Evidence map›Paper›PMID 20809203›Full record

ReviewCurrent osteoporosis reports2010

Bone loss in diabetes: use of antidiabetic thiazolidinediones and secondary osteoporosis.

Beata Lecka-Czernik

Open access · hybridAbstract readReview
In one paragraph

Review in Current osteoporosis reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
6.5field-weighted citation impact, top 2% 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

75 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Bone health in diabetes mellitus.Reviews in endocrine & metabolic disorders · 2026
    Review
  4. Small Molecule Insulin Sensitisers: New Leads and Targets for Next-Generation Insulin Sensitising Strategies.Medicinal chemistry research : an international journal for rapid communications on design and mechanisms of action of biologically active agents · 2026
    Review
  5. The association between GLP-1 receptor agonists and fractures: a nationwide Danish nested case-control study.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2026
    Article
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  16. Article
  17. Extract ofInternational journal of molecular sciences · 2023
    Article
  18. Interactive Associations betweenPharmaceuticals (Basel, Switzerland) · 2023
    Article
  19. Article
  20. Article

15 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.

Beata Lecka-CzernikDepartment of Orthopaedic Surgery, Center for Diabetes and Endocrine Research, University of Toledo Medical Center, OH, 43614, USA. Beata.LeckaCzernik@utoledo.edu
University of Toledo Medical Center · US

Funding

Bone loss with aging occurs due to increased PPAR-g activity in marrow stem cellsR01AG028935 · NIA · UNIV OF ARKANSAS FOR MED SCIS · PI LECKA-CZERNIK, BEATA ANNA · 2006 to 2010
$1.5M
NIA NIH HHS AG 028935NIA NIH HHS R01 AG028935
6 · The paper itself

Abstract

Clinical evidence indicates that bone status is affected in patients with type 2 diabetes mellitus (T2DM). Regardless of normal or even high bone mineral density, T2DM patients have increased risk of fractures. One class of antidiabetic drugs, thiazolidinediones (TZDs), causes bone loss and further increases facture risk, placing TZDs in the category of drugs causing secondary osteoporosis. Risk factors for development of TZD-induced secondary osteoporosis are gender (women), age (elderly), and duration of treatment. TZDs exert their antidiabetic effects by activating peroxisome proliferator-activated receptor-γ (PPAR-γ) nuclear receptor, which controls glucose and fatty acid metabolism. In bone, PPAR-γ controls differentiation of cells of mesenchymal and hematopoietic lineages. PPAR-γ activation with TZDs leads to unbalanced bone remodeling: bone resorption increases and bone formation decreases. Laboratory research evidence points toward a possible separation of unwanted effects of PPAR-γ on bone from its beneficial antidiabetic effects by using selective PPAR-γ modulators. This review also discusses potential pharmacologic means to protect bone from detrimental effects of clinically used TZDs (pioglitazone and rosiglitazone) by using combinational therapy with approved antiosteoporotic drugs, or by using lower doses of TZDs in combination with other antidiabetic therapy. We also suggest a possible orthopedic complication, not yet supported by clinical studies, of delayed fracture healing in T2DM patients on TZD therapy.

Indexed as

AnimalsBone DensityCell DifferentiationDiabetes Mellitus, Type 2Drug CombinationsDrug Therapy, CombinationHumansHypoglycemic AgentsOsteoporosisPioglitazonePPAR gammaRosiglitazoneThiazolidinedionesDrug CombinationsHypoglycemic AgentsPioglitazonePPAR gammaRosiglitazoneThiazolidinediones

Identifiers

PMID20809203
PMCPMC2947013
OpenAlexW2168892366

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.