Phenotypes, roles, and modulation of regulatory lymphocytes in periodontitis and its associated systemic diseases

Zou, Hang; Zhou, Niu; Huang, Yilian; Luo, Aoxiang; Sun, Jianbo

doi:10.1002/jlb.3vmr0321-027rrr

Cited by 13 publications

(8 citation statements)

References 159 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The production of opsonizing antibodies makes the targeting of microbes by phagocytic cells more efficient. B-regs are a B-cell subset, producing IL-10, IL-35, and TGF-β1 to reduce inflammation and inhibit bone resorption ( 139 , 141 ). Mice with B-cell deficiency have increased ligature induced periodontal bone loss compared to wild -type mice, suggesting that B-cells may be protective ( 142 ).…”

Section: Periodontal Diseasementioning

confidence: 99%

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

Zhou

Graves²

2022

Front. Immunol.

View full text Add to dashboard Cite

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.

show abstract

Section: Periodontal Diseasementioning

confidence: 99%

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

Zhou

Graves²

2022

Front. Immunol.

View full text Add to dashboard Cite

show abstract

“…LAPTM5, a negative regulator of T and B cell receptor and a positive modulator of macrophages, is preferentially expressed in immune cells [12,13]. T and B cells are the main immunosuppressive cells that maintain immune homeostasis [14]. B cells IgG could protect the host from periodontopathogen infection [15], and CD4 T-cell subset also plays a signi cant role in periodontitis [16].…”

Section: Discussionmentioning

confidence: 99%

Identification of hub genes and biological mechanisms associated with periodontitis and diabetes

Luo

Liang

Chen

et al. 2023

Preprint

View full text Add to dashboard Cite

Background Periodontitis is independent associated with s diabetes (DM). However, the molecular mechanisms of complex interactions between DM and periodontitis are still unclear. This study was aim to explore the shared genes and common signatures of DM and periodontitis via bioinformatic analysis. Methods The series matrix files of GSE7014 of DM and GSE16134 of periodontitis were downloaded from Gene Expression Omnibus (GEO) database. Using R package to normalize the data and the utilizing limma package to identify the differentially expressed genes (DEGs). Gene Ontology and Kyoto Encyclopedia of Genes enrichment analysis of DEGs were performed via the “cluster profiler” package in R software. Protein-protein network was conducted to analyze the potential relationship among the proteins and CytoHubba, a plug-in for Cytoscape software, was used to identify the hub genes. GSE15932 for DM and GSE10334 for periodontitis were selected to be the validation datasets. Receiver Operating Characteristic Curves analysis was performed to obtain the area under the ROC curve. Correlations between hub genes and immune cells via immune infiltration analysis. Results There were 249 common DEGs were identified. LAPTM5, RAC2, LYN were identified as the hub genes, which were all up-regulated, of DM and periodontitis. The area under the curve of the 3 hub genes were all more than 0.7. The activation of B cells, and T cells as well as the phagocytosis could be the central role in the development of the both diseases. Conclusions LAPTM5, RAC2, LYN were defined as the hub genes of DM and periodontitis. The activation of B cells, and T cells as well as the phagocytosis could be the central role in the development of the both disease, which might the potential targets for diagnosis and treatment.

show abstract

“…Periodontal inflammation may worsen systemic diseases by inducing pathological changes through the production of specific molecules by leukocytes, particularly neutrophils, that are directly responsible for the inflammatory response [ 6 ]. The immunomodulatory function of lymphocytes also plays a critical role in periodontal inflammation [ 7 ]. Several blood inflammatory markers such as neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), are considered emerging biomarkers of inflammation in blood counts, to be used as prognostic indicators in periodontitis [ 8 ].…”

Section: Introductionmentioning

confidence: 99%

Mean platelet volume is associated with periodontitis: a cross-sectional study

Zhou,

Liu,

Bai

et al. 2024

BMC Oral Health

View full text Add to dashboard Cite

Background It is uncertain if mean platelet volume and periodontitis are related. The objective of this study was to examine the association between levels of mean platelet volume and moderate/severe periodontitis in adult persons who inhabit the U.S. Methods We screened 6,809 people from the National Health and Nutrition Examination Survey (NHANES 2009–2012). Mean platelet volume was measured in the Mobile Examination Centers (MECs) using the Beckman Coulter analyzer. The category of periodontitis was defined by the CDC/AAP using clinical periodontal parameters. Multiple logistic regression models were employed to examine the distribution for covariate differences across the various independent groups. Four models were employed to examine the relationship between mean platelet volume level and periodontitis. Smoothed curve fitting was utilized to confirm the linearity of the relationships. To determine the impact of factors on the connection between MPV and periodontitis, subgroup analysis and interaction testing were utilized. Results Results from the multiple logistic regression analysis indicate a significant association between moderate/severe periodontitis and the mean platelet level, even after considering any potential confounding variables (OR = 1.090, 95% CI: 1.019–1.166, P-value = 0.01211). Additionally, those in the upper tertile of mean platelet volume levels had a 21.6% higher probability of developing periodontitis when compared with those in the least tertile of mean platelet levels (OR = 1.216, 95% CI:1.052–1.406, P-value = 0.00816). Moreover, it showed a positive correlation between mean platelet volume (MPV) and moderate/severe periodontitis. Subgroup analyses indicated a positive association between the level of mean platelet volume and moderate/severe periodontitis among individuals who were under 60 years of age, had low income, were obese, never smoked, were heavy drinkers, had hypertension, and had no cardiovascular disease (p < 0.05). However, none of the subgroups exhibited significant interactions (p for interaction > 0.05). Conclusion A correlation has been found between mean platelet volume levels and periodontal disease in individuals residing in the United States.

show abstract

Phenotypes, roles, and modulation of regulatory lymphocytes in periodontitis and its associated systemic diseases

Cited by 13 publications

References 159 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

Identification of hub genes and biological mechanisms associated with periodontitis and diabetes

Mean platelet volume is associated with periodontitis: a cross-sectional study

Contact Info

Product

Resources

About