Bone Abstracts

Objective: The incidence of eating disorders has increased in 15–19 years old¹. There is growing concern as to its impact on bone health during adolescence where peak bone mass acquisition is of paramount importance. This paper describes bone size and size adjusted bone mineral content in an adolescent/young adult eating disorder population.

Methods: A total of 68 patients (63 F/5 M, 90% anorexia nervosa and 10% atypical eating disorder), median age 15.4 years (range 10.9–19.8) median BMI SDS −1.2 (range −4.7 to 0.8) attended the bone densitometry service between January 2009 and December 2012 for total body (TB) and lumbar spine (LS) DXA scans (Lunar Prodigy DXA scanner driven by Encore Paediatric Software Version 13.3). Bone size is reported as percent predicted bone area for age (ppBA-for-age), and for size adjustment, the extent of bone mineralisation within the bone is described as percent predicted bone mineral content for bone area (ppBMC-for-BA).

Results: Median ppBA-for-age was 89% (range 66–114) at TB site, with 59% of patients presenting with ppBA-for-age ≤90. When size adjusted, median ppBMC-for-BA was 99.5% (range 89–116), with only 3% being in the ≤90% category at TB. At LS site, median ppBA-for-age was 95% (range 65–128), while median ppBMC-for-BA was 94% (range 73–131). TB ppBA-for-age correlated positively with BMI SDS (r=0.417, P=0.001), and negatively with age (r=−0.245, P=0.021). Median DXA Software derived paediatric analysis centiles were 35th (range 0–91st) for height for age (shorter bones=less linear growth), 22nd (range 0–75th) for bone area for height (thinner bones=less periosteal expansion), 27th (range 0–95th) for lean mass for height (reduced muscle mass), and 52nd (range 1–99th) for BMC for lean mass centile (adequate BMC for reduced lean mass).

Conclusion: In the adolescent/young adult eating disorder population, bones are small compared to the normal healthy population, but not obviously pathological at this stage. Muscle mass is low, but bone mineral content appears preserved at the expense of a combination of periosteal expansion and linear growth. It is likely that bone pathology in anorexia nervosa begins when restricted calorific intake is prolonged following closure of the endplates, where little scope remains for size adaptation. Long-term follow-up in these patients is required.

Reference: 1. Epidemiology of eating disorders: incidence, prevalence and mortality rates. Curr Psychiatry Rep 2012 14 406–414.