What Causes Skin Ulcers? Types and Risk Factors

Skin ulcers are open wounds that fail to heal normally, and they almost always trace back to one root problem: not enough blood, oxygen, or nutrients reaching the skin. The specific cause varies, but the four most common types are venous ulcers, arterial ulcers, diabetic ulcers, and pressure ulcers. Less common triggers include autoimmune conditions, blood disorders, and nutritional deficiencies.

Venous Ulcers: The Most Common Type

Venous ulcers account for the majority of leg ulcers and develop because of faulty blood flow in the veins. Normally, one-way valves inside your leg veins keep blood moving upward toward the heart, assisted by calf muscle contractions. When those valves stop working properly, blood flows backward and pools in the lower legs. This creates sustained high pressure inside the veins, a condition called chronic venous insufficiency.

That persistent pressure forces proteins and fluid out of the veins and into the surrounding tissue. A layer of fibrin builds up around the small blood vessels, blocking oxygen and growth factors from reaching the skin. The tissue becomes chronically inflamed, and over time, the skin breaks down into an ulcer. The ongoing inflammation also encourages blood clots, which cause further scarring and valve damage in a self-reinforcing cycle.

These ulcers typically appear on the inner lower leg, just above the ankle bone. They tend to be irregularly shaped with well-defined borders, and the wound bed often has a yellow-white discharge. The surrounding skin usually shows telltale signs: dark discoloration, hardened texture, and sometimes an “inverted champagne bottle” shape to the leg where the lower portion narrows while the calf swells.

Arterial Ulcers: Blocked Blood Supply

Arterial ulcers form when narrowed or blocked arteries can’t deliver enough blood to the legs and feet. The underlying cause is almost always atherosclerosis, the buildup of fatty deposits (plaque) inside artery walls. As plaque accumulates, the artery narrows and eventually can’t supply enough oxygen to keep tissue alive. The skin at the farthest points from the heart is the first to suffer.

These ulcers look distinctly different from venous ulcers. They appear “punched out” with sharp, well-defined edges. The wound bed is often dry and dark or necrotic, with little to no bleeding or discharge. You’ll typically find them on toes, the tops of feet, or over bony areas of the lower leg. The skin around an arterial ulcer is thin, shiny, hairless, and cool to the touch. Toenails may be thickened and brittle, and pulses in the foot are weak or absent.

Diabetic Ulcers: Nerve Damage Meets Poor Circulation

Roughly 18.6 million people worldwide develop diabetic foot ulcers each year. These wounds arise from a collision of problems that diabetes creates simultaneously: nerve damage, reduced blood flow, and impaired healing. About 50% of diabetic foot ulcers become infected, and 20% of people with these ulcers ultimately require a lower limb amputation. In fact, diabetic foot ulcers precede 80% of all diabetes-related amputations.

The process typically starts with peripheral neuropathy, the gradual destruction of nerves in the feet. This plays out in three ways. Sensory neuropathy eliminates your ability to feel pain, pressure, and temperature changes, so injuries go completely unnoticed. Motor neuropathy distorts foot anatomy, creating claw toes, high arches, and prominent bones that concentrate pressure on small areas of skin, leading to calluses and eventual breakdown. Autonomic neuropathy reduces sweating, leaving the skin dry and cracked, and disrupts the small blood vessels that regulate local blood flow.

On top of all that, peripheral artery disease is common in people with diabetes, further starving the tissue of oxygen. When neuropathy and poor circulation coexist, the result is called a neuro-ischemic ulcer, the most dangerous combination. These ulcers are most common on pressure points and the soles of the feet. They’re typically surrounded by thick callus, with undermined borders and a necrotic wound bed that can expose deeper structures like tendons or bone.

Pressure Ulcers: Sustained Force on Skin

Pressure ulcers (also called bedsores) develop when prolonged pressure on the skin cuts off blood flow to that area. They’re most common in people who are bedridden, use a wheelchair, or have limited mobility. The damage happens over bony prominences like the tailbone, heels, hips, and shoulder blades, where the bone compresses skin and tissue against a surface.

These ulcers progress through four stages. Stage I is intact skin with a persistent red area that doesn’t lighten when you press on it. Stage II involves a shallow open wound where the top layers of skin have worn away. Stage III means full-thickness skin loss, where underlying fat may be visible but bone and muscle are not. Stage IV is the most severe: full-thickness tissue loss with exposed bone, tendon, or muscle. The progression can happen surprisingly quickly, sometimes within hours in vulnerable patients, though it more commonly develops over days.

Autoimmune and Inflammatory Causes

Not all skin ulcers come from circulation problems or pressure. Pyoderma gangrenosum and vasculitis are the most common inflammatory causes of skin ulcers. Both are linked to autoimmune conditions, including inflammatory bowel disease, rheumatological disorders, and certain cancers.

Pyoderma gangrenosum starts as a small pustule or blister that rapidly expands into a deep, painful ulcer. The wound bed is necrotic and fibrinous, and the surrounding skin develops a distinctive lilac or purple ring at the border. It’s diagnosed by ruling out other causes, since there’s no single definitive test. Vasculitis, which involves inflammation and destruction of blood vessel walls, produces painful ulcers alongside purplish spots, tiny red dots on the skin, and blisters. Both conditions are extremely painful, often more so than vascular ulcers, and treatment involves suppressing the overactive immune response with systemic medications.

Sickle Cell Disease

People with sickle cell anemia develop leg ulcers in areas where the skin is thin, fat is scarce, and venous drainage is poor. The inner ankle is the most common site, though ulcers can also appear on the outer ankle, the front of the shin, or the top of the foot. These ulcers look and behave much like venous ulcers because the underlying mechanism is similar: abnormally shaped red blood cells clog small vessels, reducing oxygen delivery and triggering chronic inflammation.

Nutritional Deficiencies That Impair Healing

Several vitamin deficiencies can directly contribute to skin breakdown and ulcer formation. Vitamin C is the most well-known, since your body needs it to build collagen, the protein that gives skin its structural strength. Without adequate vitamin C, wounds heal poorly and ulcers form more easily. This is the mechanism behind scurvy, which is rare but still occurs in people with extremely limited diets.

B vitamins also play a role. Severe deficiency in vitamins B2 and B6 has been linked to skin ulcerations and chronic dermatitis that resolved with supplementation. Niacin (vitamin B3) deficiency causes pellagra, a condition where the skin hardens and becomes brittle, eventually cracking into fissures and ulcers, particularly around the perineum. These nutritional causes are less common than vascular ones, but they’re worth considering when ulcers appear without an obvious circulatory explanation, especially in older adults or people with poor dietary intake.

Early Warning Signs Before an Ulcer Forms

Skin ulcers rarely appear without warning. For venous disease, the early signs include persistent swelling in the lower legs, brownish discoloration around the ankles, skin that feels hard or leathery, and varicose veins. For arterial disease, look for skin that becomes thin, shiny, and hairless on the legs and feet, along with toenails that grow slowly and become brittle. Cold feet and pain during walking that improves with rest are classic early signals.

For people with diabetes, the warning signs are subtler precisely because nerve damage masks them. Calluses building up on pressure points of the feet, changes in foot shape, dry cracked skin on the soles, and any loss of sensation are all red flags. Regular foot checks, including looking at the bottoms of your feet with a mirror, can catch problems before they become open wounds. For pressure ulcers, the earliest sign is skin that stays red after pressure is removed, particularly over bony areas. In darker skin tones, the area may appear purple or feel warmer or firmer than the surrounding skin.