The thickness of the mucosa may be an important factor in aphthous stomatitis. Usually, ulcers form on the thinner, non-keratinizing mucosal surfaces in the mouth. Factors which decrease the thickness of mucosa increase the frequency of occurrence, and factors which increase the thickness of the mucosa correlate with decreased ulceration.

The nutritional deficiencies associated with aphthous stomatitis (B12, folate, and iron) can all cause a decrease in the thickness of the oral mucosa (atrophy).

Local trauma is also associated with aphthous stomatitis, and it is known that trauma can decrease the mucosal barrier. Trauma could occur during injections of local anesthetic in the mouth, or otherwise during dental treatments, frictional trauma from a sharp surface in the mouth such as broken tooth, or from tooth brushing.

Hormonal factors are capable of altering the mucosal barrier. In one study, a small group of females with apthous stomatitis had fewer occurrences of aphthous ulcers during the luteal phase of the menstrual cycle or with use of the contraceptive pill. This phase is associated with a fall in progestogen levels, mucosal proliferation and keratinization. This subgroup often experiences remission during pregnancy. However, other studies report no correlation between aphthous stomatitis and menstrual period, pregnancy or menopause.

Aphthous stomatitis is common in people who smoke, and there is also a correlation between habit duration and severity of the condition. Tobacco use is associated with an increase in keratinization of the oral mucosa. In extreme forms, this may manifest as leukoplakia or stomatitis nicotina (smoker's keratosis). This increased keratinization may mechanically reinforce the mucosa and reduce the tendency of ulcers to form after minor trauma, or present a more substantial barrier to microbes and antigens, but this is unclear. Nicotine is also known to stimulate production of adrenal steroids and reduce production of TNF-α, interleukin-1 and interleukin-6. Smokeless tobacco products also seem to protect against aphthous stomatitis. Cessation of smoking is known to sometimes precede the onset of aphthous stomatitis in people previously unaffected, or exacerbate the condition in those who were already experiencing aphthous ulceration. Despite this correlation, starting smoking again does not usually lessen the condition.

Various antigenic triggers have been implicated as a trigger, including L forms of streptococci, herpes simplex virus, varicella-zoster virus, adenovirus, and cytomegalovirus. Some people with aphthous stomatitis may show herpes virus within the epithelium of the mucosa, but without any productive infection. In some persons, attacks of ulceration occur at the same time as asymptomatic viral shedding and elevated viral titres.

In some instances, recurrent mouth ulcers may be a manifestation of an allergic reaction. Possible allergens include certain foods ("e.g.", chocolate, coffee, strawberries, eggs, nuts, tomatoes, cheese, citrus fruits, benzoates, cinnamaldehyde, and highly acidic foods), toothpastes, and mouthwashes. Where dietary allergens are responsible, mouth ulcers usually develop within about 12–24 hours of exposure.

Sodium lauryl sulphate (SLS), a detergent present in some brands of toothpaste and other oral healthcare products, may produce oral ulceration in some individuals. It has been shown that aphthous stomatitis is more common in people using toothpastes containing SLS, and that some reduction in ulceration occurs when a SLS-free toothpaste is used. Some have argued that since SLS is almost ubiquitously used in oral hygiene products, there is unlikely to be a true predisposition for aphthous stomatitis caused by SLS.

Many infections can cause oral ulceration (see table). The most common are herpes simplex virus (herpes labialis, primary herpetic gingivostomatitis), varicella zoster (chicken pox, shingles), and coxsackie A virus (hand, foot and mouth disease). Human immunodeficiency virus (HIV) creates immunodeficiencies which allow opportunistic infections or neoplasms to proliferate. Bacterial processes leading to ulceration can be caused by "Mycobacterium tuberculosis" (tuberculosis) and "Treponema pallidum" (syphilis).

Opportunistic activity by combinations of otherwise normal bacterial flora, such as aerobic streptococci, "Neisseria", "Actinomyces", spirochetes, and "Bacteroides" species can prolong the ulcerative process. Fungal causes include "Coccidioides immitis" (valley fever), "Cryptococcus neoformans" (cryptococcosis), and "Blastomyces dermatitidis" ("North American Blastomycosis"). Entamoeba histolytica, a parasitic protozoan, is sometimes known to cause mouth ulcers through formation of cysts.

Oral ulceration is a common reason for people to seek medical or dental advice. A breach of the oral mucosa probably affects most people at various times during life. For a discussion of the epidemiology of aphthous stomatitis, see Aphthous stomatitis#Epidemiology.

Riga–Fede disease (or syndrome) is a rare condition in infants characterized by ulceration on the ventral surface of the tongue or on the inner surface of the lower lip. It is caused by trauma to the soft tissue from erupted baby teeth.

It can be described as a sublingual traumatic ulceration. Although it begins as an ulceration, it may progress to a large fibrous mass with repeated trauma.

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.

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.

Nasal polyps resulting from chronic rhinosinusitis affect approximately 4.3% of the population. Nasal polyps occur more frequently in men than women and are more common as people get older, increasing drastically after the age of 40.

Of people with chronic rhinosinusitis, 10% to 54% also have allergies. An estimated 40% to 80% of people with sensitivity to aspirin will develop nasal polyposis. In people with cystic fibrosis, nasal polyps are noted in 37% to 48%.

Among those in the intensive care unit, ulceration resulting in bleeding is very rare.

A nasal septum perforation is a medical condition in which the nasal septum, the cartilaginous membrane dividing the nostrils, develops a hole or fissure.

This may be brought on directly, as in the case of nasal piercings, or indirectly, as by long-term topical drug application, including intranasal ethylphenidate, methamphetamine, cocaine, crushed prescription pills, or decongestant nasal sprays, chronic epistaxis, excessive nose picking and as a complication of nasal surgery like septoplasty or rhinoplasty. Much less common causes for perforated nasal septums include rare granulomatous inflammatory conditions like granulomatosis with polyangiitis. It has been reported as a side effect of anti-angiogenesis drugs like bevacizumab.

Nasal septal hematoma is a condition affecting the nasal septum. It can be associated with trauma.

Because the septal cartilage has no blood supply of its own and receives all of its nutrients and oxygen from the perichondrium, an untreated septal hematoma may lead to destruction of the septum. Immediate drainage is necessary. Failure to recognise septal hematomas, or treat in a timely fashion, can cause a saddle nose deformity.

Treatment for a nasal septal abscess is similar to that of other bacterial infections. Aggressive broad spectrum antibiotics may be used after the infected area has been drained of fluids.

They are removed under general anaesthesia . Most can be removed through anterior nares . Large ones need to be broken into pieces before removal . Some particularly hard and irregular ones may require lateral rhinotomy .

Septal perforations are managed with a multitude of options. The treatment often depends on the severity of symptoms and the size of the perforations. Generally speaking anterior septal perforations are more bothersome and symptomatic. Posterior septal perforations, which mainly occur iatrogenically, are often managed with simple observation and are at times intended portions of skull base surgery. Septal perforations that are not bothersome can be managed with simple observation. While no septal perforation will spontaneously close, for the majority of septal perforations that are unlikely to get larger observation is an appropriate form of management. For perforations that bleed or are painful, initial management should include humidification and application of salves to the perforation edges to promote healing. Mucosalization of the perforation edges will help prevent pain and recurrent epistaxis and majority of septal perforations can be managed without surgery.

For perforations in which anosmia, or the loss of smell, and a persistent whistling are a concern the use of a sillicone septal button is a treatment option. These can be placed while the patient is awake and usually in the clinic setting. While complications of button insertion are minimal, the presence of the button can be bothersome to most patients.

For patients who desire definitive close, surgery is the only option. Prior to determining candidacy for surgical closure, the etiology of the perforation must be determined. Often this requires a biopsy of the perforation to rule out autoimmune causes. If a known cause such as cocaine is the offending agent, it must be ensured that the patient is not still using the irritant.

For those that are determined to be medically cleared for surgery, the anatomical location and size of the perforation must be determined. This is often done with a combination of a CT scan of the sinuses without contrast and an endoscopic evaluation by an Ear Nose and Throat doctor. Once dimensions are obtained the surgeon will decide if it is possible to close the perforation. Multiple approaches to access the septum have been described in the literature. While sublabial and midfacial degloving approaches have been described, the most popular today is the rhinoplasty approach. This can include both open and closed methods. The open method results in a scar on the columella, however, it allows for more visibility to the surgeon. The closed method utilizes an incision all on the inside of the nose. The concept behind closure includes bringing together the edges of mucosa on each side of the perforation with minimal tension. An interposition graft is also often used. The interposition graft provides extended stability and also structure to the area of the perforation. Classically, a graft from the scalp utilizing temporalis fascia was used. Kridel, et al., first described the usage of acellular dermis so that no further incisions are required; they reported an excellent closure rate of over 90%. Overall perforation closure rates are variable and often determined by the skill of the surgeon and technique used. Often surgeons who claim a high rate of closure choose perforations that are easier to close. An open rhinoplasty approach also allows for better access to the nose to repair any concurrent nasal deformities, such as saddle nose deformity, that occur with a septal perforation.

The exact cause of nasal polyps is unclear. They are, however, commonly associated with conditions that cause long term inflammation of the sinuses. This includes chronic rhinosinusitis, asthma, aspirin sensitivity, and cystic fibrosis.

Various additional diseases associated with polyp formation include:

Chronic rhinosinusitis is a common medical condition characterized by symptoms of sinus inflammation lasting at least 12 weeks. The cause is unknown and the role of microorganisms remains unclear. It can be classified as either with or without nasal polyposis.

Cystic fibrosis (CF) is the most common cause of nasal polyps in children. Therefore, any child under 12 to 20 years old with nasal polyps should be tested for CF. Half of people with CF will experience extensive polyps leading to nasal obstruction and requiring aggressive management.

A rhinolith is a calculus present in the nasal cavity. The word is derived from the roots "" and "", literally meaning "nose stone". It is an uncommon medical phenomenon, not to be confused with dried nasal mucus. A rhinolith usually forms around the nucleus of a small exogenous foreign body, blood clot or secretion by slow deposition of calcium and magnesium salts. Over a period of time, they grow into large irregular masses that fill the nasal cavity. They may cause pressure necrosis of the nasal septum or lateral wall of nose. Rhinoliths can cause nasal obstruction, epistaxis, headache, sinusitis and epiphora. They can be diagnosed from the history with unilateral foul smelling blood stained nasal discharge or by anterior rhinoscopy. On probing probe can be passed around all its corners. In both CT and MRI rhinolith will appear like a radiopaque irregular material. Small rhinoliths can be removed by foreign body hook. Whereas large rhinoliths can be removed either by crushing with luc's forceps or by Moore's lateral rhinotomy approach.

To treat a septal haematoma it is incised & drained to prevent avascular necrosis of the septal hyaline cartilage which depends on diffusion of nutrients from its attached nasal mucosa. Small hematomas can be aspirated with a wide-bore needle. Large hematomas are drained by an incision parallel to nasal floor. Systemic antibiotics are given after the incision and drainage to prevent local infection.

The appearance of pyogenic granuloma is usually a color ranging from red/pink to purple, and can be smooth or lobulated. Younger lesions are more likely to be red because of the high number of blood vessels. Older lesions begin to change into a pink color. Size commonly ranges from a few millimeters to centimeters, though smaller or larger lesions may occur. A pyogenic granuloma can be painful, especially if located in an area of the body where it is constantly disturbed. Pyogenic granulomas can grow rapidly and will often bleed profusely with little or no trauma. They may exude an oil like substance, causing the surface to be damp. This is especially true if the granuloma is located on the scalp.

Pyogenic granulomas may be seen at any age, and are more common in females than males. In pregnant women, lesions may occur in the first trimester with an increasing incidence up until the seventh month, and are often seen on the gums. Epulis granulomatosum is a variant of pyogenic granuloma that forms only on gingiva, and is often seen forming in a recent extraction socket. Pyogenic granulomas appear on the gingiva in 75% of cases, more often in the maxillary than mandibular jaw. Anterior areas are more often affected than posterior areas. It can also be found on the lips, tongue, and inner cheek. Poor oral hygiene or trauma are usually precipitating factors.

One study has suggested a correlation between pyogenic granulomas and Bartonella seropositivity. However, this association has been questioned by others. The microscopic appearance of a pyogenic granuloma consists of highly vascular granulation tissue. Inflammation is present. The lesion may have a fibrous character if it is older, and the surface may have ulcerations. Pyogenic granulomas rarely occur in the conjunctiva, cornea or connective tissue of the eye following minor local trauma. Grossly these mass lesions resemble those occurring at more common sites. The relationship of these lesion to lobular capillary hemangiomas of skin and oropharyngeal mucosa commonly referred to as pyogenic granuloma is uncertain.

Prognosis is usually good, however recurrence may happen with rate up to 16%. Presence of myxoid structures in the pyogenic granuloma may be the main cause of recurrence.

Although pyogenic granulomas are not infectious or malignant, treatment may be considered because of bleeding or ulceration. Frequently, pyogenic granulomas are treated with electrodesiccation (cauterization) and curettage (excision), though laser treatment using pulsed dye laser or CO laser is often effective.

Several reports have demonstrated the efficacy of topical application of the beta-adrenergic antagonist timolol in the treatment of pediatric pyogenic granuloma.

There is usually no treatment if the pyogenic granuloma occurs during pregnancy since the lesion may heal spontaneously. Recurrent bleeding in either oral or nasal lesions may necessitate excision and cauterization sooner, however. If aesthetics are a concern, then treatment may be pursued as well. Usually, only minor surgery may be needed, along with a dental cleaning for oral lesions to remove any calculus or other source of irritation. For nasal lesions, nose-picking should be discouraged.

Potential complications of a nasal septal abscess include cavernous sinus thrombophlebitis, septal perforation, or saddle deformity due to cartilage necrosis.

A concha bullosa is a pneumatized (air-filled) cavity within a turbinate in the nose. (Concha is another term for turbinate.) Bullosa refers to the air-filled cavity within the turbinate. It is a normal anatomic variant seen in up to half the population. Occasionally, a large concha bullosa within a turbinate may cause it to bulge sufficiently to obstruct the opening of an adjacent sinus, possibly leading to recurrent sinusitis. In such a case the turbinate can be reduced in size by endoscopic nasal surgery (turbinectomy). The presence of a concha bullosa is often associated with deviation of the nasal septum toward the opposite side of the nasal cavity. Although it is thought that sinusitis or sinus pathology has relation to concha bullosa, no strong statistical correlation has been demonstrated.

Pseudopolyps are projecting masses of scar tissue that develop from granulation tissue during the healing phase in repeated cycle of ulceration (especially in inflammatory bowel disease). Inflammatory tissue without malignant potential, pseudopolyps may, according to Joffe (1977), represent either regenerating mucosal islands between areas of ulceration, edematous polypoid tags or granulation tissue covered by epithelium. There are reported cases when localized giant pseudopolyposis resulted in intestinal obstruction.

Residual mucosal islands between ulcerated and denuded areas of mucosa may have a polypoid appearance and are referred to as pseudopolyps. Polyposis syndromes, such as familial adenomatous polyposis, could give rise to a similar appearance on imaging, although the clinical presentation would differ from that of inflammatory pseudopolyposis.

Numerous, confluent ulcerations with bulging of the edematous residual mucosa determine a cobblestone appearance at endoscopy.

Risk factors for stress ulcer formation that have been identified are numerous and varied. However, two landmark studies and one position paper exist that addresses the topic of risk factors for stress ulcer formation:

- Non-critically ill medical patients with 2 or more of the following: respiratory failure, sepsis, heart failure, hepatic encephalopathy, jaundice, kidney failure, stroke, hypertension, previous gastrointestinal disease and treatment with corticosteroids, NSAIDS, heparin, or warfarin.

- In surgical critically ill patients, only those patients who are on a mechanical ventilator for more than 48 hours and/or those with a coagulopathy.

- The American Society of Health-System Pharmacists guideline recommends against the practice of stress ulcer prophylaxis in non-critically ill patients.

The flow of blood normally stops when the blood clots, which may be encouraged by direct pressure applied by pinching the soft fleshy part of the nose. This applies pressure to Little's area (Kiesselbach's area), the source of the majority of nose bleeds, and promotes clotting. Pressure should be firm and be applied for at least five minutes and up to 20 minutes; tilting the head forward helps decrease the chance of nausea and airway obstruction. Swallowing excess blood can irritate the stomach and cause vomiting.

The causes of nosebleeds can generally be divided into two categories, local and general factors, although a significant number of nosebleeds occur with no obvious cause.