The role of secreted osteoclastogenic factor of activated T cells in bone remodeling

Zhang, Ruonan; Peng, Shuang; Zhu, Guoxin

doi:10.1016/j.jdsr.2022.07.001

Cited by 8 publications

(4 citation statements)

References 58 publications

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“…Several co-stimulators are needed to facilitate osteoclastogenesis including osteoclast-associated receptor (OSCAR), immunoreceptor tyrosine-based activation motif (ITAM), DNAX associated protein 12kD size (DAP12) and FcϵR1 gamma chain (FcRγ) ( 31 , 32 ). Secreted osteoclastogenic factor of activated T cells (SOFAT) is produced by activated T cells and stimulates bone resorption in the absence of osteoblasts or RANKL ( 33 ). Dendritic cell-specific transmembrane protein (DC-STAMP) plays an essential role in the formation of multinucleated osteoclasts ( 34 , 35 ).…”

Section: Osteoblasts Osteocytes Periodontal Ligament and Osteoclast C...mentioning

confidence: 99%

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: Osteoblasts Osteocytes Periodontal Ligament and Osteoclast C...mentioning

confidence: 99%

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

Zhou

Graves²

2022

Front. Immunol.

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“…As a dynamic remodeling tissue, bone is continuously graded and built. Osteoblasts and osteoclasts and their interactions show crucial effects in balancing the resorption and deposition of bone (Zhang et al, 2022). Osteoblasts facilitate bone formation by generating a bone matrix (Henderson & Kaiser, 2018).…”

Section: Resultsmentioning

confidence: 99%

Mechanisms of mechanical force aggravating periodontitis: A review

Liu

Yue

et al. 2023

Oral Diseases

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Periodontitis is a widespread oral disease accompanied by uncontrolled inflammation‐related tissue destruction. Periodontitis is related to various factors. Among them, occlusal trauma can aggravate the severity of periodontitis and has been attracting a great deal of attention. We systematically searched PubMed and Web of Science databases for related articles. Keywords for the search were “mechanical force”, “mechanical stress”, “occlusal trauma” and “periodontitis”. This review focuses on the effect of mechanical forces on periodontitis and discusses the possible pivotal targets participating in this process. We elucidated and summarized 21 articles that reported on our topic. Several biological processes and pathways that participate in enhancing the inflammatory response to mechanical stress have been studied, including the regulation of osteogenesis and osteoclastic resorption balance, Yes‐associated protein signaling, induction of collagen destruction, and regulation of programmed cell death. Mechanical force enhances the process of periodontitis in multiple ways. However, currently, no studies have further examined its underlying mechanism. Understanding the specific roles of mechanical forces may assist in the treatment of periodontitis with traumatic occlusal trauma.

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“…Orthodontic tooth movement (OTM) requires bone remodeling, which results from complex processes of aseptic inflammation. Recent works have confirmed a close relationship between the immune and skeletal systems [ 1 , 2 , 3 , 4 , 5 ]. Studies have shown that bone remodeling involves osteoclasts’ (OC) and osteoblasts’ (OB) differentiation and activation, mediated by immune system [ 1 , 6 , 7 , 8 ].…”

Section: Introductionmentioning

confidence: 94%

Influence of Different Orthodontic Brackets on Cytokine and Cortisol Profile

et al. 2023

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Background and Objectives: Orthodontic tooth movement (OTM) requires bone remodeling resulting from complex processes of aseptic inflammation. Recent studies have confirmed close interaction between the immune and skeletal systems. In addition, various orthodontic appliances including fixed systems affect the sublingual microbial composition, and the likelihood of developing inflammatory reactions of the gums is high, especially early in the treatment period. It is known that these systems have both positive and negative effects on the humoral and cellular immune responses. The main aim of the study was to evaluate the influence of self-ligating and conventional brackets on the salivary concentrations of cytokines (IL-6, osteoprotegerin (OPG), TNF-alpha, and IFN-gamma) and cortisol as a marker of stress. Materials and Methods: Forty patients were analyzed at baseline (T0) and 2 months (T2) after fixing self-ligating (Ormco Damond Q) and conventional brackets (Ormco Mini Diamond). Salivary cytokine and cortisol concentrations were evaluated by commercial ELISA kits. Results: Outcomes of our study showed that after two months of treatment with either of these brackets, IFN-gamma and IL-6 levels did not change. However, TNF-alpha decreased with self-ligating brackets (13.36 to 8.32, p = 0.002). The self-ligating bracket system also affects OPG concentration and cortisol levels 2 months after orthodontic activation. The level of OPG in the group of self-ligating brackets decreased significantly (8.55 to 2.72, p = 0.003). Cortisol concentration was significantly higher in the self-ligation group (25.72 to 48.45, p = 0.001) due to the effect of sustained strength movements. Conclusions: Thus, the use of self-ligating and conventional brackets has a different effect on the concentration of cortisol and cytokines (OPG and TNF-alpha) in saliva 2 months after their fixation. Further longitudinal studies are necessary to explore why OPG levels are decreased in case of self-ligating cases and how OPG levels are related to clinical improvement.

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The role of secreted osteoclastogenic factor of activated T cells in bone remodeling

Cited by 8 publications

References 58 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

Mechanisms of mechanical force aggravating periodontitis: A review

Influence of Different Orthodontic Brackets on Cytokine and Cortisol Profile

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