Skip to main page content
U.S. flag

An official website of the United States government

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Apr;21(2):128-146.
doi: 10.1007/s11914-023-00774-x. Epub 2023 Mar 2.

Osteoimmunology in Periodontitis and Orthodontic Tooth Movement

Affiliations
Review

Osteoimmunology in Periodontitis and Orthodontic Tooth Movement

Bushra Alghamdi et al. Curr Osteoporos Rep. 2023 Apr.

Abstract

Purpose of review: To review the role of the immune cells and their interaction with cells found in gingiva, periodontal ligament, and bone that leads to net bone loss in periodontitis or bone remodeling in orthodontic tooth movement.

Recent findings: Periodontal disease is one of the most common oral diseases causing inflammation in the soft and hard tissues of the periodontium and is initiated by bacteria that induce a host response. Although the innate and adaptive immune response function cooperatively to prevent bacterial dissemination, they also play a major role in gingival inflammation and destruction of the connective tissue, periodontal ligament, and alveolar bone characteristic of periodontitis. The inflammatory response is triggered by bacteria or their products that bind to pattern recognition receptors that induce transcription factor activity to stimulate cytokine and chemokine expression. Epithelial, fibroblast/stromal, and resident leukocytes play a key role in initiating the host response and contribute to periodontal disease. Single-cell RNA-seq (scRNA-seq) experiments have added new insight into the roles of various cell types in the response to bacterial challenge. This response is modified by systemic conditions such as diabetes and smoking. In contrast to periodontitis, orthodontic tooth movement (OTM) is a sterile inflammatory response induced by mechanical force. Orthodontic force application stimulates acute inflammatory responses in the periodontal ligament and alveolar bone stimulated by cytokines and chemokines that produce bone resorption on the compression side. On the tension side, orthodontic forces induce the production of osteogenic factors, stimulating new bone formation. A number of different cell types, cytokines, and signaling/pathways are involved in this complex process. Inflammatory and mechanical force-induced bone remodeling involves bone resorption and bone formation. The interaction of leukocytes with host stromal cells and osteoblastic cells plays a key role in both initiating the inflammatory events as well as inducing a cellular cascade that results in remodeling in orthodontic tooth movement or in tissue destruction in periodontitis.

Keywords: Adaptive immune response; Gingivitis; Innate immune response; Lymphocyte; NF-kB; Neutrophil; RANKL.

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Impact of inflammation of the periodontium. Inflammation inhibits osteogenic transcription factors, growth factors, and bone matrix production of osteoblast. Simultaneously, inflammation stimulates inhibitors which block osteogenic signaling or stimulates apoptosis of bone cells [–71]
Fig. 2
Fig. 2
Compression vs. tension side in OTM. A On the compression side, the PDL is infiltrated by a large number of cells the produce inflammatory mediators (activated fibroblasts, mesenchymal stem cells, granulocytes, mononuclear phagocytes, M1 macrophages, osteoclasts, T lymphocytes). Later, anti-inflammatory T and B regulatory lymphocytes reduce the aseptic inflammatory response. B Compared to the compression side, the tension side has fewer proinflammatory leukocytes. The stretched PDL on the tension side exhibits a high degree of fibroblast activation, differentiation of mesenchymal stem cells to osteoblasts, and the presence of M2 macrophages

Similar articles

Cited by

References

    1. Lenartova M, Tesinska B, Janatova T, Hrebicek O, Mysak J, Janata J, Najmanova L. The oral microbiome in periodontal health. Front Cell Infect Microbiol. 2021;11:629723. - PMC - PubMed
    1. Wolf TG, Cagetti MG, Fisher J-M, Seeberger GK, Campus G. Non-communicable diseases and oral health: an overview. Front Oral Health. 2021;2:725460–725460. - PMC - PubMed
    1. Hajishengallis G, Lamont RJ, Graves DT. The enduring importance of animal models in understanding periodontal disease. Virulence. 2015;6:229–35. - PMC - PubMed
    1. Hajishengallis G, Lamont RJ. Polymicrobial communities in periodontal disease: their quasi-organismal nature and dialogue with the host. Periodontol. 2021;2000(86):210–30. - PMC - PubMed
    2. This review discusses the concept of the ‘polymicrobial synergy and dysbiosis’ (PSD) model of periodontal disease pathogenesis and its effect on dysregulated host inflammatory response.

    1. Xiao W, Li S, Pacios S, Wang Y, Graves DT. Bone remodeling under pathological conditions. Front Oral Biol. 2016;18:17–27. - PMC - PubMed

Publication types