Evidence map›Paper›PMID 39317350›Full record

ArticleJournal of clinical periodontology2025

Extracellular Release of a Disintegrin and Metalloproteinase Correlates With Periodontal Disease Severity.

Ahmad Aljohmani, Hakon Heinze, Federico Guillermo Gharzia, Bashar Reda, Ahmed Mohamed Mostafa Abdrabou, Sören L Becker, Markus Bischoff, Matthias Hannig, Daniela Yildiz

Abstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of clinical periodontology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Ahmad AljohmaniInstitute of Experimental and Clinical Pharmacology and Toxicology, PZMS, ZHMB, Saarland University, Homburg, Germany.ORCID 0000-0003-0982-3583
Hakon HeinzeInstitute of Experimental and Clinical Pharmacology and Toxicology, PZMS, ZHMB, Saarland University, Homburg, Germany.
Federico Guillermo GharziaInstitute of Experimental and Clinical Pharmacology and Toxicology, PZMS, ZHMB, Saarland University, Homburg, Germany.
Bashar RedaClinic of Operative Dentistry, Periodontology and Preventive Dentistry, University Hospital Saarland, Saarland University, Homburg, Germany.ORCID 0000-0001-8473-4260
Ahmed Mohamed Mostafa AbdrabouInstitute of Medical Microbiology and Hygiene, Saarland University, Homburg, Germany.
Sören L BeckerInstitute of Medical Microbiology and Hygiene, Saarland University, Homburg, Germany.ORCID 0000-0003-3634-8802
Markus BischoffInstitute of Medical Microbiology and Hygiene, Saarland University, Homburg, Germany.ORCID 0000-0001-6734-2732
Matthias HannigClinic of Operative Dentistry, Periodontology and Preventive Dentistry, University Hospital Saarland, Saarland University, Homburg, Germany.
Daniela YildizInstitute of Experimental and Clinical Pharmacology and Toxicology, PZMS, ZHMB, Saarland University, Homburg, Germany.ORCID 0000-0002-9702-8581

Funding

Deutsche Forschungsgemeinschaft DR1013/1-1German Academic Exchange Service (DAAD)HIPS-UdS TANDEM initiative
6 · The paper itself

Abstract

aimPeriodontal disease is driven by oral pathogens, including Porphyromonas gingivalis, and the release of inflammatory cytokines. These cytokines (e.g., TNF) or their receptors (e.g., IL-1R) are substrates of a disintegrin and metalloproteinases (ADAMs). In this study, we aimed to determine the effects of ADAMs on periodontal disease phenotypes. MATERIALS AND

methodsWestern blot and FRET-based activity measurements of the gingival crevicular fluid (GCF) of patients were compared with those of infected (P. gingivalis) or cytokine-stimulated oral keratinocytes and primary human neutrophils, respectively. This was accompanied by an analysis of the released extracellular vesicles and MMP9 activity.

resultsIn the GCF of patients, ADAM8 protein expression and activity were correlated with disease stage, whereas ADAM10 protein expression was inversely correlated with disease stage. Infection and the resulting cytokine release orchestrated the release of soluble ADAM8 by oral keratinocytes and primary neutrophils as soluble ectodomain and on exosomes, respectively. Furthermore, ADAM8 regulated the release of ADAM10 and MMP9.

conclusionDysregulation of cell-associated and extracellular ADAM proteolytic activity may be an essential regulatory element in the progression of periodontal disease driven by ADAM8. The influence of ADAM8 on disease onset and the evaluation of targeting ADAM8 as a potential and novel local treatment option should be addressed in future translational in vivo studies.

Indexed as

ADAM ProteinsAmyloid Precursor Protein SecretasesMembrane ProteinsPeriodontal DiseasesADAM10 ProteinAdultBacteroidaceae InfectionsCells, CulturedChronic PeriodontitisCytokinesDisease ProgressionFemaleGingival Crevicular FluidHumansKeratinocytesMaleADAM10 ProteinADAM10 protein, humanADAM8 protein, humanADAM ProteinsAmyloid Precursor Protein SecretasesCytokinesMatrix Metalloproteinase 9Membrane ProteinsMMP9 protein, humancell–matrix interactionsinfectious disease(s)matrix metalloproteinasesperiodontal diseaseproteases/proteinases

Identifiers

PMID39317350
PMCPMC11743067

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