Pulpal Inflammation Research Articles

Understanding dental pulp inflammation: from signaling to structure.

The pulp is a unique tissue within each tooth that is susceptible to painful inflammation, known as pulpitis, triggered by microbial invasion from carious lesions or trauma that affect many individuals. The host response involves complex immunological processes for pathogen defense and dentin apposition at the site of infection. The interplay of signaling between the immune and non-immune cells via cytokines, chemokines, neuropeptides, proteases, and reactive nitrogen and oxygen species leads to tissue reactions and structural changes in the pulp that escalate beyond a certain threshold to irreversible tissue damage. If left untreated, the inflammation, which is initially localized, can progress to pulpal necrosis, requiring root canal treatment and adversely affecting the prognosis of the tooth. To preserve pulp vitality and dental health, a deeper understanding of the molecular and cellular mechanisms of pulpitis is imperative. In particular, elucidating the links between signaling pathways, clinical symptoms, and spatiotemporal spread is essential to develop novel therapeutic strategies and push the boundaries of vital pulp therapy.

Tertiary Lymphoid Structure in Dental Pulp: The Role in Combating Bacterial Infections.

Tertiary lymphoid structure (TLS) is associated with various pathologies, including those of cancers and chronic infections. Depending on the organ, multiple factors regulate the formation of TLS. However, the role of TLS in immune response and the molecules that drive its formation remain uncertain. The dental pulp, includes a few immune cells surrounded by rigid mineralized tissue, and opens to the outside through the apical foramen. Owing to this special organization, the dental pulp generates a directional immune response to bacterial infection. Considering this aspect, the dental pulp is an ideal model for comprehensively studying the TLS. In the present study, single-cell RNA sequencing of healthy and inflamed human dental pulp reveals known markers of TLS, including C-C motif chemokine ligand 19 (CCL19), lysosome-associated membrane glycoprotein 3 (LAMP3), CC chemokine receptor 7 (CCR7), and CD86, present in inflamed dental pulp. Compared with the healthy pulp, types and proportions of immune cells increase, along with enhanced cellular communication. Multiple immunofluorescence staining reveals that typical TLS emerges in dental pulp with pulpitis, consistent with the high expression of CC chemokine ligand 3 (CCL3), which may be a key driver of TLS formation. Moreover, TLS is also observed in a mouse model of pulpitis. These findings collectively offer insights into the formation and function of TLS in response to infection.

The Gelatin-Chitosan-Tetraethyl Orthosilicate Calcium Hydroxide Composite as a Potential Dental Pulp Medicament (Study on Expression of COX-2, PGP 9.5, TNF-α and Neutrophils number)

Introduction Calcium hydroxide (Ca(OH)2) is the material of choice for pulp therapy. However, Ca(OH)2 has drawbacks such as toxicity, poor sealing, and tunnel defect formation. Alternative materials have been developed to provide more biocompatible materials with better dentin formation ability. The objective of this study was to evaluate the effect of composites containing gelatin (G), chitosan (CH), tetraethyl orthosilicate (TEOS), and Ca(OH)2, namely G-CH-TEOS-Ca(OH)2 (Extended data) on inflammation of the dental pulp (expression of COX-2, PGP 9.5, TNF-α, and neutrophil number). Materials and methods A total of 16 Wistar rat models of acute pulp injury were prepared and divided into two groups, treatment and control, 8 with each. In the treatment group, we applied a pulp-capping material using G-CH-TEOS-Ca(OH)2 and Ca(OH)2. On the 1st and 3rd days, rats were sacrificed. Tissue samples from 4 rats in each group were processed for histological preparation. COX-2, PGP 9.5, and TNF-α were observed using immunohistochemical (IHC) staining, and neutrophil numbers were observed using hematoxylin-eosin staining. Image analysis of COX-2, PGP 9.5, and TNF-α expression was performed using ImageJ software. Results The results showed a decrease in COX-2 expression, but not significantly while PGP 9.5 and TNF-α expression were significantly higher than those in the control group. Neutrophil numbers were lower in the treatment group than in the control group, but the difference was not statistically significant. Conclusion The G-CH-TEOS-Ca(OH)2 composite material may have potential as an exposed pulp medicament by reducing inflammation (COX-2 expression and number of neutrophils) and increasing the regeneration factor (TNF-α expression) and nerve (PGP 9.5 expression).

Efficacy of proinflamatory cytokines in the clinical and radiograpic outcomes of different primary molar pulpotomy agents: a comperative randomised study featuring a novel biomarker for pulpal diagnosis

BackgroundWhile the effect of biomaterials covering the pulp tissue is considered in the success of pulpotomy treatment, the level of pulpal inflammation is still very important for treatment success. The aim of this study was to compare IL-6 and IL-8 levels, known as good indicators of pulpal inflammation, with a new biomarker, presepsin, and to evaluate the impact of biomarker levels along with the pulp capping agents used in the treatment on the one-year success of pulpotomy treatment.MethodsThe study included 120 primary second molar teeth with pulpotomy indications from 75 children. To determine the pulpal inflammation status, pulpal bleeding samples were taken during treatment, and the levels of IL-6, IL-8, and presepsin were measured. During the pulpotomy treatment, MTA, NeoMTA™, and Biodentine™, and ZOE were randomly applied to groups of thirty teeth each. Patients were monitored for a period of 12 months post-treatment.ResultsIL-8, IL-6, and presepsin levels were significantly higher in teeth with pathology (p < 0.001). Biomarker levels were found to be higher in the NeoMTA and Biodentine groups, but this did not result in a statistically significant difference. (p > 0.05) Following pulpotomy treatment, the most successful material groups in order were MTA, ZOE, NeoMTA™, and Biodentine™.ConclusionPresepsin may be a usable indicator in predicting the level of inflammation. At the end of the one-year follow-up of pulpotomy treatment, more pathology was observed in the NeoMTA and Biodentine groups, where biomarker levels were higher, while no pathology was found in the MTA group, where biomarker levels were lower.Trial registrationNCT06398327/ 20,240,503.

Total Pulpotomy with MTA in Young Permanent Teeth: Case Series

Vital pulp therapy is a way to preserve the vitality and function of pulp damaged by trauma, caries or restorative procedures. Vital pulp therapy procedures include direct pulp capping, indirect pulp capping, partial and coronal pulpotomy treatments where diseased pulp tissue is removed. Over the years, the focus of vital pulp therapy has been on the preservation of the radicular pulp in immature permanent teeth to ensure the completion of root formation (apexogenesis). Today, it has been reported that vital pulp therapy can be considered as an alternative to root canal treatment, including in teeth with certain conditions that are considered to have irreversibly inflamed pulp. Coronal amputation therapy, a vital pulp treatment, involves complete removal of the coronal pulp, placement of a biologically acceptable material into the pulp chamber and restoration. The covering material must be able to relieve inflammation and initiate healing of the pulp tissue and allow new dentin tissue to form. The oldest material used in pulpotomy is calcium hydroxide. Mineral trioxide aggregate, which is a more recent material, is frequently preferred today due to its biocompatible and bioactive properties. In this case report, the results of 4 cases of coronal pulpotomy with mineral trioxide aggregate in young permanent teeth with a follow-up of 18 months are presented.

Ultrastructural evaluation of adverse effects on dentine formation from systemic fluoride application in an experimental mouse model.

Fluoride is widely used in dentistry for its caries prevention. To reduce dental caries, the optimal fluoride concentration of public water supplies in the United States is 0.7 ppm. However, excessive systemic fluoride consumption can lead to dental/enamel fluorosis. Numerous studies have explored the effects of fluoride on enamel and enamel-forming cells. However, research on systemic fluoride's impact on dentine is limited, particularly the effect of fluoride on the structure of the dentine-pulp complex. Therefore, this study aimed to identify how excessive fluoride affects dentine microstructure using an experimental mouse model. C57BL6/J male mice (6-9 weeks old) were randomized into four groups (Fluoride at 0, 50, 100, or 125 ppm in drinking water) (n = 4/group). Mice were provided water adlibitum for 6 weeks along with fluoride-free food. Thereafter, mandibular incisors were analysed. Enamel phenotypes were evaluated using light microscopy and quantitative light-induced fluorescence (QLF) to measure fluorosis levels. Dentine morphology was evaluated using micro-CT, scanning electron microscopy (SEM), SEM-EDX (energy-dispersive X-ray), microhardness test and histological imaging. Data were analysed using one-way ANOVA with Dunnett's multiple comparisons as a post hoc test and the Kruskal-Wallis test with Dunn's multiple comparisons post hoc test (p < .05). Mice treated with fluoride at 50-125 ppm developed enamel hypoplasia in their erupting incisors and micro-CT imaging revealed that fluoride 125 ppm caused external resorption of the growing incisor. Dentine mineral density, dentine volume decreased compared with the 0 ppm control, while pulp volume increased compared with the 0 ppm control group. SEM showed wider predentine layer and abnormalities in calcified matrix vesicles derived from odontoblasts in fluoride 100 and 125 ppm groups. Vickers microhardness of dentine significantly decreased in the high-dose group. Fluoride-induced dentine hypoplasia in a dose-dependent manner. Histological evaluation showed excessive fluoride 125 ppm induced micro abscess formation and inflammatory cell infiltration. Fluoride induced dentine dysplasia with a dentine microstructure resembling hypophosphatasia. High doses of systemic fluoride can cause dentine dysplasia. Both three-dimensional and microstructural analyses showed the structural, chemical and mechanical changes in the dentine and the mineralized tissue components, along with external resorption and pulp inflammation.

Comparative evaluation of various biomaterials as pulpotomy agents in molars with symptomatic irreversible pulpitis: A randomized single-blinded single-center control trial

Abstract Introduction: Untreated tooth decay in mature permanent dentition is a prevalent global issue, affecting 34.1% of people with 2.5 billion cases annually. Extensive decay often leads to irreversible pulpitis, characterized by pulp inflammation and pain. Pulpectomy, the standard treatment, involves complex procedures with potential complications. Modern endodontics favors minimally invasive treatment such as pulpotomy, which preserves pulp vitality. This study aims to compare the clinical as well as radiographic outcomes of different pulpotomy agents: Biodentine, mineral trioxide aggregate (MTA), Bio-C repair, and Endosequence Bio-ceramic root repair material (BCRRM) in mature permanent molars. Methodology: This single-blind, single-center study involved 80 participants randomly assigned to four groups, each receiving one of the biomaterials. Ethical approval was obtained. Participants aged 14–60 years with symptomatic irreversible pulpitis were selected. Pulpotomy procedures were performed, and follow-up evaluations occurred at 24 h, 1 week, 4 weeks, 3, 6, and 12 months. Clinical success was measured by the absence of pain, sensitivity, and tenderness. Radiographic evaluation used the periapical index (PAI) scoring system. Results: Pulpotomy significantly reduced postoperative pain in all groups. Endosequence BCRRM showed the maximum pain reduction at 24 h with a statistically significant difference from all the groups (at 1% probability level), followed by Bio-C repair, Biodentine, and MTA. At 1 week, Bio-C repair led in pain reduction with statistically nonsignificant results. All groups reported no pain at 3, 6, and 12 months. Endosequence BCRRM had the highest improvement in periapical findings at 1 year. Sensitivity to hot and cold improved significantly in all groups, with Endosequence BCRRM performing best. Conclusion: Endosequence BCRRM provided the best overall outcomes, emphasizing the importance of material choice in pulpotomy treatments. Further research on biomaterials’ long-term clinical and radiographic outcomes is needed to enhance treatment efficacy.

Investigation of Apoptosis in Healthy and Inflamed Pulp Tissue

Investigation of Apoptosis in Healthy and Inflamed Pulp Tissue

Effect of blockage of Trem1 on the M1 polarization of macrophages in the regulation dental pulp inflammation.

Dental pulp inflammation is a common and significant factor related to poor dental prognosis. Current treatment strategies primarily concentrate on managing the inflammatory response, with specific targets for intervention still under investigation. Triggering receptors expressed on myeloid cells (TREMs) are a group of receptor molecules extensively present on myeloid cell surfaces, crucial in the regulation of inflammatory process. Our analysis of transcriptomic sequencing data from clinical pulp samples of dataset GSE77459 and animal models revealed up-regulation of Trem1 during pulpitis. Administration of the Trem1-blocking peptide LP17 led to lower (more than 1-fold) levels of several pro-inflammatory factors and inhibition of M1 macrophage polarization both in vivo and in vitro. This study of the expression patterns and functions of Trem1 in the development of dental pulp inflammation provides novel insights into the therapeutic strategies for clinical pulpitis.

Effect of interleukin-17A on inflammatory mediator production in interleukin-1β-stimulated human dental pulp fibroblasts.

In response to pro-inflammatory cytokines such as interleukin (IL)-1β, dental pulp fibroblasts produce various inflammatory mediators, including IL-6, IL-8, CC chemokine ligand 20 (CCL20), and CXC chemokine ligand 10 (CXCL10), leading to the progression of pulpitis. IL-17/IL-17A (IL-17A) is a pro-inflammatory cytokine secreted by T helper (Th) 17 cells following their recruitment to inflamed sites; however, the roles of IL-17A during pulpitis remain unclear. The purpose of this study was to investigate the effect of IL-17A on IL-6, IL-8, CCL20 and CXCL10 production by human dental pulp fibroblasts (HDPFs) in vitro. IL-17A at a concentration of 100ng/ml induced the production of 10 times more IL-8 and 4 times more CXCL10, but not IL-6 and CCL20, compared to controls. Co-stimulation of HDPFs with IL-17A and IL-1β synergistically enhanced the production of IL-6, CCL20, IL-8 and CXCL10. IL-1β increased expression of IL-17 receptor/IL-17RA (IL-17R) on HDPFs. Moreover, the cell signal pathways of p38 mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) were more potently activated by simultaneous stimulation with IL-17A and IL-1β. These findings suggest that IL-17A participates in the progression of dental pulp inflammation through the enhanced production of inflammatory mediators in HDPFs.

The construction of an inflammation classification model for HDPCs applied in guiding pulpotomy based on single-cell Raman spectroscopy

The immune defense and the repair function of the pulp tissue serve as the biological foundation of pulpotomy. The precise evaluation of the pulp inflammation extent and determining its reversibility are essential for the success of pulpotomy. The objective of this study was to classify the molecular-level of dental pulp cell physiology and inflammatory state based on the biochemical changes obtained by single-cell Raman spectroscopy. Firstly, we differentiated the growth of HDPCs (human dental pulp cells) under physiological states by employing Raman spectroscopy with multivariate statistical analysis. Raman spectroscopy reflected the biochemical changes at different growth phases, including the lag phase, log phase, and stationary phase. Secondly, we evaluated the optimal concentration and duration of Porphyromonas gingivalis lipopolysaccharide (P.g.LPS) stimulation to establish a six-level inflammation classification model of HDPCs. Thirdly, we performed label-free characterization of biological component changes in cells of different inflammation grades by Raman spectroscopy. As a result, the differences of peaks in the region 600–1800 cm−1 demonstrated the biochemical molecular alterations in the different inflammation grades of HDPCs. As inflammation progresses in steps, protein peaks increased first and then decreased, while lipid and nucleic acid peaks gradually decreased compared to unstimulated cells. However, when the inflammatory stimulation reached grade V, the changes in the biological properties were characterized by a recovery in protein and lipid content, and a decrease in nucleic acid content. We then established the diagnostic model using the Raman spectra of HDPCs in physiological and inflammatory states, which had a prediction accuracy of 100 % and 97.4 %, respectively. Finally, we determined the reversibility threshold of HDPCs at different grades of inflammation. We observed that the inflammation of grade I and II cells had potential reversibility and could be attempted to be retained. In conclusion, Raman spectroscopy combined with multivariate statistical analysis has potential possibility to effectively distinguish the degree of inflammation in the dental pulp, thus providing new tools and perspectives on pulpotomy in clinical practice.

Hypoxia-induced NLRP3 inflammasome activation via the HIF-1α/NF-κB signaling pathway in human dental pulp fibroblasts

BackgroundPrevious studies have reported the link between hypoxic conditions and NLRP3 inflammasome-mediated pulpal inflammation in the progression of pulpitis. However, the underlying mechanism has not been fully elucidated. This study aimed to investigate the role of HIF-1α in the regulation of NLRP3 inflammasome pathway via NF-κB signaling under hypoxic conditions with or without LPS in human dental pulp fibroblasts (HDPFs) during the progression of pulpitis.MethodsHIF-1α plasmids or siRNAs were used to upregulate or downregulate HIF-1α in HDPFs, respectively. The effect of hypoxia with or without LPS on the NF-κB signaling and NLRP3 inflammasome pathway was analyzed by immunofluorescence staining, qRT-PCR, western blotting and ELISA.ResultsThe hypoxic conditions alone induced ASC oligomerization and NLRP3/CASP1 inflammasome pathway activation via NF-κB signaling in a time-dependent manner in HDPFs. The upregulation of HIF-1α further promoted hypoxia-induced ASC oligomerization and NLRP3/CASP1 inflammasome pathway activation via NF-κB signaling compared to the hypoxia-induced group. In comparison, downregulation of HIF-1α inhibited ASC oligomerization and NLRP3/CASP1 inflammasome pathway activation via NF-κB signaling compared to the hypoxia-induced group. Additionally, LPS plus hypoxia further promoted HIF-1α expression and NLRP3/ASC/CASP1 inflammasome pathway activation via NF-κB signaling compared to the hypoxia-induced group.ConclusionsHIF-1α served as a positive regulator of NLRP3/ASC/CASP1 inflammasome pathway activation via NF-κB signaling in HDPFs in the sterile pulpal inflammation and caries-related pulpitis microenvironment. The finding of a novel functional HIF-1α-NF-κB-NLRP3 axis provides insight into the link between the hypoxic microenvironment and pulpal inflammation, thus supporting a promising therapeutic strategy for the control of pulpal inflammation.

Impact of diabetes mellitus on endodontic treatment outcomes

Diabetes mellitus (DM) is a chronic metabolic disorder that affects various systemic functions, including oral health. Its impact on endodontic treatment outcomes has become a significant concern for dental practitioners. The relationship between DM and endodontic outcomes is complex, involving several pathophysiological mechanisms. Hyperglycemia leads to the formation of advanced glycation end-products, causing vascular dysfunction and impaired blood supply to the pulp, which exacerbates pulpal inflammation and increases the risk of necrosis. Additionally, chronic low-grade inflammation and an impaired immune response in diabetic patients contribute to a higher susceptibility to infections, delayed healing, and compromised tissue repair after endodontic procedures. Diabetic patients often experience lower success rates and prolonged recovery following endodontic treatment due to these systemic challenges. Reduced bone healing, persistent periapical lesions, and altered microbial flora are common complications that can hinder treatment success. Effective management of endodontic treatment in diabetic patients requires a multifaceted approach that includes strict glycemic control, the use of enhanced antimicrobial strategies, and the adoption of minimally invasive techniques to reduce tissue trauma. Additionally, patient education and close monitoring of the healing process are essential for minimizing complications. Understanding the pathophysiological interactions between diabetes and pulpal inflammation, as well as the factors that influence healing and success rates, is crucial for optimizing endodontic care in diabetic patients. By addressing both systemic and local factors, dental practitioners can improve the prognosis of endodontic treatment and ensure better outcomes for patients with diabetes. Ongoing research into the mechanisms underlying these complications will further enhance the ability of clinicians to manage endodontic cases effectively in this growing patient population.

MicroRNA-27a-5p Downregulates Expression of Proinflammatory Cytokines in Lipopolysaccharide-Stimulated Human Dental Pulp Cells via the NF-κB Signaling Pathway.

MicroRNA-27a-5p (miR-27a-5p) was significantly upregulated in dental pulp inflammation, yet its underlying mechanisms remain unclear. This study investigated the effect of miR-27a-5p on the expression of proinflammatory cytokines in human dental pulp cells (hDPCs) stimulated by lipopolysaccharide (LPS). LPS-stimulated hDPCs showed concurrent increases in the expression of miR-27a-5p and proinflammatory cytokines (IL-6, IL-8, and MCP1), and the increased expression was suppressed by NF-κB inhibitor BAY 11-0785. Transfection of the miR-27a-5p mimic downregulated the expression of proinflammatory cytokines, NF-κB activity, and the expression of NF-κB signaling activators (TAB1, IRAK4, RELA, and FSTL1) in LPS-stimulated hDPCs. Luciferase reporter assays revealed that miR-27a-5p bound directly to the 3'-UTR of TAB1. siTAB1 downregulated NF-κB activity and proinflammatory cytokine expression. Downregulation of proinflammatory cytokine expression, NF-κB activity, and NF-κB signaling activator expression (TAB1, IRAK4, and RELA) was also found in LPS-stimulated rat incisor pulp tissue explants following transfection with the miR-27a-5p mimic ex vivo. MiR-27a-5p, whose expression was induced by NF-κB signaling, negatively regulated the synthesis of proinflammatory cytokines via targeting NF-κB signaling. In particular, TAB1, a potent NF-κB activator, was targeted by miR-27a-5p. These results provide insights into the negative regulatory effects of miR-27a-5p, particularly those targeting the TAB1-NF-κB signaling pathway, on pulp inflammation.

Injectable Tannin-Containing Hydroxypropyl Chitin Hydrogel as Novel Bioactive Pulp Capping Material Accelerates Repair of Inflamed Dental Pulp.

Conventional pulp capping materials have limited anti-inflammatory capacity. It is necessary to develop more effective pulp capping material for the treatment of inflamed pulps. Tannic acid (TA) is a natural, water-soluble polyphenol with antimicrobial and anti-inflammatory properties. This study aimed to investigate the effects of a tannin-containing hydroxypropyl chitin hydrogel (HPCH/TA hydrogel) as an innovative pulp capping material. The physicochemical properties of the composite hydrogels were characterized. The effects of HPCH/TA hydrogel as a pulp capping material were evaluated in vitro and in vivo. The underlying mechanism of the anti-inflammatory effects of HPCH/TA hydrogel was explored. The HPCH/TA hydrogel demonstrated favorable temperature sensitivity, injectability, and antibacterial properties. In vitro, the HPCH/TA hydrogel effectively promoted the proliferation of human dental pulp cells and inhibited interleukin-1β, interleukin-6, and tumor necrosis factor-α expression, possibly by suppressing the nuclear factor kappa-B pathway. In vivo, on the fourth day after capping, the HPCH/TA hydrogel group showed lower inflammatory scores compared to the control and iRoot BP Plus (commercial pulp capping material) group. By the sixth week, complete reparative dentin formation was observed in the HPCH/TA hydrogel group, with no difference in thickness compared to the iRoot BP Plus group. Collectively, the HPCH/TA hydrogel holds promise as a bioactive pulp capping material for promoting the repair of inflamed pulp in vital pulp therapy.

A carbon dot nanozyme hydrogel enhances pulp regeneration activity by regulating oxidative stress in dental pulpitis

Preserving pulp viability and promoting pulp regeneration in pulpitis have attracted widespread attention. Restricted by the oxidative stress microenvironment of dental pulpitis, excessive reactive oxygen and nitrogen species (RONS) trigger uncontrolled inflammation and exacerbate pulp tissue destruction. However, modulating redox homeostasis in inflamed pulp tissue to promote pulp regeneration remains a great challenge. Herein, this work proposes an effective antioxidative system (C-NZ/GelMA) consisting of carbon dot nanozymes (C-NZ) with gelatin methacryloyl (GelMA) to modulate the pulpitis microenvironment for dental pulp regeneration by utilizing the antioxidant properties of C-NZ and the mechanical support of an injectable GelMA hydrogel. This system effectively scavenges RONS to normalize intracellular redox homeostasis, relieving oxidative stress damage. Impressively, it can dramatically enhance the polarization of regenerative M2 macrophages. This study revealed that the C-NZ/GelMA hydrogel promoted pulp regeneration and dentin repair through its outstanding antioxidant, antiapoptotic, and anti-inflammatory effects, suggesting that the C-NZ/GelMA hydrogel is highly valuable for pulpitis treatment.

EFFECT OF GELAM LEAF EXTRACT (Melaleuca cajuputi) AND TRICALCIUM SILICATE CEMENT AS DIRECT PULP CAPPING

Background: Reversible pulpitis is mild pulp inflammation. The treatment is direct pulpcapping. Tricalcium silicate cement has been better at inducing reparative dentin than other materials. Tricalcium silicate cement can cause inflammation 1-2 weeks after application, that natural ingredients need to improve the quality. Tricalcium silicate cement can be combined with galam leaf extract which contains anti-inflammatory properties by accelerating lymphocyte cells. Purpose: To analyzed the effect of gelam leaf extract (Melaleuca cajuputi) concentration of 100% and Tricalcium Silicate Cement on the number of lymphocyte cells on day 3 and 5 in direct pulp capping treatment. Methods: This research is a true experimental study with a post test-only with control design. This study used 24 Wistar rats, divided into 3 treatment groups with 2 different days, namely the group given a combination of Gelam leaf 100% + tricalcium silicate cement, tricalcium silicate cement as positive control, and without treatment as negative control. Results: One-way ANOVA test obtained p value=0.00&lt;0.05, which indicates there is a significant difference between each group. Post Hoc Bonferroni test showed significant difference between galam leaf extract and tricalcium silicate cement, tricalcium silicate cement, and no treatment on days 3 and 5. Conclusion: The combination of galam leaf extract and tricalcium silicate cement can increase the number of lymphocyte cells on day 3 of pulp inflammation and reduce the number of lymphocyte cells on day 5 more effectively than tricalcium silicate cement and without treatment on days 3 and 5 so that the healing process is faster.

Potential application of a combined extract of Channa striata and calcium hydroxide for inhibiting lymphocytes and interleukin-1β cells in the asymptomatic irreversible pulpitis of Wistar rats (Rattus norvegicus).

This study aimed to evaluate the effectiveness of combining Channa striata extract with calcium hydroxide (Ca(OH)2) in reducing lymphocyte counts and interleukin (IL)-1β levels in inflamed pulp teeth. A laboratory experimental setup with a posttest control group (CG) design was employed. Thirty-two rat incisor teeth were divided into four groups: a positive CG (100% Ca(OH)2), treatment 1 (25% C. striata extract + 75% Ca(OH)2), treatment 2 (50% C. striata extract + 50% Ca(OH)2), and treatment 3 (75% C. striata extract + 25% Ca(OH)2). These test materials were applied to Class 1 cavities extending to the pulp roof, with samples collected on days 1, 3, 5, and 7. Data were analyzed using analysis of variance and post hoc least significant difference tests. In all the groups, the highest levels of lymphocytes and IL-1β were observed on day 3, followed by a decline on days 5 and 7. The combination of C. striata extract with Ca(OH)2 significantly reduced inflammatory markers, particularly lymphocyte and IL-1β levels. The extract of C. striata holds significant potential as an innovative therapeutic approach for managing inflamed dental pulp.

Dysregulation of lncRNA TFAP2A-AS1 is involved in the pathogenesis of pulpitis by the regulation of microRNA-32-5p.

This study was designed to evaluate TFAP2A-AS1 expression in the dental pulp of teeth with or without pulpitis and to determine the function of TFAP2A-AS1 in pulp cells. GSE92681 was analyzed to filter out differentially expressed lncRNAs. Pulp samples from teeth with pulpitis and healthy teeth (control) were examined using real-time (RT) quantitative polymerase chain reaction (qPCR). Human dental pulp stem cells (hDPSCs) were cultured in a specific medium for osteogenic induction, or treated with lipopolysaccharide (LPS) to simulate inflammation. The viability and apoptosis of human DPSCs (hDPSCs) were determined by XTT assay and apoptosis detection kit. Inflammation was induced by LPS and assessed by measuring the expression and release of inflammatory cytokines after TFAP2A-AS1 knockdown. Osteogenic differentiation of hDPSCs was investigated by determining expression levels of osteogenic markers and alkaline phosphatase (ALP) activity after TFAP2A-AS1 overexpression. The downstream microRNA (miRNA) was predicted. Dual-luciferase reporter was used to confirm the binding between miR-32-5p and TFAP2A-AS1. The expression of TFAP2A-AS1 was evaluated in inflamed pulp using RT-qPCR. TFAP2A-AS1 had a discriminatory ability for healthy individuals and patients with pulpitis. The expression of TFAP2A-AS1 decreased upon the osteogenic differentiation of hDPSCs, and increased upon the LPS induction. TFAP2A-AS1 can reverse the osteogenic differentiation of hDPSCs, as evidenced by decreased levels of dentine sialophosphoprotein, dentin matrix protein-1, and ALP activity. TFAP2A-AS1 knockdown can promote cell proliferation of hDPSCs and relieve LPS-induced inflammation, as evidenced by decreased levels of TNF-α, IL-1β, and IL-6. miR-32-5p was identified as a downstream miRNA of TFAP2A-AS1. This study demonstrated the expression and potential function of TFAP2A-AS1 in the human dental pulp. TFAP2A-AS1 can inhibit odontogenic differentiation but promote inflammation in pulp cells.

Unveiling the Enigma of Molar Incisor Hypomineralisation: Causes, Consequences and Management Strategies

Abstract Molar incisor hypomineralisation (MIH) is a defect in the development of tooth enamel, affecting permanent first molars and incisors. This article explores MIH causes, consequences and management strategies for dental professionals. MIH is widespread, ranging from 2.4% to 40.2% globally. South America has the highest prevalence, while Africa has the lowest. Clinically, MIH presents as demarcated white, yellow or brownish opacities on the enamel surface. Affected teeth are fragile and prone to chipping, hypersensitivity and caries. MIH disrupts the tooth’s structure, increasing the risk of fractures, dentin exposure, pulp inflammation and rapid tooth decay. It can also lead to poor oral hygiene, aesthetic concerns and reduced quality of life for children. The causes of MIH are multifactorial and involve systemic or environmental factors during pre-natal or post-natal tooth development. Potential factors include childhood illnesses, antibiotic use, environmental toxins and Vitamin D deficiency. Early diagnosis and intervention are crucial for MIH management. Treatment options depend on the severity of the condition and may involve remineralisation, desensitisation, fluoride therapy, pit and fissure sealants, restorations or extractions. MIH is a common dental concern in children. Early management by dental professionals can help prevent complications and improve oral health outcomes.