ReviewAnimal cells and systems2026
Oxidative stress and metabolic dysfunction in oral lichen planus pathogenesis.
Review in Animal cells and systems, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Oral Lichen Planus and Oral Lichenoid Lesion in Pediatric Patients: A Narrative Review of Published Case Reports.Reports (MDPI) · 2026Review
- Association of Sleep Quality, Nutritional Factors, and Salivary Melatonin and Cortisol Levels with Oral Lichen Planus: A Case-Control Study.Biomedicines · 2026Article
- Melissa officinalis extract selectively suppresses STAT1 signaling in oral epithelial cells.Frontiers in immunology · 2026Article
- Hydrogen: a review of the effects and underlying mechanisms in oral diseases.Frontiers in pharmacology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oral lichen planus (OLP) is a chronic, immune-mediated inflammatory disease of the oral mucosa that can cause persistent pain and has a recognized, though relatively low, risk of malignant transformation. Recent studies have identified oxidative and nitrosative stress as key contributors to the pathophysiology of OLP. Excessive production of reactive oxygen and nitrogen species, combined with reduced antioxidant defenses, leads to cellular damage, including lipid peroxidation, protein modification, and DNA injury. This oxidative imbalance drives keratinocyte apoptosis and sustains inflammatory signaling, creating a pro-inflammatory tissue environment. In parallel, metabolic dysfunction is increasingly recognized in OLP, characterized by altered energy production and nutrient utilization that disrupt tissue homeostasis. These two processes are closely linked, as oxidative stress impairs metabolic pathways, while metabolic alterations further increase oxidative burden, forming a self-reinforcing cycle that perpetuates mucosal injury and chronic inflammation. Clinically, markers of oxidative stress and metabolic imbalance, particularly those detectable in saliva, show promise for non-invasive diagnosis and risk assessment. Therapeutic strategies aimed at restoring redox balance and improving metabolic regulation represent emerging avenues beyond conventional symptom management. Understanding the crosstalk between oxidative stress and metabolism offers new opportunities for precision medicine approaches to improve the diagnosis, treatment, and long-term outcomes of patients with OLP.
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What Socratic 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 Socratic graph.