The prevalence of diabetes mellitus is growing at epidemic proportions in the United States and worldwide. Most alarming is the steady increase in type 2 diabetes, especially among young and obese people. An estimated 7% of the US population has diabetes, and because of the increased longevity of this population, diabetes-associated complications are expected to rise in prevalence. Foot ulcerations, infections, Charcot neuroarthropathy, and peripheral arterial disease frequently result in gangrene and lower limb amputation. Consequently, foot disorders are leading causes of hospitalization for persons with diabetes and account for billion-dollar expenditures annually in the US. Although not all foot complications can be prevented, dramatic reductions in frequency have been achieved by taking a multidisciplinary approach to patient management. Using this concept, the authors present a clinical practice guideline for diabetic foot disorders based on currently available evidence, committee consensus, and current clinical practice. The pathophysiology and treatment of diabetic foot ulcers, infections, and the diabetic Charcot foot are reviewed. While these guidelines cannot and should not dictate the care of all affected patients, they provide evidence-based guidance for general patterns of practice. If these concepts are embraced and incorporated into patient management protocols, a major reduction in diabetic limb amputations is certainly an attainable goal.

Diabetic Foot Disorders: A Clinical Practice Guideline (2006 Revision)

Background—Calcification of the media of peripheral arteries is referred to as Monckeberg’s sclerosis (MS) and occurs commonly in aged and diabetic individuals. Its pathogenesis is unknown, but its presence predicts risk of cardiovascular events and leg amputation in diabetic patients. Several studies have documented expression of bone-associated genes in association with intimal atherosclerotic calcification, leading to the suggestion that vascular calcification may be a regulated process with similarities to developmental osteogenesis. Therefore, we examined gene expression in vessels with MS to determine whether there was evidence for a regulated calcification process in the vessel media. Methods and Results—In situ hybridization, immunohistochemistry, and semiquantitative reverse-transcription polymerase chain reaction were used to examine the expression of mineralization-regulating proteins in human peripheral arteries with and without MS. MS occurred in direct apposition to medial vascular smooth m...

Medial Localization of Mineralization-Regulating Proteins in Association With Mönckeberg’s Sclerosis Evidence for Smooth Muscle Cell–Mediated Vascular Calcification

Foot ulcerations, infections, and Charcot neuropathic osteoarthropathy are three serious foot complications of diabetes mellitus that can too frequently lead to gangrene and lower limb amputation. Consequently, foot disorders are one of the leading causes of hospitalization for persons with diabetes and can account for expenditures in the billions of dollars annually in the U.S. alone. Although not all foot complications can be prevented, dramatic reductions in their frequency have been obtained through the implementation of a multidisciplinary team approach to patient management. Using this concept, the authors present a Clinical Practice Guideline for diabetic foot disorders based on currently available evidence. The underlying pathophysiology and treatment of diabetic foot ulcers, infections, and the diabetic Charcot foot are thoroughly reviewed. Although these guidelines cannot and should not dictate the standard of care for all affected patients, they are intended to provide evidencebased guidance for general patterns of practice. The goal of a major reduction in diabetic limb amputations is certainly possible if these concepts are embraced and incorporated into patient management protocols.

Diabetic foot disorders: A clinical practice guideline

Pathologists have recognized arterial calcification for over a century. Recent years have witnessed a strong resurgence of interest in atherosclerotic plaque calcification because it: 1) can be easily detected noninvasively; 2) closely correlates with the amount of atherosclerotic plaque; 3) serves as a surrogate measure for atherosclerosis, allowing preclinical detection of the disease; and 4) is associated with heightened risk of adverse cardiovascular events. There are two major types of calcification in arteries: calcification of the media tunica layer (sometimes called Monckeberg's sclerosis), and calcification within subdomains of atherosclerotic plaque within the intimal layer of the artery. There are important similarities and differences between these two entities. Of particular interest are increasing parallels between cellular and molecular features of arterial calcification and bone biology, and this has led to accelerating interest in understanding how and why bone-like mineral deposits may form in arteries. Here, we review the two major pathological types of arterial calcification, the proposed models of calcification, and endocrine and genetic determinants that affect arterial calcification. In addition, we highlight areas requiring further investigation.

Molecular, endocrine, and genetic mechanisms of arterial calcification.

https://www.jvascsurg.org/article/S0741-5214(08)00936-1/pdf

The association between elevated ankle systolic pressures and peripheral occlusive arterial disease in diabetic and nondiabetic subjects.

Association of below-knee atherosclerosis to medial arterial calcification in diabetes mellitus

In diabetes mellitus, peripheral arterial occlusive disease predominantly affects the lower leg (tibial and peroneal vessel disease). Our study suggests that this feature is related to the presence of forefoot medial arterial calcification.

K.M. Lee

Papers

Association of below-knee atherosclerosis to medial arterial calcification in diabetes mellitus

Distal arterial occlusive disease in diabetes is related to medial arterial calcification.