The possible convergence between Diabetes Mellitus and the pathophysiological mechanisms underlying osteoporosis is a hotly debated topic in the medical literature. Their coexistence could be precisely interpretable in accordance with the epidemiological data compared to the age groups of their diagnosis, but emerging evidence in the medical-scientific literature is getting closer, focusing on possible common pathophysiological mechanisms, the understanding of which will become indispensable for the identification of subjects at risk for these diseases, their complications, and for appropriate clinical management.

Today we know that both type 1 and type 2 Diabetes Mellitus are associated with a decrease in bone quality which leads to an increase in low stress fractures, a condition called diabetic osteopathy. Insights into the basic cell and molecular biology as well as pathophysiological knowledge, possibly combining these two metabolic disorders, are needed to improve both the understanding of their respective clinically observable abnormalities and the relationships between anti-diabetic therapies and their eventual influence on mass and bone quality and vice versa. Further to this, we need to understand the interactions between anti-fracture drugs and their influence on glucose metabolism, carbohydrate metabolism, and musculoskeletal units to uncover new pathophysiological aspects for adequate clinical management of the diabetic patient.

This Special Issue aims to collate articles related to diabetic osteopathy. Original research and review articles are welcome.

Potential topics include but are not limited to the following:

• The skeleton and energy metabolism
• The skeleton and adjustment of glucose homeostasis
• Convergence between bone mass and energetic homeostasis
• Diabetes and osteoporosis as related diseases
• Regulation of bone cells in Diabetes Mellitus
• Bone cell changes induced by oxidative stress
• Diabetes and risk for fragility fractures
• Protein glycation, advanced glycation end products (AGEs), Reactive Oxygen Species (ROS)
• Post-translational modifications of collagen
• Hyperhomocysteinemia and DM2: reduction of bone quality and fracture risk
• Diabetes Mellitus, bone metabolism, and bone stiffness
• Hormonal alterations, bone mass, strength, and fracture risk, in male subjects with Diabetes Mellitus
• Diabetes Mellitus and clinical parameters for assessing fracture risk
• Anti-diabetic therapies, bone metabolism, and fracture risk
• Anti-fracture drugs and carbohydrate metabolism