Evidence map›Paper›PMID 25243055›Full record

ArticleTranslational endocrinology & metabolism2010

Pathogenesis of Osteoporosis.

Sundeep Khosla

Open access · greenAbstract read
In one paragraph

Article in Translational endocrinology & metabolism, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
5.7field-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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Drug discovery of sclerostin inhibitors.Acta pharmaceutica Sinica. B · 2022
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
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.

Sundeep KhoslaEndocrine Research Unit, College of Medicine, Mayo Clinic, Rochester, MN.
Mayo Clinic · US

Funding

SEX STEROIDS, GROWTH FACTORS, &BONE CELL FUNCTIONP01AG004875 · NIA · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 1985 to 2019
$30.8M
EPIDEMIOLOGY OF AGE-RELATED BONE LOSS, &FRACTURESR01AR027065 · NIAMS · MAYO CLINIC ROCHESTER · PI AMIN, SHREYASEE, KHOSLA, SUNDEEP · 1986 to 2020
$14.9M
Estrogen Regulation of the Bone Marrrow AdipocyteR01AG028936 · NIA · MAYO CLINIC ROCHESTER · PI KHOSLA, SUNDEEP · 2006 to 2010
$1.7M
NIAMS NIH HHS R01 AR027065NIA NIH HHS P01 AG004875NIA NIH HHS R01 AG028936
6 · The paper itself

Abstract

As for most multifactorial disorders, the pathogenesis of osteoporosis is complex, and a different set of mechanisms may be operative in any given individual. However, there are certain common causes of bone loss and increased fracture risk with aging in most people. These include genetic factors contributing to the acquisition of peak bone mass, illnesses affecting skeletal growth and development, sex steroid deficiency following the menopause in women and with aging in men, and intrinsic, age-related changes in bone metabolism. Superimposed on these factors are specific secondary causes of bone loss, such as corticosteroid use or other illnesses affecting bone metabolism that may contribute to fracture risk in individuals exposed to these factors. The past decade has witnessed tremendous advances in our understanding of each of these various causes of bone loss, leading to the development of novel, mechanism-based therapeutic approaches to prevent and treat this important public health disorder.

Indexed as

bone lossfracturesosteoporosis

Identifiers

PMID25243055
PMCPMC4167368
OpenAlexW1466306692

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.