AustralieFrV1, PascalFrancis, Corpus, bibRecord, 000532

Differing effects of denosumab and alendronate on cortical and trabecular bone

Identifieur interne : 000532 ( PascalFrancis/Corpus ); précédent : 000531; suivant : 000533

Differing effects of denosumab and alendronate on cortical and trabecular bone

Auteurs : Roger M. Zebaze ; Cesar Libanati ; Matthew Austin ; Ali Ghasem-Zadeh ; David A. Hanley ; Jose R. Zanchetta ; Thierry Thomas ; Stephanie Boutroy ; Cesar E. Bogado ; John P. Bilezikian ; Ego Seeman

Source :

Bone : (New York, NY) [ 8756-3282 ] ; 2014.

RBID : Pascal:14-0063034

Descripteurs français

Pascal (Inist)
- Dénosumab, Acide alendronique, Os cortical, Os spongieux, Qualité, Porosité, Morphologie, Immunomodulateur, Antiostéoporotique, Antiostéoclastique.

English descriptors

KwdEn :
- Alendronic acid, Antiosteoclastic agent, Antiosteoporotic, Cortical bone, Denosumab, Immunomodulator, Morphology, Porosity, Quality, Spongious bone.

Abstract

Vertebral fractures and trabecular bone loss are hallmarks of osteoporosis. However, 80% of fractures are non-vertebral and 70% of all bone loss is cortical and is produced by intracortical remodeling. The resulting cortical porosity increases bone fragility exponentially. Denosumab, a fully human anti-RANKL antibody, reduces the rate of bone remodeling more than alendronate. The aim of this study was to quantify the effects of denosumab and alendronate on cortical and trabecular bone. Postmenopausal women, mean age 61 years (range 50 to 70), were randomized double blind to placebo (n = 82), alendronate 70 mg weekly (n = 82), or denosumab 60 mg every 6 months (n = 83) for 12 months. Porosity of the compact-appearing cortex (CC), outer and inner cortical transitional zones (OTZ, ITZ), and trabecular bone volume/total volume (BV/TV) of distal radius were quantified in vivo from high-resolution peripheral quantitative computed tomography scans. Denosumab reduced remodeling more rapidly and completely than alendronate, reduced porosity of the three cortical regions at 6 months, more so by 12 months relative to baseline and controls, and 1.5- to 2-fold more so than alendronate. The respective changes at 12 months were [mean (95% CI)]; CC: -1.26% (-1.61, -0.91) versus -0.48% (-0.96, 0.00), p = 0.012: OTZ: -1.97% (-2.37, -1.56) versus -0.81% (-1.45, -0.17), p = 0.003; and ITZ: -1.17% (-1.38, -0.97) versus -0.78% (-1.04, -0.52), p = 0.021. Alendronate reduced porosity of the three cortical regions at 6 months relative to baseline and controls but further decreased porosity of only the ITZ at 12 months. By 12-months, CC porosity was no different than baseline or controls, OTZ porosity was reduced only relative to baseline, not controls, while ITZ porosity was reduced relative to baseline and 6 months, but not controls. Each treatment increased trabecular BV/TV volume similarly: 0.25% (0.19, 0.30) versus 0.19% (0.13, 0.30), p = 0.208. The greater reduction in cortical porosity by denosumab may be due to greater inhibition of intracortical remodeling. Head to head studies are needed to determine whether differences in porosity result in differing fracture outcomes.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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C01	`01`		`ENG`	@0 Vertebral fractures and trabecular bone loss are hallmarks of osteoporosis. However, 80% of fractures are non-vertebral and 70% of all bone loss is cortical and is produced by intracortical remodeling. The resulting cortical porosity increases bone fragility exponentially. Denosumab, a fully human anti-RANKL antibody, reduces the rate of bone remodeling more than alendronate. The aim of this study was to quantify the effects of denosumab and alendronate on cortical and trabecular bone. Postmenopausal women, mean age 61 years (range 50 to 70), were randomized double blind to placebo (n = 82), alendronate 70 mg weekly (n = 82), or denosumab 60 mg every 6 months (n = 83) for 12 months. Porosity of the compact-appearing cortex (CC), outer and inner cortical transitional zones (OTZ, ITZ), and trabecular bone volume/total volume (BV/TV) of distal radius were quantified in vivo from high-resolution peripheral quantitative computed tomography scans. Denosumab reduced remodeling more rapidly and completely than alendronate, reduced porosity of the three cortical regions at 6 months, more so by 12 months relative to baseline and controls, and 1.5- to 2-fold more so than alendronate. The respective changes at 12 months were [mean (95% CI)]; CC: -1.26% (-1.61, -0.91) versus -0.48% (-0.96, 0.00), p = 0.012: OTZ: -1.97% (-2.37, -1.56) versus -0.81% (-1.45, -0.17), p = 0.003; and ITZ: -1.17% (-1.38, -0.97) versus -0.78% (-1.04, -0.52), p = 0.021. Alendronate reduced porosity of the three cortical regions at 6 months relative to baseline and controls but further decreased porosity of only the ITZ at 12 months. By 12-months, CC porosity was no different than baseline or controls, OTZ porosity was reduced only relative to baseline, not controls, while ITZ porosity was reduced relative to baseline and 6 months, but not controls. Each treatment increased trabecular BV/TV volume similarly: 0.25% (0.19, 0.30) versus 0.19% (0.13, 0.30), p = 0.208. The greater reduction in cortical porosity by denosumab may be due to greater inhibition of intracortical remodeling. Head to head studies are needed to determine whether differences in porosity result in differing fracture outcomes.
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C03	`01`	`X`	`SPA`	`@0 Denosumab @2 FR @5 04`
C03	`02`	`X`	`FRE`	`@0 Acide alendronique @2 NK @2 FR @5 05`
C03	`02`	`X`	`ENG`	`@0 Alendronic acid @2 NK @2 FR @5 05`
C03	`02`	`X`	`SPA`	`@0 Acido alendrónico @2 NK @2 FR @5 05`
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C03	`04`	`X`	`ENG`	`@0 Spongious bone @5 08`
C03	`04`	`X`	`SPA`	`@0 Hueso esponjoso @5 08`
C03	`05`	`X`	`FRE`	`@0 Qualité @5 09`
C03	`05`	`X`	`ENG`	`@0 Quality @5 09`
C03	`05`	`X`	`SPA`	`@0 Calidad @5 09`
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C03	`07`	`X`	`ENG`	`@0 Morphology @5 14`
C03	`07`	`X`	`SPA`	`@0 Morfología @5 14`
C03	`08`	`X`	`FRE`	`@0 Immunomodulateur @5 30`
C03	`08`	`X`	`ENG`	`@0 Immunomodulator @5 30`
C03	`08`	`X`	`SPA`	`@0 Inmunomodulador @5 30`
C03	`09`	`X`	`FRE`	`@0 Antiostéoporotique @5 31`
C03	`09`	`X`	`ENG`	`@0 Antiosteoporotic @5 31`
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C03	`10`	`X`	`FRE`	`@0 Antiostéoclastique @5 32`
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Format Inist (serveur)

NO :	PASCAL 14-0063034 INIST
ET :	Differing effects of denosumab and alendronate on cortical and trabecular bone
AU :	ZEBAZE (Roger M.); LIBANATI (Cesar); AUSTIN (Matthew); GHASEM-ZADEH (Ali); HANLEY (David A.); ZANCHETTA (Jose R.); THOMAS (Thierry); BOUTROY (Stephanie); BOGADO (Cesar E.); BILEZIKIAN (John P.); SEEMAN (Ego)
AF :	Austin Health, University of Melbourne/Melbourne/Australie (1 aut., 4 aut., 11 aut.); Amgen Inc./Thousand Oaks, CA/Etats-Unis (2 aut., 3 aut.); University of Calgary/Calgary/Canada (5 aut.); Instituto de Investigacions Metabolicas/Buenos Aires/Argentine (6 aut., 9 aut.); INSERM U1059, University Hospital of St-Etienne/St-Etienne/France (7 aut.); INSERM U1033, Université de Lyon/Lyon/France (8 aut.); College of Physicians and Surgeons, Columbia University/New York, NY/Etats-Unis (10 aut.)
DT :	Publication en série; Niveau analytique
SO :	Bone : (New York, NY); ISSN 8756-3282; Pays-Bas; Da. 2014; Vol. 59; Pp. 173-179; Bibl. 51 ref.
LA :	Anglais
EA :	Vertebral fractures and trabecular bone loss are hallmarks of osteoporosis. However, 80% of fractures are non-vertebral and 70% of all bone loss is cortical and is produced by intracortical remodeling. The resulting cortical porosity increases bone fragility exponentially. Denosumab, a fully human anti-RANKL antibody, reduces the rate of bone remodeling more than alendronate. The aim of this study was to quantify the effects of denosumab and alendronate on cortical and trabecular bone. Postmenopausal women, mean age 61 years (range 50 to 70), were randomized double blind to placebo (n = 82), alendronate 70 mg weekly (n = 82), or denosumab 60 mg every 6 months (n = 83) for 12 months. Porosity of the compact-appearing cortex (CC), outer and inner cortical transitional zones (OTZ, ITZ), and trabecular bone volume/total volume (BV/TV) of distal radius were quantified in vivo from high-resolution peripheral quantitative computed tomography scans. Denosumab reduced remodeling more rapidly and completely than alendronate, reduced porosity of the three cortical regions at 6 months, more so by 12 months relative to baseline and controls, and 1.5- to 2-fold more so than alendronate. The respective changes at 12 months were [mean (95% CI)]; CC: -1.26% (-1.61, -0.91) versus -0.48% (-0.96, 0.00), p = 0.012: OTZ: -1.97% (-2.37, -1.56) versus -0.81% (-1.45, -0.17), p = 0.003; and ITZ: -1.17% (-1.38, -0.97) versus -0.78% (-1.04, -0.52), p = 0.021. Alendronate reduced porosity of the three cortical regions at 6 months relative to baseline and controls but further decreased porosity of only the ITZ at 12 months. By 12-months, CC porosity was no different than baseline or controls, OTZ porosity was reduced only relative to baseline, not controls, while ITZ porosity was reduced relative to baseline and 6 months, but not controls. Each treatment increased trabecular BV/TV volume similarly: 0.25% (0.19, 0.30) versus 0.19% (0.13, 0.30), p = 0.208. The greater reduction in cortical porosity by denosumab may be due to greater inhibition of intracortical remodeling. Head to head studies are needed to determine whether differences in porosity result in differing fracture outcomes.
CC :	002A16; 002B02Q; 002B02L
FD :	Dénosumab; Acide alendronique; Os cortical; Os spongieux; Qualité; Porosité; Morphologie; Immunomodulateur; Antiostéoporotique; Antiostéoclastique
ED :	Denosumab; Alendronic acid; Cortical bone; Spongious bone; Quality; Porosity; Morphology; Immunomodulator; Antiosteoporotic; Antiosteoclastic agent
SD :	Denosumab; Acido alendrónico; Hueso cortical; Hueso esponjoso; Calidad; Porosidad; Morfología; Inmunomodulador; Antiosteoporótico; Antiosteoclástica
LO :	INIST-19041.354000505752740230
ID :	14-0063034

Links to Exploration step

Pascal:14-0063034

Le document en format XML

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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Differing effects of denosumab and alendronate on cortical and trabecular bone</title>
<author><name sortKey="Zebaze, Roger M" sort="Zebaze, Roger M" uniqKey="Zebaze R" first="Roger M." last="Zebaze">Roger M. Zebaze</name>
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<author><name sortKey="Ghasem Zadeh, Ali" sort="Ghasem Zadeh, Ali" uniqKey="Ghasem Zadeh A" first="Ali" last="Ghasem-Zadeh">Ali Ghasem-Zadeh</name>
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<author><name sortKey="Hanley, David A" sort="Hanley, David A" uniqKey="Hanley D" first="David A." last="Hanley">David A. Hanley</name>
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<author><name sortKey="Zanchetta, Jose R" sort="Zanchetta, Jose R" uniqKey="Zanchetta J" first="Jose R." last="Zanchetta">Jose R. Zanchetta</name>
<affiliation><inist:fA14 i1="04"><s1>Instituto de Investigacions Metabolicas</s1>
<s2>Buenos Aires</s2>
<s3>ARG</s3>
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</inist:fA14>
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<author><name sortKey="Thomas, Thierry" sort="Thomas, Thierry" uniqKey="Thomas T" first="Thierry" last="Thomas">Thierry Thomas</name>
<affiliation><inist:fA14 i1="05"><s1>INSERM U1059, University Hospital of St-Etienne</s1>
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</inist:fA14>
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<author><name sortKey="Boutroy, Stephanie" sort="Boutroy, Stephanie" uniqKey="Boutroy S" first="Stephanie" last="Boutroy">Stephanie Boutroy</name>
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<author><name sortKey="Bogado, Cesar E" sort="Bogado, Cesar E" uniqKey="Bogado C" first="Cesar E." last="Bogado">Cesar E. Bogado</name>
<affiliation><inist:fA14 i1="04"><s1>Instituto de Investigacions Metabolicas</s1>
<s2>Buenos Aires</s2>
<s3>ARG</s3>
<sZ>6 aut.</sZ>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Bilezikian, John P" sort="Bilezikian, John P" uniqKey="Bilezikian J" first="John P." last="Bilezikian">John P. Bilezikian</name>
<affiliation><inist:fA14 i1="07"><s1>College of Physicians and Surgeons, Columbia University</s1>
<s2>New York, NY</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
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<author><name sortKey="Seeman, Ego" sort="Seeman, Ego" uniqKey="Seeman E" first="Ego" last="Seeman">Ego Seeman</name>
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<s2>Melbourne</s2>
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<series><title level="j" type="main">Bone : (New York, NY)</title>
<title level="j" type="abbreviated">Bone : (NY NY)</title>
<idno type="ISSN">8756-3282</idno>
<imprint><date when="2014">2014</date>
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<seriesStmt><title level="j" type="main">Bone : (New York, NY)</title>
<title level="j" type="abbreviated">Bone : (NY NY)</title>
<idno type="ISSN">8756-3282</idno>
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</fileDesc>
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<term>Antiosteoclastic agent</term>
<term>Antiosteoporotic</term>
<term>Cortical bone</term>
<term>Denosumab</term>
<term>Immunomodulator</term>
<term>Morphology</term>
<term>Porosity</term>
<term>Quality</term>
<term>Spongious bone</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Dénosumab</term>
<term>Acide alendronique</term>
<term>Os cortical</term>
<term>Os spongieux</term>
<term>Qualité</term>
<term>Porosité</term>
<term>Morphologie</term>
<term>Immunomodulateur</term>
<term>Antiostéoporotique</term>
<term>Antiostéoclastique</term>
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<front><div type="abstract" xml:lang="en">Vertebral fractures and trabecular bone loss are hallmarks of osteoporosis. However, 80% of fractures are non-vertebral and 70% of all bone loss is cortical and is produced by intracortical remodeling. The resulting cortical porosity increases bone fragility exponentially. Denosumab, a fully human anti-RANKL antibody, reduces the rate of bone remodeling more than alendronate. The aim of this study was to quantify the effects of denosumab and alendronate on cortical and trabecular bone. Postmenopausal women, mean age 61 years (range 50 to 70), were randomized double blind to placebo (n = 82), alendronate 70 mg weekly (n = 82), or denosumab 60 mg every 6 months (n = 83) for 12 months. Porosity of the compact-appearing cortex (CC), outer and inner cortical transitional zones (OTZ, ITZ), and trabecular bone volume/total volume (BV/TV) of distal radius were quantified in vivo from high-resolution peripheral quantitative computed tomography scans. Denosumab reduced remodeling more rapidly and completely than alendronate, reduced porosity of the three cortical regions at 6 months, more so by 12 months relative to baseline and controls, and 1.5- to 2-fold more so than alendronate. The respective changes at 12 months were [mean (95% CI)]; CC: -1.26% (-1.61, -0.91) versus -0.48% (-0.96, 0.00), p = 0.012: OTZ: -1.97% (-2.37, -1.56) versus -0.81% (-1.45, -0.17), p = 0.003; and ITZ: -1.17% (-1.38, -0.97) versus -0.78% (-1.04, -0.52), p = 0.021. Alendronate reduced porosity of the three cortical regions at 6 months relative to baseline and controls but further decreased porosity of only the ITZ at 12 months. By 12-months, CC porosity was no different than baseline or controls, OTZ porosity was reduced only relative to baseline, not controls, while ITZ porosity was reduced relative to baseline and 6 months, but not controls. Each treatment increased trabecular BV/TV volume similarly: 0.25% (0.19, 0.30) versus 0.19% (0.13, 0.30), p = 0.208. The greater reduction in cortical porosity by denosumab may be due to greater inhibition of intracortical remodeling. Head to head studies are needed to determine whether differences in porosity result in differing fracture outcomes.</div>
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<fA14 i1="04"><s1>Instituto de Investigacions Metabolicas</s1>
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<fA14 i1="07"><s1>College of Physicians and Surgeons, Columbia University</s1>
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<ET>Differing effects of denosumab and alendronate on cortical and trabecular bone</ET>
<AU>ZEBAZE (Roger M.); LIBANATI (Cesar); AUSTIN (Matthew); GHASEM-ZADEH (Ali); HANLEY (David A.); ZANCHETTA (Jose R.); THOMAS (Thierry); BOUTROY (Stephanie); BOGADO (Cesar E.); BILEZIKIAN (John P.); SEEMAN (Ego)</AU>
<AF>Austin Health, University of Melbourne/Melbourne/Australie (1 aut., 4 aut., 11 aut.); Amgen Inc./Thousand Oaks, CA/Etats-Unis (2 aut., 3 aut.); University of Calgary/Calgary/Canada (5 aut.); Instituto de Investigacions Metabolicas/Buenos Aires/Argentine (6 aut., 9 aut.); INSERM U1059, University Hospital of St-Etienne/St-Etienne/France (7 aut.); INSERM U1033, Université de Lyon/Lyon/France (8 aut.); College of Physicians and Surgeons, Columbia University/New York, NY/Etats-Unis (10 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Bone : (New York, NY); ISSN 8756-3282; Pays-Bas; Da. 2014; Vol. 59; Pp. 173-179; Bibl. 51 ref.</SO>
<LA>Anglais</LA>
<EA>Vertebral fractures and trabecular bone loss are hallmarks of osteoporosis. However, 80% of fractures are non-vertebral and 70% of all bone loss is cortical and is produced by intracortical remodeling. The resulting cortical porosity increases bone fragility exponentially. Denosumab, a fully human anti-RANKL antibody, reduces the rate of bone remodeling more than alendronate. The aim of this study was to quantify the effects of denosumab and alendronate on cortical and trabecular bone. Postmenopausal women, mean age 61 years (range 50 to 70), were randomized double blind to placebo (n = 82), alendronate 70 mg weekly (n = 82), or denosumab 60 mg every 6 months (n = 83) for 12 months. Porosity of the compact-appearing cortex (CC), outer and inner cortical transitional zones (OTZ, ITZ), and trabecular bone volume/total volume (BV/TV) of distal radius were quantified in vivo from high-resolution peripheral quantitative computed tomography scans. Denosumab reduced remodeling more rapidly and completely than alendronate, reduced porosity of the three cortical regions at 6 months, more so by 12 months relative to baseline and controls, and 1.5- to 2-fold more so than alendronate. The respective changes at 12 months were [mean (95% CI)]; CC: -1.26% (-1.61, -0.91) versus -0.48% (-0.96, 0.00), p = 0.012: OTZ: -1.97% (-2.37, -1.56) versus -0.81% (-1.45, -0.17), p = 0.003; and ITZ: -1.17% (-1.38, -0.97) versus -0.78% (-1.04, -0.52), p = 0.021. Alendronate reduced porosity of the three cortical regions at 6 months relative to baseline and controls but further decreased porosity of only the ITZ at 12 months. By 12-months, CC porosity was no different than baseline or controls, OTZ porosity was reduced only relative to baseline, not controls, while ITZ porosity was reduced relative to baseline and 6 months, but not controls. Each treatment increased trabecular BV/TV volume similarly: 0.25% (0.19, 0.30) versus 0.19% (0.13, 0.30), p = 0.208. The greater reduction in cortical porosity by denosumab may be due to greater inhibition of intracortical remodeling. Head to head studies are needed to determine whether differences in porosity result in differing fracture outcomes.</EA>
<CC>002A16; 002B02Q; 002B02L</CC>
<FD>Dénosumab; Acide alendronique; Os cortical; Os spongieux; Qualité; Porosité; Morphologie; Immunomodulateur; Antiostéoporotique; Antiostéoclastique</FD>
<ED>Denosumab; Alendronic acid; Cortical bone; Spongious bone; Quality; Porosity; Morphology; Immunomodulator; Antiosteoporotic; Antiosteoclastic agent</ED>
<SD>Denosumab; Acido alendrónico; Hueso cortical; Hueso esponjoso; Calidad; Porosidad; Morfología; Inmunomodulador; Antiosteoporótico; Antiosteoclástica</SD>
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Differing effects of denosumab and alendronate on cortical and trabecular bone

Differing effects of denosumab and alendronate on cortical and trabecular bone

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