Effects of Nonsurgical Periodontal Treatment on Salivary Adipokines: A Systematic Review
Abstract
OBJECTIVES: Periodontitis is a chronic inflammatory disease contributing to systemic metabolic imbalances. Adipose tissue functions as an endocrine organ, releasing adipokines that influence insulin resistance and energy homeostasis. These mediators, such as visfatin, leptin, or adiponectin, may be modulated by periodontal inflammation. This review aims to synthesize current evidence on salivary adipokine levels in periodontitis and to assess the impact of nonsurgical periodontal treatment (NSPT) on these biomarkers. METHODS: A systematic review was conducted across PubMed, Cochrane Library, and Web of Science (April 2025), following PRISMA guidelines. Studies were included if they assessed salivary levels of adipokines (visfatin, adiponectin, leptin, vaspin, adipsin, resistin) before and after NSPT in periodontitis patients. Risk of bias was assessed using the Cochrane Risk of Bias tool, version 2 (RoB2), for randomized controlled trials, and the Newcastle-Ottawa scale for nonrandomized studies. RESULTS: Fifteen studies were included. Visfatin consistently significantly decreased after NSPT, suggesting a potential mechanistic link between periodontal inflammation and systemic metabolic pathways. Results for leptin, resistin, and adiponectin were less clear. CONCLUSION: Salivary visfatin levels consistently decreased following NSPT across all nine studies reporting this outcome. However, this signal is based on very low-certainty evidence. These findings are therefore hypothesis-generating and should not be interpreted as establishing a causal relationship between periodontal inflammation and systemic metabolic dysregulation. Further methodologically rigorous studies are warranted to determine whether changes in salivary visfatin reflect a clinically meaningful systemic effect or represent a local inflammatory phenomenon. CLINICAL RELEVANCE: Salivary adipokine variations in periodontitis - even without metabolic disorders - suggest that periodontal inflammation could potentially disrupt systemic metabolic balance. This highlights that periodontitis is not only a local disease and that controlling inflammation may help prevent systemic metabolic repercussions.
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BibTeX
@article{milin2026effects,
title = {{Effects of Nonsurgical Periodontal Treatment on Salivary Adipokines: A Systematic Review}},
author = {Clement Milin and Sophie Dorval and Octave Nadile Bandiaky and Xavier Struillou and Assem Soueidan and Emmanuelle Renard},
journal = {International Dental Journal},
year = {2026},
month = sep,
doi = {10.1016/j.identj.2026.109791},
url = {https://hal.science/hal-05740429v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Effects of Nonsurgical Periodontal Treatment on Salivary Adipokines: A Systematic Review
AU - Clement Milin
AU - Sophie Dorval
AU - Octave Nadile Bandiaky
AU - Xavier Struillou
AU - Assem Soueidan
AU - Emmanuelle Renard
PY - 2026
DA - 2026/09/07
JO - International Dental Journal
DO - 10.1016/j.identj.2026.109791
UR - https://hal.science/hal-05740429v1
AB - OBJECTIVES: Periodontitis is a chronic inflammatory disease contributing to systemic metabolic imbalances. Adipose tissue functions as an endocrine organ, releasing adipokines that influence insulin resistance and energy homeostasis. These mediators, such as visfatin, leptin, or adiponectin, may be modulated by periodontal inflammation. This review aims to synthesize current evidence on salivary adipokine levels in periodontitis and to assess the impact of nonsurgical periodontal treatment (NSPT) on these biomarkers. METHODS: A systematic review was conducted across PubMed, Cochrane Library, and Web of Science (April 2025), following PRISMA guidelines. Studies were included if they assessed salivary levels of adipokines (visfatin, adiponectin, leptin, vaspin, adipsin, resistin) before and after NSPT in periodontitis patients. Risk of bias was assessed using the Cochrane Risk of Bias tool, version 2 (RoB2), for randomized controlled trials, and the Newcastle-Ottawa scale for nonrandomized studies. RESULTS: Fifteen studies were included. Visfatin consistently significantly decreased after NSPT, suggesting a potential mechanistic link between periodontal inflammation and systemic metabolic pathways. Results for leptin, resistin, and adiponectin were less clear. CONCLUSION: Salivary visfatin levels consistently decreased following NSPT across all nine studies reporting this outcome. However, this signal is based on very low-certainty evidence. These findings are therefore hypothesis-generating and should not be interpreted as establishing a causal relationship between periodontal inflammation and systemic metabolic dysregulation. Further methodologically rigorous studies are warranted to determine whether changes in salivary visfatin reflect a clinically meaningful systemic effect or represent a local inflammatory phenomenon. CLINICAL RELEVANCE: Salivary adipokine variations in periodontitis - even without metabolic disorders - suggest that periodontal inflammation could potentially disrupt systemic metabolic balance. This highlights that periodontitis is not only a local disease and that controlling inflammation may help prevent systemic metabolic repercussions.
SN - 0020-6539
ER -