Galih Sampoerno; Sukaton Sukaton; Ekarista Lussiana Ferdinandus; Najwa Nadaa Firdaus; Rista Dalila Damayanti
Abstract
Microorganism contamination can induce dental pulp inflammation and generate pain. In this process, complex communication occurs between the immune and nervous system components until ...
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Microorganism contamination can induce dental pulp inflammation and generate pain. In this process, complex communication occurs between the immune and nervous system components until pain perception occurs. An improved understanding of the interactions involved in the dental pulp inflammatory pain process can be the basis for developing potential therapeutic agents. The current study aims to analyze the inflammatory pain process that follows the application of Porphyromonas gingivalis lipopolysaccharide (LPS) to dental pulp tissue by examining the expression of calcitonin-gene-related peptide (CGRP) in neurons (neuron-CGRP) and macrophages (macrophage-CGRP) as well as the expression of NaV 1.8 in neurons (neuron-NaV 1.8). This experimental laboratory study utilized 32 Spraque Dawley rats, divided into two groups. In the mandibular incisors, the control group only had access openings, while the treatment group had access openings and P. gingivalis LPS injections. Each group was terminated after 48 hours. Then slide preparations were made, and immunohistochemical staining was done to observe the expressions of neuron-CGRP, macrophage-CGRP, and neuron-NaV 1.8 using a light microscope. The LPS administration induced a significant increase in the expression of neuron-CGRP, macrophage-CGRP in macrophages, and neuron-NaV 1.8. There was no significant difference between the neuron-CGRP and macrophage-CGRP expressions. The neuron-CGRP is significantly and positively correlated with neuron-NaV 1.8. The microbial contamination via P. gingivalis LPS application to dental pulp tissue can increase the expression level of CGRP in both neurons and macrophages. However, only neuron-CGRP has been proven to significantly cause an increase in neuron-NaV 1.8 expression.
