ulcer, open sore or circumscribed erosion, usually slow to heal, on the skin or mucous membranes. It may develop as a result of injury; because of a circulatory disturbance, e.g., in varicose veins or after prolonged bed rest; or in association with such diseases as tuberculosis, syphilis, or leprosy. Corneal ulcers, which result from infection, allergy, or foreign objects in the eye, can cause visual impairment if not treated promptly. Some ulcers may develop into cancer. The underlying cause must be treated as well as the ulcerous lesion.

Peptic ulcer occurs in the mucous membrane of the intestinal tract. An estimated 90% of peptic ulcers are caused by infection with a bacterium, Helicobacter pylori, strains of which promote the formation of ulcers by causing an inflammtory response in the cells of the stomach wall, making it more susceptible to the hydrochloric acid secreted by the stomach. Most commonly, it occurs in the stomach (gastric ulcer) or at the beginning of the small intestine (duodenal ulcer, the most common form) and causes abdominal pain, especially between meals.

Infection with the H. pylori bacterium, which is also associated with some stomach cancer, is very common, but not all strains promote the formation of ulcers. Approximately 50% of those over 60 in developed countries are infected; in developing countries the infection rate is much higher, and infection usually occurs earlier in life. Experts are as yet uncertain how the bacterium is spread. Around 20% of those infected develop ulcers. Peptic ulcer is found more frequently in men. Heavy aspirin or ibuprofen use and smoking increase the risk of ulcer development.

The connection of H. pylori infection with peptic ulcer was made in the early 1980s by Australian scientists Barry J. Marshall and J. Robin Warren. It previously was believed that peptic ulcers were caused by emotional stress, though since the early 1900s researchers had reported finding curved bacteria in the stomachs of dead patients with ulcers more often than in those without ulcers. Marshall and Warren were awarded the Nobel Prize in physiology or medicine in 2005 for their work. Treatment changed accordingly and now typically consists of antibiotics (such as clarithromycin or amoxicillin) plus metronidazole (Flagyl) and bismuth subsalicylate (e.g., Pepto-Bismol). For the relief of symptoms, drugs such as ranitidine (Zantac), famotidine (Pepcid), cimetidine (Tagamet), and omeprazole (Prilosec) may also be used. Hemorrhage or perforation of peptic ulcers requires emergency medical treatment.

The full set of genes (genome) of H. pylori was determined in 1997. This achievement will help researchers design new drugs to treat and prevent diseases caused by the bacterium.

Ulcers are healing wounds that develop on the skin, mucous membranes, or eye. Although they have many causes, they are marked by:

  1. Loss of integrity of the area
  2. Secondary infection of the site by bacteria, fungus or virus
  3. Generalized weakness of the patient
  4. Delayed healing


The word ulcer is first attested from ca. 1400 CE, deriving from Old French ulcere, which came from Latin ulcus "ulcer", ultimately from the Proto-Indo-European base *elk-es- "wound".

Skin ulcer classification schemes

The skin is the largest organ of the human body. Classification systems are used to communicate the severity and depth of an ulcer. It is an easy way to communicate changes for the better, or worse.

Raghavendra manual classification

  • Stage 1: The skin is red. The underlying tissue is soft. The redness disappears with minor pressure.
  • Stage 2: There is redness, swelling and hardening of the skin around the area. Sometimes there is blistering. Sometimes there is loss of the superficial skin.
  • Stage 3: The skin becomes necrotic. There may be exposure of the fat beneath the skin. The skin may be lost through all its layers.
  • Stage 4: There is more loss of fat and more necrosis of the skin through to the muscle beneath.
  • Stage 5: Continuing loss of fat and necrosis of muscle below.
  • Stage 6: Bone destruction begins with irritation of the bone, erosion of the bone cortex progressing to osteomyelitis. There may be sepsis of a joint, pathologic fracture or generalized body infection, septicemia.

This staging system for rating ulcers, is designed to rate the severity of pressure ulcers.

  • Stage 1: There is erythema of intact skin which does not blanch with pressure. It may be the heralding lesion of skin ulceration.
  • Stage 2: There is partial skin loss involving the epidermis, dermis, or both. The ulcer is superficial and presents as an abrasion, blister, or wound with a shallow center.
  • Stage 3: This is an entire thickness skin loss. It may involve damage to or necrosis of subcutaneous tissue that may extend down to, but not through, the underlying fascia. The ulcer presents as a deep crater with or without undermining of adjacent intact tissues.
  • Stage 4: Here there is entire thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supporting structures. Tendons, and joints may also be exposed or involved. There may be undermining and/or sinus tracts associated with ulcers at this stage.

University of Texas Health Science Center Classification

This classification system is intended to rate the severity of diabetic foot ulcerations.

  • Grade 0: Skin with prior healed ulcer scars, areas of pressure which are sometimes called pre-ulcerative lesion or the presence of bony deformity which puts pressure on an unguarded point.
  • Grade 1-A: The wound is superficial in nature, with partial or full-thickness skin involvement but does not include tendon, capsule or bone.
  • Grade 1-B: As above, the wound is superficial in nature, with partial or full thickness skin involvement but not including tendon, capsule nor bone; however the wound is infected. The definition of this wound implies superficial infection without involvement of underlying structures. If the wound shows signs of significant purulence or fluctuation, further exploration to expose a higher grade classification of infection is in order.
  • Grade 1-C: As above but with vascular compromise.
  • Grade 1-D: As above but ischemic. Because ischemia is a type of vascular compromise, the distinction between these two grades is often difficult to make.
  • Grade 2-A: Penetration through the subcutaneous tissue exposing tendon or ligament, but not bone.
  • Grade 2-B: Penetration through the deep tissues including tendon or ligament and even joint capsule but not bone.
  • Grade 2-C: As above 2B, but including ischemic.
  • Grade 2-D: As above 2C, but including infection.
  • Grade 3-A: A wound which probes to bone but shows no signs of local infection nor systemic infection.
  • Grade 3-B: A wound which probes to bone and is infected.
  • Grade 3-C: A wound which probes to bone, is infected, and is ischemic.
  • Grade 3-D: A wound which probes to bone characterized by active infection, ischemic tissues, and exposed bone.
  • Grade 4: Gangrene of the forefoot.
  • Grade 5: Gangrene of the entire foot.

Other locations

  1. Inferior members: most ulcers of the foot and leg are caused by underlying vascular insufficiency. The skin breaks down or fails to heal because of repeated trauma. Pressure of the nail can cause subungual ulceration. These are most frequently seen in diabetics who have a very low potential to heal from injury.
  2. Sacrum and ischium
  3. Mouth ulcer
  4. Peptic ulcers: This includes ulcers of the esophagus, stomach, large and small intestine
  5. Genitalia: May be penile, vulvar or labial. Most often are due to sexually transmitted diseases
  6. Eyes: corneal ulcers are the most common type. Conjunctival ulcers also occur.

Pathology of ulceration


The most common causes (not in order) are:


Some specific types of ulcers are:


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