UMMS Affiliation

Department of Pediatrics

Publication Date


Document Type



Adolescent; Anorexia Nervosa; Anthropometry; Body Composition; Bone Density; Bone Diseases, Metabolic; Bone and Bones; Child; Female; Glycoproteins; Hormones; Humans; Organ Size; Osteoprotegerin; Puberty; Receptors, Cytoplasmic and Nuclear; Receptors, Tumor Necrosis Factor


Endocrinology, Diabetes, and Metabolism | Pediatrics


Low bone mineral density (BMD) in adolescents with anorexia nervosa (AN) is associated with a low bone turnover state. Osteoprotegerin (OPG), a cytokine that acts as a decoy receptor for receptor activator of nuclear factor-kappaB ligand, decreases bone resorption by inhibiting differentiation of osteoclast precursors and activation of mature osteoclasts, and by stimulating osteoclast apoptosis. We compared OPG levels in 43 adolescent girls with AN with 38 controls and examined bone density, bone turnover, and hormonal parameters. Girls with AN had lower fat mass, lean body mass, lumbar BMD z-scores, and lumbar bone mineral apparent density than controls. OPG levels were higher in girls with AN than in controls (44.5 +/- 22.5 pg/ml vs. 34.5 +/- 12.7 pg/ml, P = 0.02). Osteocalcin, deoxypyridinoline, estradiol, free testosterone, IGF-I, and leptin were lower in AN than in healthy adolescents. OPG values correlated negatively with body mass index (r = -0.27, P = 0.02), percent fat mass (r = -0.35, P = 0.0002), leptin (r = -0.28, P = 0.02), lumbar BMD z-scores (r = -0.25, P = 0.03), and lumbar bone mineral apparent density (r = -0.26, P = 0.03). In conclusion, adolescent girls with AN have higher serum OPG values than controls. OPG values correlate negatively with markers of nutritional status and lumbar bone density z-scores and may be a compensatory response to the bone loss seen in this population.

DOI of Published Version



J Clin Endocrinol Metab. 2003 Aug;88(8):3816-22. Link to article on publisher's website

Journal/Book/Conference Title

The Journal of clinical endocrinology and metabolism

Related Resources

Link to Article in PubMed

PubMed ID