Recent advances in medicine have led to an increase in the number of children and adolescents treated for various chronic diseases and cancer. Increasingly sophisticated genetic analysis techniques have also clarified some genetic factors that contribute to bone fragility. Osteoporosis, characterized by reduced bone mass and skeletal fragility, can result from primary or secondary causes that originate in childhood and adolescence, which are critical periods for bone mineral acquisition. It is essential to identify children and adolescents at risk of fractures due to osteoporosis, and early intervention is crucial. Conservative management strategies, such as treating underlying diseases, replacing deficient hormones, providing nutritional support to meet calcium and vitamin D requirements, and encouraging regular physical activity, should be prioritized. Pharmacological treatment should be initiated in a timely manner following a comprehensive bone health examination. Intravenous pamidronate therapy has been safely and effectively administered to children and adolescents, although long-term follow-up is necessary. Further investigation is needed regarding bone fragility fractures of unknown etiology and the application of new medications for pediatric use.

Bone marrow adipose tissue (BMAT) increases with aging and once disregarded as a passive marrow space filler. However, accumulating evidence suggests that BMAT is an active modulator of bone, hematopoiesis, and metabolism. Characterization of BMAT in molecular and cellular levels identified that it is distinct from white or brown adipose tissue. This review summarizes current knowledge on changes of BMAT under physiological and pathophysiological conditions of bone and marrow. Expansion of BMAT is closely linked with increased fracture risk, therefore regulation of BMAT can be considered as a novel therapeutic approach to enhance bone strength. Regarding hematopoiesis, increase in BMAT is negatively associated with the marrow function, but it is indispensable for maintaining myelopoiesis in acute myeloid leukemia. In addition, BMAT expansion is paradoxically identified in obesity as well as anorexia nervosa. It is considered that BMAT performs a different function in different nutritional states. Future studies would involve more detailed research about regulatory factors of BMAT and its functions in health and diseases. Enhancing our understanding about BMAT would open a new avenue for combating BMAT-related diseases.

An 84-year-old woman visited our pain clinic with complaints of low back pain and severe radiating pain in the right lower extremity during walking. The patient demonstrated subacute compression fracture of L3 with vacuum change in lumbar spine plain radiographs and MRI which suggest Kummell’s disease. Despite our conservative treatments, she had little back pain relief. Therefore, we planned a percutaneous vertebroplasty. Manual compression could help perform percutaneous vertebroplasty more effectively by expanding the vertebral body. In addition, the spontaneous recovery of vacuum cleft width using negative pressure could help perform the technique more effectively. We successfully performed percutaneous vertebroplasty using these combination therapies for our patient.