ReviewBiology2022
Cellular Senescence and Periodontitis: Mechanisms and Therapeutics.
Review in Biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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.
Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Epigenetic mechanisms of gingival aging: biological basis, periodontal implications, and therapeutic perspectives.Odontology · 2026Review
- Circadian disruption and cellular senescence: emerging perspectives in periodontitis.Odontology · 2026Review
- Mechanobiological and Molecular Alterations in the Aging Dentin-Pulp Complex.Life (Basel, Switzerland) · 2026Article
- Circadian rhythm disruption affects cellular senescence through the BMAL1/CRY2/PER1 signaling pathway in periodontitis.Journal of molecular histology · 2026Article
- The Role of Cellular Senescence in Oral Health and Disease.International journal of molecular sciences · 2026Review
- Genome-wide profiling of salivary promoter-region DNA methylation in periodontitis: the Tromsø Study.BMC medical genomics · 2026Article
- Inflammation-responsive biomimetic hybrid nanovesicles reverse stem cell senescence by up-regulating SIRT1 to treat periodontitis.Journal of nanobiotechnology · 2026Article
- Identifying Shared Key Genes and Cellular Characteristics Between Chronic Periodontitis and Aging Using Integrative Single-Cell and Mendelian Randomization Analyses.BioMed research international · 2026Article
- Osteoimmune senescence in aging-related bone diseases.Frontiers in immunology · 2026Review
- Osteoimmune senescence in aging bone: from inflammaging dogma to cell-type-specific therapeutic windows.Frontiers in immunology · 2026Review
- Inflammation dynamics modulate periodontal stem cell fate and function.Frontiers in immunology · 2026Review
- CSF1R inhibitor (PLX3397) alleviates experimental periodontitis by reducing macrophage senescence through the PI3K/AKT/FOXO1 signaling pathway.Scientific reports · 2025Article
- Activating Transcription Factor 3 (ATF3) Regulates Cellular Senescence and Osteoclastogenesis via STAT3/ERK and p65/AP-1 Pathways in Human Periodontal Ligament Cells.International journal of molecular sciences · 2025Article
- ANXA2 regulates mitochondrial function and cellular senescence of PDLCs via AKT/eNOS signaling pathway under high glucose conditions.Scientific reports · 2025Article
- Association between adjustable dietary factors and periodontitis: NHANES 2009-2014 and Mendelian randomization.Journal of translational medicine · 2025Article
- Ovarian Aging: The Silent Catalyst of Age-Related Disorders in Female Body.Aging and disease · 2025Review
- Impact of Periodontitis and Oral Dysbiosis Metabolites in the Modulation of Accelerating Ageing and Human Senescence.Metabolites · 2025Review
- Integrative Transcriptomic and Machine Learning Analysis Identifies Key Senescence-Associated Secretory Phenotype Genes Associated With Immune Dysregulation in Periodontitis.Human mutation · 2025Article
- Carnosine alleviates oxidative stress to prevent cellular senescence by regulating Nrf2/HO-1 pathway: a promising anti-aging strategy for oral mucosa.Frontiers in pharmacology · 2025Article
- Cellular senescence: A new perspective on the suppression of periodontitis (Review).Molecular medicine reports · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Periodontitis is a chronic inflammatory disease which increases in prevalence and severity in the older population. Aging is a leading risk factor for periodontitis, which exacerbates alveolar bone loss and results in tooth loss in the elderly. However, the mechanism by which aging affects periodontitis is not well understood. There is considerable evidence to suggest that targeting cellular senescence could slow down the fundamental aging process, and thus alleviate a series of age-related pathological conditions, likely including alveolar bone loss. Recently, it has been discovered that the senescent cells accumulate in the alveolar bone and promote a senescence-associated secretory phenotype (SASP). Senescent cells interacting with bacteria, together with secreted SASP components altering the local microenvironment and inducing paracrine effects in neighboring cells, exacerbate the chronic inflammation in periodontal tissue and lead to more alveolar bone loss. This review will probe into mechanisms underlying excessive alveolar bone loss in periodontitis with aging and discuss potential therapeutics for the treatment of alveolar bone loss targeting cellular senescence and the SASP. Inspecting the relationship between cellular senescence and periodontitis will lead to new avenues of research in this field and contribute to developing potential translatable clinical interventions to mitigate or even reverse the harmful effects of aging on oral health.
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What OpenQuestion holds
Registered trials
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.