Many people who have chronic gastritis do not experience any noticeable symptoms. Those who do, claim to experience one or several of the following: upper abdominal pain, indigestion, bloating, nausea, vomiting, belching, loss of appetite, and weight loss. Stomach bleeding or black stool has been reported in extreme cases.

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.

Atrophic gastritis (also known as Type A or Type B Gastritis more specifically) is a process of chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells and their eventual replacement by intestinal and fibrous tissues. As a result, the stomach's secretion of essential substances such as hydrochloric acid, pepsin, and intrinsic factor is impaired, leading to digestive problems. The most common are vitamin B deficiency which results in a megaloblastic anemia and malabsorbtion of iron, leading to iron deficiency anaemia. It can be caused by persistent infection with "Helicobacter pylori", or can be autoimmune in origin. Those with the autoimmune version of atrophic gastritis are statistically more likely to develop gastric carcinoma, Hashimoto's thyroiditis, and achlorhydria.

Type A gastritis primarily affects the body/fundus of the stomach, and is more common with pernicious anemia.

Type B gastritis primarily affects the antrum, and is more common with "H. pylori" infection.

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.

The small intestine consists of the duodenum, jejunum and ileum. Inflammation of the small intestine is called enteritis, which if localised to just part is called duodenitis, jejunitis and ileitis, respectively. Peptic ulcers are also common in the duodenum.

Chronic diseases of malabsorption may affect the small intestine, including the autoimmune coeliac disease, infective Tropical sprue, and congenital or surgical short bowel syndrome. Other rarer diseases affecting the small intestine include Curling's ulcer, blind loop syndrome, Milroy disease and Whipple's disease. Tumours of the small intestine include gastrointestinal stromal tumours, lipomas, hamartomas and carcinoid syndromes.

Diseases of the small intestine may present with symptoms such as diarrhoea, malnutrition, fatigue and weight loss. Investigations pursued may include blood tests to monitor nutrition, such as iron levels, folate and calcium, endoscopy and biopsy of the duodenum, and barium swallow. Treatments may include renutrition, and antibiotics for infections.

Even though anatomically part of the GI tract, diseases of the mouth are often not considered alongside other gastrointestinal diseases. By far the most common oral conditions are plaque-induced diseases (e.g. gingivitis, periodontitis, dental caries). Some diseases which involve other parts of the GI tract can manifest in the mouth, alone or in combination, including:

- Gastroesophageal reflux disease can cause acid erosion of the teeth and halitosis.

- Gardner's syndrome can be associated with failure of tooth eruption, supernumerary teeth, and dentigerous cysts.

- Peutz–Jeghers syndrome can cause dark spots on the oral mucosa or on the lips or the skin around the mouth.

- Several GI diseases, especially those associated with malabsorption, can cause recurrent mouth ulcers, atrophic glossitis, and angular cheilitis (e.g. Crohn's disease is sometimes termed orofacial granulomatosis when it involves the mouth alone).

- Sideropenic dysphagia can cause glossitis, angular cheilitis.

Atrophic glossitis, also known as bald tongue, smooth tongue, Hunter glossitis, Moeller glossitis, or Möller-Hunter glossitis, is a condition characterized by a smooth glossy tongue that is often tender/painful, caused by complete atrophy of the lingual papillae (depapillation). The dorsal tongue surface may be affected totally, or in patches, and may be associated with a burning sensation, pain and/or erythema. Atrophic glossitis is a non-specific finding, and has a great many causes, usually related to iron-deficiency anemia, pernicious anemia, B vitamin complex deficiencies, unrecognized and untreated celiac disease (which often presents without gastrointestinal symptoms), or other factors such as xerostomia (dry mouth). Although the terms Möller and Hunter glossitis were originally used to refer to specifically the glossitis that occurs in vitamin B12 deficiency secondary to pernicious anemia, they are now used as synonyms for atrophic glossitis generally. In this article, the term glossitis, unless otherwise specified, refers to atrophic glossitis.

Candidiasis may be a concurrent finding or an alternative cause of erythema, burning, and atrophy.

Glossitis could be classified as a group of tongue diseases or gastrointestinal diseases. It may be primary, where there is no underlying cause, or secondary where it is a sign or symptom of another condition. It can be acute or chronic. Generally speaking, there are several clinical patterns of glossitis, some more common than others.

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.

Chronic atrophic rhinitis is a chronic inflammation of nose characterised by atrophy of nasal mucosa, including the glands, turbinate bones and the nerve elements supplying the nose. Chronic atrophic rhinitis may be primary and secondary. Special forms of chronic atrophic rhinitis are rhinitis sicca anterior and ozaena.

Permanent loss of smell and impairment of taste may also be a result of this disease, even after the symptoms are cured.

In health, the dorsal surface of the tongue is covered in tuft like projections called lingual papillae (some of which are associated with taste buds), which give the tongue an irregular surface texture and a white-pink color. Geographic tongue is characterized by areas of atrophy and depapillation (loss of papillae), leaving an erythematous (darker red) and smoother surface than the unaffected areas. The depapillated areas are usually well demarcated, and bordered by a slightly raised, white, yellow or grey, serpiginous (snaking) peripheral zone. A lesion of geographic tongue may start as a white patch before the depapillation occurs. In certain cases there may be only one lesion, but this is uncommon; the lesions will typically occur in multiple locations on the tongue and coalesce over time to form the typical map-like appearance. The lesions usually change in shape, size and migrate to other areas, sometimes within hours. The condition may affect only part of the tongue, with a predilection for the tip and the sides of the tongue, or the entire dorsal surface at any one time. The condition goes through periods of remission and relapse. Loss of the white peripheral zone is thought to signify periods of mucosal healing.

There are usually no symptoms other than the unusual appearance of the tongue, but in some cases persons may experience pain or burning e.g. when eating hot, acidic, spicy or other kinds of foods (e.g. cheese, tomatoes, fruit). Where there is a burning symptom, other causes of a burning sensation on the tongue are considered, such as oral candidiasis.

Geographic tongue could be considered to be a type of glossitis. It usually presents only on the dorsal 2/3 and lateral surfaces of the tongue, but less commonly an identical condition can occur on other mucosal sites in the mouth, such as the ventral surface (undersurface) of the tongue, mucosa of the cheeks or lips, soft palate or floor of mouth; usually in addition to tongue involvement. In such cases, terms such as stomatitis erythema migrans, ectopic geographic tongue, areata migrans, geographic stomatitis, or migratory stomatitis are used instead of geographic tongue. Beside the differences in locations of presentation inside the oral cavity and prevalence among the general population, in all other aspects of clinical significance, symptoms, treatment, and histopathologic appearance, these two forms are identical.

This condition is sometimes termed (oral) erythema migrans, but this has no relation to the more common use of the term erythema migrans (erythema chronicum migrans), to describe the appearance of skin lesions in Lyme disease.

Rarely is any soreness associated with the condition. Apart from the appearance of the lesion, there are usually no other signs or symptoms. The typical appearance of the lesion is an oval or rhomboid shaped area located in the midline of the dorsal surface of the tongue, just anterior (in front) of the sulcus terminalis. The lesion is usually symmetric, well demarcated, erythematous and depapillated, which has a smooth, shiny surface. Less typically, the lesion may be hyperplastic or lobulated and exophytic. There may be candidal lesions at other sites in the mouth, which may lead to a diagnosis of chronic multifocal oral candidiasis. Sometimes an approximating erythematous lesion is present on the palate as the tongue touches the palate frequently. The lesion is typically 2–3 cm in its longest dimension.

Erythematous (atrophic) candidiasis is when the condition appears as a red, raw-looking lesion. Some sources consider denture-related stomatitis, angular stomatitis, median rhombiod glossitis, and antiobiotic-induced stomatitis as subtypes of erythematous candidiasis, since these lesions are commonly erythematous/atrophic. It may precede the formation of a pseudomembrane, be left when the membrane is removed, or arise without prior pseudomembranes. Some sources state that erythematous candidiasis accounts for 60% of oral candidiasis cases. Where it is associated with inhalation steroids (often used for treatment of asthma), erythematous candidiasis commonly appears on the palate or the dorsum of the tongue. On the tongue, there is loss of the lingual papillae (depapillation), leaving a smooth area.

Acute erythematous candidiasis usually occurs on the dorsum of the tongue in persons taking long term corticosteroids or antibiotics, but occasionally it can occur after only a few days of using a topical antibiotic. This is usually termed "antibiotic sore mouth", "antibiotic sore tongue", or "antibiotic-induced stomatitis" because it is commonly painful as well as red.

Chronic erythematous candidiasis is more usually associated with denture wearing (see denture-related stomatitis).

This refers to a group of rare syndromes characterized by chronic candidal lesions on the skin, in the mouth and on other mucous membranes (i.e., a secondary oral candidiasis). These include Localized chronic mucocutaneous candidiasis, diffuse mucocutaneous candidiasis (Candida granuloma), candidiasis–endocrinopathy syndrome and candidiasis thymoma syndrome. About 90% of people with chronic mucocutaneous candidiasis have candidiasis in the mouth.

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.

Plasma cell gingivitis appears as mild gingival enlargement and may extend from the free marginal gingiva on to the attached gingiva. Sometimes it is blended with a marginal, plaque induced gingivitis, or it does not involve the free marginal gingiva. It may also be found as a solitude red area within the attached gingiva (pictures). In some cases the healing of a plaque-induced gingivitis or a periodontitis resolves a plasma cell gingivitis situated a few mm from the earlier plack-infected marginal gingiva. In case of one or few solitary areas of plasma cell gingivitis, no symptoms are reported from the patient. Most often solitary entities are therefore found by the dentist.

The gums are red, friable, or sometimes granular, and sometimes bleed easily if traumaticed. The normal stippling is lost. There is not usually any loss of periodontal attachment. In a few cases a sore mouth can develop, and if so pain is sometimes made worse by toothpastes, or hot or spicy food. The lesions can extend to involve the palate.

Plasma cell cheilitis appears as well defined, infiltrated, dark red plaque with a superficial lacquer-like glazing. Plasma cell cheilitis usually involves the lower lip. The lips appear dry, atrophic and fissured. Angular cheilitis is sometimes present.

Where the condition involves the tongue, there is an erythematous enlargement with furrows, crenation and loss of the normal dorsal tongue coating.

Rhinoscleroma has been divided into 3 stages: catarrhal/atrophic, granulomatous, and sclerotic stages. The catarrhal stage begins with a nonspecific rhinitis, which progresses into purulent, fetid rhinorrhea, and crusting, which can last for weeks or even months. The granulomatous stage results in the development of a bluish red nasal mucosa and the development of intranasal rubbery nodules or polyps. Nose bleeds, nasal deformity, and destruction of the nasal cartilage are also noted (Hebra nose). The damage may result in anesthesia of the soft palate, enlargement of the uvula, dysphonia, and various degrees of airway obstruction. The fibrotic stage is characterized by sclerosis and fibrosis. Lymphadenitis is absent.

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.

Depending upon the site of involvement, this condition could be considered a type of gingivitis (or gingival enlargement); a type of cheilitis; glossitis; or stomatitis. Sometimes the lips, the gums and the tongue can simultaneously be involved, and some authors have described this triad as a syndrome ("plasma-cell gingivostomatitis"). The mucous membranes of the genitals can also be involved by a similar condition, termed "plasma cell balanitis" or "plasma cell vulvitis".

Other synonyms for this condition not previously mentioned include atypical gingivitis, allergic gingivitis, plasmacytosis of the gingiva, idiopathic gingivostomatitis, and atypical gingivostomatitis. Some of these terms are largely historical.

Plasma cell gingivits has been subclassified into 3 types based upon the cause; namely, allergic, neoplastic and of unknown cause.

Signs of duct ectasia can include nipple retraction, inversion, pain, and sometimes bloody discharge.

Rhinoscleroma, or simply scleroma, is a chronic granulomatous bacterial disease of the nose that can sometimes infect the upper respiratory tract. It most commonly affects the nasal cavity—the nose is involved in 95–100 per cent of cases—however, it can also affect the nasopharynx, larynx, trachea, and bronchi. Slightly more females than males are affected and patients are usually 10 to 30 years of age. Rhinoscleroma is considered a tropical disease and is mostly endemic to Africa and Central America, less common in the United States.

The symptoms may vary depending on the thyroid function, i.e. hyperthyroidism or hypothyroidism. Hyperthyroidism can cause sweating, rapid heart rate, anxiety, tremors, fatigue, difficulty sleeping, sudden weight loss, and protruding eyes. Hypothyroidism can cause weight gain, fatigue, dry skin, hair loss, intolerance to cold, and constipation. The effects of this disease may be permanent but can sometimes be transient. Symptoms may come and go depending on whether the person receives treatment, and whether the treatment takes effect.

Autoimmune thyroiditis, (or Chronic Autoimmune thyroiditis), is a chronic disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid’s cells, thereby destroying it.

It may present with hypothyroidism or hyperthyroidism and with or without a goiter.