# Occlusal Overload and Periodontitis: Integrating Mechanisms, Clinical Evidence, and Emerging Perspectives—A Scoping Review

**Authors:** Pietro Leone, Julie Toby Thomas, Timo Sorsa, Mauno Könönen, Sukumaran Anil

PMC · DOI: 10.1155/ijod/9936924 · International Journal of Dentistry · 2026-03-02

## TL;DR

This review explores how excessive biting forces may worsen periodontitis by boosting inflammation and tissue breakdown, suggesting targeted interventions could improve treatment outcomes.

## Contribution

The study integrates clinical, animal, and in vitro evidence to clarify the role of occlusal overload in periodontitis progression and treatment response.

## Key findings

- Occlusal adjustment combined with periodontal therapy reduces probing depth and bacterial load more effectively than therapy alone.
- Mechanical loading increases inflammatory cytokines like IL-6 and TNF-α, and activates pathways such as IKK/NF-κB and YAP.
- MMP-8 release is consistently linked to collagen degradation in periodontal tissues under mechanical stress.

## Abstract

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.

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.

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.

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.

## Linked entities

- **Proteins:** MMP8 (matrix metallopeptidase 8), TNF (tumor necrosis factor)
- **Diseases:** periodontitis (MONDO:0005076)

## Full-text entities

- **Genes:** Vcam1 (vascular cell adhesion molecule 1) [NCBI Gene 22329] {aka CD106, Vcam-1}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}, Il6 (interleukin 6) [NCBI Gene 16193] {aka Il-6}, IL6R (interleukin 6 receptor) [NCBI Gene 3570] {aka CD126, HIES5, IL-1Ra, IL-6R, IL-6R-1, IL-6RA}, YAP1 (Yes1 associated transcriptional regulator) [NCBI Gene 10413] {aka COB1, YAP, YAP-1, YAP2, YAP65, YKI}, Pik3r1 (phosphoinositide-3-kinase regulatory subunit 1) [NCBI Gene 18708] {aka PI3K, p50alpha, p55alpha, p85alpha}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, MMP8 (matrix metallopeptidase 8) [NCBI Gene 4317] {aka CLG1, HNC, MMP-8, PMNL-CL}, ATHS (atherosclerosis susceptibility (lipoprotein associated)) [NCBI Gene 470] {aka ALP}, MMP3 (matrix metallopeptidase 3) [NCBI Gene 4314] {aka CHDS6, MMP-3, SL-1, STMY, STMY1, STR1}, Nfkb1 (nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105) [NCBI Gene 18033] {aka NF-KB1, NF-kappaB, NF-kappaB1, p105, p50, p50/p105}, Mapk8 (mitogen-activated protein kinase 8) [NCBI Gene 26419] {aka JNK, JNK1, Prkm8, SAPK1}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, Icam1 (intercellular adhesion molecule 1) [NCBI Gene 15894] {aka CD54, Icam-1, Ly-47, MALA-2}, Mmp3 (matrix metallopeptidase 3) [NCBI Gene 17392] {aka EMS-2, MMP-3, SL-1, SLN-1, SLN1, STR-1}, Yap1 (yes-associated protein 1) [NCBI Gene 22601] {aka Yap, Yap65, Yki, Yorkie}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, Cxcl15 (C-X-C motif chemokine ligand 15) [NCBI Gene 20309] {aka Il8, Scyb15, lungkine, weche}, Wnt4 (wingless-type MMTV integration site family, member 4) [NCBI Gene 22417] {aka Wnt-4}, Jun (Jun proto-oncogene, AP-1 transcription factor subunit) [NCBI Gene 16476] {aka AP-1, Junc, c-jun}, Bsp (black spleen) [NCBI Gene 103993], Ctnnb1 (catenin beta 1) [NCBI Gene 12387] {aka Bfc, Catnb, Mesc}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, TIMP1 (TIMP metallopeptidase inhibitor 1) [NCBI Gene 7076] {aka CLGI, EPA, EPO, HCI, TIMP, TIMP-1}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Ikbkb (inhibitor of kappaB kinase beta) [NCBI Gene 16150] {aka IKK-2, IKK-B, IKK-beta, IKK2, IKK[b], IKKbeta}, Nlrp3 (NLR family, pyrin domain containing 3) [NCBI Gene 216799] {aka AGTAVPRL, AII/AVP, Cias1, FCAS, FCU, MWS}, TTR (transthyretin) [NCBI Gene 7276] {aka AMYLD1, ATTR, CTS, CTS1, HEL111, HsT2651}, VCAM1 (vascular cell adhesion molecule 1) [NCBI Gene 7412] {aka CD106, INCAM-100}, TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600] {aka CD254, ODF, OPGL, OPTB2, RANKL, TNLG6B}
- **Diseases:** bone resorption (MESH:D001862), bleeding (MESH:D006470), root resorption (MESH:D012391), alveolar (MESH:D002282), CAL (MESH:D017622), tooth wear (MESH:D057085), PPD (MESH:C535387), PD (MESH:D007222), occlusal overload (MESH:D019190), Osteogenic (MESH:D012516), Periodontitis (MESH:D010518), Inflammation (MESH:D007249), injury (MESH:D014947), dysbiosis (MESH:D064806), diminished (MESH:D015354), IV (MESH:D006011), bacterial (MESH:D001424), resorption (MESH:D014091), aMMP-8 (OMIM:615401), tissue (MESH:D017695), Periodontal Disease (MESH:D010510), tissue destruction (MESH:D008105), Mobility (MESH:D014086), Occlusal trauma (MESH:D001157), bite collapse (MESH:D001261), bruxism (MESH:D002012), alveolar bone loss (MESH:D016301), RBL (MESH:D001847), aseptic (MESH:D008582)
- **Chemicals:** glyburide (MESH:D005905), LPS (MESH:D008070), BoP (-), XAV939 (MESH:C544261)
- **Species:** Treponema denticola (species) [taxon 158], Mus musculus (house mouse, species) [taxon 10090], Porphyromonas gingivalis (species) [taxon 837], Homo sapiens (human, species) [taxon 9606], Tannerella forsythia (species) [taxon 28112], Rodentia (rodent, order) [taxon 9989]
- **Cell lines:** L929 — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_AR58), MC3T3-E1 — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0409), THP-1 — Homo sapiens (Human), Childhood acute monocytic leukemia, Cancer cell line (CVCL_0006)

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## Figures

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## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12953732/full.md

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Source: https://tomesphere.com/paper/PMC12953732