There are over 100 risk factors for pressure ulcers. Factors that may place a patient at risk include immobility, diabetes mellitus, peripheral vascular disease, malnutrition, cerebral vascular accident and hypotension. Other factors are age of 70 years and older, current smoking history, dry skin, low body mass index, urinary and fecal incontinence, physical restraints, malignancy, and history of pressure ulcers.

In addition, adequate intake of protein and calories is important. vitamin C has been shown to reduce the risk of pressure ulcers. People with higher intakes of vitamin C have a lower frequency of bed sores in those who are bedridden than those with lower intakes. Maintaining proper nutrition in newborns is also important in preventing pressure ulcers. If unable to maintain proper nutrition through protein and calorie intake, it is advised to use supplements to support the proper nutrition levels. Skin care is also important because damaged skin does not tolerate pressure. However, skin that is damaged by exposure to urine or stool is not considered a pressure ulcer. These skin wounds should be classified as Incontinence Associated Dermatitis.

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.

Many drugs can cause mouth ulcers as a side effect. Common examples are alendronate (a bisphosphonate, commonly prescribed for osteoporosis), cytotoxic drugs (e.g. methotrexate, i.e. chemotherapy), non-steroidal anti-inflammatory drugs, nicorandil (may be prescribed for angina) and propylthiouracil (e.g. used for hyperthyroidism). Some recreational drugs can cause ulceration, e.g. cocaine.

The wounds from which ulcers arise can be caused by a wide variety of factors, but the main cause is impaired blood circulation. Especially, chronic wounds and ulcers are caused by poor circulation, either through cardiovascular issues or external pressure from a bed or a wheelchair. A very common and dangerous type of skin ulcers are caused by what are called pressure-sensitive sores, more commonly called bed sores and which are frequent in people who are bedridden or who use wheelchairs for long periods. Other causes producing skin ulcers include bacterial or viral infections, fungal infections and cancers. Blood disorders and chronic wounds can result in skin ulcers as well.

Venous leg ulcers due to impaired circulation or a blood flow disorder are more common in the elderly.

Compression stockings appear to prevent the formation of new ulcers in people with a history of venous ulcers.

Steps to prevent diabetic foot ulcers include frequent review by a foot specialist, good foot hygiene, diabetic socks and shoes, as well as avoiding injury.

- Foot-care education combined with increased surveillance can reduce the incidence of serious foot lesions.

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

Stem cell therapy may represent a treatment for promoting healing of diabetic foot ulcers. Diabetic foot ulcers develop their own, distinctive microbiota. Investigations into characterizing and identifying the phyla, genera and species of nonpathogenic bacteria or other microorganisms populating these ulcers may help identify one group of microbiota that promotes healing.

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.

An ulcer is a sore on the skin or a mucous membrane, accompanied by the disintegration of tissue. Ulcers can result in complete loss of the epidermis and often portions of the dermis and even subcutaneous fat. Ulcers are most common on the skin of the lower extremities and in the gastrointestinal tract. An ulcer that appears on the skin is often visible as an inflamed tissue with an area of reddened skin. A skin ulcer is often visible in the event of exposure to heat or cold, irritation, or a problem with blood circulation. They can also be caused due to a lack of mobility, which causes prolonged pressure on the tissues. This stress in the blood circulation is transformed to a skin ulcer, commonly known as bedsores or decubitus ulcers. Ulcers often become infected, and pus forms.

The main aim of the treatment is to create such an environment that allows skin to grow across an ulcer. In the majority of cases this requires finding and treating underlying venous reflux and National Institute for Health and Care Excellence (NICE) recommends referral to a vascular service for anyone with a leg ulcer that has not healed within 2 weeks or anyone with a healed leg ulcer.

Most venous ulcers respond to patient education, elevation of foot, elastic compression and evaluation, called the Bisgaard regimen. There is no evidence for intravenous or by mouth antibiotics for venous leg ulcers. Silver products are also not typically useful while there is some evidence for cadexomer iodine creams. There is a lack of quality evidence regarding the use of medical grade honey for venous leg ulcers.

These ulcers are difficult to heal by basic wound care and require advanced therapy, such as hyperbaric oxygen therapy or bioengineered skin substitutes. If not taken care of in time, there are very high chances that these may become infected and eventually may have to be amputated. Individuals with history of previous ulcerations are 36 times more likely to develop another ulcer.

This condition results from denervation of areas exposed to day-to-day friction of bony prominences. The denervation may be result of any of the following diseases:

- Spinal injuries

- Leprosy

- Peripheral nerve injury

- Diabetic neuropathy

- Tabes dorsalis

- Transverse myelitis

- Meningomyelocele

The ulcer has punched-out appearance. It is intensely painful. It has gray or yellow fibrotic base and undermining skin margins. Pulses are not palpable. Associated skin changes may be observed, such as thin shiny skin and absence of hair. They are most common on distal ends of limbs. A special type of ischemic ulcer developing in duodenum after severe burns is called Curling's ulcer.

These ulcers have punched-out edge and slough in floor, resembling gummatous ulcer. Surrounding area might have loss of sensation.

Dietary factors such as spice consumption, were hypothesized to cause ulcers until late in the 20th century, but have been shown to be of relatively minor importance. Caffeine and coffee, also commonly thought to cause or exacerbate ulcers, appear to have little effect. Similarly, while studies have found that alcohol consumption increases risk when associated with "H. pylori" infection, it does not seem to independently increase risk. Even when coupled with "H. pylori" infection, the increase is modest in comparison to the primary risk factor.

Adequate footwear is important to prevent trauma. General good health and nutrition also reduce ulcer risk. Adequate and prompt cleansing and treatment of ankle and leg skin breaks is also important. Improving hygiene and nutrition may help to prevent tropical ulcers.

There is now considerable evidence to suggest that this disease is an infection. "Mycobacterium ulcerans" has recently been isolated from lesions and is unique to tropical ulcers. Early lesions may be colonized or infected by, "Bacillus fusiformis" (Vincent's organism), anaerobes and spirochaetes. Later, tropical ulcer may become infected with a variety of organisms, notably, staphylococci and/or streptococci. The condition has been shown to be transmissible by inoculation of material from affected patients.

Stress due to serious health problems such as those requiring treatment in an intensive care unit is well described as a cause of peptic ulcers, which are termed stress ulcers.

While chronic life stress was once believed to be the main cause of ulcers, this is no longer the case. It is, however, still occasionally believed to play a role. This may be by increasing the risk in those with other causes such as "H. pylori" or NSAID use.

Corneal ulcer, or ulcerative keratitis, is an inflammatory or more seriously, infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and the agrarian societies. In developing countries, children afflicted by Vitamin A deficiency are at high risk for corneal ulcer and may become blind in both eyes, which may persist lifelong. In ophthalmology, a corneal ulcer usually refers to having an infectious cause while the term corneal abrasion refers more to physical abrasions.

Corneal ulcers are a common human eye disease. They are caused by trauma, particularly with vegetable matter, as well as chemical injury, contact lenses and infections. Other eye conditions can cause corneal ulcers, such as entropion, distichiasis, corneal dystrophy, and keratoconjunctivitis sicca (dry eye).

Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa, and chlamydia:

- Bacterial keratitis is caused by "Staphylococcus aureus", "Streptococcus viridans", "Escherichia coli", "Enterococci", "Pseudomonas", "Nocardia", "N. Gonorrhoea" and many other bacteria.

- Fungal keratitis causes deep and severe corneal ulcer. It is caused by "Aspergillus" sp., "Fusarium" sp., "Candida" sp., as also "Rhizopus", "Mucor", and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and hypopyon is usually seen.

- Viral keratitis causes corneal ulceration. It is caused most commonly by Herpes simplex, Herpes zoster and Adenoviruses. Also it can be caused by coronaviruses & many other viruses. Herpes virus cause a dendritic ulcer, which can recur and relapse over the lifetime of an individual.

- Protozoa infection like "Acanthamoeba keratitis" is characterized by severe pain and is associated with contact lens users swimming in pools.

- "Chlamydia trachomatis" can also contribute to development of corneal ulcer.

Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially dangerous and can rapidly result in corneal perforation, if not treated in time.

The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Entropion, severe dry eye and trichiasis (inturning of eyelashes) may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include Rheumatoid arthritis, rosacea, systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a circumferential crater like depression of the cornea, just inside the limbus, usually with an overhanging edge.

While emergency surgery was once the only treatment, combination therapies including enteral feeding with powerful antacids such as H-receptor antagonists or, more recently, proton pump inhibitors such as omeprazole have made Curling's ulcer a rare complication.

The drug Elmiron helps, for some patients, to prevent the formation of Hunner's Ulcers by coating the bladder wall, thus making it harder for the acid in urine to irritate the bladder wall lining, which can lead to ulceration. (not cited)

Curling's ulcer (stress ulcer) or a Curling ulcer is an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa. The condition was first described in 1823 and named for a doctor, Thomas Blizard Curling, who observed ten such patients in 1842.

These stress ulcers (actually shallow multiple erosions) were once a common complication of serious burns, presenting in over 10% of cases, and especially common in child burn victims. They result in perforation and hemorrhage more often than other forms of intestinal ulceration and had correspondingly high mortality rates (at least 80%).

A similar condition involving elevated intracranial pressure is known as Cushing's ulcer.