Evidence map›Paper›PMID 21946081›Full record

ReviewJournal of endocrinological investigation2011

Catabolic and anabolic actions of parathyroid hormone on the skeleton.

B C Silva, A G Costa, N E Cusano, S Kousteni, J P Bilezikian

Open access · greenAbstract readReview
In one paragraph

Review in Journal of endocrinological investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 5 pooled it
4.8field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

114 citing papers in PubMed, 5 syntheses or guidelines pooled it, 218 citations in OpenAlex.

  1. Pooled it
  2. Italian Guidelines for the Management of Sporadic Primary Hyperparathyroidism.Endocrine, metabolic & immune disorders drug targets · 2024
    Guideline
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Maintenance of Serum Ionized Calcium During Exercise Attenuates Parathyroid Hormone and Bone Resorption Responses.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018
    Trial
  7. Trial
  8. Treatment with intermittent PTH increases Wnt10b production by T cells in osteoporotic patients.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2015
    Trial
  9. Trial
  10. Article
  11. Observational
  12. Article
  13. Review
  14. Article
  15. Article
  16. Advances in Parathyroid Hormone-based medicines.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Review
  17. Review
  18. Article
  19. Review
  20. Review

54 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

B C SilvaMetabolic Bone Diseases Unit, Division of Endocrinology, Department of Medicine, College of Physicians and Surgeons, Columbia University, USA.
A G Costa
N E Cusano
S Kousteni
J P Bilezikian
Columbia University · US

Funding

BONE PROPERTIES IN HYPOPARATHYROIDISM: EFFECTS OF PTHR01DK069350 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BILEZIKIAN, JOHN P · 2005 to 2014
$6.1M
Treatment of Hypoparathyroidism with Parathyroid HormoneR01FD002525 · FDA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BILEZIKIAN, JOHN P · 2005 to 2012
$2.1M
FDA HHS R01 FD002525NIDDK NIH HHS R01 DK069350
6 · The paper itself

Abstract

PTH, an 84-amino acid peptide hormone synthesized by the parathyroid glands, is essential for the maintenance of calcium homeostasis.While in its traditional metabolic role, PTH helps to maintain the serum calcium concentration within narrow, normal limits and participates as a determinant of bone remodeling, more specific actions, described as catabolic and anabolic are also well known. Clinically, the catabolic effect of PTH is best represented by primary hyperparathyroidism (PHPT), while the osteoanabolic effect of PTH is best seen when PTH or its biological amino-terminal fragment [PTH(1-34)] is used as a therapy for osteoporosis. These dual functions of PTH are unmasked under very specific pathological (PHPT) or therapeutic conditions. At the cellular level, PTH favors bone resorption, mostly by affecting the receptor activator of nuclear factor κ-B (RANK) ligand (RANKL)-osteoprotegerin- RANK system, leading to an increase in osteoclast formation and activity. Increased bone formation due to PTH therapy is explained best by its ability to enhance osteoblastogenesis and/or osteoblast survival. The PTH-induced bone formation is mediated, in part, by a decrease in SOST/sclerostin expression in osteocytes. This review focuses on the dual anabolic and catabolic actions of PTH on bone, situations where one is enhanced over the other, and the cellular and molecular mechanisms by which these actions are mediated.

Indexed as

Bone RemodelingAnimalsBone and BonesBone DensityBone ResorptionFemaleFractures, BoneHumansHyperparathyroidism, PrimaryOsteoblastsOsteogenesisOsteoporosis, PostmenopausalParathyroid HormoneRANK LigandRiskTeriparatideParathyroid HormoneRANK LigandTeriparatide

Identifiers

PMID21946081
PMCPMC4315330
OpenAlexW56470165

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.