Abstract
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 cellular senescence, stem cell exhaustion, enhanced autophagy, intercellular communication, dysbiosis, chronic inflammation, and epigenetic changes including microRNA 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.