Low bone mineral density in children and adolescents with cancer

Abstract

Maximizing accumulation of bone mass during childhood and adolescence is essential to attaining optimal peak bone mass. Childhood cancer survivors (CCS) have lower bone mineral density (BMD) than the general population. Chemotherapeutic agents including steroids and radiotherapy can affect BMD. Cancer itself, hormonal insufficiency, a poor nutritional state, and a deficit of physical activities during or after treatment also influence BMD in CCS, resulting in failure to achieve appropriate peak bone mass. Low BMD in childhood and adolescence can lead to osteoporosis in adult life and complications such as bone pain, bone deformity, and fractures. Thus, BMD in CCS should be monitored with appropriate intervention. Adequate intake of calcium and vitamin D and an increase in physical activity are recommended. Timely supplements of hormones are needed in some cases. Some publications have reported that bisphosphonate therapies using pamidronate or alendronate were well tolerated in CCS and helped increase BMD.

Osteoporosis in Childhood Cancer Survivors: Physiopathology, Prevention, Therapy and Future Perspectives

“…Some studies reported that at 6 months after HSCT, nearly 50% of patients showed osteopenia at the femoral neck or lumbar spine. Almost one-third of allogeneic HSCT patients in childhood had reduced bone mineral density (BMD) before reaching adulthood, with a high prevalence of asymptomatic vertebral compression fractures [ 7 ]. Other long-term sequelae of cancer treatment, such as gonadal dysfunction, growth hormone deficiency, and altered body composition, have been shown to influence bone remodeling [ 5 ].…”

“…Estrogen has a role in attaining peak bone mass (PBM) in both sexes. Androgens enlarge the cross-sectional area of long bones and increase mechanical strength [ 7 ]. GH and insulin-like growth factor I are important for maintaining bone mass because both independently contribute to bone remodeling and apposition [ 1 ].…”

“…Childhood cancer survivors (CCS) are at increased risk of reduced BMD. It is known that CCS fail to attain peak bone mass (PBM) because of cancer itself and the related conditions (e.g., cancer treatments) [ 37 ], thus showing a high prevalence of low BMD or even OP in adulthood, with consequent higher risk of bone fragility than the general population [ 7 , 38 , 39 ]. The mechanism underlying this deficit is multifactorial and firstly depends on the cancer type and the administered therapeutic regimen [ 40 ].…”

“…The main long-term adverse consequence is the alteration of the endocrine system’s function and activity, which affects about 20–50% of CCS [ 3 ]. In CCS, there have been reports of obesity and metabolic syndrome development, impairment of the hypothalamic–pituitary axis, fertility, and bone metabolism, with osteopenia onset and, consequently, an increase in fracture risk [ 3 , 4 , 5 , 6 , 7 , 8 , 9 ]. Radiotherapy and chemotherapy are the main causes of the alteration of physiologic cellular and tissue functions, determining an increase in inflammatory processes, senescent cells number, DNA mutations, and an accumulation of reactive oxygen species (ROS) [ 10 , 11 ].…”

Effect of Vertebral Fracture on Auxological Profiles of Children Undergoing Acute Lymphoblastic Leukemia Treatment

“…ALL in childhood or adolescence is related to various endocrinopathies after the cessation of therapy, which may persist for several years (2). Most importantly, skeletal morbidities due to osteoporosis and vertebral fractures (VFs) caused by impaired mineralization are common endocrinologic complications that occur during and after ALL treatment (3)(4)(5).…”