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Updated: Aug 8, 2026

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Induction of Periodontitis via a Combination of Ligature and Lipopolysaccharide Injection in a Rat Model
Published on: February 17, 2023
Melatonin Restricts Periodontitis Related Neurodegeneration in Rats
Cem Arslan1, Nur Yorgancilar1, Oguz Kose1
1Department of Periodontology, Faculty of Dentistry, Recep Tayyip Erdoğan University, Rize, Turkey.
Oral Diseases
|August 7, 2026
Summary
Melatonin supplementation may prevent brain damage caused by periodontitis. This study shows melatonin reduces neuroinflammation, oxidative stress, and cell death in the brain, offering a potential therapeutic strategy for periodontitis-related neurological issues.
Area of Science:
- Neuroscience
- Periodontology
- Pharmacology
Background:
- Periodontitis is linked to neurodegenerative changes.
- Neuroinflammation, oxidative stress, and apoptosis are key pathological mechanisms.
- The hippocampus and cerebral cortex are vulnerable to periodontitis-associated damage.
Purpose of the Study:
- To investigate the preventive effects of melatonin on neurodegeneration in periodontitis.
- To assess melatonin's impact on neuroinflammatory, neurooxidative, and neuroapoptotic markers.
- To evaluate melatonin's role in mitigating periodontal tissue destruction.
Main Methods:
- An experimental periodontitis model was established in Sprague Dawley rats.
- Rats were divided into control, periodontitis (Ep), and periodontitis with melatonin (Ep+Mel) groups.
- Melatonin was administered systemically; tissues and serum were analyzed using various assays.
Main Results:
- Melatonin treatment significantly reduced histopathological damage, Caspase-3, GFAP, and Iba-1.
- Melatonin decreased levels of IL-1β, IL-1β/IL-10 ratio, Aβ1-42, TNF-α, TOS, and OSI.
- No significant changes were observed in TAS and IL-10 levels with melatonin treatment.
Conclusions:
- Systemic melatonin limits periodontal tissue destruction.
- Melatonin mitigates neuroinflammatory, neurooxidative, and neuroapoptotic changes in the brain.
- Melatonin shows potential as a therapeutic agent for periodontitis-associated neurological complications.

