**6. Biomechanical assessment of diabetic foot**

Peripheral neuropathy causes changes in foot function as well as in structure (due to prominent Metatarsal heads), dryness of the skin which in turn can end up in excessive callus formation [44–46]. An important risk factor for the development of Diabetic foot ulceration is high plantar foot pressure [47, 48]. In patients with Diabetes, limited joint mobility in the ankle and foot complex also had suggested to increase plantar pressure [49, 50] and also to be related with foot ulceration [51, 52]. The prevalence of limited joint mobility varies between 49% and 58% in Type I Diabetes patients and between 45% and 52% in Type II Diabetes patients [53, 54].

Most of the Diabetic foot ulcers occur in the forefoot, mainly under the metatarsal heads and under the digits (hallux). When the metatarsal head makes contact with the ground, it usually contacts at a single point because the inferior aspect of each metatarsal head is usually round.

The main structure responsible for dissipating the pressure from the lowest point of the metatarsal heads, to the sides of the metatarsal heads, then to the intermetatarsal spaces and to the points which are proximal and distal to the metatarsal heads is Metatarsal fat pad [55]. Patients with diabetes with or without neuropathy generally have decreased thickness in the metatarsal fat pads. The thinner the metatarsal fat pad, the higher the risk of developing Diabetic foot ulcers [56, 57]. The easiest way to measure fat pad thickness under the metatarsal heads is by using Ultrasound [58].

A softer metatarsal fat pad increases the shock absorption of the forefoot while hitting the ground, whereas a stiffer metatarsal fat pad decreases shock absorption thereby greater energy gets imparted to the soft tissues while landing on the forefoot [59]. The stiffer metatarsal fat pad prevents the load from being distributed medially and laterally from the deepest point of the metatarsal head. Therefore, more stress is applied to the soft tissue pad just below the metatarsophalangeal head, and less stress is applied to the part of the fat pad between the metatarsophalangeal heads [60].

In Diabetes, the collagen in the plantar fat pad not only stiffness but also the collagen tissues throughout the body stiffen. This stiffening of the entire collagen tissue causes all ligaments to become stiff and all joints to lose mobility [61]. Thus it can be a serious issue for most phase of the Gait cycle.

During the stance phase of gait, the hind foot begins with a slight inversion and then eversion. The forefoot first lands on the fifth metatarsal head, then each metatarsal lands from lateral to medial. At the end of the stance phase, the hind foot is slightly everted and the fore foot is slightly inverted. If a diabetic presents a normal amount of hind foot eversion during contact, the forefoot may be difficult to compensate by inverting at the mid tarsal joints. It can increase the pressure under the first and second metatarsal heads. On the other hand, if the forefoot cannot be fully inverted to pronate the sub talar joint, the pressure under the 4th and 5th metatarsal heads will increase. Coronal and sagittal movements are also reduced in all metatarsals with stiffer collagen tissue [62].

The glycation of the Achilles tendon increases the tendon's thickness and stiffness [63, 64]. It in turn causes several changes in the diabetic foot, including earlier forefoot loading at contact as well as an increased load on the forefoot during the stance phase of gait [65, 66]. The thickening of plantar fascia happens along with the thickening of the Achilles tendon [67]. The thickened Achilles tendon decreases the effect of windlass mechanism of the foot, which further decreases the dorsiflexion of the digits, decreased time in the propulsive period of gait and a decrease in the supination of the hind foot during foot propulsion [68, 69]. Diabetic neuropathy has a greater adverse effect on the foot. Tissue glycation is the predicting factor of other diabetic complications including neuropathy. The joint mobility of the subtalar joint is significantly reduced in the ulcerated foot than the contra lateral non ulcerated foot in Diabetic neuropathic patients [47]. Hence, combination of neuropathy and trauma results in breakdown of tissue. Increased plantar pressure can be contributed to the alterations in the foot shape, presence of callus and limited joint mobility.

Kinematic analysis was performed on the knees and ankles using 3D SIMI REALITY MOTION SYSTEM GmbH, Germany, two Basler high-speed cameras (1394a/b, GigE, 100fps @ 1Megapixel). We used Kinetik I-Step software (Aetrex, USA) and Wintrack Dynamic Scan Floor Mat (Medicapteure software, France, USA). Significant differences in kinematic and kinematic variables such as toe-off knee angle, static knee speed, heel strike, mid-stance and toe-off, static knee acceleration, heel strike and mid-stance, and ankle joint angle, Mid stance, static ankle speed, heel strike and mid stance, static ankle acceleration, heel strike, mid stance and toe off, walk cycle duration, maximum average sole pressure and maximum ankle pressure Was recognized. Therefore biomechanical analysis is an important tool and can be used for early screening and prediction of altered kinematic and kinetics in diabetes mellitus [70].
