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    • The negative long term effects of alcoholism on bone mass

    2018-11-06

    The negative, long term effects of alcoholism on bone mass have been well-established (Feskanich et al., 1999). Studies have shown that heavy chronic alcohol consumption compromises bone quality and increases the risk for osteoporosis. Other studies have shown that alcoholism is associated with a variety of risk factors that may contribute to the pathogenesis of bone disease, including poor nutrition, liver disease, malabsorption, vitamin D deficiency, hypogonadism, parathyroid dysfunction and tobacco use (Kim et al., 2003). Recent studies have reported that alcohol may affect bone formation through osteocyte apoptosis, oxidative stress, and Wnt signaling pathway modulation (Maurel et al., 2012). One study involving alcohol-binged rats suggested that following administration of 20% alcohol/saline solution for 1, 2 or 3weeks, a stimulation of bone resorption and decrease in bone mineral density was observed. However, it was interesting to note that concurrent administration of risedronate, a bisphosphonate, mitigated the response and maintained trabecular architectural indices (Callaci et al., 2009). The duration of alcohol treatment resulted in the modulation of epigallocatechin gallate profiles of RANKL and OPG, genes that regulate osteoclastogenesis. This study sheds light on the deleterious effects of bone metabolism in response to binge drinking. However, the exact mechanisms of how alcohol is related to bone loss remains unknown, but may include both direct and indirect actions, and be related to diet and other lifestyle factors. While chronic alcohol abuse has been linked to an increase in the risk for osteoporosis, light to moderate consumption has been correlated with a reduction in osteoporotic risk. Some studies have identified that light to moderate concentrations of EtOH exposure has resulted in higher bone mineral density and a reduced risk of osteoporosis (Feskanich et al., 1999; Jugdaohsingh et al., 2006). Another study found that light alcohol consumption resulted in increased lumbar spine bone mineral density (BMD) and whole body BMD in postmenopausal women (Ilich et al., 2002). In animal studies, low alcohol consumption of ethanol (5%, 2h per day) in 4-week old rats showed higher BMD and greater trabecular thickness than compared to the control groups (Yamamoto et al., 1997). However, there are few animal models related to the effects of light alcohol consumption in the literature and further investigative studies in animal models should be performed in the future to shed light on these results. In contrast, at longer durations of moderate to high alcoholic exposure, there is a dose dependent effect on bone to increase risk for stress fractures. In a rat study investigating the long-term effects of heavy alcohol consumption on cancellous and cortical bone microarchitecture, ethanol consumption resulted in lower bone mineral density and content, reduced cortical thickness, and a lower femur length as compared to controls (Johnson et al., 2014). These results suggest that chronic, heavy alcohol consumption results in a decrease in bone size, mass, and density, and negatively alters cancellous bone microarchitecture resulting in decreased skeletal integrity. In this study, we have used DPSCs as a model to examine the effect of EtOH on the mineralization process. Our findings show that EtOH treatment resulted in altered mineralization in DPSCs. The dysregulation of odontogenic/osteogenic differentiation in DPSCs treated with EtOH is reminiscent of previous findings with reductions in bone mineral density and volume. We discovered that EtOH treatment results in the reduction of several known mineralization-related gene expression profiles, including ALP, BMP2, BMP4, DLX2, OCN, and OPN. These findings appear to mirror potential biological mechanisms that are significantly dysregulated in the etiology of alcohol-induced osteoporotic events. In vitro studies are often difficult to adapt to in vivo studies due to their inability to fully simulate in vivo conditions. There are no in vitro models to study the effects of EtOH on bone formation and resorption (Turner, 2000). Furthermore, one study identified a significant discrepancy in body weight gain and bone measurements due to the delivery method of EtOH. In this study, intraperitoneal injection resulted in reduced body weight, suppression of periosteal and cancellous bone formation, and decreased mRNA levels for bone matrix proteins as compared to intragastric administration (Iwaniec and Turner, 2013). This study suggests that treatment of DPSCs in vitro using EtOH-containing media may provide a dosage that is not replicable physiologically. In addition, the effects of alcohol on epigenetic modifiers and bone loss may not be fully adaptable to human studies, as it fails to take into account co-morbidity factors including poor nutrition, vitamin deficiencies, mechanical loading, weight and smoking (Turner, 2000). The effects of alcohol related bone loss is controversial, with human studies reporting bone loss as well as no bone loss.