Animal models for glucocorticoid-induced postmenopausal osteoporosis: An updated review

Zhang, Zhida; Ren, Hui; Shen, Gengyang; Qiu, Ting; Liang, De; Yang, Zhidong; Yao, Zhensong; Tang, Jingjing; Wei, Qiushi

doi:10.1016/j.biopha.2016.09.045

Cited by 38 publications

(21 citation statements)

References 111 publications

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“…Osteoporosis is a chronic systemic skeletal disorder, characterized by bone mass reduction, microarchitectural deterioration, and raised fragility and delicacy. Consequently, the risk of bone fractures is altogether expanded leading to disability, significant morbidity and increased mortality (2)(3)(4). Generalized osteoporosis is classified into primary and secondary.…”

Section: Introductionmentioning

confidence: 99%

Effect of Bisphosphonates on the Alveolar Bone of Rats With Glucocorticoids Induced Osteoporosis

Sherif

Masry

Kawana

et al. 2019

Alexandria Dental Journal

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INTRODUCTION: Bone is a unique tissue that undergoes frequent remodeling. An imbalance between bone formation and resorption results in osteoporosis. Glucocorticoids (GCs) are widely used clinically as anti-inflammatory and immunomodulatory. However, their prolonged use may induce osteoporosis. Currently, evidences revealed that also the alveolar processes are subject to osteoporosis. Bisphosphonates, such as Alendronate, Risedronate and Zoledronate, are recommended by several international guidelines as the first-line therapy for the prevention and treatment of generalized glucocorticoids induced osteoporosis (GIOP). OBJECTIVES: To evaluate the effect of bisphosphonates (Risedronate) on the alveolar bone of rats with glucocorticoids induced osteoporosis. MATERIALS AND METHODS: Thirty female albino rats were divided into 3 equal groups (10 rats each) as follows: Group I: control group. Group II: glucocorticoids group (Dexamethasone 0.6mg/kg twice/week subcutaneously). Group III: Risedronate treated group; rats were given Dexamethasone (0.6mg/kg twice/week subcutaneously) and Risedronate (1mg/kg/day orally). After 12 weeks, rats were euthanized, and the mandibular alveolar bone was evaluated histologically by light microscope and ultra-structurally by scanning electron microscopy and energy dispersive X-ray (EDX) microanalysis. RESULTS: Group II showed deterioration of the alveolar bone in comparison to the control group I. The alveolar bone structure in Group III rats, treated by bisphosphonates (Risedronate), showed remarkable improvement both histologically and ultrastructurally in comparison to group II. Moreover, EDX analysis revealed a significant decrease of calcium levels in group II in comparison to group I. However, in group III calcium levels were restored to normal levels comparable to the control group I. CONCLUSIONS: Glucocorticoids intake induces loss of the alveolar bone; which, could be counterbalanced by bisphosphonates.

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Section: Introductionmentioning

confidence: 99%

Effect of Bisphosphonates on the Alveolar Bone of Rats With Glucocorticoids Induced Osteoporosis

Sherif

Masry

Kawana

et al. 2019

Alexandria Dental Journal

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“…In previous reports, a combination OD rat model was used. However, the high deterioration observed in the animals, the risk of induced additional disorders on the skeletal and the fact that bone loss reverses after corticoid stop [33] justify the bone histological study of the different treatment, in order to simplify the model and improve animal welfare. In general, OP condition is established through the analysis of long bones and lumbar spine but few data of the effect on the calvaria of the animals used as OP models are available [34].…”

Section: Discussionmentioning

confidence: 99%

PLGA-BMP-2 and PLA-17β-Estradiol Microspheres Reinforcing a Composite Hydrogel for Bone Regeneration in Osteoporosis

et al. 2019

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The controlled release of active substances—bone morphogenetic protein 2 (BMP-2) and 17β-estradiol—is one of the main aspects to be taken into account to successfully regenerate a tissue defect. In this study, BMP-2- and 17β-estradiol-loaded microspheres were combined in a sandwich-like system formed by a hydrogel core composed of chitosan (CHT) collagen, 2-hidroxipropil γ-ciclodextrin (HP-γ-CD), nanoparticles of hydroxyapatite (nano-HAP), and an electrospun mesh shell prepared with two external electrospinning films for the regeneration of a critical bone defect in osteoporotic rats. Microspheres were made with poly-lactide-co-glycolide (PLGA) to encapsulate BMP-2, whereas the different formulations of 17β-estradiol were prepared with poly-lactic acid (PLA) and PLGA. The in vitro and in vivo BMP-2 delivered from the system fitted a biphasic profile. Although the in vivo burst effect was higher than in vitro the second phases (lasted up to 6 weeks) were parallel, the release rate ranged between 55 and 70 ng/day. The in vitro release kinetics of the 17β-estradiol dissolved in the polymeric matrix of the microspheres depended on the partition coefficient. The 17β-estradiol was slowly released from the core system using an aqueous release medium (Deff = 5.58·10−16 ± 9.81·10−17m2s−1) and very fast in MeOH-water (50:50). The hydrogel core system was injectable, and approximately 83% of the loaded dose is uniformly discharged through a 20G needle. The system placed in the defect was easily adapted to the defect shape and after 12 weeks approximately 50% of the defect was refilled by new tissue. None differences were observed between the osteoporotic and non-osteoporotic groups. Despite the role of 17β-estradiol on the bone remodeling process, the obtained results in this study suggest that the observed regeneration was only due to the controlled rate released of BMP-2 from the PLGA microspheres.

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“…Ввиду недостаточной эффективности доступных методов диагностики и лечения ГКО патофизиология воздействия глюкокортикостероидов на костную ткань остается предметом исследований. Наиболее часто изучение ГКО производится на модели грызунов, которая, однако, имеет некоторые ограничения, основным из которых является отсутствие изменения губчатой костной ткани у мышей [4], когда именно ее потеря обусловливает наиболее частые переломы тел позвонков у людей в условиях гиперкортицизма [5]. При болезни Иценко−Кушинга из-за постоянно повышенного уровня эндогенного кортизола возникают аналогичные изменения в костной ткани, как и при длительном введении супрафизиологичных доз глюкокортикостероидов [5,6].…”

Section: актуальные вопросы эндокринологии обоснованиеunclassified

Wnt10b and Wnt3a AS BIOMARKERS OF CHANGES IN THE REGULATION OF BONE METABOLISM IN PATIENTS WITH CUSHING’S DISEASE

et al. 2018

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Background: Endogenous hypercortisolism due to Cushing’s disease (CD) is complicated by low-traumatic fractures in 50% of cases. Modern technologies allow to study pathogenetic changes in the regulation of bone remodeling in hypercortisolism and to offer new serum biomarkers.Aims: To evaluate levels of Wnt proteins related to bone remodeling regulation in serum samples from patients with CD.Materials and methods: Fasting serum samples were taken and stored in aliquot at ≤-80 °C from 42 consecutive subjects with clinically evident and biochemically confirmed active CD and 42 healthy volunteers matched by age, sex and body mass index (BMI). Evaluation of the levels of Wnt proteins (Wnt3a, Wnt10b) was measured by immunochemiluminescence assay using the WNT3a SEL818Hu (USCN) and the WNT10b SEP553Hu (USCN). Twenty-four hours urine free cortisol (24hUFC) (60−413 nmol/24h) and bone turnover markers was measured by electrochemiluminescence assay on a Cobas 6000 Module e601 (Roche). At the time of enrollment all participants were questioned regarding any low traumatic fractures for the period of the disease. Patients underwent standard spinal radiographs in anterior-posterior and lateral positions of the vertebrae Th4−L4 (Axiom Icons R200 Siemens).Results: The median (Ме Q25; Q75) age of patients with CD was 33 (21; 43) years with no difference among the groups, p=0.936; BMI ― 29 (23; 34) kg/m2, p=0.094 and without differences by sex, p=0.254. The median 24hUFC in subjects with CD ― 825 (301; 2077) nmol/24h was significantly higher as compared to the control group (p0.001). We report increased levels of Wnt3a and Wnt10b in patients with CD: Wnt3а 0.15 (0.04; 0.23) ng/ml in patients with CD vs 0,04 (0.01; 0.13) ng/ml in control group (p=0.017) and Wnt10b 2621 (2226; 3688) pg/ml vs 1917 (1721; 2549) pg/ml (p=0.008).Conclusions: The serum level of Wnt3a and Wnt10b reflects the intensity of Wnt-signaling dysregulation, and therefore they may be considered as biomarkers of bone remodeling deterioration in hypercortisolism.

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Animal models for glucocorticoid-induced postmenopausal osteoporosis: An updated review

Cited by 38 publications

References 111 publications

Effect of Bisphosphonates on the Alveolar Bone of Rats With Glucocorticoids Induced Osteoporosis

Effect of Bisphosphonates on the Alveolar Bone of Rats With Glucocorticoids Induced Osteoporosis

PLGA-BMP-2 and PLA-17β-Estradiol Microspheres Reinforcing a Composite Hydrogel for Bone Regeneration in Osteoporosis

Wnt10b and Wnt3a AS BIOMARKERS OF CHANGES IN THE REGULATION OF BONE METABOLISM IN PATIENTS WITH CUSHING’S DISEASE

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