Diabetic neuropathic arthropathy
- Lesley D Hordon, MD
Lesley D Hordon, MD
- Consultant in Rheumatology
- University of Leeds, United Kingdom
- Section Editors
- Don L Goldenberg, MD
Don L Goldenberg, MD
- Section Editor — Pain Disorders in Rheumatology
- Affiliate Assistant Professor of Medicine, Rheumatology Division, Oregon Health Science University
- Affiliate Instructor, School of Nursing Oregon Health Sciences University
- David M Nathan, MD
David M Nathan, MD
- Editor-in-Chief — Endocrinology
- Section Editor — Diabetes Mellitus
- Professor of Medicine
- Harvard Medical School
A variety of musculoskeletal conditions have been associated with diabetes mellitus. These include specific arthropathies of the hand and shoulder, spontaneous infarction of skeletal muscle, and limited joint mobility. (See "Musculoskeletal complications in diabetes mellitus" and "Diabetic muscle infarction" and "Limited joint mobility in diabetes mellitus".)
In addition, the loss of sensation to a joint may result in a chronic, progressive, and destructive arthropathy. The prototype of this disorder was described by Charcot in relation to tabes dorsalis. Similar changes are seen with other neurologic disorders, such as syringomyelia and diabetic neuropathy. Diabetes is the most common cause of neuropathic (Charcot) arthropathy in the western world. Diabetic neuropathic arthropathy is also called diabetic osteoarthropathy.
The pathogenesis of this condition remains uncertain, but it is probably due to a combination of mechanical and vascular factors resulting from diabetic peripheral neuropathy (algorithm 1) [1-3]. As an example, lack of proprioception secondary to peripheral neuropathy may result in ligamentous laxity, increased range of joint movement, instability, and damage by minor trauma, to which the relatively insensitive neuropathic foot is prone.
An alternative theory suggests that autonomic neuropathy results in vasomotor changes and in the formation of arteriovenous shunts. These, in turn, result in reductions in effective skin and bone blood flow, despite the good and sometimes bounding foot pulses in these patients. Another unproven hypothesis is that an exaggerated local inflammatory response to trauma, mediated by proinflammatory cytokines, results in the osteoarthropathy .
A possible cytokine-associated effect is suggested by the finding of enhanced osteoclastic activity in surgical specimens from patients with Charcot arthropathy . Other laboratory studies suggest that both receptor activator of nuclear factor (NF) kappa B (RANK) Ligand (RANKL)-dependent and -independent pathways may be involved in the increased bone resorption seen in this condition .
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