Thyroid-stimulating hormone decreases the risk of osteoporosis by regulating osteoblast proliferation and differentiation

Abstract

Background As the incidence of secretory osteoporosis has increased, bone loss, osteoporosis and their relationships with thyroid-stimulating hormone (TSH) have received increased attention. In this study, the role of TSH in bone metabolism and its possible underlying mechanisms were investigated. Methods We analyzed the serum levels of free triiodothyronine (FT3), free thyroxine (FT4), and TSH and the bone mineral density (BMD) levels of 114 men with normal thyroid function. In addition, osteoblasts from rat calvarial samples were treated with different doses of TSH for different lengths of time. The related gene and protein expression levels were investigated. Results A comparison of the BMD between the high-level and low-level serum TSH groups showed that the TSH serum concentration was positively correlated with BMD. TSH at concentrations of 10 mU/mL and 100 mU/mL significantly increased the mRNA levels of ALP, COI1 and Runx2 compared with those of the control (P < 0.05, P < 0.01). Bone morphogenetic protein (BMP)2 activity was enhanced with both increased TSH concentration and increased time. The protein levels of Runx2 and osterix were increased in a dose-dependent manner. Conclusions The circulating concentrations of TSH and BMD were positively correlated with normal thyroid function in males. TSH promoted osteoblast proliferation and differentiation in rat primary osteoblasts.

A Causality between Thyroid Function and Bone Mineral Density in Childhood: Abnormal Thyrotropin May Be Another Pediatric Predictor of Bone Fragility

“…TSH signals the thyroid follicular cells to produce T3 and T4, whose excess exerts an inhibitory action via a negative feedback loop system on the anterior pituitary gland, thus suppressing the TSH secretion. TSH receptor expression was observed not only in the thyroid tissue but also in normal osteoblasts, implying the direct action of TSH on bone formation [ 21 ]. Several observational studies conducted in an adult population concluded that individuals with low normal TSH levels, regardless of TH levels, are at risk of developing osteoporosis [ 22 ].…”

Trifloroside Induces Bioactive Effects on Differentiation, Adhesion, Migration, and Mineralization in Pre-Osteoblast MC3T3E-1 Cells

“…Osteoblast-mediated bone formation is induced by complex processes via migration and adhesion to bone formation, remodeling, and repair sites; their subsequent differentiation; and osteoblast maturation, leading to osteoid formation and mineral apposition [ 22 , 23 ]. Thus, damage to complex processes causes bone loss in bone diseases such as osteoporosis and periodontitis [ 7 , 8 ]. As is well established, the ALP (a key osteoblast differentiation marker) enzyme is required for the formation of hydroxyapatite crystals through the hydrolysis of organic phosphomonoesters and inorganic pyrophosphate [ 5 , 6 , 24 , 25 ].…”

“…Consequently, osteoblast differentiation and maturation produce osteoids through synthesis and secretion to construct the bone matrix, which then leads to mineralization of the bone matrix filled around collagen rope containing dense and irregular crystals of hydroxyapatite that bestow rigidity to the bone [ 5 , 6 ]. In contrast, the dysregulation and impairment of osteoblast differentiation and maturation are mainly responsible for the pathogenesis of diseases including osteoporosis-induced bone fractures and periodontitis-induced alveolar bone loss [ 7 , 8 ].…”

A Multicenter, Randomized, Double-Blind, Placebo-Controlled Clinical Study of Jianyao Migu Granules in the Treatment of Osteopenic Low Back Pain

“… 31 , 32 TSH promotes the proliferation and differentiation of osteoblasts. Deng et al 33 treated rat skull osteoblasts with different doses of TSH and reported that high-dose TSH effectively promotes the proliferation of osteoblasts and increases the expressions of key osteoblast differentiation genes ( ALP, BMP2, COL2 , and Runx2 ).…”