title: Anorexia nervosa and bone.
abstract: Anorexia nervosa (AN) is a condition of severe low weight that is associated with low bone mass, impaired bone structure, and reduced bone strength, all of which contribute to increased fracture risk. Adolescents with AN have decreased rates of bone accrual compared with normal-weight controls, raising additional concerns of suboptimal peak bone mass and future bone health in this age group. Changes in lean mass and compartmental fat depots, and hormonal alterations secondary to nutritional factors contribute to impaired bone metabolism in AN. The best strategy to improve bone density is to regain weight and menstrual function. Oral estrogen-progesterone combinations are not effective in increasing bone density in adults or adolescents with AN, and transdermal testosterone replacement is not effective in increasing bone density in adult women with AN. However, physiological estrogen replacement as transdermal estradiol with cyclic progesterone does increase bone accrual rates in adolescents with AN to approximate that in normal-weight controls, leading to a maintenance of bone density Z-scores. A recent study has shown that risedronate increases bone density at the spine and hip in adult women with AN. However, bisphosphonates should be used with great caution in women of reproductive age, given their long half-life and potential for teratogenicity, and should be considered only in patients with low bone density and clinically significant fractures when non-pharmacological therapies for weight gain are ineffective. Further studies are necessary to determine the best therapeutic strategies for low bone density in AN.
authors.affiliation: BUL 457Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USAPediatric Endocrine UnitMassachusetts General Hospital for Children and Harvard Medical School, Boston, Massachusetts 02114, USABUL 457Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USAPediatric Endocrine UnitMassachusetts General Hospital for Children and Harvard Medical School, Boston, Massachusetts 02114, USA mmisra@partners.org.
authors.forename: Madhusmita
authors.initials: M
authors.lastname: Misra
authors.affiliation: BUL 457Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, 55 Fruit Street, Boston, Massachusetts 02114, USAPediatric Endocrine UnitMassachusetts General Hospital for Children and Harvard Medical School, Boston, Massachusetts 02114, USA.
authors.forename: Anne
authors.initials: A
authors.lastname: Klibanski
mesh_terms: D000293:Adolescent; D000328:Adult; D000856:Anorexia Nervosa / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D001823:Body Composition / Q000502:physiology; D015519:Bone Density; D001842:Bone and Bones / Q000378:metabolism / Q000503:physiopathology*; D050723:Fractures, Bone / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D010024:Osteoporosis / Q000150:complications / Q000503:physiopathology*; D015430:Weight Gain / Q000502:physiology
keywords: IGF1; PYY; adipokines; adolescents; adults; anorexia nervosa; bisphosphonates; bone density; eating disorders; estrogen; fracture; ghrelin; growth hormone; leptin; microarchitecture; strength; testosterone