Pulpitis, an inflammation of the dental pulp, is generated by bacterial invasion through different ways as caries. In the establishment and development of this disease, different biological processes are involved. Long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) are transcripts with regulatory capacity participating in different biological functions and have been implicated in different diseases. The aim of this narrative review is to critically analyze available evidence on the biological role of lncRNAs and circRNAs in pulpitis and discuss possible new research prospects. LncRNAs and circRNAs involved in pulpitis were explored, addressing their expression, molecular mechanisms, targets and biological effects studied in animal and in vitro models, as well as in studies in human patients. LncRNAs and circRNAs are emerging as key regulators of diverse biological functions in pulpitis including apoptosis, proliferation, differentiation, oxidative stress, autophagy, ferroptosis, inflammation and immune response. The molecular mechanisms performed by these non-coding RNAs (ncRNAs) involved interactions with miRNAs and the formation of regulatory networks in the context of pulpitis. Further studies more deeply analyzing the participation of lncRNAs and circRNAs in pulpitis will reveal the potential applications of these ncRNAs as biomarkers or their use in therapeutic strategies in pulp inflammation.

El objetivo de esta revisión bibliográfica es analizar la evidencia existente sobre la relación de la microbiota oral con el establecimiento y progresión de enfermedad periodontal y diabetes. La microbiota es un ecosistema de microorganismos que se encuentran en nuestro organismo, donde aproximadamente más de 700 bacterias diferentes se encuentran en la cavidad bucal, y su disbiosis da inicio a características clínicas sumado con otros factores sistémicos y locales. En los últimos años se ha analizado la composición de la microbiota como firma biológica como estados de salud o enfermedad. La enfermedad periodontal se considera de origen multifactorial y su mecanismo etiopatogénico se basa en la disbiosis oral. La relación bidireccional de la periodontitis con pacientes de enfermedades endocrinas como la diabetes mellitus tipo 2 contribuye a perpetuar un estado inflamatorio que por consecuencia ocasiona la pérdida de tejidos periodontales de soporte.

Background: Periodontitis is one of the most common inflammatory diseases in humans, mostly caused by bacterial infection and with diverse populations of immune cells involved. Myeloid-derived suppressor cells (MDSCs), a heterogeneous group of immature myeloid cells derived from hematopoietic precursor cells, have exhibited immunomodulatory functions by production of different molecules such as inducible NO synthase (iNOS) and it is thought to be involved in periodontitis. However, reports of characterization of cells with MDSC phenotypes in gingival tissues are very scarce. This study aimed to characterize gingival cells with MDSC phenotypes in healthy gingiva and periodontitis tissues. Methods and Results: Human healthy gingival tissues and those with periodontitis were included to analyze cells with MDSC phenotypes by flow cytometry. Additionally, a mouse model of experimental periodontitis was used to identify cells with MDSC phenotypes and production of iNOS. Results showed an increased accumulation of CD45 ⁺ HLA-DR ^neg/low CD11b ⁺ CD33 ⁺ cells in human gingival tissues with periodontitis. Experimental periodontitis promotes accumulation of CD45 ⁺ CD11b ⁺ Gr-1 ⁺ and CD45 ⁺ CD11b ⁺ Ly6G ⁺ cells in gingival tissues. Experimental periodontitis did not promote accumulation of these subpopulations in other tissues as spleen. Additionally, gingival CD45 ⁺ Gr-1 ⁺ iNOS ⁺ cells were identified. Conclusions: cells with MDSC phenotypes are resident in healthy gingival tissues and their accumulation is locally triggered by periodontitis. Cells with capacity of iNOS production could be implicated in generation of reactive nitrogen species, suggesting immunomodulatory properties.

Very good article, wich shows us the alterations of periodontal tissues, which may occur whith the relationship of periodontal disease whith external alteration. This leads to future epigenetic studies. I would have liked to see more information abou...