Introduction and aimsThe traditional thought of vascular inflammation has been an “inside-out” reaction, concentrated on the monocyte adherence to the intima of blood vessels and the oxidative lipid hypotheses. The relevancy of the “outside-in” procedure in vascular disorders will be better clarified in future investigations. In this study, we tried to investigate the origin of inflammation in the form of outside-in and inside-out in the vascular wall of diabetic patients.Material and MethodsA random sampling technique was used to enroll patients in this pilot study (10 Samples). Specimens were prepared when the diabetic foot with lesion was mainly amputated from the tissue, comprising the dermal layer and muscle from the lesion site and the transitory site with a minimal 1 cm length, width, and height. The specimens were placed in pathology battles containing 10% formalin for pathological tests. Slides were stained based on the Hematoxylin and Eosin Staining Protocol, Elastin staining and Trichrome staining. Immunohistochemistry was performed for IL-1, IL-6, VECAM-1, PECAM-1 and 4-HNE markers.ResultsAccording to the results of pathological studies and the level of inflammatory markers, it was shown that in diabetic tissues with vascular damage, the source of inflammation is more from the wound and from outside the body than internal factors such as hyperglycemia. On the other hand, the same inflammation the wound can spread from the outer vascular layers of the adventitia to the inner layers of the intima vascular in the form of outside-in.ConclusionIt is concluded that the source of vascular wall-destroying inflammation is from the outside to the inside and according to the (outside- in) assumption in patients with diabetic foot, ulceration leads to limb amputation.
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