RNA-seq analysis of RNA extracted from control alveolar bone samples and alveolar bone under apical periodontitis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE221990 | GEO | 2023/02/11
REPOSITORIES: GEO
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Project description:Single-cell gene expression of mandibular bone marrow cells and mandibular bone marrow cells under the stimulation of apical periodontitis were determined by scRNAseq.
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Project description:Apical periodontitis (AP) is a painful disease that develops quickly following dental infections and is primarily characterized by robust inflammation surrounding the tissues of the affected tooth, resulting in disruption of bone homeostasis and periradicular bone loss. Moreover, there are distinct clinical presentations, symptoms, and responses to AP treatment between males and females, creating a desperate need to further understand the sex-specific mechanisms of AP. With the growing evidence that nociceptors modulate AP development, we utilized RNA sequencing in nociceptor-ablated (Nav1.8 cre+/-, Diphtheria Toxin Alox+/-) transgenic mice to study nociceptor regulation of the periapical lesion transcriptome using a rodent model of AP in female mice over 14 days. Overall, we found that female mice exhibit unique patterns of differentially expressed genes throughout AP infection compared to male mice, and that the expression of these genes is regulated by nociceptors. Additionally, nociceptor-ablation results in a more significant enrichment of biological processes related to immune responses earlier compared to cre-control (Nav1.8 cre+/-) females as well as greater expression of genes involved in inflammatory processes and osteolytic activity. Therefore, while nociceptor-ablation augments inflammatory and bone resorption responses in both males and females in a mouse model of AP, transcriptomic analyses demonstrate the mechanisms through which nociceptors modulate AP are distinct between sexes. These studies will provide the foundation needed to study further mechanisms of sex differences in AP, an area with a desperate need for investigation to treat current AP patients. Understanding these mechanisms can ultimately inform treatment options to alleviate suffering for millions of patients suffering from AP.
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Project description:Neutrophil recruitment and activation are hallmarks of the prevalent inflammatory disease, periodontitis. However, the mechanisms by which neutrophils contribute to in inflammatory bone destruction remain unclear. Herein, we document that neutrophil extracellular traps (NETs) have a direct role in mediating inflammatory pathology. In an established animal model of periodontitis, we demonstrate that genetic or pharmacologic inhibition of NETs formation, or removal of NETs by DNase-Ⅰ, alleviates inflammatory bone loss in vivo. Investigating the mechanisms by which NETs drive periodontal inflammation, we find that extracellular histones have a direct role in disease progression. Consistent with findings in animal models, histones bearing classic NET-associated post-translational modifications are correlated with disease severity and are significantly elevated in local lesions and systemic circulation of patients with periodontitis. Our work reveals NETs-associated components as pathogenic mediators, potential biomarkers, and therapeutic targets for periodontitis.
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Project description:Apical periodontitis (AP) is an inflammatory disease occurring following tooth infection with distinct osteolytic activity. Despite increasing evidence that sensory neurons participate in regulation of non-neuronal cells, their role in the development of AP is largely unknown. We hypothesized that Nav1.8+ nociceptors regulate bone metabolism changes in response to AP. Methods: A selective ablation of nociceptive neurons in Nav1.8Cre/ DTALox mouse line was used to evaluate the development and progression of AP using murine model of infection-induced AP. Micro-computed tomography examination was applied to quantify osteolytic lesions following induction of AP. Additionally, RT-PCR, RNAscope, and immunohistochemical (IHC) analysis were used to investigate the expression of immune cells, osteoblasts, and osteoclasts. Co-culture of trigeminal ganglia (TG) neurons from DTALox (control) and Nav1.8Cre/ DTALox mice with either IDG-SW3 or MC3T3-E1 osteoblast precursor cell lines or RAW264.7 murine macrophages were used to assess osteoblast and osteoclast function, by RNA sequencing, mineralization, and osteoclastic assays. Results: Ablation of Nav1.8+ nociceptors had earlier progression of AP with larger osteolytic lesions compared to the controls. IHC and RNAscope analysis demonstrated greater number of macrophages, T-cells, osteoclast and osteoblast precursors as well as an increased RANKL:OPG ratio at earlier time points among Nav1.8Cre/ DTALox mice. There was an increased expression of IL-1a and IL-6 within lesions of nociceptor-ablated mice. Further, co-culture experiments demonstrated that TG neurons promoted osteoblast mineralization and inhibited osteoclastic function. Conclusion: The findings suggest that TG Nav1.8+ neurons contribute to modulation of the AP development by delaying the influx of immune cells, promoting osteoblastic differentiation, and decreasing osteoclastic activities. This newly uncovered mechanism could become a therapeutic strategy for the treatment of AP and minimize the persistence of osteolytic lesions in refractory cases.
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