Medication-induced osteoporosis

Weng, Meng Yi; Lane, Nancy E.

doi:10.1007/s11914-007-0008-y

Cited by 24 publications

(16 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These agents, however, have not been proved to significantly increase bone formation. Therefore, the ideal agent would not only improve bone strength by decreasing bone breakdown but also promote bone formation in the ultimate quest to prevent fractures [1].The decrease in bone volume associated with osteoporosis, age-related osteopenia, and other diseases is accompanied by an increase in marrow adipose tissue as seen following ovariectomy [2], immobilization [3], medication [4], aging [5], chronic obstructive pulmonary disease [6], and inflammatory cytokines such as tumor necrosis factor-a (TNF-a) that leads to bone loss [7]. TNF-a, a proinflammatory cytokine secreted by inflammatory cells, plays a key role in abnormal bone remodeling and inflammatory bone diseases.…”

Section: Introductionmentioning

confidence: 99%

Simvastatin attenuates TNF-α-induced growth inhibition and apoptosis in murine osteoblastic MC3T3-E1 cells

et al. 2009

View full text Add to dashboard Cite

Objective and design Tumor necrosis factor-a (TNF-a) is a proinflammatory cytokine that induces apoptosis in a number of cell systems, including osteoblasts. Simvastatin is a potent 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor known as a stimulator for bone formation via promoting osteoblast differentiation and mineralization. This study was designed to examine the role of simvastatin on TNF-a-induced growth inhibition and apoptosis in murine osteoblastic MC3T3-E1 cells. Materials and methods MC3T3-E1 cells were cultured in DMEM essential medium supplemented with 10% fetal bovine serum and antibiotics, and 3-(4,5-dimethylthiazol2yl-)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to evaluate cell viability. A trypan blue exclusion assay was used to determine the level of cytotoxicity. Hoechst staining for cells treated with TNF-a was visualized under a microscope equipped with an epifluorescence illumination. Apoptosis of MC3T3-E1 cells was further examined by flow cytometric analysis after Annexin V/7-AAD double staining.Results MC3T3-E1 cells exposed to low concentrations (10 -10 -10 -7 M) of simvastatin increased in both growth and viability. In contrast, high concentrations of simvastatin (10 -6 -10 -5 M) have no effect on growth and viability of MC3T3-E1 cells. TNF-a-induced decrease in cell viability and growth were antagonized by simvastatin in a concentration-dependent manner. MC3T3-E1 cells treated with TNF-a at 10 ng/ml showed typical pyknotic fragmented nuclei and apoptotic bodies assessed by Hoechst staining. Moreover, Annexin V/7-AAD double staining indicated that MC3T3-E1 cells treated with 10 ng/ml of TNF-a resulted in a significant increase of the proportion of apoptotic cells up to 39.5% of total cell population, and the proportion of apoptotic cells were dose-dependently decreased after simvastatin treatment (10 -10 -10 -7 M); the inhibitory rates were approximately 31.34, 48.5, 52.11, and 65.73%, respectively. Conclusions Our data demonstrate that simvastatin increases growth and viability of osteoblastic cells and decreases TNF-a-induced growth inhibition and apoptosis in murine osteoblastic MC3T3-E1 cells.

show abstract

Section: Introductionmentioning

confidence: 99%

Simvastatin attenuates TNF-α-induced growth inhibition and apoptosis in murine osteoblastic MC3T3-E1 cells

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Corticosteroids, anti-rheumatic drugs, cancer chemotherapeutic agents or even with osteoporosis medications can adversely affect bone [26,58,76,106]. These skeletal side effects should be considered when assessing a patient's fracture risk.…”

Section: Discussionmentioning

confidence: 99%

“…Many of these conditions affect more than one of the components of bone strength. For example, glucocorticoids not only increase bone turnover, resulting in increased bone resorption, but also affect mineral homeostasis by reducing calcium absorption and causing secondary hyperparathyroidism [44,106,109]. For the purpose of discussion, we categorized conditions affecting bone quality based on their impact to the most affected component of bone quality.…”

Section: Conditions and Diseases Affecting Bone Quality Besides Osteomentioning

confidence: 99%

“…Evidence shows daily doses of corticosteroids for less than 6 months can cause rapid bone loss [106], although the mechanism of bone loss from corticosteroids has not been fully elucidated. It is known that after several days of corticosteroid therapy, osteoclast and osteoblast activity and maturation are affected [5,58,106].…”

Section: The Effect Of Drugs On Bone Qualitymentioning

confidence: 99%

“…It is known that after several days of corticosteroid therapy, osteoclast and osteoblast activity and maturation are affected [5,58,106]. This results in less osteoblast to form bone.…”

Section: The Effect Of Drugs On Bone Qualitymentioning

confidence: 99%

See 2 more Smart Citations

Diseases Affecting Bone Quality: Beyond Osteoporosis

Unnanuntana

Rebolledo

Khair

et al. 2011

Clinical Orthopaedics &Amp; Related Research

View full text Add to dashboard Cite

Background Bone quantity, quality, and turnover contribute to whole bone strength. Although bone mineral density, or bone quantity, is associated with increased fracture risk, less is known about bone quality. Various conditions, including disorders of mineral homeostasis, disorders in bone remodeling, collagen disorders, and drugs, affect bone quality. Questions/purposes The objectives of this review are to (1) identify the conditions and diseases that could adversely affect bone quality besides osteoporosis, and (2) evaluate how these conditions influence bone quality. Methods We searched PubMed using the keywords ''causes'' combined with ''secondary osteoporosis'' or ''fragility fracture.'' After identifying 20 disorders/conditions, we subsequently searched each condition to evaluate its effect on bone quality. Results Many disorders or conditions have an effect on bone metabolism, leading to fragility fractures. These disorders include abnormalities that disrupt mineral homeostasis, lead to an alteration of the mineralization process, and ultimately reduce bone strength. The balance between bone formation and resorption is also essential to prevent microdamage accumulation and maintain proper material and structural integrity of the bone. As a result, diseases that alter the bone turnover process lead to a reduction of bone strength. Because Type I collagen is the most abundant protein found in bone, defects in Type I collagen can result in alterations of material property, ultimately leading to fragility fractures. Additionally, some medications can adversely affect bone. Conclusions Recognizing these conditions and diseases and understanding their etiology and pathogenesis is crucial for patient care and maintaining overall bone health.

show abstract

Fragility Fracture Incidence in Chronic Obstructive Pulmonary Disease (COPD) Patients Associates With Nanoporosity, Mineral/Matrix Ratio, and Pyridinoline Content at Actively Bone-Forming Trabecular Surfaces

Paschalis

Gamsjaeger

Dempster

et al. 2016

Journal of Bone and Mineral Research

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is associated with low areal bone mineral density (aBMD) by dual-energy X-ray absorptiometry (DXA) and altered microstructure by bone histomorphometry and micro-computed tomography. Nevertheless, not all COPD patients sustain fragility fractures. In the present study, we used Raman microspectroscopic analysis to determine bone compositional properties at actively forming trabecular surfaces (based on double fluorescent labels) in iliac crest biopsies from 19 postmenopausal COPD patients (aged 62.1 ± 7.3 years). Additionally, we analyzed trabecular geometrical centers, representing tissue much older than the forming surfaces. Eight of the patients had sustained fragility fractures, and 13 had received treatment with inhaled glucocorticoids. None of the patients had taken oral glucocorticoids. The monitored parameters were mineral/matrix ratio (MM), nanoporosity, and relative glycosaminoglycan (GAG), lipid, and pyridinoline contents (PYD). There were no significant differences between the glucocorticoid-treated patients and those who did not receive any. On the other hand, COPD patients sustaining fragility fractures had significantly lower nanoporosity and higher MM and PYD values compared with COPD patients without fragility fractures. To the best of our knowledge, this is the first study to discriminate between fracture and non-fracture COPD patients based on differences in the material properties of bone matrix. Given that these bone material compositional differences are evident close to the cement line (a major bone interface), they may contribute to the inferior bone toughness and coupled with the lower lumbar spine bone mineral density values result in the fragility fractures prevalent in these patients. © 2016 American Society for Bone and Mineral Research.

show abstract

Medication-induced osteoporosis

Cited by 24 publications

References 54 publications

Simvastatin attenuates TNF-α-induced growth inhibition and apoptosis in murine osteoblastic MC3T3-E1 cells

Simvastatin attenuates TNF-α-induced growth inhibition and apoptosis in murine osteoblastic MC3T3-E1 cells

Diseases Affecting Bone Quality: Beyond Osteoporosis

Fragility Fracture Incidence in Chronic Obstructive Pulmonary Disease (COPD) Patients Associates With Nanoporosity, Mineral/Matrix Ratio, and Pyridinoline Content at Actively Bone-Forming Trabecular Surfaces

Contact Info

Product

Resources

About