Evidence map›Paper›PMID 25879791›Full record

ArticleJournal of periodontology2015

Odanacatib, A Cathepsin K-Specific Inhibitor, Inhibits Inflammation and Bone Loss Caused by Periodontal Diseases.

Liang Hao, Jianwei Chen, Zheng Zhu, Michael S Reddy, John D Mountz, Wei Chen, Yi-Ping Li

Open access · bronzeAbstract read
In one paragraph

Article in Journal of periodontology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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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.

Liang HaoDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL.
Jianwei ChenDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL.
Zheng ZhuDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL.
Michael S ReddyDepartment of Periodontology, University of Alabama at Birmingham School of Dentistry, Birmingham, AL.
John D MountzDepartment of Medicine, University of Alabama at Birmingham.
Wei ChenDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL.
Yi-Ping LiDepartment of Pathology, University of Alabama at Birmingham, Birmingham, AL.
University of Alabama at Birmingham · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
UAB Core Center for Musculoskeletal DisordersP30AR046031 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI PONNAZHAGAN, SELVARANGAN · 2001 to 2010
$5.6M
Inhibiting Periodontitis by Targeting Cathepsin K and Attenuating TLR SignalingR01DE023813 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2014 to 2023
$3.9M
NIAMS NIH HHS P30 AR046031NIDCR NIH HHS R01 DE023813NIDCR NIH HHS R01DE023813NIDDK NIH HHS P30 DK079626NIDDK NIH HHS P30DK079626NINDS NIH HHS P30 NS0474666
6 · The paper itself

Abstract

backgroundPeriodontitis is a bacteria-induced inflammatory disease mainly affecting periodontal tissues, leading to periodontal inflammation, bone breakdown, and loss of the tooth. The main obstacle for treating periodontitis effectively is the difficulty in finding a target that can inhibit bone loss and inflammation simultaneously. Recent studies showed that cathepsin K (CTSK) might have functions in the immune system besides its role in osteoclasts. Thus, targeting CTSK would have a potential therapeutic effect in both the bone system and the immune system during the progression of periodontitis.

methodsIn the current study, a small molecular inhibitor (odanacatib [ODN]) is explored to inhibit the function of CTSK in a bacteria-induced periodontitis mouse model.

resultsThe application of ODN decreased the number of osteoclasts, macrophages, and T cells, as well as the expression of Toll-like receptors (TLRs) in the periodontitis lesion area. Furthermore, lack of CTSK inhibited the expression of TLR4, TLR5, and TLR9 and their downstream cytokine signaling in the gingival epithelial cells in periodontitis lesions, demonstrating that the innate immune response was inhibited in periodontitis.

conclusionThe present results show that inhibition of CTSK can prevent bone loss and the immune response during the progression of periodontitis, indicating that CTSK is a promising target for treating inflammatory diseases such as periodontitis by affecting both osteoclasts and the immune system.

Indexed as

Alveolar Bone LossAnimalsAnti-Inflammatory AgentsBacteroidaceae InfectionsBiphenyl CompoundsCathepsin KDisease Models, AnimalEpithelial CellsFemaleGingivaGram-Negative Bacterial InfectionsImmunity, InnateMacrophagesMaleMiceMice, Inbred BALB CAnti-Inflammatory AgentsBiphenyl CompoundsCathepsin KCtsk protein, mouseodanacatibTlr4 protein, mouseTlr9 protein, mouseToll-Like Receptor 4Toll-Like Receptor 5Toll-Like Receptor 9Bone resorptioncathepsin Kmacrophagesosteoclastsperiodontal diseasesToll-like receptors

Identifiers

PMID25879791
PMCPMC4648620
OpenAlexW2096947296

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.