## 1 Introduction
### Background
In addition, factors such as persistent hyperglycemia, structural deformities, inappropriate footwear, repeated trauma, calluses and dry skin significantly increase the risk of ulceration [7]. Due to the loss of sensation and poor tissue perfusion, patients often do not detect these lesions early on, which allows them to progress to severe infections and, in advanced cases, can culminate in the amputation of the affected limb [8]. Peripheral neuropathy affects the functioning of the peripheral nerves, compromising sensory, motor and autonomic fibers. Sensory dysfunction results in a loss of protective sensitivity, making it difficult to perceive stimuli such as pain, pressure, temperature or injuries [1]. As a result, it becomes difficult to detect damage to the feet at an early stage, allowing small injuries to develop silently into more serious conditions [9]. At the same time, motor neuropathy causes muscle imbalances and structural changes, such as hallux rigidus and hammer toes, which increase pressure points in the foot. Autonomic neuropathy compromises the regulation of sweating, leading to dry skin, cracks and greater vulnerability to infections [9]. In addition, peripheral vascular disease is attributed to increased oxidative stress and atherosclerosis, phenomena that are exacerbated by hyperglyaemia. The accumulation of glucose in the blood results in the weakening, narrowing and obstruction of the arteries. Furthermore, oxidative stress prolongs the inflammatory state in the microcirculation and reduces the elasticity of the capillaries, while atherosclerosis affects the blood vessels associated with the femoral artery and the knee. In this way, blood flow to the lower limbs is compromised, reducing tissue oxygenation, delaying wound healing and significantly increasing the risk of ischaemia. These conditions are further aggravated by biomechanical changes, which can alter the patient's gait, increasing pressure on certain areas of the foot and raising the risk of ulceration [10]. A summary of the etiology of diabetic foot ulcers is illustrated in Figure 1.  
According to the World Health Organization, one of the main indicators of diabetic foot is the appearance of a foot ulcer, usually below the malleolus, associated with the presence of autonomic neuropathy, ischemic disorders and local infections. It is estimated that more than 10% of people with DM are at risk of developing foot ulcers throughout their lives. Furthermore, this predisposition increases the likelihood of injuries caused by peripheral neuropathy in 80 to 90% of cases, as well as peripheral vascular disease and deformities [11]. Ulcers can be classified by their aetiology as neuropathic or ischemic. Neuropathic ulcers result from peripheral nerve damage, often in diabetic patients, and tend to occur on weight-bearing areas like plantar surface or metatarsal heads. They usually have callused borders, a painless presentation, and warm, well-perfused surrounding tissue due to preserved blood flow but lost sensation. Ischemic ulcers, on the other hand, arise because of insufficient circulation and are often located on the tips of the toes or lateral foot. They present punched-out margins, minimal bleeding, and surrounding pale or cool skin. There are often painful due to intact nerves [12]. The precise location of the wound and the existance of pain are relevant for diagnose. Assessing the risk of ulceration is an essential  
Figure 1: Causes of diabetic foot ulcers (adapted from [9]; images from Biorender.com). step in avoiding serious complications. This process should be an integral part of the regular physical examination of diabetic patients and should be carried out thoroughly. To identify loss of sensation associated with neuropathy, the Semmes-Weinstein 10 g monofilament is used [13], where the patient's foot is touched in order to assess its response. This can be complemented with vibration sensitivity tests (128 Hz tuning fork), tactile sensitivity and patellar and achilles reflexes.