Aims. In our previous research, we have found that melatonin (MEL) affects the osteoporotic process. By balancing bone remoulding, autophagy is involved in age-related bone loss. However, as a regulator of autophagy, whether MEL influences senile osteoporosis via regulating autophagy remains unclear. Methods. Cellular, radiological, and histopathological evaluations were performed on 36 16-month-old male C57BL6/L mice or aged bone marrow-derived mesenchymal stem cells. A MEL-gelatin methacrylamide system was constructed to aid osteoporotic fracture healing. Results. In this study, we found that bone loss, low level of MEL, and decreased autophagy coexisted in aged C57BL6/L mice. A physiological (low, 10 nM but not 100 nM) concentration of MEL restored bone loss, transformed the cytokine framework, and increased the autophagic level in aged mice, whereas inhibition of autophagy unfavourably reduced the positive effects of MEL on bone mass. The autophagy-conducted increased osteogenic lineage commitment and extracellular matrix mineralization, but not matrix synthesis of aged bone marrow-derived mesenchymal stem cells, was responsible for MEL anabolic effects on bone. PIK3C-AKT-MTOR signal was tested to be a main pathway that is involved in MEL-induced autophagy. Conclusion. Our data suggest that the application of MEL can restore degenerative osteogenesis of aged bone marrow-derived mesenchymal stem cells, and has the potential to regain bone mass in aged mice through activating autophagy via the PIK3C-AKT-MTOR pathway. MEL therefore may serve as a potential clinical therapy to treat senile osteoporosis. Cite this article: Bone Joint Res 2025;14(2):97–110

Aims

Alcoholism is a well-known detrimental factor in fracture healing. However, the underlying mechanism of alcohol-inhibited fracture healing remains poorly understood.

Aims

Exosomes derived from bone marrow mesenchymal stem cells (BMSCs) have been reported to be a promising cellular therapeutic approach for various human diseases. The current study aimed to investigate the mechanism of BMSC-derived exosomes carrying microRNA (miR)-136-5p in fracture healing.

Aims. Cigarette smoking has a negative impact on the skeletal system, causes a decrease in bone mass in both young and old patients, and is considered a risk factor for the development of osteoporosis. In addition, it disturbs the bone healing process and prolongs the healing time after fractures. The mechanisms by which cigarette smoking impairs fracture healing are not fully understood. There are few studies reporting the effects of cigarette smoking on new blood vessel formation during the early stage of fracture healing. We tested the hypothesis that cigarette smoke inhalation may suppress angiogenesis and delay fracture healing. Methods. We established a custom-made chamber with airflow for rats to inhale cigarette smoke continuously, and tested our hypothesis using a femoral osteotomy model, radiograph and microCT imaging, and various biomechanical and biological tests. Results. In the smoking group, Western blot analysis and immunohistochemical staining revealed less expression of vascular endothelial growth factor (VEGF) and von Willebrand factor (vWF). The smoking group also had a lower microvessel density than the control group. Image and biochemical analysis also demonstrated delayed bone healing. Conclusion. Cigarette smoke inhalation was associated with decreased expression of angiogenic markers in the early bone healing phase and with impaired bone healing. Cite this article:Bone Joint Res. 2020;9(3):99–107

Objectives

The aim of this study was to review the impact of smoking tobacco on the musculoskeletal system, and on bone fractures in particular.