Pediatric Osteoporosis Linked to Anti-Inflammatory Meds
Adolescent mice—reportedly easier to work with that adolescent humans—are helping us understand how cells that age prematurely (senescent cells) may emanate from poor bone mass in youth…and how glucocorticoid given during puberty for inflammation resulting from rheumatoid disorders and other diseases might be the origin of that premature aging.
The article, “Programmed cell senescence in skeleton during late puberty,” was published in the November 3, 2017 edition of Nature Communications.
Mei Wan, Ph.D., a professor of Orthopaedics at Johns Hopkins University in Baltimore, and co-author on the study, told OTW, “Childhood and adolescence are critical periods for optimizing bone growth and mineral accrual. Bone mass and strength in this period are influenced by genetic/epigenetic factors, activity, nutrition, and hormones. For children with genetic skeletal disorders or chronic disease, bone growth and mineral accrual are often compromised, leading to osteoporosis and high bone fracture rate.”
“In childhood, fractures are a common event, with an annual fracture incidence of 205 per 10,000 person-years in those under the age of 16 years, with the highest rate during the rapid growth spurts of puberty.”
“Moreover, bone mineral accrual in childhood and adolescence influences long-term bone health. Epidemiologic studies suggest that 60% of the risk for osteoporosis later in life can be explained by the bone mineral acquired by childhood and early adulthood. However, little is known about the cellular changes and the regulatory mechanisms in the skeleton during the transition from fast growing childhood/early puberty to slow growing late puberty/young adulthood.”
“Childhood osteoporosis is typically divided into primary and secondary causes, with osteogenesis imperfecta (OI) representing the prototypical primary osteoporosis of childhood.”
“There is a growing list of secondary pediatric osteoporosis (i.e., osteoporosis caused by underlying diseases and/or their treatment), with most falling into two broad categories: glucocorticoid-treated diseases and the disorders which compromise normal weight-bearing and mobility such as cerebral palsy, Rett syndrome, Duchenne muscular dystrophy, spina bifida, and spinal muscular atrophy.”
