Evidence map›Paper›PMID 15936915›Full record

ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2005

Cellular basis for age-related changes in fracture repair.

Chuanyong Lu, Theodore Miclau, Diane Hu, Erik Hansen, Kathy Tsui, Christian Puttlitz, Ralph S Marcucio

Open access · greenAbstract read
In one paragraph

Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

117 citing papers in PubMed, 229 citations in OpenAlex.

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  13. Bioengineering (Basel, Switzerland) · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Geriatric trauma: there is more to it than just the implant!OTA international : the open access journal of orthopaedic trauma · 2024
    Review
  19. Review
  20. Review

57 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

7 authors at 1 institution in 1 country.

Chuanyong LuDepartment of Orthopaedic Surgery, San Francisco General Hospital, University of California at San Francisco, 1001 Potrero Avenue, San Francisco, CA 94110, USA.
Theodore Miclau
Diane Hu
Erik Hansen
Kathy Tsui
Christian Puttlitz
Ralph S Marcucio
San Francisco General Hospital · US

Funding

ROLE OF ANGIOGENESIS IN BONE REPAIRK08AR002164 · NIAMS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI MICLAU, THEODORE · 2000 to 2004
$574k
NIAMS NIH HHS K08 AR002164NIAMS NIH HHS KO8-AR002164
6 · The paper itself

Abstract

The goal of this work was to define cellular and molecular changes that occur during fracture healing as animals age. We compared the molecular, cellular, and histological progression of skeletal repair in juvenile (4 weeks old), middle-aged (6 months old), and elderly (18 months old) mice at 3, 5, 7, 10, 14, 21, 28, and 35 days post-fracture, using a non-stabilized tibia fracture model. Our histological and molecular analyses demonstrated that there was a sharp decline in fracture healing potential between juvenile and middle-aged animals, while a more subtle decrease in healing potential was apparent between middle-aged and elderly mice. By three days after fracture, chondrocytes expressing Collagen type II, and osteoblasts expressing osteocalcin, were present in calluses of juvenile, but not middle-aged or elderly, mice. At day 5 immature chondrocytes and osteoblasts were observed in calluses of middle-aged and elderly mice. While at this time, chondrocytes in juvenile mice were expressing Collagen type X (ColX) indicating that chondrocyte maturation was already underway. At day 7, chondrocytes expressing ColX were abundant in middle-aged mice while a small domain of ColX-positive chondrocytes were observed in elderly mice. Further, in juvenile and middle-aged mice, but not elderly mice, vascular invasion of the cartilage was underway by day 7. Juvenile mice had replaced nearly all of the cartilage by day 14, while cartilage was still present in the callus of middle-aged mice at day 21 and in elderly mice at day 28. In addition to these delays, histomorphometry revealed that elderly and middle-aged mice formed less bone than juveniles (p<0.001), while cartilage production was unaffected (p>0.22). Collectively, these data suggest that enhancing cell differentiation, improving osteoblast function, and accelerating endochondral ossification may significantly benefit the elderly.

Indexed as

Fracture HealingAgingAnimalsBony CallusCell DifferentiationChondrocytesMaleMiceOsteoblastsOsteogenesis

Identifiers

PMID15936915
PMCPMC2844440
OpenAlexW2087125520

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.