Why are adolescent females at increased risk for bone fractures during puberty?

Why Pubescent Girls Are at Risk for Bone Fracture

Adolescent girls face increased fracture risk during puberty primarily because they are in the critical window of peak bone mass acquisition—approximately 86% of adult spine bone mass is gained before skeletal age 14 or within the first two years after menarche—and any disruption to this process (nutritional deficits, menstrual irregularities, low physical activity) creates permanent skeletal deficits that manifest as increased fracture susceptibility. 1

The Critical Timing of Pubertal Bone Development

Peak Bone Mass Acquisition Window

• Skeletal mass approximately doubles during adolescence, with the most dramatic increases occurring between skeletal ages 10-14 years or until the first year after menarche 2, 1
• After skeletal age 17 or the fourth year after menarche, there is no significant further increase in bone mineral density (BMD) or bone mineral content (BMC), meaning the window for optimal bone development has essentially closed 1
• Bone values achieved during puberty become the major determinant of peak bone mass and thereby determine the risk of osteoporotic fractures during advanced age 2

Hormonal Orchestration

• The main determinants of pubertal bone mass gain are sex steroids (estrogen and progesterone), growth hormone, insulin-like growth factors (through effects on bone and muscle mass), 1,25-dihydroxyvitamin D (by stimulating calcium absorption), and muscle mass (by regulating bone modeling/remodeling thresholds) 2
• Serum osteocalcin peaks at skeletal ages 11-12 years, while IGF-1 peaks at 13-14 skeletal years or at the first year after menarche, indicating the intense metabolic activity during this period 1

Sex-Specific Vulnerabilities in Girls

Structural Disadvantages Emerge Early

• Sexual dimorphism in tibial bone strength is evident even in prepuberty, with boys demonstrating 6-15% greater bone strength indices compared to girls after adjusting for tibial length and muscle cross-sectional area 3
• This sex difference in bone strength is due largely to greater bone areas (4-6%) in boys, establishing a structural disadvantage for girls that persists into adulthood 3
• Girls who sustain fractures during skeletal development show substantial deficits in both structural and strength components of the radius that persist into young adulthood, unlike boys who show no such persistent deficits 4

The Female Athlete Triad and Energy Deficiency

• Menstrual dysfunction (amenorrhea or oligomenorrhea) resulting from low energy availability is a major contributor to low BMD in young women 5
• Functional hypothalamic amenorrhea commonly results from inadequate energy intake relative to energy expenditure, disrupting the hormonal environment necessary for optimal bone development 5
• Weight gain of 5-9% body weight has been shown to restore menstrual function and improve BMD in amenorrheic young women, demonstrating the reversibility of some deficits if caught early 5

Clinical Implications and Risk Stratification

Fracture History as a Marker

• In girls reporting low physical activity intensity, there is a significant negative association between previous fracture history and both total hip aBMD and femoral neck BMC, suggesting that fractures in less active girls may indicate underlying skeletal fragility rather than high activity levels 6
• Childhood fractures in girls may be an early marker of persistent skeletal fragility that tracks into young adulthood, contrasting with boys where fractures during development do not predict adult bone deficits 6, 4

Common Pitfalls in Assessment

• Do not use T-scores for diagnosis or treatment decisions in premenopausal women or adolescents—only Z-scores are appropriate for this age group, as WHO T-score criteria do not apply 5, 7
• A Z-score above -2.0 is classified as "within the expected range for age," but this does not mean the bone health is optimal if other risk factors (menstrual irregularities, nutritional deficits, fracture history) are present 5
• In children with short stature or growth delay, spine and total body BMD results should be adjusted using either bone mineral apparent density or height Z-score to avoid misinterpretation 8

Prevention and Intervention Strategy

Non-Pharmacological Interventions Are Primary

• Ensure calcium intake of at least 1000 mg/day through diet or supplementation 5
• Maintain vitamin D supplementation at 800-1000 IU/day 5
• If low energy availability is identified, increase energy intake by 300-600 kcal/day (1.2-2.4 MJ/day) 5
• Muscle cross-sectional area is the primary explanatory variable of tibial bone geometry and strength in both sexes, accounting for 10-16% of variance, emphasizing the importance of weight-bearing physical activity 3

When Pharmacological Treatment Is NOT Indicated

• Pharmacological treatment is NOT recommended for premenopausal women with Z-scores above -2.0 without fragility fractures 5
• Bisphosphonates have a very long half-life and should be used with extreme caution in women of childbearing age due to concerns of teratogenicity, and there are no published studies of bisphosphonate use in exercising and athletic women with bone health disorders 8
• The decision to initiate treatment with bisphosphonates should only be made on a case-by-case basis by or in consultation with a board-certified endocrinologist or specialist in metabolic bone diseases 8

Monitoring Strategy

• Repeat DXA scan in 12 months to assess response to interventions, using the same DXA machine for accurate comparison 5
• Monitor menstrual function monthly—resumption of menses is a key indicator of successful treatment and restoration of the hormonal environment necessary for bone health 5