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.

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

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.

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)

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.

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.

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.

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

The ulcers can be removed through fulguration (burned off with the use of electricity or a laser) or resection (cutting around the ulcer, removing both the ulcer and the surrounding inflamed tissue). Some ulcers may recur in the same location.

Many patients choose to live with the ulcers and treat the symptoms associated with them through bladder instillations and/or pain medication/therapy.

Patients with interstitial cystitis may find relief by modifying their diet to remove foods and beverages that trigger symptoms. Caffeinated beverages, particularly coffee (regular and decaf), tea, green tea, soda, artificial sugars and fruit juices. Cranberry juice may also trigger intense pain and discomfort. However, studies about the impact of specific foods and drinks on Hunner's ulcer symptoms are limited.

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.

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.

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.

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.

Venous ulcers (venous insufficiency ulceration, stasis ulcers, stasis dermatitis, varicose ulcers, or ulcus cruris) are wounds that are thought to occur due to improper functioning of venous valves, usually of the legs (hence leg ulcers). They are the major occurrence of chronic wounds, occurring in 70% to 90% of leg ulcer cases. Venous ulcers develop mostly along the medial distal leg, and can be very painful with significant effects on quality of life.

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.

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.

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.

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

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.

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.

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.

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.

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

The disorder typically appears among young girls and adolescents but cases in children as young as 17 months have been reported.