Evidence map›Paper›PMID 40011000›Full record

ArticleIn vivo (Athens, Greece)

Analysis of Risedronate Analog on Extraction Socket Healing in Mice.

Moeka Kasagawa, Yuichi Mine, Mizuho Sano, Yukinaga Kurokui, Ayano Ueda, Masato Kaku, Hiroki Nikawa, Takeshi Murayama

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

8 authors.

Moeka Kasagawa *Department of Medical Systems Engineering, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yuichi Mine *Department of Medical Systems Engineering, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan; mine@hiroshima-u.ac.jp.
Mizuho SanoDepartment of Medical Systems Engineering, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yukinaga KurokuiDepartment of Medical Systems Engineering, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Ayano UedaDepartment of Medical Systems Engineering, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Masato KakuDepartment of Anatomy and Functional Restorations, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hiroki NikawaDepartment of Oral Biology & Engineering, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Takeshi MurayamaDepartment of Medical Systems Engineering, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimMedication-related osteonecrosis of the jaw (MRONJ) is a severe adverse effect associated with anti-resorptive medications like nitrogen-containing bisphosphonates (N-BPs), particularly zoledronate (ZOL). This study aimed to investigate whether a BP analog with high bone affinity but minimal anti-resorptive activity, NE-58051, could induce MRONJ-like lesions in a mouse model. MATERIALS AND

methodsFemale C57BL/6J mice (n=6 per group) were administered ZOL (250 μg/kg intravenously, twice weekly) for one or two weeks, or NE-58051 (250 μg/kg intravenously, twice weekly) for two weeks. Two weeks after initiation of study, the bilateral first molars were extracted. Mice were euthanized after a total duration of four weeks. Histological assessments evaluated necrotic bone area and osteoclast activity at extraction sites. Serum tartrate-resistant acid phosphatase isoform 5b (TRAcP-5b) levels were measured.

resultsMice treated with ZOL for two weeks exhibited significant increases in empty osteocytic lacunae and necrotic bone area compared to the saline group, indicating the development of MRONJ-like lesions. NE-58051-treated mice did not show significant differences in necrotic bone area or osteoclast activity compared to controls. No significant differences were observed in serum TRAcP-5b levels among all groups.

conclusionHigh bone affinity without potent inhibition of bone resorption does not induce MRONJ-like lesions in mice. These findings suggest that the potent anti-resorptive activity of N-BPs is a key factor in MRONJ development, highlighting the importance of bone turnover suppression in the pathogenesis of this condition.

Indexed as

Bisphosphonate-Associated Osteonecrosis of the JawBone Density Conservation AgentsRisedronic AcidTooth ExtractionTooth SocketWound HealingAnimalsDiphosphonatesDisease Models, AnimalFemaleMiceMice, Inbred C57BLOsteoclastsTartrate-Resistant Acid PhosphataseZoledronic AcidBone Density Conservation AgentsDiphosphonatesRisedronic AcidTartrate-Resistant Acid PhosphataseZoledronic Acidbisphosphonate analogmouse model of ONJOsteonecrosis of the jaw (ONJ)

Identifiers

PMID40011000
PMCPMC11884466

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Registered trials

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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.