The financial and social cost of hypertension and osteoporosis, clinically silent diseases, are determined by the consequences, such as a vascular disease and fractures. The relationship between these illnesses has not been clearly established, although many alterations in extracellular metabolism of calcium, which could determine the level of bone mineral density (BMD) in these patients, have been associated to hypertension. Despite these alterations, the lack of studies relating these two important diseases is surprising, and hypertension is not identified as a risk factor for osteoporosis.Interestingly, there is a lack of information of the long-term effects of antihypertensive treatment on bone mineral density, although 50 % of the hypertensive population is made up of postmenopausal women. Most studies analyzed the effects of thiazides and, to a lesser degree, the effects of calcium antagonist.The purpose of this review is evaluate the effect of the antihypertensive therapeutic group (diuretics, β-blockers, calcium antagonists, angiotensin converting enzyme) on the bone mineral density (BMD) and osteoporotic fracture.

Several clinical trials have shown an association between osteoporosis and an increase in cardiovascular mortality, especially in patients with vertebral fracture. In addition to their action on a decrease in cholesterol levels and a reduction of mortality in individuals with ischemic heart disease, statins can have a beneficial effect on other chronic diseases, including osteoporosis.Statins can have anabolic and anticatabolic effects on bone. Mundy published the first in vitro study with animals and demonstrated an anabolic effect of the statins on bone. On the other hand, through its action on the 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase, it inhibits the mevalonate synthesis by reducing the prenylation of glutamyltranspeptidase (Ras, Rho, Rai, Rab) necessary to osteoclast activity and the decrease in the apoptosis, which results in a decrease in bone resorption. Studies on humans have alnalyzed the effect of statins on bone remodeling markers, bone mass fracture risks. Retrospective studies (case-control, cohort studies) followed, which showed a beneficial effect of the statins on the reduction of fractures, although not all the results are consistent. The prospective studies have been undertaken with a small number of patients and only the bone mineral density has been evaluated. A meta-analysis of prospective and observational studies has shown a protective effect on hip fracture (OR: 0.43, 95 % CI 0.25-0.75) and non-vertebral fracture (OR: 0.69, 95 % CI 0.75-0.88).The objective of this article is to review the available evidence, experimental and clinical, of the effect of statins on bone mass and the reduction of fractures. These drugs may be an alternative for the treatment of osteoporosis, keeping in mind that osteoporosis and atherosclerosis affect similar age groups.

The objective of this study was to evaluate the relationship between coronary disease and osteoporosis and determine the effect of osteoprotegerin (OPG) on bone remodeling and bone mineral density (BMD) in a group of patients with acute coronary syndrome. Eightythree patients (52 males and 31 women) with acute coronary syndrome (75 patients with acute myocardial infarction and 8 with unstable angina) with an average age of 61 ± 10 years were studied. Levels of osteocalcin, urinarydeoxypyridinoline, OPG and the receptor activator of nuclear factor-κB ligand (RANKL) were determined during the hospital stay. Femoral neck, trochanter and lumbar spine densitometry was carried out using a DXA densitometer. Thirty percent of patients presented osteoporosis (39% of females and 26% of males). Osteoporotic patients were older and had a lower weight and height and elevated serum levels of osteocalcin (3.6 ± 2.25 2.63 versus ± 1.55, p = 0.05). Levels of OPG and RANKL were similar in both groups and showed no relationship with BMD. In conclusion, no relationship was observed between the OPG/RANKL system and BMD in these patients.

Abstract. Objectives. To evaluate the effect of atorvastatin on bone mass and markers of bone remodeling in patients with acute coronary syndrome according to the Lys656Asn leptin receptor gene polymorphism. Methods. Sixty-two patients with acute coronary syndrome were included. Patients were allocated to low and high doses of atorvastatin according to baseline levels of cholesterol and triglycerides and the index of vascular risk and were studied at hospital admission and at 12 months. Cholesterol, triglycerides, total calcium, phosphorus, magnesium, osteocalcin and urinary deoxypyridinoline were determined in all patients at baseline and at 12 months of follow up. Densitometric studies were conducted in the lumbar spine and hip. Patients with a T-score<-2.5 were considered osteoporotic. The Lys656Asn leptin receptor gene polymorphism was determined by PCR. Results. Forty-two patients were Lys/Lys homozygotic and 20 Lys/Asn heterozygotic. The prevalence of osteoporosis was 31% for the Lys/Lys genotype and 27% for the Lys/Asn genotype with no significant differences between groups. There was a significant increase in bone mineral density in the lumbar spine (1.117 ± 0.24 versus 1.135 ± 0.24, P = 0.008) in patients with the Lys/Lys genotype. Conclusion. Atorvastatin increases lumbar spine bone mineral density only in patients with the Lys/Lys genotype of the Lys656Asn polymorphism. . Inflammatory cytokines play an important role in the imbalance between bone formation and resorption that leads to the reduced bone mass seen in osteoporosis [3]. In addition, drugs such as statins are effective in both diseases, diminishing vascular events in patients with atherosclerosis and increasing bone mass in those with high levels of cholesterol [4]. Human leptin is a protein of 167 amino acids manufactured in fat cells which is involved in regulating the ingestion and consumption of energy. It intervenes in the regulation of bone mass by means of a central hypothalamic mechanism, exerting a double antagonistic effect on bone formation and resorption through activation of the sympathetic nervous system and the Cocaine Amphetamine Regulated Transcript (CART) [5]. In addition, studies have shown that hyperleptinemia can exert atherogenic effects [6]. In North American patients, elevated leptin levels have been associated with an increased risk of myocardial infarction in both males (3.16, 95% CI 1.40-7.37) and females (3.95, 95% CI 1.29-12.72) [7].Leptin exerts its biological effect by bonding with a receptor from the cytokine-receptor family. The leptin

Aims: To evaluate the effect of atorvastatin on bone mass and markers of bone remodeling in patients with acute coronary syndrome depending on the tumor necrosis factor-α (TNFα)-308 G/A polymorphism. Methods: Sixty-two patients with acute coronary syndrome (35 males and 27 females), average age 60 ± 10 years, were included. Patients were given low (10–20 mg) and high doses (40–80 mg) atorvastatin according to their baseline levels of cholesterol and triglycerides and their index of vascular risk. Patients were studied during hospital admission (baseline) and at 12 months of follow-up. Cholesterol, triglycerides, total calcium, phosphorus, magnesium, osteocalcin and urinary deoxypyridinoline were determined in all patients at baseline and at 12 months of follow-up. Densitometric studies were conducted in the lumbar spine (L₂–L₄), femoral neck and trochanter using an X-ray densitometer. The TNFα-308 G/A polymorphism was determined by the polymerase chain reaction.Results:Forty-five patients were homozygous for G/G (72.5%) and 17 were heterozygous for G/A (27.5%). The prevalence of osteoporosis (T score ≤2.5 in the lumbar spine and/or hip) was 33% for the G/G genotype and 35% for the G/A genotype, with no statistically significant differences between groups. There was a statistically significant increase in bone mineral density (BMD) in the lumbar spine (1.107 ± 0.32 vs. 1.129 ± 0.23; p = 0.0001) in patients with the G/G genotype. No changes were observed in patients with the G/A genotype. Conclusion: In patients with acute coronary syndrome, atorvastatin increases lumbar spine BMD solely in patients with the G/G genotype of the TNFα-308 G/A polymorphism.