure to heartburn may erode the lining of the esophagus, leading potentially to Barrett's esophagus which is associated with an increased risk of adenocarcinoma most commonly found in the distal one-third of the esophagus.

Some people also experience a sensation known as globus esophagus, where it feels as if a ball is lodged in the lower part of the esophagus.

The following are additional diseases and conditions that affect the esophagus:

- Achalasia

- Acute esophageal necrosis

- Barrett's esophagus

- Boerhaave syndrome

- Caustic injury to the esophagus

- Chagas disease

- Diffuse esophageal spasm

- Esophageal atresia and Tracheoesophageal fistula

- Esophageal cancer

- Esophageal dysphagia

- Esophageal varices

- Esophageal web

- Esophagitis

- GERD

- Hiatus hernia

- Jackhammer esophagus (hypercontractile peristalsis)

- Killian–Jamieson diverticulum

- Mallory-Weiss syndrome

- Neurogenic dysphagia

- Nutcracker esophagus

- Schatzki's ring

- Zenker's Diverticulum

Cystitis glandularis is a term describing a metaplasial transformation of mucosal cells lining the urinary bladder. The main importance is in histopathology, distinguishing the metaplastic change from urothelial cell carcinoma. It is a very common finding in bladder biopsies and cystectomies, and most often found in the trigone area. Cystitis glandularis lesions are usually present as small microscopic foci; however, occasionally it can form raised intramucosal or polypoid lesions. The cystitis glandularis lesions are within the submucosa.

Since many, if not most, anal cancers derive from HPV infections, and since the HPV vaccine before exposure to HPV prevents infection by some strains of the virus and has been shown to reduce the incidence of potentially precancerous lesions, scientists surmise that HPV vaccination may reduce the incidence of anal cancer.

On 22 December 2010, the U.S. Food and Drug Administration approved Gardasil vaccine to prevent anal cancer and pre-cancerous lesions in males and females aged 9 to 26 years. The vaccine has been used before to help prevent cervical, vulvar, and vaginal cancer, and associated lesions caused by HPV types 6, 11, 16, and 18 in women.

The American Cancer Society estimated that in 2014 about 7,060 new cases of anal cancer would be diagnosed in the United States (4,430 in women and 2,630 in men) . It is typically found in adults, average age early 60s.

In the United States, an estimated 800 to 900 people die of anal cancer annually.

A Schatzki ring or Schatzki–Gary ring is a narrowing of the lower esophagus that can cause difficulty swallowing (dysphagia). The narrowing is caused by a ring of mucosal tissue (which lines the esophagus) or muscular tissue. A Schatzki ring is a specific type of "esophageal ring", and Schatzki rings are further subdivided into those above the esophagus/stomach junction (A rings), and those found at the squamocolumnar junction in the lower esophagus (B rings).

Patients with Schatzki rings can develop intermittent difficulty swallowing or, more seriously, a completely blocked esophagus. The ring is named after the German-American physician Richard Schatzki.

The two major risk factors for esophageal squamous-cell carcinoma are tobacco (smoking or chewing) and alcohol. The combination of tobacco and alcohol has a strong synergistic effect. Some data suggest that about half of all cases are due to tobacco and about one-third to alcohol, while over three-quarters of the cases in men are due to the combination of smoking and heavy drinking. Risks associated with alcohol appear to be linked to its aldehyde metabolite and to mutations in certain related enzymes. Such metabolic variants are relatively common in Asia.

Other relevant risk factors include regular consumption of very hot drinks (over 65 °C)(149 Fahrenheit) and ingestion of caustic substances. High levels of dietary exposure to nitrosamines (chemical compounds found both in tobacco smoke and certain foodstuffs) also appear to be a relevant risk factor. Unfavorable dietary patterns seem to involve exposure to nitrosamines through processed and barbecued meats, pickled vegetables, etc., and a low intake of fresh foods. Other associated factors include nutritional deficiencies, low socioeconomic status, and poor oral hygiene. Chewing betel nut (areca) is an important risk factor in Asia.

Physical trauma may increase the risk. This may include the drinking of very hot drinks.

Zenker's diverticulum mainly affects older adults. It has an incidence of 2 per 100,000 per year in the UK, but there is significant geographical variation around the world.

Barrett's esophagus occurs due to chronic inflammation. The principal cause of the chronic inflammation is gastroesophageal reflux disease, GERD (UK: GORD). In this disease, acidic stomach, bile, and small intestine and pancreatic contents cause damage to the cells of the lower esophagus. Recently, bile acids were shown to be able to induce intestinal differentiation, in gastroesophageal junction cells, through inhibition of the epidermal growth factor receptor (EGFR) and the protein kinase enzyme Akt. This results in the eventual up-regulation of the p50 subunit of protein complex NF-κB ("NFKB1"), and ultimately activation of the homeobox gene "CDX2", which is responsible for the expression of intestinal enzymes such as guanylate cyclase 2C. This mechanism also explains the selection of HER2/neu (also called ERBB2) and the overexpressing (lineage-addicted) cancer cells during the process of carcinogenesis, and the efficacy of targeted therapy against the Her-2 receptor with trastuzumab (Herceptin) in the treatment of adenocarcinomas at the gastroesophageal junction.

Researchers are unable to predict who with heartburn will develop Barrett's esophagus. While no relationship exists between the severity of heartburn and the development of Barrett's esophagus, a relationship does exist between chronic heartburn and the development of Barrett's esophagus. Sometimes, people with Barrett's esophagus have no heartburn symptoms at all. In rare cases, damage to the esophagus may be caused by swallowing a corrosive substance such as lye.

Cervical ectropion is a normal phenomenon, especially in the ovulatory phase in younger women, during pregnancy, and in women taking the oral contraceptive pill, which increases the total estrogen level in the body. It also may be a congenital problem by persistence of the squamocolumnar junction which is normally present prior to birth.

Mucopurulent cervicitis may increase the size of the cervical ectropion.

The squamocolumnar junction, where the columnar secretory epithelium of the endocervical canal meets the stratified squamous covering of the ectocervix, is located at the external os before puberty. As estrogen levels rise during puberty, the cervical os opens, exposing the endocervical columnar epithelium onto the ectocervix. This area of columnar cells on the ectocervix forms an area that is red and raw in appearance called an ectropion (cervical erosion). It is then exposed to the acidic environment of the vagina and, through a process of squamous metaplasia, transforms into stratified squamous epithelium.

It can be caused by or associated with gastroesophageal reflux disease, esophagitis, a dysfunctional lower esophageal sphincter, disordered motility, lye ingestion, or a hiatal hernia. Strictures can form after esophageal surgery and other treatments such as laser therapy or photodynamic therapy. While the area heals, a scar forms, causing the tissue to pull and tighten, leading to difficulty in swallowing.

Male predominance is particularly strong in this type of esophageal cancer, which occurs about 7 to 10 times more frequently in men. This imbalance may be related to the characteristics and interactions of other known risk factors, including acid reflux and obesity.

The long-term erosive effects of acid reflux (an extremely common condition, also known as gastroesophageal reflux disease or GERD) have been strongly linked to this type of cancer. Longstanding GERD can induce a change of cell type in the lower portion of the esophagus in response to erosion of its squamous lining. This phenomenon, known as Barrett's esophagus, seems to appear about 20 years later in women than in men, maybe due to hormonal factors. Having symptomatic GERD or bile reflux makes Barrett's esophagus more likely, which in turn raises the risk of further changes that can ultimately lead to adenocarcinoma. The risk of developing adenocarcinoma in the presence of Barrett's esophagus is unclear, and may in the past have been overestimated.

Being obese or overweight both appear to be associated with increased risk. The association with obesity seems to be the strongest of any type of obesity-related cancer, though the reasons for this remain unclear. Abdominal obesity seems to be of particular relevance, given the closeness of its association with this type of cancer, as well as with both GERD and Barrett's esophagus. This type of obesity is characteristic of men. Physiologically, it stimulates GERD and also has other chronic inflammatory effects.

"Helicobacter pylori" infection (a common occurrence thought to have affected over half of the world's population) is not a risk factor for esophageal adenocarcinoma and actually appears to be protective. Despite being a cause of GERD and a risk factor for gastric cancer, the infection seems to be associated with a reduced risk of esophageal adenocarcinoma of as much as 50%. The biological explanation for a protective effect is somewhat unclear. One explanation is that some strains of "H. pylori" reduce stomach acid, thereby reducing damage by GERD. Decreasing rates of "H. pylori" infection in Western populations over recent decades, which have been linked to better hygiene and increased refrigeration of food, could be a factor in the concurrent increase in esophageal adenocarcinoma.

Female hormones may also have a protective effect, as EAC is not only much less common in women but develops later in life, by an average of 20 years. Although studies of many reproductive factors have not produced a clear picture, risk seems to decline for the mother in line with prolonged periods of breastfeeding.

Tobacco smoking increases risk, but the effect in esophageal adenocarcinoma is slight compared to that in squamous cell carcinoma, and alcohol has not been demonstrated to be a cause.

There is risk of perforation of the esophagus with the use of dilators for treatment. Furthermore, it is one of the risk factors for developing squamous cell carcinoma of the oral cavity, esophagus, and hypopharynx.

It is not clear exactly what causes esophageal spasms. Sometimes esophageal spasms start when someone eats hot or cold foods or drinks. However, they can also occur with eating or drinking. The increased release of acetylcholine may also be a factor, but the triggering event is not known.

There are two main types of cystitis glandularis, non-mucinous and mucinous (intestinal). The difference is in the cellular production of mucin, a normal feature of colonic and intestinal epithelial cells but not of urothelial cells. Another distinction is made between focal areas and diffuse involvement of the bladder. Whereas focal areas are more common, diffuse involvement is seen in chronically irritated bladders, such as in paraplegics or those with bladder stones or indwelling catheters. Individuals with diffuse intestinal-type cystitis glandularis are at increased risk for developing bladder cancer.

Neonates with TEF or esophageal atresia are unable to feed properly. Once diagnosed, prompt surgery is required to allow the food intake. Some children do experience problems following TEF surgery; they can develop dysphagia and thoracic problems. Children with TEF can also be born with other abnormalities, most commonly those described in VACTERL association - a group of anomalies which often occur together, including heart, kidney and limb deformities. 6% of babies with TEF also have a laryngeal cleft.

In simple words, when there is excessive pressure within the lower pharynx, the weakest portion of the pharyngeal wall balloons out, forming a diverticulum which may reach several centimetres in diameter.

More precisely, while traction and pulsion mechanisms have long been deemed the main factors promoting development of a Zenker's diverticulum, current consensus considers occlusive mechanisms to be most important: uncoordinated swallowing, impaired relaxation and spasm of the cricopharyngeus muscle lead to an increase in pressure within the distal pharynx, so that its wall herniates through the point of least resistance (known as Killian's triangle, located superior to the cricopharyngeus muscle and inferior to the Thyropharyngeus muscle. Thyropharyngeus and Laryngopharyngeus are the superior and inferior parts of inferior constrictor muscle of pharynx respectively). The result is an outpouching of the posterior pharyngeal wall, just above the esophagus.

While it may be asymptomatic, Zenker diverticulum can present with the following symptoms:

- Dysphagia (difficulty swallowing), and sense of a lump in the throat

- Food might get trapped in the outpouching, leading to:

- Regurgitation, reappearance of ingested food in the mouth

- Cough, due to food regurgitated into the airway

- Halitosis, smelly breath, as stagnant food is digested by microorganisms

- Infection

It rarely, if ever, causes any pain.

Cervical webs are seen associated in 50% of patients with this condition.

Rarer forms of cervical esophageal diverticula are the Killian's diverticulum and the Laimer's diverticulum. Killian's diverticulum is formed in the Killian-Jamiseon triangle (located inferior to the cricopharyngeus on both sides of this muscle's insertion into the cricoid cartilage). Laimer's diverticulum is formed in Laimer's triangle (located inferior to the cricopharyngeus in the posterior midline above the confluence of the longitudinal layer of esophageal muscle). Laimer's triangle is covered only by the circular layer of esophageal muscle.

Esophageal stricture, or narrowing of the esophagus, is usually a complication of acid reflux, most commonly due to gastroesophageal reflux (GERD). These patients are usually older and have had GERD for a long time. Esophageal stricture can also be due to other causes, such as acid reflux from Zollinger-Ellison syndrome, trauma from a nasogastric tube placement, and chronic acid exposure in patients with poor esophageal motility from scleroderma. Other non-acid related causes of peptic strictures include infectious esophagitis, ingestion of chemical irritant, pill irritation, and radiation. Peptic stricture is a progressive mechanical dysphagia, meaning patients will complain of initial intolerance to solids followed by inability to tolerate liquids. When the diameter of the stricture is less than 12 mm the patient will always have dysphagia, while dysphagia is not seen when the diameter of the stricture is above 30 mm. Symptoms relating to the underlying cause of the stricture usually will also be present.

Esophageal cancer also presents with progressive mechanical dysphagia. Patients usually come with

rapidly progressive dysphagia first with solids then with liquids, weight loss (> 10 kg), and anorexia (loss of appetite). Esophageal cancer usually affects the elderly. Esophageal cancers can be either squamous cell carcinoma or adenocarcinoma. Adenocarcinoma is the most prevalent in the US and is associated with patients with chronic GERD who have developed Barrett's esophagus (intestinal metaplasia of esophageal mucosa). Squamous cell carcinoma is more prevalent in Asia and is associated with tobacco smoking and alcohol use.

Esophageal rings and webs, are actual rings and webs of tissue that may occlude the esophageal lumen.

- "Rings" --- Also known as Schatzki rings from the discoverer, these rings are usually mucosal rings rather than muscular rings, and are located near the gastroesophageal junction at the squamo-columnar junction. Presence of multiple rings may suggest eosinophilic esophagitis. Rings cause intermittent mechanical dysphagia, meaning patients will usually present with transient discomfort and regurgitation while swallowing solids and then liquids, depending on the constriction of the ring.

- "Webs" --- Usually squamous mucosal protrusion into the esophageal lumen, especially anterior cervical esophagus behind the cricoid area. Patients are usually asymptomatic or have intermittent dysphagia. An important association of esophageal webs is to the Plummer-Vinson syndrome in iron deficiency, in which case patients will also have anemia, koilonychia, fatigue, and other symptoms of anemia.

Achalasia is an idiopathic motility disorder characterized by failure of lower esophageal sphincter (LES) relaxation as well as loss of peristalsis in the distal esophagus, which is mostly smooth muscle. Both of these features impair the ability of the esophagus to empty contents into the stomach. Patients usually complain of dysphagia to both solids and liquids. Dysphagia to liquids, in particular, is a characteristic of achalasia. Other symptoms of achalasia include regurgitation, night coughing, chest pain, weight loss, and heartburn. The combination of achalasia, adrenal insufficiency, and alacrima (lack of tear production) in children is known as the triple A (Allgrove) syndrome. In most cases the cause is unknown (idiopathic), but in some regions of the world, achalasia can also be caused by Chagas disease due to infection by "Trypanosoma cruzi".

Scleroderma is a disease characterized by atrophy and sclerosis of the gut wall, most commonly of the distal esophagus (~90%). Consequently, the lower esophageal sphincter cannot close and this can lead to severe gastroesophageal reflux disease (GERD). Patients typically present with progressive dysphagia to both solids and liquids secondary to motility problems or peptic stricture from acid reflux.

Spastic motility disorders include diffuse esophageal spasm (DES), nutcracker esophagus, hypertensive lower esophageal sphincter, and nonspecific spastic esophageal motility disorders (NEMD).

- "DES" can be caused by many factors that affect muscular or neural functions, including acid reflux, stress, hot or cold food, or carbonated drinks. Patients present with intermittent dysphagia, chest pain, or heartburn.

Rare causes of esophageal dysphagia not mentioned above

- Diverticulum

- Aberrant subclavian artery, or (dysphagia lusoria)

- Cervical osteophytes

- Enlarged aorta

- Enlarged left atrium

- Mediastinal tumor