DOCSLIB.ORG

Free PDF Download

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Free PDF Download European Review for Medical and Pharmacological Sciences 2018; 22: 4669-4676 Ipriflavone promotes osteogenesis of MSCs derived from osteoporotic rats A.-G. GAO1,2, Y.-C. ZHOU2, Z.-J. HU2, B.-B. LU2 1Department of Orthopedics, The First Affiliated Hospital Of Soochow University, Suzhou, China 2Department of Orthopedics, Wuxi People’s Hospital Affiliated to Nanjing Medical University, Wuxi, China Abstract. – OBJECTIVE: To explore whether celerated bone resorption, bone mass decrease, Ipriflavone could prevent postmenopausal oste- microstructure destruction and bone fragility oporosis (PMOP) and improve bone quality via elevation, thus eventually leading to high risk of promoting osteogenesis of bone marrow-de- fracture5. Therefore, PMOP is a serious problem rived mesenchymal stem cell (MSCs). 6 MATERIALS AND METHODS: MSCs were ex- that poses a great challenge in public health . In tracted from rats and identified using flow cy- recent years, hormone replacement therapy and tometry. Osteogenic specific genes and adipo- calcitonin intervention are the main treatments genic specific genes in MSCs were detected by for PMOP7. However, the long-term use of es- quantitative Real-time polymerase chain reac- trogen significantly increases the prevalence of tion (qRT-PCR). The effect of Ipriflavone on os- endometrial cancer and breast cancer8. Besides, teogenesis was detected by CCK-8 (cell count- the long-term use of calcitonin injection is incon- ing kit-8) assay, ALP activity detection, alizarin 3 red staining and Western blot, respectively. Fur- venient and expensive . Currently, Ipriflavone has thermore, ovariectomized PMOP rat model was been well recognized since it could effectively constructed. The effects of Ipriflavone on osteo- prevent PMOP9,10. genesis, BMD and bone biomechanical proper- Ipriflavone is a phytoestrogenic drug derived ties of ovariectomized rats were detected. from isoflavones. However, Ipriflavone has no es- RESULTS: MSCs derived from ovariectomized trogenic effect in the human body11. It has been rats exerted multiple differentiation potentials. shown that Ipriflavone can directly act on the CCK-8 assay indicated that 0.8 μM Ipriflavone 12 were the maximal dose that did not affect MSCs bone and inhibits bone resorption . Meanwhile, proliferation, which was selected for the follow- Ipriflavone stimulates calcitonin release from the ing experiments. In vitro researches demonstrat- thyroid gland, thereby exerting therapeutic ef- ed that Ipriflavone remarkably promoted MSCs fects as estrogen and calcitonin but without their osteogenesis. In vivo results indicated that side effects13. Therefore, Ipriflavone has a promis- BMD, BV/TV, Tb.N and Tb.Th were decreased in ovariectomized rats than those of rats in sh- ing prospect in preventing PMOP. am group. Ipriflavone treatment remarkably pre- In this study, we constructed ovariectomized vented osteoporosis via promoting MSCs osteo- rat model of PMOP to observe the effect of Ipri- genesis in ovariectomized rats. flavone on MSCs differentiation, BMD, and bone CONCLUSIONS: Ipriflavone prevents post- biomechanical properties. Our results provide menopausal osteoporosis, improves bone quali- solid basis for the better application of Ipriflavone ty and protects bone tissue via promoting MSCs in clinical prevention and treatment of PMOP. osteogenesis. Key Words: Ipriflavone, MSCs, Osteogenesis, Osteoporosis. Materials and Methods Isolation and Culture of MSCs Introduction 3-month-old female Sprague Dawley (SD) rats weighing from 280-300 g were obtained Postmenopausal osteoporosis (PMOP) is a from the Model Animal Research Center of common disease in postmenopausal women1, Nanjing University. After one-week adaptive which is manifested as ovarian dysfunction2 and feeding, rats were randomly assigned into reduced estrogen secretion3,4. PMOP leads to ac- sham group, ovariectomy group (OVX group) Corresponding Author: Aiguo Gao, MM; e-mail: [email protected] 4669 A.-G. Gao, Y.-C. Zhou, Z.-J. Hu, B.-B. Lu and ovariectomy + Ipriflavone treatment group Lipid Differentiation of MSCs (OVX + Ipriflavone group), with 20 rats in each Third-passage MSCs were seeded in the 6-well group. 8 weeks later, rats were sacrificed with plates at a density of 2.0×104 per well. Lipid differen- dislocation of cervical vertebra. The femur tiation was induced by α-MEM supplemented with and tibia were collected under aseptic condi- 0.5 mmol/L 3-isobutyl-1-methylxanthine (IBMX), tion, washed with 75% ethanol for 10-30 s and 5 mg/L insulin and 1 μmol/L dexamethasone for 3 D-Hanks solution for 5-8 times. The marrow days. On the 4th day, MSCs were cultured with Dul- cavity was washed with α-MEM (α-Modified becco’s Modified Eagle Medium (DMEM) contain- Eagle Medium) containing 10% fetal bovine ing 5 mg/L insulin for a total of 14-21 d. serum (FBS). After centrifugation at 1000 r/ min for 5 min, MSCs were re-suspended inα- RNA Extraction and qRT-PCR MEM and maintained in a 5% CO2 incubator (Quantitative Real-Time Polymerase at 37°C (Gibco, Rockville, MD, USA). MSCs Chain Reaction) were then seeded in 6-well plates at a density of The TRIzol kit (Invitrogen, Carlsbad, CA, 1.0×10 9/L. Half of culture medium was replaced USA) was used to extract the total RNA, fol- 24 h later and total medium was replaced after lowed by reverse transcription into complemen- 48 h. Third-passage MSCs were collected for tary Deoxyribose Nucleic Acid (cDNA). QRT- the following studies. All animal experiments PCR was performed to detect the expressions of were approved by The First Affiliated Hospital related genes according to the instructions of 2 of Soochow University Ethics Committee. × SYBR Green PCR MasterMix (Thermo Fisher Scientific, Waltham, MA, USA). PCR reaction Ovariectomized PMOP Rat Model was performed as follows: denaturalization at Rats were anesthetized with intraperitoneal in- 95°C for 15 s, extension at 60°C for 15 s and an- jection of 1% pentobarbital sodium (4 mL/kg) and nealing at 72°C for 32 s, for a total of 40 cycles. placed on the surgical table. A midline incision Each experiment was repeated in triplicate. The was cut to expose the abdominal cavity. Bilateral relative gene expression was calculated as 2ΔΔCt. ovariectomy was performed in rats of OVX group Primers used in the study were: ALP, F: 5’-TTC- and OVX + Ipriflavone group. The abdominal CACAACAGGCCACTTACT-3’, R: 5’-GAG- cavity was sutured layer by layer. Rats in sham CATCTCTGCTTGTCTATCTG-3’; Bglap, F: group were only cut with a small piece of adipose 5’-CACTCCTCGCCCTATTGGC-3’, R: 5’-CCCTCCT- tissue near the ovary. All rats recovered well after GCTTGGACACAAAG-3’; RUNX2, F: 5’-TG- the procedures. GTTACTGTCATGGCGGGTA-3’, R: 5’-TCT- CAGATCGTTGAACCTTGCTA-3’; PPARG, F: MSCs Identification 5’-GGGATCAGCTCCGTGGATCT-3’, R: 5’-TG- MSCs identification was performed using flow CACTTTGGTACTCTTGAAGTT-3’; CEBPA, cytometry. In brief, MSCs were resuspended in F:5’- CCGCCTCAGTGATTTAGGGC-3’, R: PBS (phosphate-buffered saline) at a density of 5’-GGGTCTGTAATCTGACTCTGTCC-3’; KLF5, 1.0×10 6/mL. After washing with PBS twice, 500 F: 5’-TCAGTCGTAGACCAGTTCTTCA-3’, R: μL of suspension were incubated with 5 μL of 5’-CTGGGATTTGTAGAGGCCAGT-3’; GAP- CD45 and CD73 at room temperature without DH, F: 5’- ACCCACTCCTCCACCTTTGA-3’, light for 30 min. After PBS washing for three R: 5’-CTGTTGCTGTAGCCAAATTCGT-3’. times, cells were centrifuged and resuspended in 500 μL of PBS, followed by flow cytometric CCK-8 (Cell Counting Kit-8) Assay detection. MSCs treated with different doses of Iprifla- vone were seeded in the 96-well plates at a density Osteogenic Differentiation of MSCs of 1.0×10 4 per well. After culturing for 24 h, 10 μL Third-passage MSCs were seeded in the 6-well of CCK-8 solution (Dojindo, Kumamoto, Japan) plates at a density of 2.0×104 per well. After the were added into each well. The absorbance values cell confluence was up to 70-80%, osteogenic dif- at the wavelength of 450 nm were detected by the ferentiation was induced by α-MEM containing microplate reader (Bio-Rad, Hercules, CA, USA). 10 mmol/L sodium β-glycerophosphate, 50 μg/ mL Vitamin C, 10 μmol/L dexamethasone and ALP Activity Detection 100 mL/L FBS. Culture medium was replaced MSCs were seeded in the 6-well plates at a every 3 days for a total of 14-21 d. dose of 1.0×108/L. Each group had 6 replicates. 4670 Ipriflavone promotes osteogenesis of MSCs derived from osteoporotic rats After cell culture with serum-free α-MEM for 24 volume/total volume), Tb.N (trabecular number) h, complete α-MEM supplemented with different and Tb.Th (trabecular thickness). doses of Ipriflavone was added into each well. 72 h later, cells were washed with D-Hanks and in- Statistical Analysis cubated with 1 mL of lysate at 4°C for 30 min. We used Statistical Product and Service Solu- ALP activity was then detected according to the tions (SPSS) 19.0 software (IBM, Armonk, NY, instructions of the commercial kit. USA) for statistical analysis. The quantitative data were represented as mean ± standard devi- Western Blot ation (x–±s). The t-test was used for comparing The total protein of MSCs was extracted by differences between the two groups. p<0.05 was the radioimmunoprecipitation assay (RIPA) ly- considered statistically significant. sate (Yeasen, Shanghai, China). The concentra- tion of each protein sample was determined by a BCA (bicinchoninic acid) kit (Abcam, Cam- Results bridge, MA, USA). Briefly, total protein was se- parated by a 12% SDS-PAGE (sodium dodecyl Identification of MSCs Purity and sulphate-polyacrylamide gel electrophoresis) gel Multiple Differentiation Potential under denaturing conditions and transferred to Elongated MSCs were observed using a micro- PVDF (polyvinylidene difluoride) membranes scope. The typical morphology of MSCs on the 2nd (Merck Millipore, Billerica, MA, USA). Mem- and 3rd day were shown in Figure 1A. Third-pas- branes were blocked with 5% skimmed milk sage MSCs were collected for surface antigen for 1 h, followed by the incubation of specific identification.
Load more

Recommended publications
  • Ipriflavone in the Treatment of Postmenopausal Osteoporosis a Randomized Controlled Trial
    ORIGINAL CONTRIBUTION Ipriflavone in the Treatment of Postmenopausal Osteoporosis A Randomized Controlled Trial Peter Alexandersen, MD Context Data on the efficacy and safety of ipriflavone for prevention of postmeno- Anne Toussaint, MD pausal bone loss are conflicting. Claus Christiansen, MD, PhD Objectives To investigate the effect of oral ipriflavone on prevention of postmeno- pausal bone loss and to assess the safety profile of long-term treatment with iprifla- Jean-Pierre Devogelaer, MD, PhD vone in postmenopausal osteoporotic women. Christian Roux, MD, PhD Design and Setting Prospective, randomized, double-blind, placebo-controlled, 4-year Jacques Fechtenbaum, MD, PhD study conducted in 4 centers in Belgium, Denmark, and Italy from August 1994 to July 1998. Carlo Gennari, MD, PhD Participants Four hundred seventy-four postmenopausal white women, aged 45 Jean Yves Reginster, MD, PhD to 75 years, with bone mineral densities (BMDs) of less than 0.86 g/cm2. for the Ipriflavone Multicenter Interventions Patients were randomly assigned to receive ipriflavone, 200 mg 3 times European Fracture Study per day (n = 234), or placebo (n = 240); all received 500 mg/d of calcium. TUDIES OF IPRIFLAVONE, A SYN- Main Outcome Measures Efficacy measures included spine, hip, and forearm BMD thetic isoflavone derivative, have and biochemical markers of bone resorption (urinary hydroxyproline corrected for cre- atinine and urinary CrossLaps [Osteometer Biotech, Herlev, Denmark] corrected for suggested that it inhibits bone re- creatinine), assessed every 6 months. Laboratory safety measures and adverse events sorption and stimulates osteo- were recorded every 3 months. Sblast activity in vitro in cell cultures1,2 and Results Based on intent-to-treat analysis, after 36 months of treatment, the annual in vivo in experimental models of osteo- 3 percentage change from baseline in BMD of the lumbar spine for ipriflavone vs pla- porosis.
    [Show full text]
  • Botanicals in Postmenopausal Osteoporosis
    nutrients Review Botanicals in Postmenopausal Osteoporosis Wojciech Słupski, Paulina Jawie ´nand Beata Nowak * Department of Pharmacology, Wroclaw Medical University, ul. J. Mikulicza-Radeckiego 2, 50-345 Wrocław, Poland; [email protected] (W.S.); [email protected] (P.J.) * Correspondence: [email protected]; Tel.: +48-607-924-471 Abstract: Osteoporosis is a systemic bone disease characterized by reduced bone mass and the deterioration of bone microarchitecture leading to bone fragility and an increased risk of fractures. Conventional anti-osteoporotic pharmaceutics are effective in the treatment and prophylaxis of osteoporosis, however they are associated with various side effects that push many women into seeking botanicals as an alternative therapy. Traditional folk medicine is a rich source of bioactive compounds waiting for discovery and investigation that might be used in those patients, and therefore botanicals have recently received increasing attention. The aim of this review of literature is to present the comprehensive information about plant-derived compounds that might be used to maintain bone health in perimenopausal and postmenopausal females. Keywords: osteoporosis; menopause; botanicals; herbs 1. Introduction Women’s health and quality of life is modulated and affected strongly by hormone status. An oestrogen level that changes dramatically throughout life determines the Citation: Słupski, W.; Jawie´n,P.; development of women’s age-associated diseases. Age-associated hormonal imbalance Nowak, B. Botanicals in and oestrogen deficiency are involved in the pathogenesis of various diseases, e.g., obesity, Postmenopausal Osteoporosis. autoimmune disease and osteoporosis. Many female patients look for natural biological Nutrients 2021, 13, 1609. https:// products deeply rooted in folk medicine as an alternative to conventional pharmaceutics doi.org/10.3390/nu13051609 used as the prophylaxis of perimenopausal health disturbances.
    [Show full text]
  • Nutriceuticals: Over-The-Counter Products and Osteoporosis
    serum calcium levels are too low, and adequate calcium is not provided by the diet, calcium is taken from bone. Osteoporosis: Clinical Updates Long- term dietary calcium deficiency is a known risk Osteoporosis Clinical Updates is a publication of the National factor for osteo porosis. The recommended daily cal- Osteoporosis Foundation (NOF). Use and reproduction of this publication for educational purposes is permitted and cium intake from diet and supplements combined is encouraged without permission, with proper citation. This 1000 mg/day for people aged 19 to 50 and 1200 mg/ publication may not be used for commercial gain. NOF is a day for people older than 50. For all ages, the tolerable non-profit, 501(c)(3) educational organization. Suggested upper limit is 2500 mg calcium per day. citation: National Osteoporosis Foundation. Osteoporosis Clinical Updates. Issue Title. Washington, DC; Year. Adequate calcium intake is necessary for attaining peak bone mass in early life (until about age 30) and for Please direct all inquiries to: National Osteoporosis slowing the rate of bone loss in later life.3 Although Foundation 1150 17th Street NW Washington, DC 20037, calcium alone (or with vitamin D) has not been shown USA Phone: 1 (202) 223-2226 to prevent estrogen-related bone loss, multiple stud- Fax: 1 (202) 223-1726 www.nof.org ies have found calcium consumption between 650 mg Statement of Educational Purpose and over 1400 mg/day reduces bone loss and increases Osteoporosis Clinical Updates is published to improve lumbar spine BMD.4-6 osteoporosis patient care by providing clinicians with state-of-the-art information and pragmatic strategies on How to take calcium supplements: prevention, diagnosis, and treatment that they may apply in Take calcium supplements with food.
    [Show full text]
  • Ipriflavone: an Important Bone-Building Isoflavone
    Ipriflavone: An Important Bone-Building Isoflavone Kathleen A. Head, N.D. Abstract Ipriflavone, an isoflavone synthesized from the soy isoflavone daidzein, holds great promise in the prevention and treatment of osteoporosis and other metabolic bone diseases. It has been widely studied in humans and found effective for inhibiting bone resorption and enhancing bone formation, the net result being an increase in bone density and a decrease in fracture rates in osteoporotic women. While ipriflavone appears to enhance estrogen’s effect, it does not possess intrinsic estrogenic activity, making it an attractive adjunct or alternative to conventional hormone replacement therapy. Preliminary studies have also found ipriflavone effective in preventing bone loss associated with chronic steroid use, immobility, ovariectomy, renal osteodystro- phy, and gonadotrophin hormone-releasing hormone agonists. In addition, it holds prom- ise for the treatment of other metabolic diseases affecting the bones, including Paget’s disease of the bone, hyperparathyroidism, and tinnitus caused by otosclerosis. (Altern Med Rev 1999;4(1):10-22) Introduction Ipriflavone (chemical structure: 7-isopropoxyisoflavone), derived from the soy isoflavone, daidzein, holds great promise for osteoporosis prevention and treatment (see Figure 1). Ipriflavone (IP) was discovered in the 1930s but has only recently begun to be embraced by the medical community in this country. Over 150 studies on safety and effective- ness, both animal and human, have been conducted in Italy, Hungary, and Japan. As of 1997, 2,769 patients had been treated a total of 3,132 patient years.1 Pharmacokinetics IP is metabolized mainly in the liver and excreted in the urine. Food appears to enhance its absorption.
    [Show full text]
  • PRODUCT MONOGRAPH Pr Zoledronic Acid
    PRODUCT MONOGRAPH Pr Zoledronic Acid - A (zoledronic acid injection) 5 mg/100 mL solution for intravenous infusion Bone Metabolism Regulator Sandoz Canada Inc. Date of Revision: 145 Jules-Léger June 01, 2016 Boucherville, QC, Canada J4B 7K8 Control No. : TBD Zoledronic Acid – A Page 1 of 62 Table of Contents PART I: HEALTH PROFESSIONAL INFORMATION ............................................................ 3 SUMMARY PRODUCT INFORMATION ........................................................................... 3 INDICATIONS AND CLINICAL USE ................................................................................. 3 CONTRAINDICATIONS ....................................................................................................... 4 WARNINGS AND PRECAUTIONS ..................................................................................... 4 ADVERSE REACTIONS ..................................................................................................... 10 DOSAGE AND ADMINISTRATION ................................................................................. 25 OVERDOSAGE ..................................................................................................................... 27 ACTION AND CLINICAL PHARMACOLOGY............................................................... 27 STORAGE AND STABILITY ............................................................................................. 30 SPECIAL HANDLING INSTRUCTIONS .......................................................................... 30
    [Show full text]
  • Current and Potential Future Drug Treatments for Osteoporosis
    700 Annals ofthe Rheumatic Diseases 1996;55:700-714 REVIEW Ann Rheum Dis: first published as 10.1136/ard.55.10.700 on 1 October 1996. Downloaded from Current and potential future drug treatments for osteoporosis Sanjeev Patel Osteoporosis is the most common metabolic ture risk increases by a factor of 1.5 to 3.0.6 bone disease in the developed world and is Other determinants of osteoporotic fracture increasingly recognised as an important public are shown in table 1. health problem.' There is marked worldwide Drugs active on bone can be simplistically variation in its incidence. It is predicted that classified as those that inhibit bone resorption the incidence of hip fractures caused by or those that stimulate bone formation (table osteoporosis will increase, particularly in 2). The effects of these drugs on bone mineral developing countries.2 The human burden of density are summarised in fig 1. Drugs that osteoporosis is considerable, with increased stimulate bone formation lead to a direct morbidity and mortality, especially following increase in bone mineral density, whereas those osteoporotic hip fractures.' The current finan- that inhibit bone resorption result in limited cial burden is substantial, with estimated yearly increases in bone mineral density by costs of £750 million in the UK,' $10 billion in uncoupling bone turnover and allowing forma- the USA, and FF3.7 billion in France.3 The tion to continue in excess of resorption. This ability to measure bone mineral density and leads to an increase in bone mineral density thereby monitor response to intervention has due to filling in of the remodelling space (the been vital in the development ofpharmacologi- remodelling transient).7 It has been suggested cal treatments.
    [Show full text]
  • [Product Monograph Template
    PRODUCT MONOGRAPH Pr ZOLEDRONIC ACID INJECTION 5 mg / 100 mL zoledronic acid (as zoledronic acid monohydrate) Solution for intravenous infusion Bone Metabolism Regulator Manufacturer: Dr. Reddy’s Laboratories Limited Bachupally 500 090 – INDIA Imported/Distributed By: Date of Revision: August 1, 2019 Dr. Reddy’s Laboratories Canada Inc. Mississauga, ON L4W 4Y1 Canada Submission Control Number: 228238 1 Table of Contents PART I: HEALTH PROFESSIONAL INFORMATION ..................................................................... 3 SUMMARY PRODUCT INFORMATION .................................................................................... 3 INDICATIONS AND CLINICAL USE ......................................................................................... 3 CONTRAINDICATIONS ............................................................................................................... 4 WARNINGS AND PRECAUTIONS ............................................................................................. 4 ADVERSE REACTIONS ............................................................................................................. 10 DRUG INTERACTIONS.............................................................................................................. 24 DOSAGE AND ADMINISTRATION ......................................................................................... 25 OVERDOSAGE ............................................................................................................................ 27 ACTION AND CLINICAL
    [Show full text]
  • Clinical Practice Guidelines AMERICAN ASSOCIATION OF
    Clinical Practice Guidelines AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS/ AMERICAN COLLEGE OF ENDOCRINOLOGY CLINICAL PRACTICE GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS— 2020 UPDATE Pauline M. Camacho, MD, FACE1; Steven M. Petak, MD, JD, FACP, FCLM, MACE, CCD2; Neil Binkley, MD3; Dima L. Diab, MD, FACE, FACP, CCD4; Leslie S. Eldeiry, MD5; Azeez Farooki, MD6; Steven T. Harris, MD, FACP, FASBMR7; Daniel L. Hurley, MD, FACE8; Jennifer Kelly, DO, FACE9; E. Michael Lewiecki, MD, FACE, FACP, CCD10; Rachel Pessah-Pollack, MD, FACE11; Michael McClung, MD, FACP, FACE12; Sunil J. Wimalawansa, MD, PhD, MBA, FCCP, FACP, FRCP, DSc, FACE13; Nelson B. Watts, MD, FACP, CCD, FASBMR, MACE14 The American Association of Clinical Endocrinologists’ Medical Guidelines for Practice are systematically developed statements to assist health-care professionals in medical decision-making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflect the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. The presented recommendations may not be appropriate in all situations. Any decision by practitioners to apply these guidelines must be made considering local resources and individual patient circumstances.
    [Show full text]
  • AACE/ACE Guidelines AMERICAN ASSOCIATION of CLINICAL
    AACE/ACE Guidelines AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY CLINICAL PRACTICE GUIDELINES FOR THE DIAGNOSIS AND TREATMENT OF POSTMENOPAUSAL OSTEOPOROSIS — 2016 Pauline M. Camacho, MD, FACE; Steven M. Petak, MD, MACE, FACP, FCLM, JD; Neil Binkley, MD; Bart L. Clarke, MD, FACP, FACE; Steven T. Harris, MD, FACP Daniel L. Hurley, MD, FACE; Michael Kleerekoper, MBBS, MACE; E. Michael Lewiecki, MD, FACP, FACE; Paul D. Miller, MD; Harmeet S. Narula, MD, FACP, FACE; Rachel Pessah-Pollack, MD, FACE; Vin Tangpricha, MD, PhD, FACE; Sunil J. Wimalawansa, MD, PhD, MBA, FCCP, FACP, FRCP, DSc, FACE; Nelson B. Watts, MD, FACP, MACE The American Association of Clinical Endocrinologists/American College of Endocrinology Medical Guidelines for Practice are systematically developed statements to assist healthcare professionals in medical decision-making for specific clinical conditions. Most of the content herein is based on literature reviews. In areas of uncertainty, professional judgment was applied. These guidelines are a working document that reflects the state of the field at the time of publication. Because rapid changes in this area are expected, periodic revisions are inevitable. We encourage medical professionals to use this information in conjunction with their best clinical judgment. The presented recommendations may not be appropriate in all situations. Any decision by practitioners to apply these guidelines must be made in light of local resources and individual patient circumstances. From 1Professor
    [Show full text]
  • Ipriflavone Bone Health
    PRODUCT DATA DOUGLAS LABORATORIES® 07/2014 1 Ipriflavone Bone Health DESCRIPTION Ipriflavone capsules, provided by Douglas Laboratories®, contain 300 mg of ipriflavone, a type of isoflavone. Ipriflavone is a phytonutrient that supports normal bone turnover and decreased bone resorption for healthy bone structure.† FUNCTIONS Ipriflavone helps promote bone density by inhibiting bone resorption. Numerous studies of postmenopausal women and individuals whose bones are showing signs of demineralization have investigated the benefits of ipriflavone on bone health. Laboratory and clinical studies have documented ipriflavone’s positive effect on bone density. Experts agree that ipriflavone appears to directly inhibit osteoclast activity, thereby decreasing bone resorption. Osteoclasts and osteoblasts are two primary types of bone cells. Osteoblasts, the more exterior cells, are responsible for bone mineralization. Osteoclasts, found beneath the osteoblasts, are responsible for bone resorption. When calcium levels in the blood drop, the osteoblasts change shape, allowing the osteoclasts to become exposed and release calcium from the bones to the rest of the body. Scientists suspect ipriflavone may also stimulate osteoblast activity. Since osteoblasts are responsible for laying down new bone, an increase in osteoblast activity would result in increased bone mineralization. This suggests Ipriflavone may not only inhibit the breakdown of existing bone, but also encourage the formation of new bone. Bone is constantly turning over in a continuous process of formation and resorption. During certain stages of life, the balance between bone mineralization and resorption may be tipped. During childhood and adolescence, while the body is growing, bone mineralization generally exceeds bone resorption. Once one reaches peak bone mass, sometime between the age of 20 and 30, bone formation slows down.
    [Show full text]
  • Diagnosis and Treatment of Osteoporosis
    Supporting Evidence: Diagnosis and Treatment of Osteoporosis The subdivisions of this section are: • References Copyright © 2017 by Institute for Clinical Systems Improvement 1 Diagnosis and Treatment of Osteoporosis Ninth Edition/July 2017 References Abrahamsen B, Eiken P, Eastell R. Cumulative alendronate dose and the long-term absolute risk of subtrochanteric and diaphyseal femur fractures: a register-based national cohort analysis. J Clin Endocrinol Metab 2010;95:5258-65. Adami S, Libanati C, Boonen S, et al. Denosumab treatment in postmenopausal women with osteo- porosis does not interfere with fracture-healing. J Bone Joint Surg Am 2012;94:2113-19. Adler RA, El-Hajj Fuleihan G, Bauer DC, et al. Managing osteoporosis in patients on long-term bisphos- phonate treatment: report of a task force of the American society for bone and mineral research. J Bone Miner Res 2016;31:16-35. Alekel DL, St Germain A, Peterson CT, et al. Isoflavone-rich soy protein isolate attenuates bone loss in the lumbar spine of perimenopausal women. Am J Clin Nutr 2000;72:844-52. Alexandersen P, Toussaint A, Christiansen, et al. for the Ipriflavone Multicenter European Fracture Study. Ipriflavone in the treatment of postmenopausal osteoporosis: a randomized controlled trial. JAMA 2001;285:1482-88. Anastasilakis AD, Polyzos SA, Makras P, et al. Clinical features of 24 patients with rebound-associated vertebral fractures after denosumab discontinuation: systematic review and additional cases. J Bone Miner Res 2017. Andrews EB, Gilsenan AW, Midkiff K, et al. The US postmarketing surveillance study of adult osteosarcoma and teriparatide: study design and findings from the first 7 years.
    [Show full text]
  • Phyto-Oestrogen Excretion and Rate of Bone Loss in Postmenopausal Women
    European Journal of Clinical Nutrition (1998) 52, 850±855 ß 1998 Stockton Press. All rights reserved 0954±3007/98 $12.00 http://www.stockton-press.co.uk/ejcn Phyto-oestrogen excretion and rate of bone loss in postmenopausal women AFM Kardinaal1, MS Morton2, IEM BruÈggemann-Rotgans3 and ECH van Beresteijn4 1Department of Consumer Research and Epidemiology, TNO Nutrition and Food Research Institute, Zeist, The Netherlands; 2Tenovus Cancer Research Centre, University of Wales College of Medicine, Cardiff, UK; 3Department of Biopharmaceutical Analysis, TNO Nutrition and Food Research Institute, Zeist, The Netherlands; and 4Department of Nutrition and Health, Netherlands Institute for Dairy Research (NIZO), Ede, The Netherlands Objective: The hypothesis was tested that the rate of postmenopausal bone loss is inversely associated with long- term urinary excretion of phyto-oestrogens, as a marker of habitual dietary intake. Design: Secondary analysis of a 10-year follow-up study (1979 ± 1989) among postmenopausal women in the Netherlands. Subjects: From the original population of 154 women, 32 women were selected with an annual rate of radial bone loss of 0.5% over the ®rst 5 years of the study and 35 women with a rate of 2.5% per year. Methods: The iso¯avonoids genistein, daidzein and equol, and the lignan enterolactone were determined by gas chromatography ± mass spectrometry in aggregate samples from annually collected urine samples. Cortical bone density of the radius had previously been measured annually by single-photon absorptiometry. Results: Excretion of iso¯avonoids did not differ between both groups, although in multivariate analysis equol excretion was weakly positively associated with rate of bone loss in the 5 years after the menopause.
    [Show full text]