Chronic consumption of alcohol has an adverse effect on the skeletal system, which may lead to osteoporosis, delayed fracture healing and osteonecrosis of the femoral head. Currently, the treatment is limited, therefore, there is an urgent need to determine the underline mechanism and develop a new treatment. It is well-known that normal bone remodeling relies on the balance between osteoclast-mediated bone resorption and - mediated bone formation. Various factors can destroy the balance, including the dysfunction of the immune system. In this review, we summarized the relevant research in the alcoholic osteopenia with a focus on the abnormal osteoimmunology signals. We provided a new theoretical basis for the prevention and treatment of the alcoholic bone.

We searched PubMed for publications from 1 January 1980 to 1 February 2020 to identify relevant and recent literature, summarizing evaluation and the prospect of alcoholic osteopenia. Detailed search terms were 'alcohol', 'alcoholic osteoporosis', 'alcoholic osteopenia' 'immune', 'osteoimmunology', 'bone remodeling', 'osteoporosis treatment' and 'osteoporosis therapy'.

A total of 135 papers are included in the review. About 60 papers described the mechanisms of alcohol involved in bone remodeling. Some papers were focused on the pathogenesis of alcohol on bone through osteoimmune mechanisms.

There is a complex network of signals between alcohol and bone remodeling and intercellular communication of osteoimmune may be a potential mechanism for alcoholic bone. Studying the osteoimmune mechanism is critical for drug development specific to the alcoholic bone disorder.

To assess the association between alcohol consumption and healthy Korean young women bone by Alcohol Use Disorders Identification Test (AUDIT) scores and drinking consumption; frequency and amount.

Cross-sectional study composed of three parts: health interview, health examination, nutrition survey.

2008-2011 Korea National Health and Nutrition Examination Survey.

Of the 21,303 participants whose bone mineral density (BMD) was assessed, 1176 healthy women aged 19-30 years were selected.

Mean BMD T-scores of the total femur (TF), femur neck (FN) and lumbar spine (LB) by drinking consumption and AUDIT scores, and the odds of having a low BMD (T-score <-1) at the sites by AUDIT scores.

After adjustment, lower BMD was found at three sites in those who drank more and had higher AUDIT scores. These associations were significant by AUDIT scores at TF (p=0.002) and FN (p=0.004) and by drinking frequency and amount at FN (p=0.029 and 0.039, respectively). The adjusted OR of having low BMD increased significantly, particularly at FN, in those who had higher AUDIT scores such as 16-17 harmful drinking (OR 4.31; 95% CI 1.16 to 16.06) and 20-40 alcohol dependence (OR 5.99; 95% CI 1.69 to 21.21), compared with young women who scored 0-7 low-risk drinking or abstinence. No beneficial effect of moderate drinking was observed at any of the sites and the association between alcohol consumption and bone health was most evident at FN.

It is crucial to promote the awareness of alcohol harm on Korean young women's bone health. At the same time, since alcohol's effect on the bone is complex with cumulative effects of various factors over the years and there is an absence of studies with young women in their twenties, more studies, in particular for FN, are needed with more precise and appropriate design to confirm our findings.

To evaluate the association between alcoholic liver disease (ALD) and bone fractures or osteoporosis.

Non-randomized studies were identified from databases (PubMed, EMBASE, and the Cochrane Library). The search was conducted using Boolean operators and keywords, which included "alcoholic liver diseases", "osteoporosis", or "bone fractures". The prevalence of any fractures or osteoporosis, and bone mineral density (BMD) were extracted and analyzed using risk ratios and standardized mean difference (SMD). A random effects model was applied.

In total, 15 studies were identified and analyzed. Overall, ALD demonstrated a RR of 1.944 (95%CI: 1.354-2.791) for the development of bone fractures. However, ALD showed a RR of 0.849 (95%CI: 0.523-1.380) for the development of osteoporosis. BMD was not significantly different between the ALD and control groups, although there was a trend toward lower BMD in patients with ALD (SMD in femur-BMD: -0.172, 95%CI: -0.453-0.110; SMD in spine-BMD: -0.169, 95%CI: -0.476-0.138). Sensitivity analyses showed consistent results.

Current publications indicate significant associations between bone fractures and ALD, independent of BMD or the presence of osteoporosis.

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.

The osteolytic activity of metastases of prostate cancer was evaluated in relation to total body bone mineral content (TBBMC) and regional bone mineral content (RBMC).

Bone mass was determined by dual-energy X-ray absorptiometry (DXA). Tartrate-resistant acid phosphatase (TRAP) was measured as a biochemical marker of bone resorption.

In 32 patients (mean age 72+/-4 years) compared with 32 controls (mean age 73+/-5 years), there were significant differences in TRAP (P < 0.0001), TBBMC (P < 0.0001), and RBMC in the pelvis (P < 0.0001), legs (P=0.0001), and trunk (P<0.05), but not in the arms and head (P=ns). In the overall group of subjects, the correlation between TBBMC and TRAP was r=-0.68, P < 0.0001. The correlations remained significant in the patient and control groups separately.

The loss of bone mass observed in patients with metastatic prostate cancer was caused mainly by the predominance of bone resorption in the osteoblastic metastases.

Seventy-two postmenopausal osteoporotic women having more than one nontraumatic vertebral crush fracture were studied. Thirty-six of them, aged 68.8 +/- 1.2 years (18 +/- 4 YSM-years since menopause), were treated with 100 IU/day of salmon calcitonin i.m. plus 500 mg of elemental calcium for 10 days each month. The remaining 36 patients, aged 69.6 +/- 1.4 years (19 +/- 3 YSM), were given only 500 mg of elemental calcium for 10 days each month. All patients underwent clinical and analytical evaluation every 3 months. Radiological evaluation, assessment of vertebral deformities, and metacarpal radiogrammetry were done every 6 months. Densitometric measurements of total and regional bone mass were made every 12 months. At 24 months, the calcitonin group showed a 60% reduction in the number of new fractures and the group receiving only calcium had a 45% increase (P < 0.001). The incidence of vertebral fractures was 0.07 per patient-year in the group treated with calcitonin and 0.45 per patient-year in the group treated with calcium (P < 0.001). At 2 years, the calcitonin group showed a 12% increase in cortical bone mass on metacarpal radiogrammetry, a 16% increase in the axial skeleton on trunk densitometry, a 3.5% increase in total body bone mineral content, a 30.7% increase in pelvic bone mineral content, and a 6.2% increase in arm bone mineral content (all P < 0.001). In the group treated with calcium alone there was a loss of bone mass in every region. These findings suggest that salmon calcitonin is effective in the treatment of osteoporosis and show that it acts on cortical and trabecular bone.

Changes in bone mineral content induced by GnRH agonists were investigated by measuring total body bone mineral content (TBBM) and regional bone mineral content (BMC) (arms, legs, trunk, pelvis) and densities with dual energy X-ray absorptiometry in 25 premenopausal women before and after a 6-month treatment with gonadotropin-releasing hormone (GnRH) agonists. Biological markers of bone remodeling, estrogens, luteinizing hormone, and follicle-stimulating hormone were also measured. Weight and body mass index increased significantly after treatment (P < 0.05), and TBBM, corrected for weight (TBBM/W), decreased (P < 0.001). The changes in BMC that we observed ranged from +2.5% to -6.9%. The greatest decrease in regional BMC occurred in the trunk (4.4%, P < 0.001), with TBBM decreasing by 2.1% (P < 0.001). No significant changes were observed in the limbs. Tartrate-resistant acid phosphatase (TRAP) increased significantly after treatment (P < 0.001) and a significant negative correlation between TRAP and TBBM (P < 0.001) and between TRAP and estradiol (P < 0.001) were observed before treatment. The lack of changes observed in the BMC of the limbs indicate that GnRH agonists cause a preferential loss of BMC in trunk osseous structures, a situation similar to that of the first years of menopause.

Bibliographic references seem very controversial regarding the most appropriate anatomical area for bone mass estimation. Since some overlapping in the different bone mass measurements among normal and osteoporotic females has been observed, we have studied the bone mineral content of the pelvic bone through DEXA, and have correlated it with the total body bone mineral content, a highly discriminating measure, in order to observe whether pelvic bone mineral may be a useful measure in bone mass assessment. Pelvic and total body bone mineral values did not decrease until menopause in 104 normal premenopausal females aged 20 to 49 years. On the other hand, these values decreased in normal postmenopausal women (n = 44) aged 50 to 65 years (p < 0.001), with a 16% pelvic bone mineral content and an 11% total body bone mineral content decrease. Osteoporotic females (n = 30), showed lower values for both levels than normal postmenopausal ones (p < 0.001), with a 54% pelvic and a 24% total decrease. A 15% overlap was observed when pelvic values between normal postmenopausal and osteoporotic females were compared. The greater percentage decrease in pelvic BMC compared to total body bone mineral content and the lower overlap observed suggest that the pelvis may be an ideal anatomical area for bone mass evaluations.