The main pathogenic factors of diabetic foot disease include peripheral neuropathy, peripheral vascular disease, restricted joint movement, increased local pressure and infection. Other chronic complications can also affect the occurrence and development of diabetic foot disease. 1, diabetic neuropathy Diabetic peripheral neuropathy can involve sensory nerves, motor nerves and autonomic nerves. Studies have found that sensory neuropathy is the primary cause of diabetic foot disease. Symptoms of diabetic sensory neuropathy include numbness of the foot, insensitivity, pins and needles or burning sensation, and abnormal sensation on the bottom of the foot. Foot insensitivity is the most serious risk factor for podiatry and can cause unnoticeable trauma and ulcers. Abnormal foot sensation makes the patient unstable in walking and prone to falls and trauma. Sensory neuropathy can also cause plantar calluses, which in turn cause increased local pressure and neuropathic ulcers. Motor neuropathy causes restricted joint motion of the foot, and restricted joint motion increases pressure on the plantar aspect of the foot, which can lead to tissue inflammation and eventual ulcer formation. Autonomic neuropathy can cause dryness of the skin of the foot and lower extremities, abnormal sweating, arteriovenous shunts in the lower extremities, and vascular dysfunction of diastole and contraction, causing abnormal blood supply and hypoxia in the lower extremities. Dry skin also tends to cause skin cracking and induce ulcers and infections. The above abnormalities promote the occurrence of foot disease and are the main factors for the difficulty of healing of foot ulcers. 2, diabetic peripheral vasculopathy Diabetic patients have a high incidence of peripheral vascular atherosclerosis, early age of onset of vascular disease, and more diffuse lesions. Due to atherosclerotic occlusion of small and medium-sized arteries in the lower limbs, thrombosis, thickening of microvascular basement membrane, lumen narrowing, microcirculatory disorders cause skin-nerve nutritional disorders and aggravate neurological damage. Podiatry combined with vascular lesions has a poorer prognosis than podiatry due to neuropathy alone. Tissue repair requires blood to provide nutrition and its various components, and ischemia makes it difficult to recover from existing ulcers in podiatry. Moreover, on the basis of vascular lesions in the lower extremities, foot infections are more likely to occur, and the effect of antibiotic treatment is poor and the infection is likely to recur. 3, skin lesions diabetic patients often have extensive collagen abnormalities in the skin tissue, the main pathological mechanism is the glycosylation of collagen fibers, causing thickening and hinging of collagen bundles, one of the clinical manifestations of this change is thickened, tight and waxy skin. Diabetic lower extremity dermatosis is often recurrent and can lead to anterior tibial and foot skin ulcers and infections. Peripheral neuropathy can also cause skin dystrophy and skin dryness in the lower extremities and feet, resulting in decreased skin healing. Diabetic neuropathy and persistent hyperglycemia cause anterior tibial rash and progressive fat necrosis in the lower extremities, inducing local infection. Callus formation can cause increased plantar pressure and dry skin, further increasing abnormal foot pressure and thus inducing ulcers. Improper treatment of plantar calluses and corns can also cause skin damage, and bleeding and infection can occur under the calluses. In addition, diabetic maculopathy of the herpes skin off is very easy to form ulcers. 4, abnormal bone tissue of the foot Abnormal bone tissue of the foot can increase the pressure on the bottom of the foot. Long-term excessive pressure acting intermittently on the bottom of the foot, just like the abnormal pressure acting on the bottom of the foot when walking excessively, can lead to tissue inflammation and eventually the formation of ulcers. Foot deformities such as bunions, herniated metatarsal heads, hammertoes, and ankle dorsiflexion can all cause increased pressure on the bottom of the patient’s foot, which can predispose to ulceration after prolonged friction. Charcot’s arthropathy is also a common cause of recurrent foot ulcers in patients. In its acute phase, there is usually no skin breakdown, and in the chronic phase, the foot forms deformities, which can be accompanied by ulcer formation in 40% of patients. Deformities such as foot drop and horseshoe foot cause recurrent ulcers at the site of pressure, which cannot be eradicated without orthopedic correction. The extension disorder of the big toe, the so-called “hammer-like stiffness”, can impair the adaptive extension of the toe and prone to ulceration. 5, infection Infection aggravates metabolic disorders, resulting in increased blood sugar, and if ketosis occurs during infection, it further impairs immune function. In addition, more than 80% of podiatrists combined with at least three chronic complications of diabetes or cardiovascular risk factors, once the foot infection, the comorbidities are often difficult to control, not only with long medication, costly and ineffective. Infection and its complications of edema, can further aggravate local ischemia and cause tissue necrosis, serious cases require amputation (toe). 6, other pathogenic factors Other factors that cause diabetic foot include: trauma, decreased resistance, smoking, complications of diabetes, especially the combination of severe kidney disease.