Abstract
Long-term heavy alcohol consumption could result in a range of health, social, and behavioral problems. People who abuse alcohol are at high risks of seriously having osteopenia, periodontal disease, and compromised oral health. However, the role of ethanol (EtOH) in the biological functions of human dental pulp cells (DPCs) is unknown. Whether EtOH affects the odontoblastic differentiation of DPCs through the mechanistic target of rapamycin (mTOR) remains unexplored. The objective of this study was to investigate the effects of EtOH on DPC differentiation and mineralization. DPCs were isolated and purified from human dental pulps. The proliferation and odontoblastic differentiation of DPCs treated with EtOH were subsequently investigated. Different doses of EtOH were shown to be cytocompatible with DPCs. EtOH significantly activated the mTOR pathway in a dose-dependent manner. In addition, EtOH downregulated the alkaline phosphatase activity, attenuated the mineralized nodule formation, and suppressed the expression of odontoblastic markers including ALP, DSPP, DMP-1, Runx2, and OCN. Moreover, the pretreatment with rapamycin, a specific mTOR inhibitor, markedly reversed the EtOH-induced odontoblastic differentiation and cell mineralization. Our findings show for the first time that EtOH can suppress DPC differentiation and mineralization in a mTOR-dependent manner, indicating that EtOH may be involved in negatively regulating the dental pulp repair.
Highlights
Alcohol is widely consumed throughout the world and has attracted human concernment for thousands of years
An increase in calcified nodule formation (Figure 4(c)) and calcium content (Figure 4(d)) was observed in cells treated with EtOH in the presence of rapamycin. These results suggest that the downstream effects of EtOH on the odontoblastic maturation of dental pulp cells (DPCs) were mediated through the activation of the mammalian target of rapamycin (mTOR) signaling pathway
Previous studies showed that heavy chronic alcohol consumption is associated with a variety of risk factors that may contribute to the pathogenesis of bone disease, including malabsorption, hypogonadism, poor nutrition, vitamin D deficiency, liver
Summary
Alcohol is widely consumed throughout the world and has attracted human concernment for thousands of years. Alcohol abuse can place the health of an individual at risk for a series of diseases. According to the World Health Organization, heavy alcohol consumptions are associated with many chronic diseases, including low bone mass, hepatitis, and cardiovascular diseases [1]. Chronic and heavy alcohol consumption is known to result in bone loss, decreased bone formation, increased risks for bone fracture, and delayed fracture healing [2,3,4]. Moderate alcohol consumption may have a modest favorable effect on bone density, in postmenopausal women, not all studies agree [5,6,7,8]. Alcohol intake of three or more drinks per day is detrimental to bone health [9]. Recent experimental evidences indicated that the mammalian target of rapamycin (mTOR) signal may contribute to the maintenance of bone homeostasis and the differentiation of mesenchymal stem cells [10, 11]
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