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Updated: Mar 6, 2026

Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
Occlusal Overload and Periodontitis: Integrating Mechanisms, Clinical Evidence, and Emerging Perspectives-A Scoping
Pietro Leone1, Julie Toby Thomas2,3, Timo Sorsa2,4
1Independent Researcher, SmileLongevityCare360 Centre, Naples, Italy.
Background:
Occlusal trauma has long been debated as a contributing factor in periodontitis. Excessive occlusal loading acting on inflamed tissues may accelerate periodontal breakdown through inflammatory and proteolytic pathways. This scoping review synthesizes current evidence from clinical, animal, and in vitro studies on the mechanistic and clinical interplay between occlusal trauma and periodontal degradation.
Methods:
In accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for scoping reviews (PRISMA-ScR), PubMed, Web of Science, Scopus, Embase, and Cochrane Library were searched for studies published 2014-2025. Clinical trials, observational studies, animal models, and in-vitro experiments evaluating occlusal loading in periodontitis were eligible. Study selection followed the PECO framework and targeted inflammatory mediators, aMMP-8 activity, and clinical periodontal outcomes.
Results:
Eighteen studies met the inclusion criteria: eight clinical, seven animal, and three in vitro. Clinical studies have reported that occlusal adjustment, when combined with periodontal therapy, yields greater reductions in probing depth (PD), bleeding on probing (BoP), and pathogenic bacterial load compared to periodontal therapy alone. Animal and in vitro studies consistently demonstrate that mechanical loading amplifies inflammatory cytokine production (e.g., interleukin [IL]-6 and TNF-α), activates signaling pathways (inhibitor of kappa B kinase/nuclear factor kappa [IKK/NF-κB] and yes-associated protein [YAP]), and suppresses osteogenic differentiation. The release of matrix metalloproteinases (MMPs), particularly MMP-8, was a recurring feature associated with collagen degradation.
Conclusions:
Occlusal trauma functions as a modifying factor that may exacerbate periodontitis progression in susceptible individuals, though it should not be considered an initiating cause of disease. The integration of occlusal assessment, active MMP-8 (aMMP-8) biomarker analysis, and targeted therapies may enhance periodontal treatment outcomes. However, the modest effect sizes observed in clinical studies suggest that selective rather than routine occlusal intervention may optimize the benefit-to-burden ratio. Further longitudinal and interventional studies are warranted to validate these findings and establish clinical guidelines.
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