pitavastatin and Osteoporosis

pitavastatin has been researched along with Osteoporosis* in 4 studies

Reviews

1 review(s) available for pitavastatin and Osteoporosis

ArticleYear
Statins and osteoporosis: new role for old drugs.
    The Journal of pharmacy and pharmacology, 2006, Volume: 58, Issue:1

    Osteoporosis is the most common bone disease, affecting millions of people worldwide and leading to significant morbidity and high expenditure. Most of the current therapies available for its treatment are limited to the prevention or slowing down of bone loss rather than enhancing bone formation. Recent discovery of statins (HMG-CoA reductase inhibitors) as bone anabolic agents has spurred a great deal of interest among both basic and clinical bone researchers. In-vitro and some animal studies suggest that statins increase the bone mass by enhancing bone morphogenetic protein-2 (BMP-2)-mediated osteoblast expression. Although a limited number of case-control studies suggest that statins may have the potential to reduce the risk of fractures by increasing bone formation, other studies have failed to show a benefit in fracture reduction. Randomized, controlled clinical trials are needed to resolve this conflict. One possible reason for the discrepancy in the results of preclinical, as well as clinical, studies is the liver-specific nature of statins. Considering their high liver specificity and low oral bioavailability, distribution of statins to the bone microenvironment in optimum concentration is questionable. To unravel their exact mechanism and confirm beneficial action on bone, statins should reach the bone microenvironment in optimum concentration. Dose optimization and use of novel controlled drug delivery systems may help in increasing the bioavailability and distribution of statins to the bone microenvironment. Discovery of bone-specific statins or their bone-targeted delivery offers great potential in the treatment of osteoporosis. In this review, we have summarized various preclinical and clinical studies of statins and their action on bone. We have also discussed the possible mechanism of action of statins on bone. Finally, the role of drug delivery systems in confirming and assessing the actual potential of statins as anti-osteoporotic agents is highlighted.

    Topics: Animals; Atorvastatin; Bone and Bones; Clinical Trials as Topic; Drug Delivery Systems; Fatty Acids, Monounsaturated; Fluorobenzenes; Fluvastatin; Fractures, Bone; Heptanoic Acids; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Indoles; Liver; Lovastatin; Osteogenesis; Osteoporosis; Pharmacokinetics; Pravastatin; Pyridines; Pyrimidines; Pyrroles; Quinolines; Rosuvastatin Calcium; Simvastatin; Sulfonamides

2006

Trials

1 trial(s) available for pitavastatin and Osteoporosis

ArticleYear
Short-term effects of pitavastatin on biochemical markers of bone turnover in patients with hypercholesterolemia.
    Internal medicine (Tokyo, Japan), 2007, Volume: 46, Issue:24

    No consensus has been reached whether clinical use of statins has beneficial effects on bone health, partly due to lower statin concentrations because of first-pass metabolism by the liver. We thus evaluated the effects of pitavastatin, which does not undergo first-pass metabolism, on bone metabolism.. According to the therapeutic regimen, the subjects were divided into two groups (group A, 66 with pitavastatin; group B, 35 without pitavastatin). Bone-specific alkaline phosphatase (BAP) and serum N-terminal telopeptide of type I collagen (NTx) as bone turnover markers (BTMs) were compared between the two groups and between at baseline and after 3 months of treatment in each group. Correlations between baseline characteristics and deltaBTMs, and between delta lipid profile and deltaBTMs were investigated using both Pearson's correlation analysis and multivariate analysis.. The subjects were 101 patients with untreated hypercholesterolemia.. After 3 months of treatment, BAP in group A did not change significantly compared with either the baseline value or that in group B. However, NTx in group A significantly decreased compared with both the baseline value and that in group B. In addition, deltaNTx was negatively correlated with NTx at baseline, and the significance of this correlation persisted after multiple regression analysis.. Our findings suggest that pitavastatin may have potentially beneficial effects on bone metabolism primarily by reducing bone resorption rather than by stimulating bone formation. Further studies with more patients and longer duration are warranted to evaluate its effects, if any, on prevention of osteoporosis and subsequent fractures.

    Topics: Adult; Aged; Alkaline Phosphatase; Biomarkers; Bone and Bones; Bone Resorption; Collagen Type I; Enzyme Inhibitors; Female; Humans; Hypercholesterolemia; Male; Middle Aged; Multivariate Analysis; Osteogenesis; Osteoporosis; Peptides; Prospective Studies; Quinolines; Time Factors

2007

Other Studies

2 other study(ies) available for pitavastatin and Osteoporosis

ArticleYear
Pitavastatin prevents ovariectomy-induced osteoporosis by regulating osteoclastic resorption and osteoblastic formation.
    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2021, Volume: 139

    Excessive osteoclast activity, along with relatively weak osteoblast function, is strongly associated with bone disease. Therefore, studies to identify novel anti-osteoporosis candidates with dual actions of inhibiting osteoclastogenesis and increasing osteoblastogenesis may provide an ideal approach for treating osteoporosis. Pitavastatin, an inhibitor of 3-hydroxy-3 methyl-glutaryl coenzyme A reductase, has demonstrated various pharmacological activities, including anti-inflammation, bone anabolic effects, vasodilation, and inhibition of revascularization; however, the precise effects and mechanisms of pitavastatin on the regulation of osteoblast and osteoclast activity need to be comprehensively elucidated. Herein, we demonstrated that pitavastatin is a potential candidate for treating osteoporosis by enhancing osteoblast differentiation and bone growth and inhibiting osteoclast differentiation and bone resorption. Pitavastatin exerted dose-dependent inhibitory effects on receptor activator of nuclear factor kappa-B ligand-induced osteoclast formation, bone resorption, and osteoclast-specific marker gene expression. These inhibitory effects were achieved by inhibiting the Akt, NF-κB, and mitogen-activated protein kinase (p38, ERK, and JNK) signaling pathways, resulting in the downregulation of major transcription factors c-Fos and NFATc1. Furthermore, pitavastatin potentially stimulated osteoblast differentiation by activating alkaline phosphatase (ALP), enhancing mineralization by Alizarin Red S, and increasing the expression of osteoblastogenic marker genes such as runt-related transcription factor 2, ALP, osteocalcin, and collagen type 1 alpha. Furthermore, we evaluated the therapeutic potential of pitavastatin in ovariectomy-induced systematic bone loss based on micro-computed tomography and histological analysis of femurs. Our findings demonstrated a new function and mechanism for pitavastatin in bone remodeling, indicating its potential as a therapeutic candidate in treating osteoporosis by inhibiting osteoclastic resorption and promoting osteoblastic formation.

    Topics: Animals; Biomarkers; Bone Remodeling; Bone Resorption; Cell Differentiation; Female; Femur; Male; Mice, Inbred C57BL; Mice, Inbred ICR; Osteoblasts; Osteoclasts; Osteogenesis; Osteoporosis; Ovariectomy; Quinolines; Signal Transduction

2021
Role of Pitavastatin in Prevention of Osteopenic Changes in Ovariectomized Rats.
    Journal of the College of Physicians and Surgeons--Pakistan : JCPSP, 2016, Volume: 26, Issue:1

    To determine the effect of pitavastatin, a third generation statin, on development of osteopenia in ovariectomized rats.. Experimental study.. Department of Pharmacology, Basic Medical Sciences Institute, Jinnah Postgraduate Medical Center, Karachi, from January to July 2013.. Forty female Sprague Dawley rats were divided into ovariectomized (OVX), Sham OVX and OVX given pitavastatin 0.4 mg/kg/day, 0.8 mg/kg/day, for 8 weeks. Bone density measurements using CT scan and Archimedes’ principle were made on femora and tibiae. Blood samples were analyzed for acid phosphatase (ACP) and alkaline phosphatase (ALP) levels.. Ovariectomy-induced osteopenic changes were indicated by significant decrease in bone densities and Hounsfield (HU) index of distal femoral and proximal tibial metaphyses and elevation of ACP and ALP levels. 0.4 mg/kg pitavastatin did not significantly alter the evaluated parameters. 0.8 mg/kg produced a restoration of HU of lower femur and femoral density comparable to Sham. HU of upper tibia and tibial density following 0.8 mg/kg was significantly higher than OVX but was not approximate to Sham. ALP and ACP with 0.8 mg/kg were comparable to Sham.. Supra-therapeutic dose of pitavastatin was effective in preventing estrogen deficiency-induced decrease in bone density of ovariectomized rates, over an 8-week period.

    Topics: Animals; Bone Density; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Osteoporosis; Ovariectomy; Quinolines; Rats; Rats, Sprague-Dawley

2016