posted on 2014-08-10, 00:00authored byAnne Tsampalieros, Carol K. L. Lam, Jenna C. Spencer, Meena Thayu, Justine Shults, Babette S. Zemel, Rita M. Herskovitz, Robert N. Baldassano, Mary B. Leonard
Context: Glucocorticoids and inflammation inhibit bone formation; however, the impact on skeletal modeling is unknown.
Objectives: The objectives of the study were to examine changes inbonemineral density(BMD) and cortical structure after Crohn disease (CD) diagnosis and identify associations with growth, glucocorticoids, and disease activity.
Design/Participants: This was a prospective cohort study among 76 CD participants, aged 5-21 years. Tibia quantitative computed tomography trabecular BMD and cortical dimensions were obtained at diagnosis and 6 and 12 and a median of 42 months later; 51 completed the final visit.
Outcomes: Sex, race, and age-specific Z-scores were generated for outcomes based on more than 650 reference participants, and cortical dimension Z-scores were further adjusted for tibia length. Generalized estimating equations were used to model changes in Z-scores.
Results: Disease activity improved over the study interval (P <.001). TrabecularBMDZ-scoresimproved over the first 6 months; increases were associated with improved disease activity (P <.001), younger age (P <.005), and increases in vitamin D levels (P = .02). Greater increases in tibia length were associated with greater increases in cortical area Z-scores (P <.001). Greater glucocorticoid doses and disease activity were significantly associated with failure to accrue cortical area and were more pronounced with greater linear growth (interaction P <.05). Mean (+/- SD) trabecular BMD (similar to 1.0 +/- 1.21) and cortical area (similar to 0.57 +/- 1.10) Z-scores at the final visit were significantly reduced.
Conclusions: CD was associated with persistent deficits in trabecular BMD, although younger participantsdemonstratedagreater potential for recovery. In addition, greater lineargrowthwasassociated with a greater recovery of cortical dimensions, especially among participants with less glucocorticoid exposure and inflammation. These data suggest that younger age and concurrent growth provide a window of opportunity for skeletal recovery.