A comprehensive overview on osteoporosis and its risk factors

Pouresmaeili, Farkhondeh; Kamalıdehghan, Behnam; Kamarehei, Maryam; Goh, Yong Meng

doi:10.2147/tcrm.s138000

Cited by 267 publications

(190 citation statements)

References 306 publications

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“…Many factors affect atherosclerosis 18,19 ; however, recent studies have emphasized the influence of the serum concentrations of the small peptide molecules salusin-a and salusin-b. 1,[6][7][8] A reduction in the serum salusin-a concentration or an increase in the serum salusin-b concentration promotes the progression of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Salusin-β is superior to salusin-α as a marker for evaluating coronary atherosclerosis

Wang

Zhang

et al. 2020

J Int Med Res

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Objective: This study was performed to evaluate the interaction effect of salusin-a and salusin-b on coronary artery injury or stenosis. Methods: The salusin-a and salusin-b concentrations were measured by enzyme-linked immunosorbent assay in 256 patients who underwent coronary angiography for chest pain, and coronary artery stenosis was assessed by the SYNTAX scoring system. Multivariate logistic regression was used to analyze the correlation between variables and coronary artery stenosis. The interaction of salusin-a and salusin-b on coronary artery stenosis was further explored by multiple linear regression. Results: The model goodness of fit (R) for the interaction effect of salusin-a and salusin-b on coronary artery stenosis was 0.863, and the adjusted R value revealed that the interaction could explain 74.3% of the variation in SYNTAX scores. The F-statistic exceeded F 0.05 (3.031485935) and P < 0.001, further showing that salusin-a and salusin-b had a significant interaction effect on coronary artery stenosis. The standard coefficient for salusin-b (0.797) was higher than that for salusin-a (À0.367, indicating an inhibitory effect), showing that salusin-b had a greater effect on coronary artery stenosis. Conclusions: Salusin-b, a potential marker for assessing coronary atherosclerosis, was superior to salusin-a, contributing to our understanding of the etiology of coronary artery stenosis.

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Section: Discussionmentioning

confidence: 99%

Salusin-β is superior to salusin-α as a marker for evaluating coronary atherosclerosis

Wang

Zhang

et al. 2020

J Int Med Res

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“…For example, inflammatory factors play an important role in the progression of schizophrenia and BD [25,26]. Some inflammatory factors have been shown to have detrimental effects on BMD and increase the fracture risk through the promotion of osteoclast differentiation and apoptosis in osteoblast populations [27]. Other risk factors of bone loss, such as age, sex, genetic susceptibility, estrogen and daily activity, were also associated with schizophrenia, BD and AD [3,27,28].…”

Section: Discussionmentioning

confidence: 99%

“…Some inflammatory factors have been shown to have detrimental effects on BMD and increase the fracture risk through the promotion of osteoclast differentiation and apoptosis in osteoblast populations [27]. Other risk factors of bone loss, such as age, sex, genetic susceptibility, estrogen and daily activity, were also associated with schizophrenia, BD and AD [3,27,28]. However, it remained unclear whether these factors were causes or consequences of the three neuropsychiatric diseases.…”

Section: Discussionmentioning

confidence: 99%

Schizophrenia, Bipolar Disorder, and Alzheimer’s Disease are not Causal Factors of Bone Mineral Density: A Mendelian Randomization Analysis

et al. 2019

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Until recently, it remains unclear whether schizophrenia, bipolar disorder (BD), and Alzheimer's disease (AD) is associated with bone mineral density (BMD). We aimed to investigate the causal effects of schizophrenia, BD and AD on BMD with Mendelian randomization (MR) analysis. Single-nucleotide polymorphisms (SNPs) strongly associated with these three neuropsychiatric diseases as instrumental variables were selected from genome-wide association studies in the MR Base database. We analyzed the effects of these SNPs on the femoral neck BMD (FN-BMD), lumbar spine BMD (LS-BMD) and forearm BMD (FA-BMD), and evaluated the heterogeneities and pleiotropy of these genetic variants. We also evaluated the potential confounding factors in the association between these three neuropsychiatric diseases and the BMD level. It was found that none of these genetic variants were significantly associated with BMD or confounding factors. Using these genetic variants, we did not find statistically significant causal effects of per unit increase in the log-odds of having schizophrenia, BD or AD with FN-BMD, LS-BMD and FA-BMD changes (e.g. schizophrenia and FN-BMD, MR-Egger OR 0.9673, 95% CI 0.8382 to 1.1163, p = 0.6519). The MR results also revealed that directional pleiotropy was unlikely to bias the causality (e.g., schizophrenia and FN-BMD, intercept = 0.0023, p = 0.6887), and no evidence of heterogeneity was found between the genetic variants (e.g., schizophrenia and FN-BMD, MR-Egger Q = 46.1502, I 2 = 0.0899, p = 0.3047). Our MR study did not support causal effects of increased risk of schizophrenia, BD and AD status with BMD level.

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“…Among the risk factors for osteoporosis, it is possible to identify modifiable factors, including diet and lifestyle factors, and non-modifiable factors such as gender, age, genetic factors, history of prior fractures, diseases and pharmacological treatments [13,14]. The modifiable factors, such as a balanced diet and exercise, have an important role already in childhood.…”

Section: Physiological Mechanisms Of Bone Remodelingmentioning

confidence: 99%

How Physical Activity across the Lifespan Can Reduce the Impact of Bone Ageing: A Literature Review

Faienza

Lassandro

Chiarito

et al. 2020

IJERPH

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Bone remodeling is a lifelong process, due to the balanced activity of the osteoblasts (OBs), the bone-forming cells, and osteoclasts (OCs), the bone-resorbing cells. This equilibrium is mainly regulated by the WNT-ß-cathenin pathway and the RANK-RANKL/OPG system, respectively. Bone ageing is a process which normally occurs during life due to the imbalance between bone formation and bone resorption, potentially leading to osteoporosis. Bone loss associated with bone ageing is determined by oxidative stress, the result of the increasing production of reactive oxygen species (ROS). The promotion of physical exercise during growth increases the chances of accruing bone and delaying the onset of osteoporosis. Several studies demonstrate that physical exercise is associated with higher bone mineral density and lower fracture incidence, and the resulting bone mineral gain is maintained with ageing, despite a reduction of physical activity in adulthood. The benefits of exercise are widely recognized, thus physical activity is considered the best non-pharmacologic treatment for pathologies such as osteoporosis, obesity, diabetes and cardiovascular disease. We reviewed the physiological mechanisms which control bone remodeling, the effects of physical activity on bone health, and studies on the impact of exercise in reducing bone ageing.

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A comprehensive overview on osteoporosis and its risk factors

Cited by 267 publications

References 306 publications

Salusin-β is superior to salusin-α as a marker for evaluating coronary atherosclerosis

Salusin-β is superior to salusin-α as a marker for evaluating coronary atherosclerosis

Schizophrenia, Bipolar Disorder, and Alzheimer’s Disease are not Causal Factors of Bone Mineral Density: A Mendelian Randomization Analysis

How Physical Activity across the Lifespan Can Reduce the Impact of Bone Ageing: A Literature Review

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