Polarization Profiles of T Lymphocytes and Macrophages Responses in Periodontitis

Cavalla, Franco; Hernández, Marcela

doi:10.1007/978-3-030-96881-6_10

Cited by 16 publications

(14 citation statements)

References 72 publications

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“…Th2/Treg-secreted cytokines also upregulate OPG to inhibit bone resorption ( 132 , 133 ). Th9 cells increase T-cell expansion and survival and Tfh cells found in the spleen and lymph nodes enhance antibody production by B-cells ( 133 , 137 , 138 ). CD8 + cytotoxic T-lymphocytes (CTL) release vesicles containing perforin and granzyme, inducing death of target cells.…”

Section: Periodontal Diseasementioning

confidence: 99%

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Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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Periodontitis involves the loss of connective tissue attachment and alveolar bone. Single cell RNA-seq experiments have provided new insight into how resident cells and infiltrating immune cells function in response to bacterial challenge in periodontal tissues. Periodontal disease is induced by a combined innate and adaptive immune response to bacterial dysbiosis that is initiated by resident cells including epithelial cells and fibroblasts, which recruit immune cells. Chemokines and cytokines stimulate recruitment of osteoclast precursors and osteoclastogenesis in response to TNF, IL-1β, IL-6, IL-17, RANKL and other factors. Inflammation also suppresses coupled bone formation to limit repair of osteolytic lesions. Bone lining cells, osteocytes and periodontal ligament cells play a key role in both processes. The periodontal ligament contains cells that exhibit similarities to tendon cells, osteoblast-lineage cells and mesenchymal stem cells. Bone lining cells consisting of mesenchymal stem cells, osteoprogenitors and osteoblasts are influenced by osteocytes and stimulate formation of osteoclast precursors through MCSF and RANKL, which directly induce osteoclastogenesis. Following bone resorption, factors are released from resorbed bone matrix and by osteoclasts and osteal macrophages that recruit osteoblast precursors to the resorbed bone surface. Osteoblast differentiation and coupled bone formation are regulated by multiple signaling pathways including Wnt, Notch, FGF, IGF-1, BMP, and Hedgehog pathways. Diabetes, cigarette smoking and aging enhance the pathologic processes to increase bone resorption and inhibit coupled bone formation to accelerate bone loss. Other bone pathologies such as rheumatoid arthritis, post-menopausal osteoporosis and bone unloading/disuse also affect osteoblast lineage cells and participate in formation of osteolytic lesions by promoting bone resorption and inhibiting coupled bone formation. Thus, periodontitis involves the activation of an inflammatory response that involves a large number of cells to stimulate bone resorption and limit osseous repair processes.

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Section: Periodontal Diseasementioning

confidence: 99%

“…The various cell populations from each major group respond to challenge and interact to generate an inflammatory host response. This table was adapted from information in ref: ( 138 ) and ( 140 ).…”

Section: Periodontal Diseasementioning

confidence: 99%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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“…The primary immunological factor is the destructive host inflammatory response, with a large amount of inflammatory cell infiltration, oxidative stress, osteoblast disorder, and osteoclast hyperactivity (Zhang et al, 2021). Despite the difficulty in defining the mechanisms of periodontitis, the consensus has been reached that the immune status of the periodontitis microenvironment is unbalanced, in which several immune cells like macrophages, DCs, and T cells are involved (Cavalla & Hernández, 2022; Darveau, 2009). Zinc affects a variety of different signaling pathways in myelocytes and lymphocytes in a concentration‐dependent manner (Glesne et al, 2006; Haase et al, 2008; Haase & Rink, 2009).…”

Section: The Role Of Zinc In Periodontal Inflammationmentioning

confidence: 99%

The changes and potential effects of zinc homeostasis in periodontitis microenvironment

Liu

et al. 2022

Oral Diseases

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Zinc is a very important and ubiquitous element, which is present in oral environment, daily diet, oral health products, dental restorative materials, and so on. However, there is a lack of attention to the role of both extracellular or intracellular zinc in the progression of periodontitis and periodontal regeneration. This review summarizes the characteristics of immunological microenvironment and host cells function in several key stages of periodontitis progression, and explores the regulatory effect of zinc during this process. We find multiple evidence indicate that zinc may be involved and play a key role in the stages of immune defense, inflammatory response and bone remodeling. Zinc supplementation in an appropriate dose range or regulation of zinc transport proteins can promote periodontal regeneration by either enhancing immune defense or up‐regulating local cells proliferation and differentiation functions. Therefore, zinc homeostasis is essential in periodontal remodeling and regeneration. More attention is suggested to be focused on zinc homeostasis regulation and consider it as a potential strategy in the studies on periodontitis treatment, periodontal‐guided tissue regeneration, implant material transformation, and so on.

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“…Although the phagocytosis of antigens initially activates macrophages, their function can be further enhanced by various factors such as IFN-γ secreted by activated T cells. Macrophages and T cells interact during immune responses, which facilitates the activation of macrophages [ 57 , 58 ].…”

Section: Damage and Repair Functions Of Macrophagesmentioning

confidence: 99%

Regulation of the Host Immune Microenvironment in Periodontitis and Periodontal Bone Remodeling

Han

Liu

et al. 2023

IJMS

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The periodontal immune microenvironment is a delicate regulatory system that involves a variety of host immune cells including neutrophils, macrophages, T cells, dendritic cells and mesenchymal stem cells. The dysfunction or overactivation of any kind of local cells, and eventually the imbalance of the entire molecular regulatory network, leads to periodontal inflammation and tissue destruction. In this review, the basic characteristics of various host cells in the periodontal immune microenvironment and the regulatory network mechanism of host cells involved in the pathogenesis of periodontitis and periodontal bone remodeling are summarized, with emphasis on the immune regulatory network that regulates the periodontal microenvironment and maintains a dynamic balance. Future strategies for the clinical treatment of periodontitis and periodontal tissue regeneration need to develop new targeted synergistic drugs and/or novel technologies to clarify the regulatory mechanism of the local microenvironment. This review aims to provide clues and a theoretical basis for future research in this field.

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Polarization Profiles of T Lymphocytes and Macrophages Responses in Periodontitis

Cited by 16 publications

References 72 publications

Impact of the host response and osteoblast lineage cells on periodontal disease

Impact of the host response and osteoblast lineage cells on periodontal disease

The changes and potential effects of zinc homeostasis in periodontitis microenvironment

Regulation of the Host Immune Microenvironment in Periodontitis and Periodontal Bone Remodeling

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