The impact of hyperthyroidism on bone microarchitecture and its changes with therapy among women

By: Reza Behdani, Terra Arnason (PI), Masud Rana, Saija Kontulainen, & David Cooper

Thyroid hormones play an important role in bone physiology. Hyperthyroidism drives high bone turnover and bone remodelling which is associated with net loss of bone mineral density (BMD). The gold standard of measuring BMD has long been Dual Energy X-ray Absorptiometry (DEXA). Notably, biochemical thyroid hormone normalization improves BMD towards normal, yet an increased risk of fractures remains lifelong. Therefore, DEXA cannot explain the underlying etiology for fracture risk which may be due to undetected changes in bone microarchitecture.

Our primary objective was to utilize the newest 3-dimensional bone imaging technology, High Resolution peripheral Quantitative Computed Tomography (HR-pQCT), to study bone microarchitecture in actively hyperthyroid women to determine if bone remodelling is cortical, trabecular or both.

We enrolled 20 hyperthyroid women (age 20-76) with TSH suppression for > 3 month (TSH< 0.5, normal reference range: 0.5-4.49 mU/L) without secondary causes for bone loss. Their HR-pQCT scans of the radius were compared to age-matched scans of the normal female population. A subset of participants were scanned again after 6 months of TSH normalization to determine reversibility.

The observed data showed statistically significant difference in some parameters of bone microarchitecture, including cortical thickness, trabecular thickness and failure load, between case and control groups (p-value<0.05). Despite the lower cortical thickness on average among hyperthyroid patients, the difference in volumetric bone density (cortical, trabecular and total) was insignificant. These findings were not associated with hyperthyroidism etiology. Repeat scan following successful treatment revealed some improvement in bone microarchitecture, but did not fully normalize microarchitectural elements.

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