Evidence map›Paper›PMID 20601287›Full record

ArticleBone2010

Malfunction of bone marrow-derived osteoclasts and the delay of bone fracture healing in diabetic mice.

Toshiyuki Kasahara, Sinji Imai, Hideto Kojima, Miwako Katagi, Hiroshi Kimura, Lawrence Chan, Yoshitaka Matsusue

Abstract read
In one paragraph

Article in Bone, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  14. Altered microRNA profile during fracture healing in rats with diabetes.Journal of orthopaedic surgery and research · 2020
    Article
  15. Macrophage Control of Incipient Bone Formation in Diabetic Mice.Frontiers in cell and developmental biology · 2020
    Article
  16. Review
  17. Impact of Diabetes Mellitus on Bone Health.International journal of molecular sciences · 2019
    Review
  18. Article
  19. Article
  20. Article
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

7 authors at 2 institutions in 2 countries.

Toshiyuki KasaharaDepartment of Orthopedic Surgery, Shiga University of Medical Science, Otsu, Shiga 520-2192, Japan. tkasa@belle.shiga-med.ac.jp
Sinji Imai
Hideto Kojima
Miwako Katagi
Hiroshi Kimura
Lawrence Chan
Yoshitaka Matsusue
Shiga University of Medical Science · JPBaylor College of Medicine · US

Funding

MODELS FOR ATHEROSCLEROSIS RESEARCHR01HL051586 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CHAN, LAWRENCE · 1994 to 2014
$5.5M
NHLBI NIH HHS HL-51586NHLBI NIH HHS R01 HL051586
6 · The paper itself

Abstract

It is well known that bone fracture healing is delayed in diabetes mellitus, but the mechanism remains to be elucidated. Since several studies have demonstrated that diabetes causes abnormalities in bone marrow-derived cells, we used the streptozotocin (STZ)-induced diabetic mouse model after bone marrow transfer from green fluorescent protein (GFP) transgenic mice, and examined fracture healing. Compared with nondiabetic mice, diabetic mice at 3 weeks after fracture showed a decrease in mineralized callus, with the remainder consisting of cartilage. Bone formation parameters and mineralization rate were not altered in the STZ mice, but bone resorption parameters were significantly decreased. Therefore, the delayed bone formation in the STZ mice may have resulted from an impairment of cartilage resorption. Interestingly, we found that 80% of the osteoclasts in the callus were derived from bone marrow and the sizes of the osteoclasts as well as the resorption pits formed were significantly smaller in the diabetic mice. Moreover, transcript analysis using RNA isolated by laser capture microdissection (LCM) showed that the expression of DC-STAMP, a putative pivotal gene for osteoclast fusion, was decreased in osteoclasts from diabetic mice. Since the sustainability of osteoclast function depends on the controlled renewal of multinuclear osteoclasts, impaired osteoclast function in diabetes may contribute to decreased cartilage resorption and delayed endochondral ossification.

Indexed as

Fractures, BoneAnimalsBone Marrow CellsBone ResorptionCartilageDiabetes Mellitus, ExperimentalFracture HealingMaleMiceMice, Inbred C57BLMice, TransgenicOsteoclasts

Identifiers

PMID20601287
PMCPMC2926189
OpenAlexW1985416777

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.