Neuropathy and the vascular-bone axis in diabetes: Lessons from Charcot osteoarthropathy

N. L. Petrova, C. M. Shanahan*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

29 Citations (Scopus)

Abstract

Emerging evidence from the last two decades has shown that vascular calcification (VC) is a regulated, cell-mediated process orchestrated by vascular smooth muscle cells (VSMCs) and that this process bears many similarities to bone mineralization. While many of the mechanisms driving VSMC calcification have been well established, it remains unclear what factors in specific disease states act to promote vascular calcification and in parallel, bone loss. Diabetes is a condition most commonly associated with VC and bone abnormalities. In this review, we describe how factors associated with the diabetic milieu impact on VSMCs, focusing on the role of oxidative stress, inflammation, impairment of the advanced glycation end product (AGE)/receptor for AGE system and, importantly, diabetic neuropathy. We also explore the link between bone and VC in diabetes with a specific emphasis on the receptor activator of nuclear factor κβ ligand/osteoprotegerin system. Finally, we describe what insights can be gleaned from studying Charcot osteoarthropathy, a rare complication of diabetic neuropathy, in which the occurrence of VC is frequent and where bone lysis is extreme.

Original languageEnglish
Pages (from-to)1197-1207
Number of pages11
JournalOsteoporosis International
Volume25
Issue number4
DOIs
Publication statusE-pub ahead of print - 3 Oct 2013

Keywords

  • Bone fracture
  • Charcot osteoarthropathy
  • Diabetes
  • Neuropathy
  • RANKL/OPG
  • Vascular calcification

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