Evidence map›Paper›PMID 24736703›Full record

ReviewAdvances in dental research2014

Alveolar bone loss: mechanisms, potential therapeutic targets, and interventions.

G Intini, Y Katsuragi, K L Kirkwood, S Yang

Open access · greenAbstract readReview
In one paragraph

Review in Advances in dental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Review
  6. Drug design, development and therapy · 2020
    Article
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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

4 authors at 4 institutions in 2 countries.

G IntiniDepartment of Oral Medicine, Infection, and Immunity, Harvard School of Dental Medicine, 188 Longwood Avenue, REB 513, Boston, MA 02115, USA.
Y Katsuragi
K L Kirkwood
S Yang
Harvard Stem Cell Institute · USHarvard University · USMedical University of South Carolina · USSunstar (Japan) · JP

Funding

Pilot and Feasibility Project ProgramP30GM103331 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KERN, MICHAEL J · 2012 to 2016
$5.2M
Role of RGS12, a Regulator of G protein Signaling, in Bone RemodelingR01AR066101 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$1.8M
Negative Regulation of Innate Immune Responses through MAPK PhosphatasesR01DE018290 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIRKWOOD, KEITH L · 2007 to 2011
$1.8M
Function of Regulator of G protein signaling in aging skeletonR01AG048388 · NIA · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$1.7M
BMP2 regulation of the intramembranous bone stem cell nicheR00DE021069 · NIDCR · HARVARD MEDICAL SCHOOL · PI INTINI, GIUSEPPE · 2012 to 2014
$738k
Regulation of (Ca2+)i oscillation and osteoclast differentiation by RGS12K08AR055678 · NIAMS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI YANG, SHUYING · 2008 to 2010
$311k
BMP2 regulation of the intramembranous bone stem cell nicheK99DE021069 · NIDCR · HARVARD MEDICAL SCHOOL · PI INTINI, GIUSEPPE · 2010 to 2011
$260k
The Role and Mechanism of RGS12 in Bone ResorptionR03DE016857 · NIDCR · FORSYTH INSTITUTE · PI YANG, SHUYING · 2005 to 2006
$178k
NIAMS NIH HHS AR055678NIAMS NIH HHS K08 AR055678NIAMS NIH HHS R01 AR066101NIA NIH HHS R01 AG048388NIDCR NIH HHS DE016857NIDCR NIH HHS K99 DE021069NIDCR NIH HHS R00 DE021069NIDCR NIH HHS R01 DE018290NIDCR NIH HHS R01DE018290NIDCR NIH HHS R03 DE016857NIGMS NIH HHS P30 GM103331NIGMS NIH HHS P30GM103331
6 · The paper itself

Abstract

This article reviews recent research into mechanisms underlying bone resorption and highlights avenues of investigation that may generate new therapies to combat alveolar bone loss in periodontitis. Several proteins, signaling pathways, stem cells, and dietary supplements are discussed as they relate to periodontal bone loss and regeneration. RGS12 is a crucial protein that mediates osteoclastogenesis and bone destruction, and a potential therapeutic target. RGS12 likely regulates osteoclast differentiation through regulating calcium influx to control the calcium oscillation-NFATc1 pathway. A working model for RGS10 and RGS12 in the regulation of Ca(2+) oscillations during osteoclast differentiation is proposed. Initiation of inflammation depends on host cell-microbe interactions, including the p38 mitogen-activated protein kinase (MAPK) signaling pathway. Oral p38 inhibitors reduced lipopolysaccharide (LPS)-induced bone destruction in a rat periodontitis model but showed unsatisfactory safety profiles. The p38 substrate MK2 is a more specific therapeutic target with potentially superior tolerability. Furthermore, MKP-1 shows anti-inflammatory activity, reducing inflammatory cytokine biosynthesis and bone resorption. Multipotent skeletal stem cell (SSC) populations exist within the bone marrow and periosteum of long bones. These bone-marrow-derived SSCs and periosteum-derived SSCs have shown therapeutic potential in several applications, including bone and periodontal regeneration. The existence of craniofacial bone-specific SSCs is suggested based on existing studies. The effects of calcium, vitamin D, and soy isoflavone supplementation on alveolar and skeletal bone loss in post-menopausal women were investigated. Supplementation resulted in stabilization of forearm bone mass density and a reduced rate of alveolar bone loss over 1 yr, compared with placebo. Periodontal attachment levels were also well-maintained and alveolar bone loss suppressed during 24 wk of supplementation.

Indexed as

Alveolar Bone LossBone ResorptionCalciumFemaleHumansImmunity, InnateIsoflavonesMiddle AgedPostmenopauseRGS ProteinsSignal TransductionStem CellsVitamin DCalciumIsoflavonesRGS ProteinsVitamin Dmenopausemesenchymal stem cellsp38 inhibitorsp38 MAPKregulator of G protein signalingskeletal stem cells

Identifiers

PMID24736703
PMCPMC6636231
OpenAlexW2165943443

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.