Aphthous stomatitis (also termed recurrent aphthous stomatits, RAS, and commonly called "canker sores") is a very common cause of oral ulceration. 10–25% of the general population suffer from this non-contagious condition. The appearance of aphthous stomatitis varies as there are 3 types, namely minor aphthous ulceration, major aphthous ulceration and herpetiform ulceration. Minor aphthous ulceration is the most common type, presenting with 1–6 small (2-4mm diameter), round/oval ulcers with a yellow-grey color and an erythematous (red) "halo". These ulcers heal with no permanent scarring in about 7–10 days. Ulcers recur at intervals of about 1–4 months. Major aphthous ulceration is less common than the minor type, but produces more severe lesions and symptoms. Major aphthous ulceration presents with larger (>1 cm diameter) ulcers that take much longer to heal (10–40 days) and may leave scarring. The minor and major subtypes of aphthous stomatitis usually produce lesions on the non-keratinized oral mucosa (i.e. the inside of the cheeks, lips, underneath the tongue and the floor of mouth), but less commonly major aphthous ulcers may occur in other parts of the mouth on keratinized mucosal surfaces. The least common type is herpetiform ulceration, so named because the condition resembles primary herpetic gingivostomatitis. Herpetiform ulcers begin as small blisters (vesicles) which break down into 2-3mm sized ulcers. Herpetiform ulcers appear in "crops" sometimes hundreds in number, which can coalesce to form larger areas of ulceration. This subtype may cause extreme pain, heals with scarring and may recur frequently.

The exact cause of aphthous stomatitis is unknown, but there may be a genetic predisposition in some people. Other possible causes include hematinic deficiency (folate, vitamin B, iron), stopping smoking, stress, menstruation, trauma, food allergies or hypersensitivity to sodium lauryl sulphate (found in many brands of toothpaste). Aphthous stomatitis has no clinically detectable signs or symptoms outside the mouth, but the recurrent ulceration can cause much discomfort to sufferers. Treatment is aimed at reducing the pain and swelling and speeding healing, and may involve systemic or topical steroids, analgesics (pain killers), antiseptics, anti-inflammatories or barrier pastes to protect the raw area(s).

As a result of radiotherapy to the mouth, radiation-induced stomatitis may develop, which can be associated with mucosal erosions and ulceration. If the salivary glands are irradiated, there may also be xerostomia (dry mouth), making the oral mucosa more vulnerable to frictional damage as the lubricating function of saliva is lost, and mucosal atrophy (thinning), which makes a breach of the epithelium more likely. Radiation to the bones of the jaws causes damage to osteocytes and impairs the blood supply. The affected hard tissues become hypovascular (reduced number of blood vessels), hypocellular (reduced number of cells), and hypoxic (low levels of oxygen). Osteoradionecrosis is the term for when such an area of irradiated bone does not heal from this damage. This usually occurs in the mandible, and causes chronic pain and surface ulceration, sometimes resulting in non-healing bone being exposed through a soft tissue defect. Prevention of osteradionecrosis is part of the reason why all teeth of questionable prognosis are removed before the start of a course of radiotherapy.

This subtype makes up about 10% of all cases of aphthous stomatitis. It is termed major aphthous ulceration (MaAU) or major recurrent aphthous stomatitis (MaRAS). Major aphthous ulcers (major aphthae) are similar to minor aphthous ulcers, but are more than 10 mm in diameter and the ulceration is deeper. Because the lesions are larger, healing takes longer (about twenty to thirty days), and may leave scars. Each episode of ulceration usually produces a greater number of ulcers, and the time between attacks is less than seen in minor aphthous stomatitis. Major aphthous ulceration usually affects non keratinized mucosal surfaces, but less commonly keratinized mucosa may also be involved, such as the dorsum (top surface) of the tongue or the gingiva (gums). The soft palate or the fauces (back of the throat) may also be involved, the latter being part of the oropharynx rather than the oral cavity. Compared to minor aphthous ulceration, major aphthae tend to have an irregular outline.

This is the most common type of aphthous stomatitis, accounting for about 80–85% of all cases. This subtype is termed minor aphthous ulceration (MiAU), or minor recurrent aphthous stomatitis (MiRAS). The lesions themselves may be referred to as minor aphthae or minor aphthous ulcers. These lesions are generally less than 10 mm in diameter (usually about 2–3 mm), and affect non-keratinized mucosal surfaces (i.e. the labial and buccal mucosa, lateral borders of the tongue and the floor of the mouth). Usually several ulcers appear at the same time, but single ulcers are possible. Healing usually takes seven to ten days and leaves no scar. Between episodes of ulceration, there is usually an ulcer-free period of variable length.

Skin ulcers appear as open craters, often round, with layers of skin that have eroded. The skin around the ulcer may be red, swollen, and tender. Patients may feel pain on the skin around the ulcer, and fluid may ooze from the ulcer. In some cases, ulcers can bleed and, rarely, patients experience fever. Ulcers sometimes seem not to heal; healing, if it does occur, tends to be slow. Ulcers that heal within 12 weeks are usually classified as acute, and longer-lasting ones as chronic.

Ulcers develop in stages. In stage 1 the skin is red with soft underlying tissue. In the second stage the redness of the skin becomes more pronounced, swelling appears, and there may be some blisters and loss of outer skin layers. During the next stage, the skin may become necrotic down through the deep layers of skin, and the fat beneath the skin may become exposed and visible. In stage 4, deeper necrosis usually occurs, the fat underneath the skin is completely exposed, and the muscle may also become exposed. In the last two stages the sore may cause a deeper loss of fat and necrosis of the muscle; in severe cases it can extend down to bone level, destruction of the bone may begin, and there may be sepsis of joints.

Chronic ulcers may be painful. Most patients complain of constant pain at night and during the day. Chronic ulcer symptoms usually include increasing pain, friable granulation tissue, foul odour, and wound breakdown instead of healing. Symptoms tend to worsen once the wound has become infected.

Venous skin ulcers that may appear on the lower leg, above the calf or on the lower ankle usually cause achy and swollen legs. If these ulcers become infected they may develop an unpleasant odour, increased tenderness and redness. Before the ulcer establishes definitively, there may be a dark red or purple skin over the affected area as well as a thickening, drying, and itchy skin.

Although skin ulcers do not seem of great concern at a first glance, they are worrying conditions especially in people suffering from diabetes, as they are at risk of developing diabetic neuropathy.

Ulcers may also appear on the cheeks, soft palate, the tongue, and on the inside of the lower lip. These ulcers usually last from 7 to 14 days and can be painful.

Different types of discharges from ulcer are:

- Serous, usually seen in healing ulcer

- Purulent, seen in infected ulcer. Yellow creamy discharge is observed in staphylococcal infection; bloody opalescent discharge in streptococcal infection, while greenish discharge is seen in pseudomonas ulcer

- Bloody (sanguineous), usually seen in malignant ulcers and in healing ulcers with healthy granulation tissue

- Seropurulent

- Serosanguinous

- Serous with sulphur granules, seen in actinomycosis

- Yellowish, as seen in tuberculous ulcer

The definitions of the four pressure ulcer stages are revised periodically by the National Pressure Ulcer Advisor Panel (NPUAP) in the United States and the European Pressure Ulcer Advisor Panel (EPUAP) in Europe. Briefly, they are as follows:

- Stage 1: Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area differs in characteristics such as thickness and temperature as compared to adjacent tissue. Stage 1 may be difficult to detect in individuals with dark skin tones. May indicate "at risk" persons (a heralding sign of risk).

- Stage 2: Partial thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising. This stage should not be used to describe skin tears, tape burns, perineal dermatitis, maceration or excoriation.

- Stage 3: Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling. The depth of a stage 3 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and stage 3 ulcers can be shallow. In contrast, areas of significant adiposity can develop extremely deep stage 3 pressure ulcers. Bone/tendon is not visible or directly palpable.

- Stage 4: Full thickness tissue loss with exposed bone, tendon or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling. The depth of a stage 4 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have (adipose) subcutaneous tissue and these ulcers can be shallow. Stage 4 ulcers can extend into muscle and/or supporting structures (e.g., fascia, tendon or joint capsule) making osteomyelitis likely to occur. Exposed bone/tendon is visible or directly palpable. In 2012, the NPUAP stated that pressure ulcers with exposed cartilage are also classified as a stage 4.

- Unstageable: Full thickness tissue loss in which actual depth of the ulcer is completely obscured by slough (yellow, tan, gray, green or brown) and/or eschar (tan, brown or black) in the wound bed. Until enough slough and/or eschar is removed to expose the base of the wound, the true depth, and therefore stage, cannot be determined. Stable (dry, adherent, intact without erythema or fluctuance) eschar on the heels is normally protective and should not be removed.

- Suspected Deep Tissue Injury: A purple or maroon localized area of discolored intact skin or blood-filled blister due to damage of underlying soft tissue from pressure and/or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer or cooler as compared to adjacent tissue. A deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over a dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid exposing additional layers of tissue even with optimal treatment.

Plasma cell cheilitis is a very rare presentation of a condition which more usually occurs on the gingiva (termed "plasma cell gingivitis") or sometimes the tongue. 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 also present.

Geographic tongue, also termed benign migratory glossitis, is a common condition which usually affects the dorsal surface of the tongue. It is characterized by patches of depapillation and erythema bordered by a whitish peripheral zone. These patches give the tongue the appearance of a map, hence the name. Unlike glossitis due to nutritional deficiencies and anemia, the lesions of geographic tongue move around the tongue over time. This is because in geographic tongue, new areas of the tongue become involved with the condition whilst previously affected areas heal, giving the appearance of a moving lesion. The cause is unknown, and there is no curative treatment. Rarely are there any symptoms associated with the lesions, but occasionally a burning sensation may be present, which is exacerbated by eating hot, spicy or acidic foodstuffs. Some consider geographic tongue to be an early stage of fissured tongue, since the two conditions often occur in combination.

This condition is characterized by a persistent erythematous, rhomboidal depapillated lesion in the central area of the dorsum of the tongue, just in front of the circumvallate papillae. Median rhomboid glossitis is a type of oral candidiasis, and rarely causes any symptoms. It is treated with antifungal medication. Predisposing factors include use of corticosteroid sprays or inhalers or immunosuppression.

Common causes of drug-related cheilitis include Etretinate, Indinavir, Protease inhibitors, Vitamin A and Isotretinoin (a retinoid drug). Uncommon causes include Atorvastatin, Busulphan, Clofazimine, Clomipramine, Cyancobalamin, Gold, Methyldopa, Psoralens, Streptomycin, Sulfasalazine and Tetracycline. A condition called "drug-induced ulcer of the lip" is described as being characterized by painful or tender, well-defined ulcerations of the lip without induration. It is the result of oral administration of drugs, and the condition resolves when the drugs are stopped.

Pressure ulcers, also known as pressure sores, pressure injuries, bedsores, and decubitus ulcers, are localized damage to the skin and/or underlying tissue that usually occur over a bony prominence as a result of pressure, or pressure in combination with shear and/or friction. The most common sites are the skin overlying the sacrum, coccyx, heels or the hips, but other sites such as the elbows, knees, ankles, back of shoulders, or the back of the cranium can be affected.

Pressure ulcers occur due to pressure applied to soft tissue resulting in completely or partially obstructed blood flow to the soft tissue. Shear is also a cause, as it can pull on blood vessels that feed the skin. Pressure ulcers most commonly develop in individuals who are not moving about, such as those being bedridden or confined to a wheelchair. It is widely believed that other factors can influence the tolerance of skin for pressure and shear, thereby increasing the risk of pressure ulcer development.

These factors are protein-calorie malnutrition, microclimate (skin wetness caused by sweating or incontinence), diseases that reduce blood flow to the skin, such as arteriosclerosis, or diseases that reduce the sensation in the skin, such as paralysis or neuropathy. The healing of pressure ulcers may be slowed by the age of the person, medical conditions (such as arteriosclerosis, diabetes or infection), smoking or medications such as anti-inflammatory drugs.

Although often prevented and treatable if detected early, pressure ulcers can be very difficult to prevent in critically ill people, frail elders, and individuals with impaired mobility such as wheelchair users (especially where spinal injury is involved). Primary prevention is to redistribute pressure by regularly turning the person. The benefit of turning to avoid further sores is well documented since at least the 19th century. In addition to turning and re-positioning the person in the bed or wheelchair, eating a balanced diet with adequate protein and keeping the skin free from exposure to urine and stool is very important.

The rate of pressure ulcers in hospital settings is high; the prevalence in European hospitals ranges from 8.3% to 23% and 26% in Canadian healthcare settings. In 2013, there were 29,000 documented deaths globally, up from 14,000 deaths in 1990.

A stress ulcer is a single or multiple mucosal defect which can become complicated by upper gastrointestinal bleeding during the physiologic stress of serious illness. Ordinary peptic ulcers are found commonly in the gastric antrum and the duodenum whereas stress ulcers are found commonly in fundic mucosa and can be located anywhere within the stomach and proximal duodenum.

The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage.

The vast majority of the tropical ulcers occur below the knee, usually around the ankle. They may also occur on arms. They are often initiated by minor trauma, and subjects with poor nutrition are at higher risk. Once developed, the ulcer may become chronic and stable, but also it can run a destructive course with deep tissue invasion, osteitis, and risk of amputation. Unlike Buruli ulcer, tropical ulcers are very painful. Lesions begin with inflammatory papules that progress into vesicles and rupture with the formation of an ulcer. Chronic ulcers involve larger area and may eventually develop into squamous epithelioma after 10 years or more.

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.

Edema and fibrinous exudate leads to fibrosis of subcutaneous tissues with localized pigment loss and dilation of capillary loops. This is called atrophic blanche. This can occur around ankles and gives an appearance of inverted champagne bottle to legs. Large ulcers may encircle the leg.

Lymphedema results from obliteration of superficial lymphatics. There is hypertrophy of overlying epidermis giving polypoid appearance, known as lipodermatosclerosis.

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

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.

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.

Corneal ulcers are extremely painful due to nerve exposure, and can cause tearing, squinting, and vision loss of the eye. There may also be signs of anterior uveitis, such as miosis (small pupil), aqueous flare (protein in the aqueous humour), and redness of the eye. An axon reflex may be responsible for uveitis formation—stimulation of pain receptors in the cornea results in release inflammatory mediators such as prostaglandins, histamine, and acetylcholine.

Sensitivity to light (photophobia) is also a common symptom of corneal ulcer.

Tropical ulcer, more commonly known as jungle rot, is a chronic ulcerative skin lesion thought to be caused by polymicrobial infection with a variety of microorganisms, including mycobacteria. It is common in tropical climates.

Ulcers occur on exposed parts of the body, primarily on anterolateral aspect of the lower limbs and may erode muscles and tendons, and sometimes, the bones. These lesions may frequently develop on preexisting abrasions or sores sometimes beginning from a mere scratch.

Arterial insufficiency ulcers (also known as Ischemic ulcers or Ischemic wounds) are mostly located on the lateral surface of the ankle or the distal digits. They are commonly caused by peripheral artery disease (PAD).

Malum perforans (also known as neurotrophic ulcer and trophic ulcer) is a long-lasting, usually painless ulcer that penetrates deep into or through the skin, usually on the sole of the foot (in which case it may be called malum perforans pedis). It is often a complication in diabetes mellitus and other conditions affecting the nerves.

Assessment of diabetic foot ulcer includes identifying risk factors such as diabetic peripheral neuropathy, noting that 50 percent of people are asymptomatic, and ruling out other causes of peripheral neuropathy such as alcohol abuse and spinal injury.

The location of the ulcer, its size, shape, depth and whether the tissue is granulating or sloughy needs to be considered. Further considerations include whether the there is malodour, condition of the border of the wound and palpable bone and sinus formation should be investigated. Signs of infection require to be considered such as development of grey or yellow tissue, purulent discharge, unpleasant smell, sinus, undermined edges and exposure of bone or tendon.

Identification of diabetic foot in medical databases, such as commercial claims and prescription data, is complicated by the lack of a specific ICD-9 code for diabetic foot and variation in coding practices. The following codes indicate ulcer of the lower limb or foot:

- 707.1 Ulcer of lower limbs, except pressure ulcer

- 707.14 Ulcer of heel and midfoot

- 707.15 Ulcer of other part of foot

- 707.19 Ulcer of other part of lower limb

One or more codes, in combination with a current or prior diagnosis of diabetes may be sufficient to conclude diabetic foot:

- 250.0 Diabetes Mellitus

- 250.8 Diabetes with other specified manifestations