Evidence map›Paper›PMID 17517365›Full record

ReviewBone2007

Molecular and cellular mechanisms of the anabolic effect of intermittent PTH.

Robert L Jilka

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Bone, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 322 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
322citing papers in PubMed, 1 pooled it
20.1field-weighted citation impact, top 1% 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

322 citing papers in PubMed, 1 synthesis or guideline pooled it, 701 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  12. The cellular effect of intermittent PTH treatment on bone remodeling and modeling in humans-a histomorphometry centered scoping review.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2025
    Article
  13. 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
  14. Article
  15. Review
  16. Bidirectional Interaction Between the Brain and Bone in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  17. Review
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  19. Review
  20. Article

262 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

1 author at 1 institution in 1 country.

Robert L JilkaDivision of Endocrinology and Metabolism, Slot 587 Center for Osteoporosis and Metabolic Bone Diseases, Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, 4301 W. Markham, Little Rock, AR 72205, USA. rljilka@uams.edu
University of Arkansas for Medical Sciences · US

Funding

TRANSGENIC MOUSE COREP01AG013918 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI WEINSTEIN, ROBERT STEWART · 1996 to 2016
$25.7M
PTH STIMULATED BONE FORMATIONR01AR046823 · NIAMS · UNIVERSITY OF ARKANSAS MED SCIS LTL ROCK · PI JILKA, ROBERT L · 2000 to 2004
$1.3M
NIAMS NIH HHS R01 AR046823NIAMS NIH HHS R01 AR46823NIA NIH HHS P01 AG013918NIA NIH HHS P01 AG13918
6 · The paper itself

Abstract

Intermittent administration of parathyroid hormone (PTH) stimulates bone formation by increasing osteoblast number, but the molecular and cellular mechanisms underlying this effect are not completely understood. In vitro and in vivo studies have shown that PTH directly activates survival signaling in osteoblasts; and that delay of osteoblast apoptosis is a major contributor to the increased osteoblast number, at least in mice. This effect requires Runx2-dependent expression of anti-apoptotic genes like Bcl-2. PTH also causes exit of replicating progenitors from the cell cycle by decreasing expression of cyclin D and increasing expression of several cyclin-dependent kinase inhibitors. Exit from the cell cycle may set the stage for pro-differentiating and pro-survival effects of locally produced growth factors and cytokines, the level and/or activity of which are known to be influenced by PTH. Observations from genetically modified mice suggest that the anabolic effect of intermittent PTH requires insulin-like growth factor-I (IGF-I), fibroblast growth factor-2 (FGF-2), and perhaps Wnts. Attenuation of the negative effects of PPAR gamma may also lead to increased osteoblast number. Daily injections of PTH may add to the pro-differentiating and pro-survival effects of locally produced PTH related protein (PTHrP). As a result, osteoblast number increases beyond that needed to replace the bone removed by osteoclasts during bone remodeling. The pleiotropic effects of intermittent PTH, each of which alone may increase osteoblast number, may explain why this therapy reverses bone loss in most osteoporotic individuals regardless of the underlying pathophysiology.

Indexed as

AnimalsApoptosisCell DifferentiationHumansMiceModels, BiologicalOsteoblastsOsteogenesisParathyroid HormoneParathyroid Hormone

Identifiers

PMID17517365
PMCPMC1995599
OpenAlexW2099028287

What OpenQuestion holds

Textmetadata
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.