4.5 Review

Alterations of tendons in diabetes mellitus: what are the current findings?

Journal

INTERNATIONAL ORTHOPAEDICS
Volume 39, Issue 8, Pages 1465-1473

Publisher

SPRINGER
DOI: 10.1007/s00264-015-2775-x

Keywords

Diabetes mellitus; Tendon stem/progenitor cells; Tendon repair and regeneration

Categories

Funding

  1. National Natural Science Foundation of China [81201422, 81172177]
  2. China Postdoctoral Science Foundation [2012 M520983]
  3. National Student Innovation Training Program of China [1210286090]
  4. Jiangsu Province Science Foundation for Youths [BK2012334]
  5. Innovative Foundation of Southeast University [3290002401]
  6. Shenzhen Science and Technology Bureau Grant [JCYJ20130401171935811]
  7. National Basic Science and Development Programme (973 Programme) [2012CB518105]
  8. SMART program seed funding, Institute of Innovative Medicine, The Chinese University of Hong Kong

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As a connective tissue, tendon connects the muscle and bone, and plays the key role in the locomotor system. Some previous studies have shown the pathological alternations in diabetic tendons, which might result in the structural and functional changes, and even accelerate the process of diabetic foot. In this review, we examined the current findings of the diabetic tendons in the form of various aspects, and summarized the clinical presentation, imaging, biomechanical, histopathological, cellular and molecular abnormalities in the diabetic tendons. The progress of diabetic tendon damage is complicated and the main hypotheses include the excessive accumulation of AGEs, the altered inflammatory response, neovascularization and insensitive neuropathy. However, the cellular and molecular mechanisms of these alterations are still ambiguous. Tendon stem/progenitor cells (TSPCs) have been discovered to play important roles in both tendon physiology and tendon pathology. Recently, we identified TSPCs from patellar tendons in our well-established diabetic rat model and found impaired tenogenic differentiation potential of these cells. We proposed a new hypothesis that the impaired cell functions of diabetic TSPCs might be the underlying cellular and molecular mechanism of the diabetic tendon alternations. These findings should be helpful to establish a better therapeutic strategy for diabetic tendon repair and regeneration.

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