Type 2 diabetes may promote bone fragility through aging-like processes that impair bone cell function and bone quality.
Evidence
This review synthesizes recent findings on type 2 diabetes, accelerated aging biology, , stem cell exhaustion, autophagy, dysbiosis, inflammation, and epigenetic change.
Caveat
The accelerated-aging framework is a proposed unifying model, and the abstract states that no unified mechanism for diabetic fracture risk is established.
Simplified
PURPOSE OF REVIEW: This review summarizes recent findings of the pathophysiology of bone fragility with a particular focus on type 2 diabetes (T2D). It proposes that T2D is a condition of accelerated aging, highlighting mechanisms related to aging as key contributors to bone fragility.
RECENT FINDINGS: Multiple mechanisms have been proposed to explain the increased fracture risk in individuals with T2D; however, a unified model is still lacking. In this review, we propose that T2D represents a state of accelerated aging, with age-related processes, such as , stem cell exhaustion, enhanced autophagy, intercellular communication, dysbiosis, chronic inflammation, and epigenetic changes including expression, driving the development of diabetic bone fragility. These mechanisms predominantly impair bone cell function, ultimately compromising bone quality. The pathophysiology of bone fragility in T2D is discussed within the broader context of aging, emphasizing how fundamental biological mechanisms of the aging process contribute to diabetic bone disease.
Key numbers
1.2
Relative Risk of Hip Fracture
Summary relative risk based on 15 studies.
5%
Increase in Fracture Risk per HbA1c
Each 1% increase in HbA1c levels.
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