LPS-Induced Neuron Cell Apoptosis through TNF-α and Cytochrome c Expression in Dental Pulp.

OBJECTIVES: Inflammation of the dental pulp tissue caused by bacteria, creating an immunology response of death of the dental pulp, is called apoptosis. The Porphyromonas gingivalis that cause apoptosis is lipopolysaccharide (LPS) through toll-like receptor (TLR) via two different mechanisms, intracellular and extracellular pathways. This study analyzed the role of LPS exposure of neuron cells, tumor necrosis factor-α (TNF-α), and cytochrome c (cyt-c) expression in the dental pulp to predict the possible mechanism of apoptosis. MATERIALS AND METHODS: The lower tooth of Sprague Dawley rats was opened and exposed to LPS for 48 hours. Then the neuron cell analyzed histopathology using hematoxylin-eosin, whereas the TNF-α and cyt-c expression with indirect immunohistochemistry using a light microscope. The relationship between neuron cells with TNF-α and cyt-c was analyzed using stepwise regression linear analysis. RESULT: The LPS exposure showed a lower number of neuron cells and had a relationship with TNF-α expression but not with cyt-c, while compared with control, both TNF-α and cyt-c expression were higher in neuron cells. CONCLUSION: LPS exposure in dental pulp is possible to stimulate the apoptosis process through extracellular pathways marked by higher TNF-α expression.

Effect of Lipopolysaccharide-Induced Apical Periodontitis in Diabetes Mellitus Rats on Periapical Inflammation.

OBJECTIVES: To evaluate periapical inflammation through immunohistochemical analysis of interleukin 6 (IL-6) and tumor necrosis factor α (TNF-a) expression resulting from lipopolysaccharide (LPS)-induced apical periodontitis in diabetes mellitus rats, observed at 14, 28, and 42 days. MATERIALS AND METHODS: Diabetes model on rats was induced by streptozotocin (STZ). Fifteen rats were injected with low-dose STZ for 5 days and waited for 5 days until the blood glucose level was stable and measured above 300 mg/dL confirmed by a digital glucometer. LPS was used to induce apical periodontitis. After performing access cavity, pulpal and root canal extirpation was done on the right mandibular first molar's root canal space of rats, under anesthesia. LPS of 1 mg/mL dose was induced in the pulpal and root canal space. Apical periodontitis was expected 14 days afterward and then, the rats were randomly allocated to three groups. The first group was terminated 14 days after induction and used as control. The second group was observed 28 days after induction, and the third group was observed 42 days after induction. IL-6 and TNF-a expression was analyzed by immunohistochemistry on macrophages in the periapical area. STATISTICAL ANALYSIS: Data were analyzed using one-way ANOVA and continued with the post hoc Tukey HSD test. Significance was considered if p < 0.05. RESULTS: LPS induced apical periodontitis in diabetes mellitus rats at control (14 days), 28 and 42 days observation showed a significant increase in the expression of IL-6 and TNF-a. There were significant differences between the control and observed groups (p < 0.05). The expression of IL-6 in the apical area was not significant at 14 and 28 days (p > 0.05) but increased significantly at 42 days (p < 0.05). The expression of TNF-a in the apical area was significantly increased after 14 days (p < 0.05) and remained stable at 28 and 42 days (p > 0.05). CONCLUSIONS: The periapical inflammation of LPS-induced apical periodontitis in diabetes mellitus rats increased macrophages' expression of IL-6 at 42 days and TNF-a at 28 days.

Expression of NaV-1.7, TNF-α and HSP-70 in experimental flare-up post-extirpated dental pulp tissue through a neuroimmunological approach.

BACKGROUND: Dental caries continue to represent a major problem which, if left untreated, will cause irreversible pulpitis. Root canal treatment constitutes one potential treatment intended to preserve teeth afflicted with irreversible pulpitis. During root canal treatment, pain or swelling, referred to as flare-ups, can occur at any point in the process. AIM: To analyze the molecular aspect of the phenomenon of flare-up in vital dental pulp tissue following mechanical and bacterial trauma (extirpation and lipopolysaccharide [LPS] induction respectively) through a neurological approach, based on the expression of NaV-1.7 in neuron cells, and HSP-70, TNF-α in macrophage cells. METHOD: This laboratory experimental study was conducted using 15 Spraque Dawley rats as subjects which were divided into three groups of five subjects: a control group, a pulp tissue extirpation group and an LPS induction followed by extirpation of pulp tissue group. Test samples were collected from the apical field of the mandibular incisor and subsequently examined using immunohistochemical methods. RESULTS: There were significant differences in NaV1.7, HSP70 and TNFα expression between the treatment groups. While a marked increase in the expression of HSP70 occurred, both Nav1.7, and TNFα expression decreased significantly. CONCLUSION: Extirpating the dental pulp tissue will induce a more pronounced flare-up response from the molecules of the pulp tissue in vital teeth than those in inflamed vital pulp tissue.