Low bone accrual is associated with osteocyte apoptosis in alcohol-induced osteopenia

Maurel, Daniel; Jaffré, Christelle; Rochefort, Gaël Y.; Aveline, Priscilla; Boisseau, Nathalie; Uzbekov, Rustem; Gosset, D.; Pichon, Chantal; Fazzalari, Nicola L.; Pallu, Stéphane; Benhamou, Claude-Laurent

doi:10.1016/j.bone.2011.06.001

Cited by 51 publications

(47 citation statements)

References 52 publications

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“…Recently, apoptosis has been reported in rat tibia after chronic consumption of EtOH for 17 weeks (Maurel et al, 2011). We observed an increase in apoptosis as measured by qualitative in situ TUNEL staining in tibial bone marrow after chronic EtOH exposure (Fig.…”

Section: Vitamin D Supplementation Prevents Etoh-mediated Bone Loss 407supporting

confidence: 56%

Vitamin D Supplementation Protects against Bone Loss Associated with Chronic Alcohol Administration in Female Mice

Mercer

Wynne

Lazarenko

et al. 2012

J Pharmacol Exp Ther

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Chronic alcohol abuse results in decreased bone mineral density (BMD), which can lead to increased fracture risk. In contrast, low levels of alcohol have been associated with increased BMD in epidemiological studies. Alcohol's toxic skeletal effects have been suggested to involve impaired vitamin D/calcium homeostasis. Therefore, dietary vitamin D supplementation may be beneficial in reducing bone loss associated with chronic alcohol consumption. Six-week-old female C57BL/6J mice were pair-fed ethanol (EtOH)-containing liquid diets (10 or 36% total calories) for 78 days. EtOH exposure at 10% calories had no effects on any measured bone or serum parameter. EtOH consumption at 36% of calories reduced BMD and bone strength (P Ͻ 0.05), decreased osteoblastogenesis, increased osteoclastogenesis, suppressed 1,25-hydroxyvitamin D 3 [1,25(OH) 2 D 3 ] serum concentrations (P Ͻ 0.05), and increased apoptosis in bone cells compared with pair-fed controls. In a second study, female mice were pair-fed 30% EtOH diets with or without dietary supplementation with vitamin D 3 (cholecalciferol; VitD) for 40 days. VitD supplementation in the EtOH diet protected against cortical bone loss, normalized alcohol-induced hypocalcaemia, and suppressed EtOHinduced expression of receptor of nuclear factor-B ligand mRNA in bone. In vitro, pretreatment of 1,25(OH) 2 D 3 in osteoblastic cells inhibited EtOH-induced apoptosis. In EtOH/ VitD mice circulating 1,25(OH) 2 D 3 was lower compared with mice receiving EtOH alone (P Ͻ 0.05), suggesting increased sensitivity to feedback control of VitD metabolism in the kidney. These findings suggest dietary VitD supplementation may prevent skeletal toxicity in chronic drinkers by normalizing calcium homeostasis, preventing apoptosis, and suppressing EtOH-induced increases in bone resorption.

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Section: Vitamin D Supplementation Prevents Etoh-mediated Bone Loss 407supporting

confidence: 56%

Vitamin D Supplementation Protects against Bone Loss Associated with Chronic Alcohol Administration in Female Mice

Mercer

Wynne

Lazarenko

et al. 2012

J Pharmacol Exp Ther

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“…Furthermore, apoptosis is regarded as one of the most crucial changes in the pathological process of ONFH [10, 27]. We carried out TUNEL staining of femoral head specimens to detect apoptosis.…”

Section: Resultsmentioning

confidence: 99%

“…Animal studies also indicated decreased osteogenesis and bone volume after long-term alcohol consumption [9, 10]. Human bone mesenchymal stem cells (hBMSCs) are regarded as the main source of self-renewal and regeneration of bone tissue [11-13], whereas recent studies demonstrated that ethanol treatment could impair the osteogenic differentiation of hBMSCs [2, 14].…”

Section: Introductionmentioning

confidence: 99%

The Protective Effect of Cordycepin On Alcohol-Induced Osteonecrosis of the Femoral Head

Chen¹,

Zhu²,

Xu³

et al. 2017

Cell Physiol Biochem

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Background: Alcohol abuse is known to be a leading risk factor for atraumatic osteonecrosis of the femoral head (ONFH), in which the suppression of osteogenesis plays a critical role. Cordycepin benefits bone metabolism; however, there has been no study to determine its effect on osteonecrosis. Methods: Human bone mesenchymal stem cells (hBMSCs) were identified by multi-lineage differentiation. Alkaline phosphatase (ALP) activity, RT-PCR, western blots, immunofluorescent assay and Alizarin red staining of BMSCs were evaluated. A rat model of alcohol-induced ONFH was established to investigate the protective role of cordycepin against ethanol. Hematoxylin & eosin (H&E) staining and micro-computerized tomography (micro-CT) were performed to observe ONFH. Apoptosis was assessed by TdT-mediated dUTP nick end labeling (TUNEL). Immunohistochemical staining was carried out to detect OCN and COL1. Results: Ethanol significantly suppressed ALP activity, decreased gene expression of OCN and BMP2, lowered levels of RUNX2 protein, and reduced immunofluorescence staining of OCN and COL1 and calcium formation of hBMSCs. However, these inhibitory effects were attenuated by cordycepin co-treatment at concentrations of 1 and 10 µg/mL Moreover, it was revealed that the osteo-protective effect of cordycepin was associated with modulation of the Wnt/β-catenin pathway. In vivo, by micro-CT, TUNEL and immunohistochemical staining of OCN and COL1, we found that cordycepin administration prevented alcohol-induced ONFH. Conclusion: Cordycepin treatment to enhance osteogenesis may be considered a potential therapeutic approach to prevent the development of alcohol-induced ONFH.

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“…Leptin is able to affect the central nervous system (CNS) as well as peripheral tissues: it decreases bone mass through the CNS while also having an anabolic effect on bone by driving stem cell differentiation to the osteoblastic cell lineage [88,89]. Alcohol consumption decreases leptin concentrations in men and rats [41,90,91], as well as decreasing osteoblastogenesis and increasing adipogenesis concomitantly in the bone marrow, modifying the balance between osteogenesis and adipogenesis [92,93]. Consistent with this, an increase of the adipogenesis indicator PPARgamma and a decrease in osteocalcin have been observed in vitro on cloned bone marrow stem cells from mice and on human mesenchymal stem cells cultured with ethanol [94,95].…”

Section: Leptinmentioning

confidence: 99%

Alcohol and bone: review of dose effects and mechanisms

et al. 2011

Self Cite

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Alcohol is widely consumed across the world. It is consumed in both social and cultural settings. Until recently, two types of alcohol consumption were recognized: heavy chronic alcohol consumption or light consumption. Today, there is a new pattern of consumption among teenagers and young adults namely: binge drinking. Heavy alcohol consumption is detrimental to many organs and tissues, including bones, and is known to induce secondary osteoporosis. Some studies, however, have reported benefits from light alcohol consumption on bone parameters. To date, little is known regarding the effects of binge drinking on bone health. Here, we review the effects of three different means of alcohol consumption: light, heavy, and binge drinking. We also review the detailed literature on the different mechanisms by which alcohol intake may decrease bone mass and strength. The effects of alcohol on bone are thought to be both direct and indirect. The decrease in bone mass and strength following alcohol consumption is mainly due to a bone remodeling imbalance, with a predominant decrease in bone formation. Recent studies, however, have reported new mechanisms by which alcohol may act on bone remodeling, including osteocyte apoptosis, oxidative stress, and Wnt signalling pathway modulation. The roles of reduced total fat mass, increased lipid content in bone marrow, and a hypoleptinemia are also discussed.

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Low bone accrual is associated with osteocyte apoptosis in alcohol-induced osteopenia

Cited by 51 publications

References 52 publications

Vitamin D Supplementation Protects against Bone Loss Associated with Chronic Alcohol Administration in Female Mice

Vitamin D Supplementation Protects against Bone Loss Associated with Chronic Alcohol Administration in Female Mice

The Protective Effect of Cordycepin On Alcohol-Induced Osteonecrosis of the Femoral Head

Alcohol and bone: review of dose effects and mechanisms

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