The Charcot Foot in Diabetes

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

The diabetic Charcot foot syndrome is a serious and potentially limb-threatening lower-extremity complication of diabetes. First described in 1883, this enigmatic condition continues to challenge even the most experienced practitioners. Now considered an inflammatory syndrome, the diabetic Charcot foot is characterized by varying degrees of bone and joint disorganization secondary to underlying neuropathy, trauma, and perturbations of bone metabolism. An international task force of experts was convened by the American Diabetes Association and the American Podiatric Medical Association in January 2011 to summarize available evidence on the pathophysiology, natural history, presentations, and treatment recommendations for this entity.

Related collections

Most cited references 76

Record: found
Abstract: found
Article: not found

Functions of RANKL/RANK/OPG in bone modeling and remodeling.

Brendan F Boyce, Lianping Xing (2008)

The discovery of the RANKL/RANK/OPG system in the mid 1990s for the regulation of bone resorption has led to major advances in our understanding of how bone modeling and remodeling are regulated. It had been known for many years before this discovery that osteoblastic stromal cells regulated osteoclast formation, but it had not been anticipated that they would do this through expression of members of the TNF superfamily: receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG), or that these cytokines and signaling through receptor activator of NF-kappaB (RANK) would have extensive functions beyond regulation of bone remodeling. RANKL/RANK signaling regulates osteoclast formation, activation and survival in normal bone modeling and remodeling and in a variety of pathologic conditions characterized by increased bone turnover. OPG protects bone from excessive resorption by binding to RANKL and preventing it from binding to RANK. Thus, the relative concentration of RANKL and OPG in bone is a major determinant of bone mass and strength. Here, we review our current understanding of the role of the RANKL/RANK/OPG system in bone modeling and remodeling.

0 comments Cited 518 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Osteoporosis in patients with diabetes mellitus.

Lorenz Hofbauer, Harald Dobnig, Avtar Singh … (2007)

Demographic trends with longer life expectancy and a lifestyle characterized by low physical activity and high-energy food intake contribute to an increasing incidence of diabetes mellitus and osteoporosis. Diabetes mellitus is a risk factor for osteoporotic fractures. Patients with recent onset of type 1 diabetes mellitus may have impaired bone formation because of the absence of the anabolic effects of insulin and amylin, whereas in long-standing type 1 diabetes mellitus, vascular complications may account for low bone mass and increased fracture risk. Patients with type 2 diabetes mellitus display an increased fracture risk despite a higher BMD, which is mainly attributable to the increased risk of falling. Strategies to improve BMD and to prevent osteoporotic fractures in patients with type 1 diabetes mellitus may include optimal glycemic control and aggressive prevention and treatment of vascular complications. Patients with type 2 diabetes mellitus may additionally benefit from early visual assessment, regular exercise to improve muscle strength and balance, and specific measures for preventing falls.

0 comments Cited 125 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

The role of proinflammatory cytokines in the cause of neuropathic osteoarthropathy (acute Charcot foot) in diabetes.

Fran Game, W Jeffcoate, P. Cavanagh (2005)

The pathogenesis of the acute Charcot foot of diabetes remains unclear. All patients with this condition have evidence of peripheral neuropathy, with loss of protective sensation and abnormal foot biomechanics. However, the acute Charcot foot is also characterised by a pronounced inflammatory reaction and the pathogenic significance of this inflammation has received little attention. We suggest that an initial insult--which may or may not be detected--is sufficient to trigger an inflammatory cascade through increased expression of proinflammatory cytokines, including TNFalpha and interleukin 1beta. This cascade then leads to increased expression of the nuclear transcription factor, NF-kappaB, which results in increased osteoclastogenesis. Osteoclasts cause progressive bone lysis, leading to further fracture, which in turn potentiates the inflammatory process. The potential role of proinflammatory cytokines suggests the possibility of new treatments for this sometimes devastating complication of diabetes.

0 comments Cited 70 times – based on 0 reviews      Review now

All references

Author and article information

Journal

Journal ID (nlm-ta): Diabetes Care

Journal ID (hwp): diacare

Journal ID (pmc): dcare

Journal ID (publisher-id): Diabetes Care

Title: Diabetes Care

Publisher: American Diabetes Association

ISSN (Print): 0149-5992

ISSN (Electronic): 1935-5548

Publication date (Print): September 2011

Publication date (Electronic): 19 August 2011

Volume: 34

Issue: 9

Pages: 2123-2129

Affiliations

[1]From the ¹Amputation Prevention Center at Valley Presbyterian Hospital, Los Angeles, California; the

[2] ²Carl T. Hayden Veterans Affairs Medical Center, Phoenix, Arizona; the

[3] ³Southern Arizona Limb Salvage Alliance (SALSA), University of Arizona College of Medicine, Tucson, Arizona; the

[4] ⁴Department of Medicine, University of Manchester, Manchester, U.K.; the

[5] ⁵Diabetic Foot Clinic, King's College Hospital, London, U.K.; the

[6] ⁶Diabetes and Metabolic Diseases Department, Pitié-Salpêtrière University Hospital, Paris, France; the

[7] ⁷Department of Diabetes and Endocrinology, Nottingham University Hospitals NHS Trust, Nottingham, U.K.; the

[8] ⁸Institute for Clinical and Experimental Medicine, Diabetes Centre, Prague, Czech Republic; the

[9] ⁹Department of Diabetes and Angiology, Marienkrankenhaus, Soest, Germany; the

[10] ¹⁰Department of Radiology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania; the

[11] ¹¹Department of Orthopedic Surgery, Loyola University Health System, Maywood, Illinois; the

[12] ¹²Diabetes Center and Foot Care Unit A, Gemelli Hospital, Catholic University, Rome, Italy; the

[13] ¹³Podiatry Service, Veterans Affairs Medical Center, Lebanon, Pennsylvania; the

[14] ¹⁴Department of Orthopedic Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania; and the

[15] ¹⁵Department of Internal Medicine, University of Rome Tor Vergata, Rome, Italy

Author notes

Corresponding author: Lee C. Rogers, lee.c.rogers@ 123456gmail.com .

This article is copublished in Diabetes Care and the Journal of the American Podiatric Medical Association, under joint copyright.

Article

Publisher ID: 0844

DOI: 10.2337/dc11-0844

PMC ID: 3161273

PubMed ID: 21868781

SO-VID: e6e566a7-a679-4578-a940-0967cb957dcb

License:

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

The Charcot Foot in Diabetes

Read this article at

Abstract

Related collections

Journal of the ASEAN Federation of Endocrine Societies

Most cited references 76

Functions of RANKL/RANK/OPG in bone modeling and remodeling.

Osteoporosis in patients with diabetes mellitus.

The role of proinflammatory cytokines in the cause of neuropathic osteoarthropathy (acute Charcot foot) in diabetes.

Author and article information

Journal

Affiliations

Author notes

Article

History

Categories

Comments

Comment on this article

Similar content 1,134

Cited by 102