Patients with atrophic gastritis are also at increased risk for the development of gastric adenocarcinoma. The optimal endoscopic surveillance strategy is not known but all nodules and polyps should be removed in these patients.

Recent research has shown that AMAG is a result of the immune system attacking the parietal cells.

"Environmental Metaplastic Atrophic Gastritis" (EMAG) is due to environmental factors, such as diet and "H. pylori" infection. EMAG is typically confined to the body of the stomach. Patients with EMAG are also at increased risk of gastric carcinoma.

This is the most common form of chronic gastritis. Involvement tends to occur in either an antral-predominant or multifocal atrophic pattern. "H. pylori" infection is also associated with development of peptic ulcer disease, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue (MALT) lymphomas.

Chronic gastritis is a chronic inflammation of the gastric mucosa.

Diseases of the hepatobiliary system affect the biliary tract (also known as the "biliary tree"), which secretes bile in order to aid digestion of fats. Diseases of the gallbladder and bile ducts are commonly diet-related, and may include the formation of gallstones that impact in the gallbladder (cholecystolithiasis) or in the common bile duct (choledocholithiasis).

Gallstones are a common cause of inflammation of the gallbladder, called cholecystitis. Inflammation of the biliary duct is called cholangitis, which may be associated with autoimmune disease, such as primary sclerosing cholangitis, or a result of bacterial infection, such as ascending cholangitis.

Disease of the biliary tree may cause pain in the upper right abdomen, particularly when pressed. Disease might be investigated using ultrasound or ERCP, and might be treated with drugs such as antibiotics or UDCA, or by the surgical removal of the gallbladder.

Oesophageal diseases include a spectrum of disorders affecting the oesophagus. The most common condition of the oesophagus in Western countries is gastroesophageal reflux disease, which in chronic forms is thought to result in changes to the epithelium of the oesophagus, known as Barrett's oesophagus.

Acute disease might include infections such as oesophagitis, trauma caused ingestion of corrosive substances, or rupture of veins such as oesophageal varices, Boerhaave syndrome or Mallory-Weiss tears. Chronic diseases might include congenital diseases such as Zenker's diverticulum and esophageal webbing, and oesophageal motility disorders including the nutcracker oesophagus, achalasia, diffuse oesophageal spasm, and oesophageal stricture.

Oesophageal disease may result in a sore throat, throwing up blood, difficulty swallowing or vomiting. Chronic or congenital diseases might be investigated using barium swallows, endoscopy and biopsy, whereas acute diseases such as reflux may be investigated and diagnosed based on symptoms and a medical history alone.

Many conditions can cause glossitis via malnutrition or malabsorption, which creates the nutritional deficiencies described above, although other mechanisms may be involved in some of those conditions listed.

- Alcoholism

- Sprue (celiac disease, or tropical sprue), secondary to nutritional deficiencies

- Crohn’s disease

- Whipple disease

- Glucagonoma syndrome

- Cowden disease

- Acquired immunodeficiency syndrome (AIDS)

- Carcinoid syndrome

- Kwashiorkor amyloidosis

- Veganism and other specialized diets,

- Poor hydration and low saliva in the mouth, which allows bacteria to grow more readily

- Mechanical irritation or injury from burns, rough edges of teeth or dental appliances, or other trauma

- Tongue piercing Glossitis can be caused by the constant irritation by the ornament and by colonization of Candida albicans in site and on the ornament

- Exposure to irritants such as tobacco, alcohol, hot foods, or spices

- Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in confectionery, plastic in dentures or retainers, or certain blood-pressure medications (ACE inhibitors)

- Administration of ganglion blockers (e.g., Tubocurarine, Mecamylamine).

- Oral lichen planus, erythema multiforme, aphthous ulcer, pemphigus vulgaris

- Heredity

- Albuterol (bronchodilator medicine)

- Schizophrenia

A painful tongue may be an indication of an underlying serious medical condition and nearly always merits assessment by a physician or dental surgeon.

Bacterial, viral or fungal infections can cause glossitis. "Candida" species are involved in median rhomboid glossitis.

Syphilis is now relatively rare, but the tertiary stage can cause diffuse glossitis and atrophy of lingual papillae, termed "syphilitic glossitis", "luetic glossitis" or "atrophic glossitis of tertiary syphilis". It is caused by Treponema pallidum and is a sexually transmitted infection.

Causes can be remembered by mnemonic HERNIA:

- Hereditary factors: the disease runs in families

- Endocrine imbalance: the disease tends to start at puberty and mostly involves females

- Racial factors: whites are more susceptible than natives of equatorial Africa

- Nutritional deficiency: vitamins A or D, or iron

- Infection: "Klebsiella ozaenae", diphtheroids, "Proteus vulgaris", "E. coli", etc.

- Autoimmune factors: viral infection or some other unidentified insult may trigger antigenicity of the nasal mucosa.

Specific infections, such as syphilis, lupus, leprosy and rhinoscleroma, may cause destruction of the nasal structures leading to atrophic changes. Atrophic rhinitis can also result from long-standing purulent sinusitis or radiotherapy of the nose, or as a complication of surgery of the turbinates. The United Kingdom National Health Service has stated that "Most cases of atrophic rhinitis in the UK occur when the turbinates are damaged or removed during surgery". Some authors refer to as Atrophic rhinitis secondary to sinus surgery as the empty nose syndrome.

Smoking, especially heavy smoking, is an important predisposing factor but the reasons for this relationship are unknown. One hypothesis is that cigarette smoke contains nutritional factors for "C. albicans", or that local epithelial alterations occur that facilitate colonization of candida species.

Malnutrition, whether by malabsorption, or poor diet, especially hematinic deficiencies (iron, vitamin B12, folic acid) can predispose to oral candidiasis, by causing diminished host defense and epithelial integrity. For example, iron deficiency anemia is thought to cause depressed cell-mediated immunity. Some sources state that deficiencies of vitamin A or pyridoxine are also linked.

There is limited evidence that a diet high in carbohydrates predisposes to oral candidiasis. "In vitro" and studies show that Candidal growth, adhesion and biofilm formation is enhanced by the presence of carbohydrates such as glucose, galactose and sucrose.

The cause is unknown. Geographic tongue does not usually cause any symptoms, and in those cases where there are symptoms, an oral parafunctional habit may be a contributory factor. Persons with parafunctional habits related to the tongue may show scalloping on the sides of the tongue (crenated tongue). Some suggest that hormonal factors may be involved, because one reported case in a female appeared to vary in severity in correlation with oral contraceptive use. People with geographic tongue frequently claim that their condition worsens during periods of psychologic stress. Geographic tongue is inversely associated with smoking and tobacco use. Sometimes geographic tongue is said to run in families, and it is reported to be associated with several different genes, though studies show family association may also be caused by similar diets. Some have reported links with various human leukocyte antigens, such as increased incidence of HLA-DR5, HLA-DRW6 and HLA-Cw6 and decreased incidence in HLA-B51. Vitamin B2 deficiency (ariboflavinosis) can cause several signs in the mouth, possibly including geographic tongue, although other sources state that geographic tongue is not related to nutritional deficiency. Fissured tongue often occurs simultaneously with geographic tongue, and some consider fissured tongue to be an end stage of geographic tongue.

In the past, some research suggested that geographic tongue was associated with diabetes, seborrheic dermatitis and atopy, however newer research does not corroborate these findings. Others suggest allergy as a major factor, e.g. to nickel sulphate. Some studies have reported a link between geographic tongue and psoriasis, although 90% of children who are diagnosed with geographic tongue do not develop psoriasis. Again however, modern research studies do not support any link between psoriasis and geographic tongue. Lesions that are histologically indistinguishable from geographic tongue may also be diagnosed in reactive arthritis (arthritis, uveitis/conjunctivitis and urethritis).

It is an uncommon condition, occurring with equal prevalence in males and females and at any age.

Plasma cell gingivits is rare, and plasma cell cheilitis is very rare. Most people with plasma cell cheilitis have been elderly.

Geographic tongue is a common condition, affecting 2-3% of the adult general population, although other sources report a prevalence of up to 14%. It is one of the most common tongue disorders that occurs in children. The condition often starts in childhood, sometimes at an early age, but others report that the highest incidence occurs in the over 40 age group. Females are sometimes reported to be more commonly affected than males, in a 2:1 ratio, although others report that the gender distribution is equal.

It has been shown that “the prevalence of positive tests for thyroid antibodies increases with age, with a frequency as high as 33 percent in women 70 years old or older.” The mean age of prevalence in women is higher than in men by one year, (58 and 59 years old respectively).

Autoimmune thyroiditis can affect children. It is very rare in children under the age of five, but can occur;it accounts for around 40 percent of cases in adolescents with goiters.

People with hypothyroidism over the age of 40 have an increased chance of developing autoimmune thyroiditis.

Intestinal Connective tissue abnormality may cause Intestinal Desmosis The absence of the tendinous plexus layer was first described in 1998 by Meier-Ruge. Desmosis is implicated in disturbed gut motility.

Normal peristalsis depends upon the interaction between muscles, nerve cells and tendinous connective tissue. A malfunction of any of these leads to intestinal motility disorders.

Desmosis may be congenital (aplastic form) or acquired (atrophic form).

The "aplastic" form is rare. Typical clinical findings are hypoperistalsis, and pseudo-obstruction. These are found in premature infants, associated with low birth weight. The "atrophic" form is more frequent. Inflammation of the muscularis propria releases enzymes including collagenases which destroy the connective tissue of the bowel wall. Primarily newborns and small children are affected, although this manifestation can also be found in adults. The most common location is the colon with a necrotizing enterocolitis as well as Crohn Disease and diverticulitis. If the taenia are also affected, the disease is defined as complete atrophic desmosis, all other forms without involvement of the taenia are referred to as incomplete. Clinically, patients demonstrate chronic constipation.

As proposed by Giuseppe Martucciello, microscopic diagnosis requires laparoscopic intestinal full-thickness biopsies from colon. Histological findings are absence of the tendinous plexus layer and connective tissue fibers in longitudinal and circular muscle layer.

Autoimmune thyroiditis has a higher prevalence in societies that have a higher intake of iodine in their diet, such as the United States and Japan. Also, the rate of lymphocytic infiltration increased in areas where the iodine intake was once low, but increased due to iodine supplementation. “The prevalence of positive serum tests in such areas rises to over 40 percent within 0.5 to 5 years.”

Predisposing factors include smoking, denture wearing, use of corticosteroid sprays or inhalers and human immunodeficiency virus (HIV) infection. "Candida" species even in healthy people mainly colonizes the posterior dorsal tongue. Median rhombiod glossitis is thought to be a type of chronic atrophic (or erythematous) candidiasis. Microbiological culture of the lesion usually shows "Candida" mixed with bacteria.

It is not lethal in nature and is responsive to tetracycline or ciprofloxacin. Surgical treatment include rhinoplasty. However, if left untreated the disease can lead to sepsis, bleeding, or other chronic conditions that can be fatal.

Plasma cell gingivits and plasma cell cheilitis are thought to be hypersensitivity reactions to some antigen. Possible sources of antigens include ingredients in toothpastes, chewing gum, mints, pepper, or foods. Specifically, cinnamonaldehyde and cinnamon flavoring are often to blame. However, the exact cause in most is unknown.

A precancerous condition or premalignant condition, sometimes called a potentially precancerous condition or potentially premalignant condition, is a state of disordered morphology of cells that is associated with an increased risk of cancer. If left untreated, these conditions may lead to cancer. Such conditions are usually either dysplasia or benign neoplasia (and the dividing line between those is sometimes blurry). Sometimes the term "precancer" is used to describe carcinoma in situ, which is a noninvasive cancer that has not progressed to an aggressive, invasive stage. Not all carcinoma in situ will progress to invasive disease.

Premalignant lesions are morphologically atypical tissue which appears abnormal under microscopic examination, and in which cancer is more likely to occur than in its apparently normal counterpart.

Examples of premalignant conditions include:

- actinic keratosis

- Barrett's esophagus

- atrophic gastritis

- ductal carcinoma in situ

- dyskeratosis congenita

- sideropenic dysphagia

- lichen planus

- oral submucous fibrosis

- solar elastosis

- cervical dysplasia

- leukoplakia

- erythroplakia

The term was coined in 1875 by Romanian physician Victor Babeş.

It is caused by "Klebsiella rhinoscleromatis"—subspecies of

"Klebsiella pneumoniae"— a gram-negative, encapsulated, nonmotile, rod-shaped bacillus (diplobacillus), member of the Enterobacteriaceae family. It is sometimes referred to as the "Frisch bacillus," named for Anton von Frisch who identified the organism in 1882. It is contracted directly by droplets or by contamination of material that is subsequently inhaled.

Severe protein deficiency can cause Laennec's cirrhosis.

Two causes have been identified. The first is malnutrition, or, more specifically, protein deprivation. This is seen in starving children who have insufficient supplies of protein and therefore manufacture insufficient amounts of lipoproteins. They develop fatty livers: it is presumed that if they survive, cirrhosis will develop.

Chronic alcoholism can cause Laennec's cirrhosis. Whether or not alcohol alone can produce fatty nutritional cirrhosis has been debated for decades. Current evidence is that it can. If so, the condition should be renamed "alcoholic cirrhosis". Those who do not subscribe to the "alcohol-as-a-poison" school state that the changes to be described are the result of malnutrition common to alcoholics. They argue that alcoholics, in a sense, are no different from those in a state of chronic protein deprivation — both have protein deprivations.