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Article ; Online: Time present and time past are both perhaps present in time future, and time future contained in time past - TSEliot, The Four Quartets.

Seeman, Ego

2020 Volume 137, Page(s) 115427

MeSH term(s)	Bone Remodeling ; Female ; Humans ; Osteoporosis ; Postmenopause ; Women
Language	English
Publishing date	2020-09-02
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	632515-4
ISSN	1873-2763 ; 8756-3282
ISSN (online)	1873-2763
ISSN	8756-3282
DOI	10.1016/j.bone.2020.115427
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Zs.A 1571: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 332: Show issues

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Article: Bone Remodeling and Modeling: Cellular Targets for Antiresorptive and Anabolic Treatments, Including Approaches Through the Parathyroid Hormone (PTH)/PTH-Related Protein Pathway.

Martin, Thomas John / Seeman, Ego

Neurospine

2023 Volume 20, Issue 4, Page(s) 1097–1109

Abstract: Bone is continuously in a state of building and renewal, though the process of remodeling that takes place at many sites asynchronously throughout the skeleton, with bone formation and resorption equal at these sites (bone multicellular units). ... ...

Abstract	Bone is continuously in a state of building and renewal, though the process of remodeling that takes place at many sites asynchronously throughout the skeleton, with bone formation and resorption equal at these sites (bone multicellular units). Remodeling takes place on bone surfaces, both on trabeculae and in the cortex, and serves the purposes of replacing old bone or that damaged by microfractures throughout the skeleton. The bone loss and consequent osteoporotic fractures that result from excess resorption over formation have mainly been prevented or treated by antiresorptive drugs that inhibit osteoclast formation and/or activity. Virtually all of the evidence leading to acceptance of antiresorptive drugs as treatment has depended upon their prevention of vertebral fractures. In recent decades, new prospects came of anabolic treatments that partly restore bone volume and microstructure restore bone that has been lost. The first of these was parathyroid hormone (PTH), shown by daily injection to increase markers of bone formation and prevent fractures. This field of interest enlarged with the discovery of PTH-related protein (PTHrP), so closely related in structure and action to PTH. The structural relationship between PTH and PTHrP is important in assessing their physiological and pharmacological roles, with the N-terminal domains of the 2 having virtually equal actions on target cells. Abaloparatide, a peptide analogue based on the structures of PTHrP and PTH, has been approved in some countries as a therapy for osteoporosis. Treatment through the PTH receptor activation pathway, and probably with any anabolic therapy, needs to be followed by antiresorptive treatment in order to maintain bone that has been restored. No matter how effective anabolic therapies for the skeleton become, it seems highly likely that there will be a continuing need for antiresorptive drugs.
Language	English
Publishing date	2023-12-31
Publishing country	Korea (South)
Document type	Journal Article
ZDB-ID	3031654-6
ISSN	2586-6591 ; 2586-6583
ISSN (online)	2586-6591
ISSN	2586-6583
DOI	10.14245/ns.2346966.483
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Book ; Conference proceedings: Proceedings of a Symposium Advances in the Epidemiology, Prevention, and Treatment of Osteoporosis and Fractures

Seeman, Ego

held on September 5 - 6, 1996, in San Francisco, California

(The American journal of medicine ; 103,2A)

1997

Title variant	Advances in the epidemiology, prevention, and treatment of osteoporosis and fractures
Event/congress	Symposium Advances in the Epidemiology, Prevention, and Treatment of Osteoporosis and Fractures (1996, SanFranciscoCalif.)
Author's details	guest ed. Ego Seeman
Series title	The American journal of medicine ; 103,2A
Collection
Keywords	Osteoporosis / congresses ; Fractures / congresses
Language	English
Size	92S S. : Ill., graph. Darst.
Publisher	Excerpta Medica
Publishing place	New York, NY
Publishing country	United States
Document type	Book ; Conference proceedings
HBZ-ID	HT007808182
Database	Catalogue ZB MED Medicine, Health

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Ua VI Zs 289 -103,2A-	verfügbar in Königswinter	Königswinter

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Article ; Online: Overview of bone microstructure, and treatment of bone fragility in chronic kidney disease.

Seeman, Ego

Nephrology (Carlton, Vic.)

2017 Volume 22 Suppl 2, Page(s) 34–35

MeSH term(s)	Bone Density/drug effects ; Bone Density Conservation Agents/adverse effects ; Bone Density Conservation Agents/therapeutic use ; Bone Remodeling/drug effects ; Bone and Bones/diagnostic imaging ; Bone and Bones/drug effects ; Bone and Bones/physiopathology ; Chronic Kidney Disease-Mineral and Bone Disorder/diagnosis ; Chronic Kidney Disease-Mineral and Bone Disorder/drug therapy ; Chronic Kidney Disease-Mineral and Bone Disorder/etiology ; Chronic Kidney Disease-Mineral and Bone Disorder/physiopathology ; Fractures, Bone/diagnostic imaging ; Fractures, Bone/etiology ; Fractures, Bone/physiopathology ; Fractures, Bone/prevention & control ; Humans ; Predictive Value of Tests ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/diagnosis ; Renal Insufficiency, Chronic/physiopathology ; Renal Insufficiency, Chronic/therapy ; Risk Factors
Chemical Substances	Bone Density Conservation Agents
Language	English
Publishing date	2017-04-21
Publishing country	Australia
Document type	Journal Article
ZDB-ID	1303661-0
ISSN	1440-1797 ; 1320-5358
ISSN (online)	1440-1797
ISSN	1320-5358
DOI	10.1111/nep.13024
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Zs.A 4822: Show issues

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Article: Growth and Age-Related Abnormalities in Cortical Structure and Fracture Risk.

Seeman, Ego

Endocrinology and metabolism (Seoul, Korea)

2015 Volume 30, Issue 4, Page(s) 419–428

Abstract: Vertebral fractures and trabecular bone loss have dominated thinking and research into the pathogenesis and the structural basis of bone fragility during the last 70 years. However, 80% of all fractures are non-vertebral and occur at regions assembled ... ...

Abstract	Vertebral fractures and trabecular bone loss have dominated thinking and research into the pathogenesis and the structural basis of bone fragility during the last 70 years. However, 80% of all fractures are non-vertebral and occur at regions assembled using large amounts of cortical bone; only 20% of fractures are vertebral. Moreover, ~80% of the skeleton is cortical and ~70% of all bone loss is cortical even though trabecular bone is lost more rapidly than cortical bone. Bone is lost because remodelling becomes unbalanced after midlife. Most cortical bone loss occurs by intracortical, not endocortical remodelling. Each remodelling event removes more bone than deposited enlarging existing canals which eventually coalesce eroding and thinning the cortex from 'within.' Thus, there is a need to study the decay of cortical as well as trabecular bone, and to develop drugs that restore the strength of both types of bone. It is now possible to accurately quantify cortical porosity and trabecular decay in vivo. The challenges still to be met are to determine whether measurement of porosity identifies persons at risk for fracture, whether this approach is compliments information obtained using bone densitometry, and whether changes in cortical porosity and other microstructural traits have the sensitivity to serve as surrogates of treatment success or failure.
Language	English
Publishing date	2015-12
Publishing country	Korea (South)
Document type	Journal Article ; Review
ZDB-ID	2802452-7
ISSN	2093-5978 ; 2093-596X
ISSN (online)	2093-5978
ISSN	2093-596X
DOI	10.3803/EnM.2015.30.4.419
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Article: Reduced Bone Modeling and Unbalanced Bone Remodeling: Targets for Antiresorptive and Anabolic Therapy.

Ramchand, Sabashini K / Seeman, Ego

Handbook of experimental pharmacology

2020 Volume 262, Page(s) 423–450

Abstract: Bone loss during advancing age is the net result of reduced modeling-based bone formation upon the outer (periosteal) envelope and unbalanced remodeling by basic multicellular units (BMUs) upon the three (intracortical, endocortical, and trabecular) ... ...

Abstract	Bone loss during advancing age is the net result of reduced modeling-based bone formation upon the outer (periosteal) envelope and unbalanced remodeling by basic multicellular units (BMUs) upon the three (intracortical, endocortical, and trabecular) components of the inner (endosteal) bone envelope. Each BMU deposits less bone than resorbed, reducing total bone volume and deteriorating the microstructure of the diminished residual bone volume.Antiresorptive agents like bisphosphonates reduce, but do not abolish, the rate of bone remodeling - fewer BMUs remodel, "turn over," the volume of bone. Residual unbalanced remodeling continues to slowly reduce total bone volume and deteriorate bone microstructure. By contrast, denosumab virtually abolishes remodeling so the decrease in bone volume and the deterioration in microstructure cease. The less remodeled matrix remains, leaving more time to complete the slow process of secondary mineralization which reduces the heterogeneity of matrix mineralization and allows it to become glycosylated, changes that may make the smaller and microstructurally deteriorated bone volume more brittle. Neither class of antiresorptive restores bone volume or its microstructure, despite increases in bone mineral density misleadingly suggesting otherwise. Nevertheless, these agents reduce vertebral and hip fractures by 50-60% but only reduce nonvertebral fractures by 20-30%.Restoring bone volume, microstructure, and material composition, "curing" bone fragility, may be partly achieved using anabolic therapy. Teriparatide, and probably abaloparatide, produce mainly remodeling-based bone formation by acting on BMUs existing in their resorption, reversal, or formation phase at the time of treatment and by promoting bone formation in newly initiated BMUs. Romosozumab produces modeling-based bone formation almost exclusively and decreases the surface extent of bone resorption. All three anabolic agents reduce vertebral fracture risk relative to untreated controls; parathyroid hormone 1-34 and romosozumab reduce vertebral fracture risk more greatly than risedronate or alendronate, respectively. Evidence for nonvertebral or hip fracture risk reduction relative to untreated or antiresorptive-treated controls is lacking or inconsistent. Only one study suggests sequential romosozumab followed by alendronate reduces vertebral, nonvertebral, and hip fracture risk compared to continuous alendronate alone. Whether combined antiresorptive and anabolic therapy result in superior fracture risk reduction than monotherapy is untested.
MeSH term(s)	Bone Density/physiology ; Bone Density Conservation Agents ; Bone Remodeling/physiology ; Bone and Bones ; Humans ; Osteoporosis
Chemical Substances	Bone Density Conservation Agents
Language	English
Publishing date	2020-03-30
Publishing country	Germany
Document type	Journal Article
ISSN	0171-2004
ISSN	0171-2004
DOI	10.1007/164_2020_354
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Sign. bis Bd. 125 (1997): 1982 A 2146: Show issues
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Article ; Online: Reducing hip and non-vertebral fractures in institutionalised older adults by restoring inadequate intakes of protein and calcium is cost-saving.

Baek, Yeji / Iuliano, Sandra / Robbins, Judy / Poon, Shirley / Seeman, Ego / Ademi, Zanfina

Age and ageing

2023 Volume 52, Issue 6

Abstract: Background: older adults in aged care account for 30% of the population burden of hip fractures. Nutritional interventions to correct under nutrition reduce these debilitating fractures, perhaps partly by reducing falls and slowing deterioration in bone ...

Abstract	Background: older adults in aged care account for 30% of the population burden of hip fractures. Nutritional interventions to correct under nutrition reduce these debilitating fractures, perhaps partly by reducing falls and slowing deterioration in bone morphology. Objective: to determine whether a nutritional approach to fracture risk reduction in aged care homes is cost-effective. Design: cost-effectiveness was estimated based on results from a prospective 2-year cluster-randomised controlled trial and secondary data. Intervention residents consumed a total of 3.5 daily servings of milk, yoghurt and/or cheese, resulting in 1,142 mg of calcium and 69 g of protein compared with the daily intakes of 700 mg of calcium and 58 g of protein consumed by the control group. Setting: fifty-six aged care homes. Participants: residents for 27 intervention (n = 3,313) and 29 control (n = 3,911) homes. Methods: ambulance, hospital, rehabilitation and residential care costs incurred by fracture were estimated. The incremental cost-effectiveness ratios per fracture averted within a 2-year time horizon were estimated from the Australian healthcare perspective applying a 5% discount rate on costs after the first year. Results: intervention providing high-protein and high-calcium foods reduced fractures at a daily cost of AU$0.66 per resident. The base-case results showed that the intervention was cost-saving per fracture averted, with robust results in a variety of sensitivity and scenario analyses. Scaling the benefits of intervention equates to a saving of AU$66,780,000 annually in Australia and remained cost-saving up to a daily food expenditure of AU$1.07 per resident. Conclusions: averting hip and other non-vertebral fractures in aged care residents by restoring nutritional inadequacy of protein and calcium is cost-saving.
MeSH term(s)	Humans ; Aged ; Calcium ; Prospective Studies ; Australia ; Hip Fractures/prevention & control ; Ambulances
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2023-05-05
Publishing country	England
Document type	Randomized Controlled Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186788-x
ISSN	1468-2834 ; 0002-0729
ISSN (online)	1468-2834
ISSN	0002-0729
DOI	10.1093/ageing/afad114
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Zs.A 877: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 448: Show issues

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Article ; Online: Physiological and Pharmacological Roles of PTH and PTHrP in Bone Using Their Shared Receptor, PTH1R.

Martin, T John / Sims, Natalie A / Seeman, Ego

Endocrine reviews

2021 Volume 42, Issue 4, Page(s) 383–406

Abstract: Parathyroid hormone (PTH) and the paracrine factor, PTH-related protein (PTHrP), have preserved in evolution sufficient identities in their amino-terminal domains to share equivalent actions upon a common G protein-coupled receptor, PTH1R, that ... ...

Abstract	Parathyroid hormone (PTH) and the paracrine factor, PTH-related protein (PTHrP), have preserved in evolution sufficient identities in their amino-terminal domains to share equivalent actions upon a common G protein-coupled receptor, PTH1R, that predominantly uses the cyclic adenosine monophosphate-protein kinase A signaling pathway. Such a relationship between a hormone and local factor poses questions about how their common receptor mediates pharmacological and physiological actions of the two. Mouse genetic studies show that PTHrP is essential for endochondral bone lengthening in the fetus and is essential for bone remodeling. In contrast, the main postnatal function of PTH is hormonal control of calcium homeostasis, with no evidence that PTHrP contributes. Pharmacologically, amino-terminal PTH and PTHrP peptides (teriparatide and abaloparatide) promote bone formation when administered by intermittent (daily) injection. This anabolic effect is remodeling-based with a lesser contribution from modeling. The apparent lesser potency of PTHrP than PTH peptides as skeletal anabolic agents could be explained by lesser bioavailability to PTH1R. By contrast, prolongation of PTH1R stimulation by excessive dosing or infusion, converts the response to a predominantly resorptive one by stimulating osteoclast formation. Physiologically, locally generated PTHrP is better equipped than the circulating hormone to regulate bone remodeling, which occurs asynchronously at widely distributed sites throughout the skeleton where it is needed to replace old or damaged bone. While it remains possible that PTH, circulating within a narrow concentration range, could contribute in some way to remodeling and modeling, its main physiological role is in regulating calcium homeostasis.
MeSH term(s)	Animals ; Bone Density Conservation Agents ; Calcium ; Cyclic AMP/metabolism ; Humans ; Mice ; Parathyroid Hormone/pharmacology ; Parathyroid Hormone-Related Protein/genetics ; Parathyroid Hormone-Related Protein/metabolism ; Parathyroid Hormone-Related Protein/pharmacology ; Peptides ; Receptor, Parathyroid Hormone, Type 1/metabolism
Chemical Substances	Bone Density Conservation Agents ; PTH1R protein, human ; Parathyroid Hormone ; Parathyroid Hormone-Related Protein ; Peptides ; Receptor, Parathyroid Hormone, Type 1 ; Cyclic AMP (E0399OZS9N) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-02-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603096-8
ISSN	1945-7189 ; 0163-769X
ISSN (online)	1945-7189
ISSN	0163-769X
DOI	10.1210/endrev/bnab005
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Article ; Online: Antiresorptive and anabolic agents in the prevention and reversal of bone fragility.

Seeman, Ego / Martin, T J

Nature reviews. Rheumatology

2019 Volume 15, Issue 4, Page(s) 225–236

Abstract: Bone volume, microstructure and its material composition are maintained by bone remodelling, a cellular activity carried out by bone multicellular units (BMUs). BMUs are focally transient teams of osteoclasts and osteoblasts that respectively resorb a ... ...

Abstract	Bone volume, microstructure and its material composition are maintained by bone remodelling, a cellular activity carried out by bone multicellular units (BMUs). BMUs are focally transient teams of osteoclasts and osteoblasts that respectively resorb a volume of old bone and then deposit an equal volume of new bone at the same location. Around the time of menopause, bone remodelling becomes unbalanced and rapid, and an increased number of BMUs deposit less bone than they resorb, resulting in bone loss, a reduction in bone volume and microstructural deterioration. Cortices become porous and thin, and trabeculae become thin, perforated and disconnected, causing bone fragility. Antiresorptive agents reduce fracture risk by reducing the rate of bone remodelling so that fewer BMUs are available to remodel bone. Bone fragility is not abolished by these drugs because existing microstructural deterioration is not reversed, unsuppressed remodelling continues producing microstructural deterioration and unremodelled bone that becomes more mineralized can become brittle. Anabolic agents reduce fracture risk by stimulating new bone formation, which partly restores bone volume and microstructure. To guide fracture prevention, this Review provides an overview of the structural basis of bone fragility, the mechanisms of remodelling and how anabolic and antiresorptive agents target remodelling defects.
MeSH term(s)	Anabolic Agents/therapeutic use ; Animals ; Bone Demineralization, Pathologic/prevention & control ; Bone Demineralization, Pathologic/therapy ; Bone Density Conservation Agents/therapeutic use ; Bone Remodeling/drug effects ; Bone Resorption/drug therapy ; Humans
Chemical Substances	Anabolic Agents ; Bone Density Conservation Agents
Language	English
Publishing date	2019-02-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2491532-4
ISSN	1759-4804 ; 1759-4790
ISSN (online)	1759-4804
ISSN	1759-4790
DOI	10.1038/s41584-019-0172-3
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Article ; Online: Age- and menopause-related bone loss compromise cortical and trabecular microstructure.

Seeman, Ego

The journals of gerontology. Series A, Biological sciences and medical sciences

2013 Volume 68, Issue 10, Page(s) 1218–1225

Abstract: All factors influencing the material composition and structure of bone do so through the final common cellular pathways of modeling and remodeling. During growth, modeling, the formation of new bone in different locations without prior bone resorption, ... ...

Abstract	All factors influencing the material composition and structure of bone do so through the final common cellular pathways of modeling and remodeling. During growth, modeling, the formation of new bone in different locations without prior bone resorption, deposits matrix upon the periosteum, enlarging the cross-sectional area of bone. Concurrently, endocortical resorption excavates the medullary canal while remodeling, the resorption and deposition of bone in the same location, assembles cortical osteons, each with their central Haversian canal. The Haversian canals and the connecting Volkmann canals form an intracortical canal network that occupies 30% of the total cortical volume. The remaining 70% is mineralized bone matrix volume. Around midlife, in women, remodeling balance becomes negative; less bone is deposited than it is resorbed by each bone's basic multicellular units (BMUs), and remodeling rate increases; there are more BMUs removing bone upon its intracortical, endocortical, and trabecular surfaces. Canals enlarge and coalesce creating giant pores. Remodeling upon trabeculae removes them, whereas intracortical and endocortical remodeling cavitates and fragments the cortex. Bone loss becomes almost entirely cortical as trabeculae disappear. Remodeling removes more bone from a diminishing total mineralized bone matrix volume so that by old age, total mineralized bone matrix volume is halved; 70% of all bone loss is cortical because 80% of the skeleton is cortical; 30% of the bone loss arises from the 20% of the skeleton that is trabecular. Of all fractures occurring, 80% are nonvertebral and 20% are vertebral. The notion of osteoporosis as a disease of trabecular bone loss and vertebral fractures needs to be revised.
MeSH term(s)	Bone Density ; Bone Density Conservation Agents/therapeutic use ; Bone Remodeling ; Bone and Bones/pathology ; Bone and Bones/physiopathology ; Female ; Haversian System/pathology ; Humans ; Osteoporosis/drug therapy ; Osteoporosis/pathology ; Osteoporosis/physiopathology ; Osteoporosis, Postmenopausal/drug therapy ; Osteoporosis, Postmenopausal/pathology ; Osteoporosis, Postmenopausal/physiopathology
Chemical Substances	Bone Density Conservation Agents
Language	English
Publishing date	2013-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glt071
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