Evidence map›Paper›PMID 33187558›Full record

ArticleBMC pharmacology & toxicology2020

A new anabolic compound, LLP2A-Ale, reserves periodontal bone loss in mice through augmentation of bone formation.

Min Jiang, Lixian Liu, Ruiwu Liu, Kit S Lam, Nancy E Lane, Wei Yao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC pharmacology & toxicology, 2020. 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
0.2field-weighted citation impact, top 46% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

6 authors at 4 institutions in 2 countries.

Min JiangDepartment of Internal Medicine, University of California, Davis Medical Center, 4625 2nd Avenue, Sacramento, CA, 95817, USA.
Lixian LiuDepartment of Internal Medicine, University of California, Davis Medical Center, 4625 2nd Avenue, Sacramento, CA, 95817, USA.
Ruiwu LiuDepartment of Biochemistry & Molecular Medicine, University of California Davis, Sacramento, CA, 95817, USA.
Kit S LamDepartment of Biochemistry & Molecular Medicine, University of California Davis, Sacramento, CA, 95817, USA.
Nancy E LaneDepartment of Internal Medicine, University of California, Davis Medical Center, 4625 2nd Avenue, Sacramento, CA, 95817, USA.
Wei YaoDepartment of Internal Medicine, University of California, Davis Medical Center, 4625 2nd Avenue, Sacramento, CA, 95817, USA. yao@ucdavis.edu.ORCID 0000-0002-1198-1161
University of California, Davis · USUniversity of California Davis Medical Center · USShanghai Jiao Tong University · CNYunnan Vocational College of Mechanical and Electrical Technology · CN

Funding

Center for Dental, Oral, and Craniofacial Tissue and Organ Regeneration (C-DOCTOR)U24DE026914 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAI, YANG, CHEN, YONG · 2017 to 2019
$12.0M
6 · The paper itself

Abstract

backgroundCurrently, there are no effective medications to reverse periodontal disease (PD)-induced bone loss. The objective of this study was to test a new anabolic compound, LLP2A-Ale, or with the combination treatment of mesenchymal stromal cell (MSC), in the treatment of bone loss secondary to PD.

methodsPD was induced in mice by placing a ligature around the second right molar. At one week after disease induction, the mice were treated with placebo, LLP2A-Ale, MSCs, or combination of LLP2A-Ale + MSCs, and euthanized at week 4.

resultsWe found that PD induced alveolar bone loss that was associated with reduced bone formation. LLP2A-Ale alone or in combination with MSCs sustained alveolar bone formation and reversed alveolar bone loss. Additionally, PD alone caused systemic inflammation and increased the circulating levels of G-CSF, IP-10, MIP-1a, and MIP2, which were suppressed by LLP2A-Ale +/- MSCs. LLP2A-Ale +/- MSCs increased bone formation at the peripheral skeletal site (distal femur), which was otherwise suppressed by PD.

conclusionOur findings indicated that LLP2A-Ale treatment rescued alveolar bone loss caused by PD, primarily by increasing bone formation. LLP2A-Ale also attenuated the circulating levels of a series of inflammatory cytokines and reversed the PD-induced suppression of systemic bone formation.

Indexed as

Disease Models, AnimalAlveolar Bone LossAnimalsDipeptidesMaleMaxillary DiseasesMiceMice, Inbred BALB COsteogenesisPeriodontitisPhenylurea CompoundsDipeptidesLLP2A compoundPhenylurea Compounds

Identifiers

PMID33187558
PMCPMC7664094
OpenAlexW3100654491

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.