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Charcot neuroarthropathy (CN) is a devastating condition affecting the feet in patients with diabetes. The pathophysiology of (CN) is still incompletely understood, although main etiological components have been identified. The cornerstone of treatment of acute CN is immediate effective offloading, typically with total contact casting, and reduction in weight-bearing. The main current targets of pharmacological intervention are the inhibition of excess osteoclast activation and suppression of an excess pro-inflammatory cytokine response. Anti-resorption therapy, especially with bisphosphonates, has been used in randomized trials. The trials so far have demonstrated improved symptom control, a more rapid decline in foot temperature and a significant decrease in bone turnover markers. An understanding of the molecular pathways of bone resorption will help in the development of novel adjunctive pharmacological therapies which might further improve the outcome in patients with CN.

Accurate identification of infection in diabetic foot lesions is essential as the alternative can result in complicated medical and/or surgical interventions. The aim should be the differentiation between colonization and infection to avoid premature initiation of antimicrobial therapy. Diabetic foot ulcers provide a suitable environment for a diversity of microorganisms to first contaminate then subsequently colonize the wound. Infection can occur when a pathogenic factor produced by one or more microorganisms exceeds the capacity of the host immune system causing tissue damage and triggering both local and systemic inflammatory responses. The progression from wound colonization to infection is influenced by various factors including type and depth of the wound, blood supply, immune status of the patient. The quantity of microbial flora and pathogenicity expressed by the microorganisms involved will also have an effect.

High plantar pressures lead to ulceration in the diabetic foot, particularly in the forefoot region around the metatarsal heads. High plantar pressures persist during gait due to factors such as peripheral neuropathy, foot deformities, limited ankle dorsi flexion range of motion and reduced plantar tissue thickness. Strategies impinging upon gait such as the use of appropriate therapeutic footwear, custom-moulded insoles and injectable silicone can help to reduce plantar pressures and attenuate the risk for ulceration. Shoes adapted with external rocker profiles facilitate plantar flexion and restrict sagittal plane motion of the metatarsophalangeal joint, reducing pressures in the region of the metatarsal heads. Insoles custom-moulded to patient's feet help to reduce plantar pressures and minimise the risk of ulceration in the forefoot region. The loss of subcutaneous fat tissue in the diabetic foot enhances bony prominences and predisposes the foot to high-pressure areas. Silicone is a biocompatible material that can be safely injected into plantar soft tissue to augment tissue thickness and prevent the development of ulceration. This enhancement to the subcutaneous layer is remarkably well retained and is a generally well-adopted procedure in the clinical setting.