Bone disease in diabetes: another manifestation of microvascular disease?
Abstract
Type 1 and type 2 diabetes are generally accepted to be associated with increased bone fracture risk. However, the pathophysiological mechanisms of diabetic bone disease are poorly understood, and whether the associated increased skeletal fragility is a comorbidity or a complication of diabetes remains under debate. Although there is some indication of a direct deleterious effect of microangiopathy on bone, the evidence is open to question, and whether diabetic osteopathy can be classified as a chronic, microvascular complication of diabetes remains uncertain. Here, we review the current knowledge of potential contributory factors to diabetic bone disease, particularly the association between diabetic microangiopathy and bone mineral density, bone structure, and bone turnover. Additionally, we discuss and propose a pathophysiological model of the effects of diabetic microvascular disease on bone, and examine the progression of bone disease alongside the evolution of diabetes.
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Advanced glycation end-product deposition, impaired osseous angiogenesis and dysregulated glucose-insulin axis collectively suppress osteogenic differentiation, impair bone turnover, and compromise healing capacity.
“Additionally, the advanced glycation end-product deposition, impaired osseous angiogenesis and dysregulated glucose-insulin axis, collectively suppress osteogenic differentiation, impair bone turnover, and compromise healing capacity2,7.”
From Microenvironment-responsive multifunctional enzyme-linked hydrogel for diabetic bone defect regeneration. (2025) · cites this paper as [7]
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Flagged first, then by citations
Cited by
Sorted by citations
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“Additionally, the advanced glycation end-product deposition, impaired osseous angiogenesis and dysregulated glucose-insulin axis, collectively suppress osteogenic differentiation, impair bone turnover, and compromise healing capacity 2,7 .”
- Authors
- Shanbhogue, V. V., Hansen, S., Frost, M., Brixen, K., & Hermann, A. P.
- Affiliations
- Odense University Hospital (DK)
- Corresponding author
- Shanbhogue, Vikram V
- Venue
- The Lancet Diabetes & Endocrinology
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 5
- Issue
- 10
- Pages
- 827-838
- ISSN
- 2213-8587 (ISSN-L)
- OpenAlex
- W2619718872
- Cited by
- 158
- References
- 127
- Citations by year
- 2026: 14 · 2025: 20 · 2024: 20 · 2023: 19 · 2022: 19 · 2021: 18 · 2020: 19 · 2019: 12 · 2018: 14 · 2017: 2
- FWCI
- 2.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Lancet Diabetes & Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Funders
- Danish Diabetes Academy
- Novo Nordisk Fonden
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Management and Research
- Keywords
- diabetic bone disease, diabetic osteopathy, microangiopathy, diabetic microvascular complications, bone mineral density, bone structure, bone turnover, fracture risk, type 1 diabetes, type 2 diabetes, pathophysiological model
- MeSH terms
- Animals, Bone Diseases, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Diabetic Angiopathies, Humans, Risk Factors, Bone Density, Comorbidity, Fractures, Bone, Microvessels
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