Causes
The underlying mechanism behind diabetic dermopathy is unknown, although many theories have been suggested. As the lesions are asymptomatic, patients often do not notice their appearance and may assume they have arisen due to trauma. Melin explored the theory that the lesions of diabetic dermopathy occurred secondary to trauma; however attempts to experimentally reproduce the lesions by striking the skin with a rubber hammer were unsuccessful. Another theory is that the lesions were caused by areas of relative ischaemia caused by changes in local temperature. Binkley suggested that the predilection for the shins was due to decreased skin temperature, slow blood flow, increased plasma viscosity and vessel fragility. Experimental attempts to induce diabetic dermopathy in patients with diabetes revealed that application of thermal stimuli, both hot and cold, induced atrophic circumscribed skin lesions in elderly patients with diabetes, or those with diabetes of long duration. However, similar lesions were also elicited in the skin of patients with amyloidosis, suggesting that they were not specific for diabetes. Local ischaemia was postulated as a possible cause for diabetic dermopathy, but blood flow in the lesions has been shown to be increased, rather than decreased, making this theory less likely. The authors concluded that diabetic dermopathy does not occur due to ischaemia and represents a scarring process due to defective wound healing. A subsequent study confirmed increased blood flow in the actual lesions, but found decreased blood flow in normal appearing skin on the shins of patients with diabetic dermopathy. The authors proposed that the decreased blood flow predisposed patients with diabetes to inadequate wound healing, which led to the formation of the characteristic lesions of diabetic dermopathy. Another suggested mechanism is that diabetic neuropathy causes subcutaneous nerve degeneration, which leads to diabetic dermopathy.