Chronic excess iodine intake inhibits bone reconstruction leading to osteoporosis in rats.

BACKGROUND: Although iodine modulates bone metabolism in the treatment of thyroid disease, the iodine intake on bone metabolism remains less known.

OBJECTIVE: This study evaluated excess iodine intake on bone reconstruction using rats in the 6th and 12th month of intervention.

METHOD: We used a different dose of iodinated water-treated rat model, split into 5 groups: the normal group (NI, 6.15 μg/day), 5-fold high iodine group (5HI, 30.75 μg/day), 10-fold high iodine group (10HI, 61.5 μg/day), 50-fold high iodine group (50HI, 307.5 μg/day), and 100-fold high iodine group (100HI, 615 μg/day). Thyroid hormones were determined by a chemiluminescent immunoassay. Morphometry and microstructure of bone trabecula were observed by HE staining and Micro-CT, respectively. Alkaline phosphatase (ALP) and tartrate-resistant acid phosphatase (TRAP) staining were performed to evaluate the activity of osteoblasts and osteoclasts, respectively.

RESULTS: The 24-h urine iodine concentration increased with the iodine intake. The rats in the HI groups presented higher serum sTSH in the 12th month than in the NI group, and decreased serum FT4 (all P<0.05). The percent of the trabecular bone area and osteoblast perimeter in the 100HI group were significantly lower than those in the NI group (P<0.05). Increased structure model index was observed in the 50HI and 100HI groups compared to the NI group in the 6th month, and increased trabecular separation in the 12th month (all P<0.05). ALP and TRAP staining revealed osteoblastic bone formation reduced and the number of TRAP+ multinucleated cells decreased with increasing iodine intake.

CONCLUSIONS: Excess iodine intake may increase the risk of hypothyroidism in rats. Chronic excess iodine intake can lead to abnormal changes in skeletal structure, resulting in reduced activity of osteoblasts and osteoclasts, which inhibits the process of bone reconstruction and may lead to osteoporosis.