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Age at onset of puberty predicts adult osteoporosis risk
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A team of researchers determined that the onset of puberty is the primary influence on adult bone mineral density. Later puberty resulted in lower bone mass and increased the risk for fracture, and length of puberty did not affect bone density, they found.
The Bone Mineral Density in Childhood Study is an ongoing multicenter study examining bone development in healthy US children and adolescents. For this analysis, the researchers studied 78 girls and 84 boys who had just entered puberty and followed them until they reached sexual maturity.
“Puberty has a significant role in bone development,” Vicente Gilsanz, MD, PhD, said in a press release. “During this time, bones lengthen and increase in density. At the end of puberty, the epiphyseal plates close, terminating the ability of the bones to lengthen. When this occurs, the teenager has reached their maximum adult height and peak bone mass. We found that early puberty was associated with greater bone mass, while later puberty resulted in less.”
Timing of puberty
According to results of the study, the age of onset of puberty was a strong negative predictor of DXA bone measurements at skeletal maturity. This finding was independent of bone values at the start of puberty, as well as the length of puberty. Further, the negative relationship was observed for all bone mineral content and BMD measurements at all skeletal sites in boys and girls.
“On average, healthy girls starting puberty a year earlier had approximately 5% greater bone mineral content measures and 2.5% greater BMD values at skeletal maturity, but those starting a year later had 5% and 2.5% less,” Gilsanz and colleagues wrote in The Journal of Pediatrics. “Similar findings of a slightly smaller magnitude were observed in healthy boys.”
Predicting adults bone mass, density
The researchers said these findings “provide further evidence of the importance of timing of pubertal commencement as a strong independent predictor of bone mass and bone density in healthy young adults.”
In addition, the data may be of interest to health care professionals who consider medical intervention to delay puberty in adolescents with short stature. Gilsanz and colleagues concluded that prolonging the growth period by delaying puberty may have “unexpected consequences” later in life and may result in a deficit in peak bone mass.
“Because the rate of decline in bone mass in adulthood is approximately 1% to 2% per year, a 10% to 20% difference in bone density because of the normal variations in the timing of puberty corresponds to an additional 10 to 20 years of protection against the normal age-related decline in skeletal mass,” the researchers wrote.
The results open the door to further studies to evaluate whether deficiencies in peak bone mass can be prevented with nutritional, mechanical or pharmacologic intervention in adolescents with delayed pubertal commencement, they said.
For more information:
- Gilsanz V. J Pediatr. 2011;158:100-105.
Disclosure: The researchers report no relevant financial disclosures.
This study demonstrates a negative relation between the timing of the onset of puberty and peak bone mass and peak BMD in normal children. Children whose onset of puberty occurs earlier than average end up with higher peak bone mass and BMD than those whose onset of puberty occurs later than average, even though the total duration of puberty is similar.
Implicit in these findings is a word of caution in delaying puberty via methods such as gonadotropin-releasing hormone analogues or other means to prolong growth and increase height. Missing from these important but provocative data are two important pieces of information. First, has the full peak bone mass and BMD been reached at the time of analysis (closed epiphyses)? In males, peak BMD is reached in the mid to late 20s — is it possible that the difference between ‘early- and late-bloomers’ within the normal range of puberty is made up over the ensuing decade such that those with later onset of puberty continue to gain peak bone mass and BMD and eventually reach the same values as those who started puberty earlier but reached their peaks earlier? It would appear important to assess peak bone mass and BMD in these subjects a decade later to determine if differences persist, or have narrowed or widened. Second, what is the mechanism by which early puberty ‘outperforms’ later puberty in achieving BMD and peak bone mass? Is puberty, via sex hormones or other mechanisms, regulating bone metabolism or does bone metabolism signal the onset of puberty? Recent findings on the relationship between osteoblasts and metabolism (Clemens TL. J Bone Miner Res. 2010;doi:10.1002/jbmr.321) certainly warrant that these questions should be investigated.
— Mark A. Sperling, MD
Pediatric Endocrinology, Diabetes & Metabolism, University of Pittsburgh Medical Center