Diabetic foot syndrome is one of the most costly complications of diabetes. Damage to the soft tissue structure is one of the primary causes of diabetic foot ulcers and most of the current literature focuses on factors such as neuropathy and excessive load. Although the role of blood supply has been reported in the context of macro-circulation, soft tissue damage and its healing in the context of skin microcirculation have not been adequately investigated. Previous research suggested that certain microcirculatory responses protect the skin and their impairment may contribute to increased risk for occlusive and ischemic injuries to the foot. The purpose of this narrative review was to explore and establish the possible link between impairment in skin perfusion and the chain of events that leads to ulceration, considering the interaction with other more established ulceration factors. This review highlights some of the key skin microcirculatory functions in response to various stimuli. The microcirculatory responses observed in the form of altered skin blood flow are divided into three categories based on the type of stimuli including occlusion, pressure and temperature. Studies on the three categories were reviewed including: the microcirculatory response to occlusive ischemia or Post-Occlusive Reactive Hyperaemia (PORH); the microcirculatory response to locally applied pressure such as Pressure-Induced Vasodilation (PIV); and the interplay between microcirculation and skin temperature and the microcirculatory responses to thermal stimuli such as reduced/increased blood flow due to cooling/heating. This review highlights how microcirculatory responses protect the skin and the plantar soft tissues and their plausible dysfunction in people with diabetes. Whilst discussing the link between impairment in skin perfusion as a result of altered microcirculatory response, the review describes the chain of events that leads to ulceration. A thorough understanding of the microcirculatory function and its impaired reactive mechanisms is provided, which allows an understanding of the interaction between functional disturbances of microcirculation and other more established factors for foot ulceration.

糖尿病足综合征是糖尿病最昂贵的并发症之一。软组织结构的损伤是糖尿病足溃疡的主要原因之一，目前大多数文献都集中在神经病变和过度负荷等因素上。尽管血液供应在宏观循环中的作用已有报道，但软组织损伤及其在皮肤微循环中的愈合尚未得到充分研究。先前的研究表明，某些微循环反应可以保护皮肤，而它们的损伤可能会增加足部发生闭塞性和缺血性损伤的风险。本叙述性审查的目的是探索和确定皮肤灌注损伤与导致溃疡的事件链之间可能存在的联系，考虑与其他更确定的溃疡因素的相互作用。本综述重点介绍了响应各种刺激的一些关键皮肤微循环功能。以皮肤血流改变的形式观察到的微循环反应根据刺激类型分为三类，包括闭塞、压力和温度。对三类研究进行了审查，包括：对闭塞性缺血或闭塞后反应性充血 (PORH) 的微循环反应；对局部施加压力的微循环反应，例如压力诱导的血管舒张 (PIV)；以及微循环和皮肤温度之间的相互作用以及微循环对热刺激的反应，例如由于冷却/加热而减少/增加的血流量。这篇综述强调了微循环反应如何保护皮肤和足底软组织及其在糖尿病患者中可能出现的功能障碍。在讨论微循环反应改变导致皮肤灌注受损之间的联系时，该评价描述了导致溃疡的事件链。提供了对微循环功能及其受损反应机制的透彻了解，从而可以了解微循环功能障碍与足部溃疡的其他更确定因素之间的相互作用。该评价描述了导致溃疡的一系列事件。提供了对微循环功能及其受损反应机制的透彻了解，从而可以了解微循环功能障碍与足部溃疡的其他更确定因素之间的相互作用。该评价描述了导致溃疡的一系列事件。提供了对微循环功能及其受损反应机制的透彻了解，从而可以了解微循环功能障碍与足部溃疡的其他更确定因素之间的相互作用。