Evidence map›Paper›PMID 25680368›Full record

ReviewJournal of dental research2015

Molecular and clinical aspects of drug-induced gingival overgrowth.

P C Trackman, A Kantarci

Open access · greenAbstract readReview
In one paragraph

Review in Journal of dental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
25.6field-weighted citation impact, top 1% 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

52 citing papers in PubMed, 152 citations in OpenAlex.

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  13. Genetic Variants in theInternational journal of molecular sciences · 2024
    Article
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  15. Review
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  18. Drug-Induced Gingival Overgrowth-Molecular Aspects of Drug Actions.International journal of molecular sciences · 2023
    Review
  19. 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

2 authors at 1 institution in 1 country.

P C TrackmanBoston University Henry M. Goldman School of Dental Medicine, Department of Molecular and Cell Biology, Boston, MA, USA trackman@bu.edu.
A KantarciForsyth Institute, Department of Applied Oral Sciences, Center for Periodontology, Cambridge, MA, USA.
Boston University · US

Funding

GROWTH FACTORS AND GINGIVAL FIBROSISR01DE011004 · NIDCR · BOSTON UNIVERSITY MEDICAL CAMPUS · PI TRACKMAN, PHILIP C · 2002 to 2011
$3.1M
NIDCR NIH HHS R01 DE011004NIDCR NIH HHS R01DE011004
6 · The paper itself

Abstract

Drug-induced gingival overgrowth is a tissue-specific condition and is estimated to affect approximately one million North Americans. Lesions occur principally as side-effects from phenytoin, nifedipine, or ciclosporin therapy in approximately half of the people who take these agents. Due to new indications for these drugs, their use continues to grow. Here, we review the molecular and cellular characteristics of human gingival overgrowth lesions and highlight how they differ considerably as a function of the causative drug. Analyses of molecular signaling pathways in cultured human gingival fibroblasts have provided evidence for their unique aspects compared with fibroblasts from the lung and kidney. These findings provide insights into both the basis for tissue specificity and into possible therapeutic opportunities which are reviewed here. Although ciclosporin-induced gingival overgrowth lesions exhibit principally the presence of inflammation and little fibrosis, nifedipine- and especially phenytoin-induced lesions are highly fibrotic. The increased expression of markers of gingival fibrosis, particularly CCN2 [also known as connective tissue growth factor (CTGF)], markers of epithelial to mesenchymal transition, and more recently periostin and members of the lysyl oxidase family of enzymes have been documented in phenytoin or nifedipine lesions. Some oral fibrotic conditions such as leukoplakia and oral submucous fibrosis, after subsequent additional genetic damage, can develop into oral cancer. Since many pathways are shared, the study of gingival fibrosis and comparisons with characteristics and molecular drivers of oral cancer would likely enhance understandings and functional roles of molecular drivers of these oral pathologies.

Indexed as

AnticonvulsantsCalcium Channel BlockersFibroblastsGingival OvergrowthHumansImmunosuppressive AgentsMolecular BiologySignal TransductionAnticonvulsantsCalcium Channel BlockersImmunosuppressive Agentscell signalingcollagen(s)connective tissue biologygingivainflammationinnate immunity

Identifiers

PMID25680368
PMCPMC4485217
OpenAlexW2163127301

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.