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 effect of iodine intake on bone metabolism remains less known. OBJECTIVE: This study evaluated the effect of excess iodine intake in rats on bone reconstruction in the 6th and 12th month of intervention. METHOD: Rats were treated with different doses of iodinated water: the normal group (NI, 6.15 µg/d), 5-fold high iodine group (5HI, 30.75 µg/d), 10-fold high iodine group (10HI, 61.5 µg/d), 50-fold high iodine group (50HI, 307.5 µg/d), and 100-fold high iodine group (100HI, 615 µg/d). Thyroid hormone concentrations were determined by a chemiluminescent immunoassay. Morphometry and microstructure of bone trabecula were observed by hematoxylin and eosin staining and microcomputed tomography, 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 iodine intake. The rats in the HI groups had higher serum thyroid-stimulating hormone and decreased serum free thyroxine concentrations in the 12th month than the NI group (all P < 0.05). The percentage 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 with 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 was 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.

Chronic Iodine Intake Excess Damages the Structure of Articular Cartilage and Epiphyseal Growth Plate.

This study aimed to explore the influence of excess iodine on the articular cartilage and epiphyseal growth plate in rats. Wistar rats (n = 200) were randomly divided into five groups with 40 rats in each: normal iodine (NI), 5-fold high iodine group (5HI), 10-fold high iodine group (10HI), 50-fold high iodine group (50HI), and 100-fold high iodine group (100HI). The rats were executed in 6 and 12 months. 24-h urinary iodine concentration (UIC) was monitored by arsenic-cerium catalytic spectrophotometry. The chemiluminescence method was used to determine the thyroid function. The pathological changes in the epiphyseal plate, articular cartilage, and thickness of the epiphyseal plate were observed. The mRNA expression of collagen II (ColII), collagen X, matrix metalloproteinase-13 (MMP-13), and fibroblast growth factor receptor 1 in articular chondrocytes was detected by RT-PCR. 24-h UIC increased as iodine intake increased. In the 12th month, there was a significant increase in serum sTSH and a decrease in serum FT4 in HI groups, compared to the NI group. There was a decrease in the number of proliferating cells in the epiphyseal plate and an increase in the number of mast cell layers. The chondrocytes appeared disorganized, and the tidal lines were disturbed or even broken. Growth plate thickness decreased with increasing iodine intake. Compared with the NI group, ColII and MMP-13 mRNA expression in chondrocytes in all HI groups significantly increased. Chronic iodine overdose increases the risk of hypothyroidism. Chronic iodine overdose leads to abnormal morphology of epiphyseal growth plates and articular cartilage, increasing the risk of osteoarthritis.

Genetic evidence strengthens the bidirectional connection between gut microbiota and periodontitis: insights from a two-sample Mendelian randomization study.

BACKGROUND: Recent research has established the correlation between gut microbiota and periodontitis via oral-gut axis. Intestinal dysbiosis may play a pivotal bridging role in extra-oral inflammatory comorbidities caused by periodontitis. However, it is unclear whether the link is merely correlative or orchestrated by causative mechanistic interactions. This two-sample Mendelian randomization (MR) study was performed to evaluate the potential bidirectional causal relationships between gut microbiota and periodontitis. MATERIALS AND METHODS: A two-sample MR analysis was performed using summary statistics from genome-wide association studies (GWAS) for gut microbiota (n = 18,340) and periodontitis (cases = 12,251; controls = 22,845). The inverse-variance weighted (IVW) method was used for the primary analysis, and we employed sensitivity analyses to assess the robustness of the main results. The PhenoScanner database was then searched for pleiotropy SNPs associated with potential confounders. In order to identify the possibly influential SNPs, we further conducted the leave-one-out analysis. Finally, a reverse MR analysis was performed to evaluate the possibility of links between periodontitis and genetically predicted gut microbiota alternation. RESULTS: 2,699 single nucleotide polymorphisms (SNPs) associated with 196 microbiota genera were selected as instrumental variables (IVs). IVW method suggested that order Enterobacteriales (OR: 1.35, 95% CI 1.10-1.66), family Bacteroidales S24.7group (OR: 1.22, 95% CI 1.05-1.41), genus Lachnospiraceae UCG008 (OR: 1.16, 95% CI 1.03-1.31), genus Prevotella 7 (OR: 1.11, 95% CI 1.01-1.23), and order Pasteurellales (OR: 1.12, 95% CI 1.00-1.26) may be associated with a higher risk of periodontitis, while genus Ruminiclostridium 6 may be linked to a lower risk (OR: 0.82, 95% CI 0.70-0.95). The sensitivity and heterogeneity analyses yielded no indication of horizontal pleiotropy or heterogeneity. Only the association between order Enterobacteriales and the likelihood of periodontitis remained consistent across all alternative MR approaches. In the reverse MR analysis, four microbiota genera were genetically predicted to be down-regulated in periodontitis, whereas two were predicted to be up-regulated. CONCLUSIONS: The present MR analysis demonstrated the potential bidirectional causal relationships between gut microbiota and periodontitis. Our research provided fresh insights for the prevention and management of periodontitis. Future research is required to support the finding of our current study.

Mothers' experiences of neonatal intensive care: A systematic review and implications for clinical practice.

BACKGROUND: Preterm birth is on the rise worldwide. Neonatal intensive care units (NICUs) have enabled many critically ill newborns to survive. When a premature baby is admitted to the NICU, the mother-infant relationship may be interrupted, affecting the mother's mental health. AIM: To examine the maternal emotions associated with having a child in the NICU and provide suggestions for clinical practice. METHODS: MEDLINE, CINAHL, PsychARTICLES, and PsychINFO were searched for relevant articles between 2005 to 2019, and six qualitative articles were chosen that explored the experiences of mothers who had a preterm infant in the NICU. The thematic analysis method was used to identify the most common themes. RESULTS: Four main themes of the experience of mothers who had a preterm infant in the NICU were identified: Negative emotional impacts on the mother, support, barriers to parenting, and establishment of a loving relationship. CONCLUSION: NICU environment is not conducive to mother-child bonding, but we stipulate steps that health care professionals can take to reduce the negative emotional toll on mothers of NICU babies.