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Asian Journal of Periodontics and Orthodontics

2025 Volume 5

Shared Inflammatory Pathways in Periodontitis and Orthodontic Tooth Movement: Implications for Bone Remodeling


, ,
  1. Department of Periodontics and Orthodontics, School of Dentistry, University of Michigan, Ann Arbor, United States.
  2. Department of Periodontics and Orthodontics, Faculty of Dentistry, Cairo University, Cairo, Egypt.
Abstract

Periodontitis and orthodontic tooth movement (OTM) represent two distinct yet interconnected processes in oral health, both characterized by inflammatory responses that drive bone remodeling. Periodontitis, a chronic bacterial-induced inflammatory disease, leads to progressive destruction of periodontal tissues, including alveolar bone loss through dysregulated immune responses and osteoclast activation. In contrast, OTM is a controlled, aseptic inflammatory process triggered by mechanical forces, facilitating tooth repositioning via coordinated bone resorption and formation within the periodontal ligament (PDL) and alveolar bone. Despite their differences—one pathological and the other therapeutic—these conditions share common inflammatory pathways, including cytokine signaling (e.g., IL-1, IL-6, TNF-α), RANKL/OPG axis, and immune-stromal cell interactions, which modulate osteoclastogenesis and osteoblast activity. This narrative review synthesizes recent evidence from peer-reviewed studies (2020–2025) to elucidate these shared mechanisms and their implications for bone remodeling. In periodontitis, bacterial dysbiosis activates innate and adaptive immunity, promoting pro-inflammatory mediators that uncouple bone resorption from formation, resulting in net bone loss. Similarly, in OTM, mechanical stress induces a sterile inflammation, with compression-side resorption and tension-side apposition, but excessive or dysregulated inflammation can lead to complications like root resorption. Overlapping pathways, such as NF-κB, MAPK, and Wnt signaling, highlight how systemic factors (e.g., obesity, diabetes) exacerbate both conditions. Advanced glycation end products (AGEs), glycolysis reprogramming, and mechanosensitive channels like Piezo1/2 further link metabolic and mechanical cues to inflammation. Understanding these convergences offers therapeutic insights, including immunomodulation (e.g., targeting CCR2+ macrophages or sclerostin) to enhance OTM efficiency while mitigating periodontitis progression. Adjunctive therapies like low-intensity pulsed ultrasound (LIPUS) or photobiomodulation (PBM) may optimize bone remodeling by dampening inflammation. This review underscores the osteoimmunological framework uniting periodontitis and OTM, paving the way for integrated clinical strategies to preserve alveolar bone integrity.


How to cite this article
Vancouver
Reed TB, El Sherif AK, Petrenko OV. Shared Inflammatory Pathways in Periodontitis and Orthodontic Tooth Movement: Implications for Bone Remodeling. Asian J Periodontics Orthod. 2025;5:288-97. https://doi.org/10.51847/bYMBjPPnbg
APA
Reed, T. B., El Sherif, A. K., & Petrenko, O. V. (2025). Shared Inflammatory Pathways in Periodontitis and Orthodontic Tooth Movement: Implications for Bone Remodeling. Asian Journal of Periodontics and Orthodontics, 5, 288-297. https://doi.org/10.51847/bYMBjPPnbg
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