Prevalence of pulp canal obliteration after traumatic dental injuries: a systematic review and meta-analysis.

This systematic review aimed to answer the following question: What is the estimated prevalence of pulp canal obliteration in subtypes of traumatic dental injury (TDI) in deciduous and permanent teeth? The searches were conducted in PubMed, Embase, Scopus, Web of Science, LILACS, Grey Literature, and Google Scholar, and complemented by a manual search, until April 16th, 2023. Observational studies were selected based on population, exposure, and outcome (PEO) (P, deciduous or permanent teeth; E, TDI; O, pulp canal obliteration). Two reviewers (kappa 0.90) applied the eligibility criteria, extracted qualitative data, and assessed the methodological quality using the Newcastle-Ottawa tool. A meta-analysis was performed using MedCalc 17.2. Thirty-four articles were selected after screening. The methodological quality was moderate to high. The estimated prevalence of pulp canal obliteration was 27.6% (95%CI: 18.7-37.7) and 21.9% (95%CI:16.0-28.4), for permanent and deciduous teeth, respectively. Considering the TDI subtypes, the prevalence of pulp canal obliteration was higher in root fractures of the permanent teeth (78.6 %, 95%CI: 62.8-90.9) and lateral luxation injuries in deciduous teeth (29.4%, 95%CI:19.1-41.0). Our review of 34 articles of moderate and high methodological quality found that the prevalence of pulpal canal obliteration ranges from 21.9% to 27.6%. Pulp canal obliteration was most frequently detected following lateral luxation injuries of the deciduous teeth and root fractures of the permanent teeth (PROSPERO CRD42020179438).

Decellularized extracellular matrix derived from dental pulp stem cells promotes gingival fibroblast adhesion and migration.

BACKGROUND: Decellularized extracellular matrix (dECM) has been proposed as a useful source of biomimetic materials for regenerative medicine due to its biological properties that regulate cell behaviors. The present study aimed to investigate the influence of decellularized ECM derived from dental pulp stem cells (DPSCs) on gingival fibroblast (GF) cell behaviors. Cells were isolated from dental pulp and gingival tissues. ECM was derived from culturing dental pulp stem cells in growth medium supplemented with ascorbic acid. A bioinformatic database of the extracellular matrix was constructed using Metascape. GFs were reseeded onto dECM, and their adhesion, spreading, and organization were subsequently observed. The migration ability of the cells was determined using a scratch assay. Protein expression was evaluated using immunofluorescence staining. RESULTS: Type 1 collagen and fibronectin were detected on the ECM and dECM derived from DPSCs. Negative phalloidin and nuclei were noted in the dECM. The proteomic database revealed enrichment of several proteins involved in ECM organization, ECM-receptor interaction, and focal adhesion. Compared with those on the controls, the GFs on the dECM exhibited more organized stress fibers. Furthermore, cultured GFs on dECM exhibited significantly enhanced migration and proliferation abilities. Interestingly, GFs seeded on dECM showed upregulation of FN1, ITGB3, and CTNNB1 mRNA levels. CONCLUSIONS: ECM derived from DSPCs generates a crucial microenvironment for regulating GF adhesion, migration and proliferation. Therefore, decellularized ECM from DPSCs could serve as a matrix for oral tissue repair.

Immunomodulatory properties of naïve and inflammation-informed dental pulp stem cell derived extracellular vesicles.

Mesenchymal stem cell derived extracellular vesicles (MSC EVs) are paracrine modulators of macrophage function. Scientific research has primarily focused on the immunomodulatory and regenerative properties MSC EVs derived from bone marrow. The dental pulp is also a source for MSCs, and their anatomical location and evolutionary function has primed them to be potent immunomodulators. In this study, we demonstrate that extracellular vesicles derived from dental pulp stem cells (DPSC EVs) have pronounced immunomodulatory effect on primary macrophages by regulating the NFκb pathway. Notably, the anti-inflammatory activity of DPSC-EVs is enhanced following exposure to an inflammatory stimulus (LPS). These inhibitory effects were also observed in vivo. Sequencing of the naïve and LPS preconditioned DPSC-EVs and comparison with our published results from marrow MSC EVs revealed that Naïve and LPS preconditioned DPSC-EVs are enriched with anti-inflammatory miRNAs, particularly miR-320a-3p, which appears to be unique to DPSC-EVs and regulates the NFκb pathway. Overall, our findings highlight the immunomodulatory properties of DPSC-EVs and provide vital clues that can stimulate future research into miRNA-based EV engineering as well as therapeutic approaches to inflammation control and disease treatment.

Asiatic acid reduces lipopolysaccharides-induced pulp inflammation through activation of nuclear factor erythroid 2-related factor 2 in rats.

Background: Dental pulp inflammation, often initiated by Gram-negative microorganisms and lipopolysaccharides (LPS), can lead to pulpitis and, subsequently, dental pulp necrosis, compromising tooth structure and increasing susceptibility to fracture. Asiatic acid, derived from Centella asiatica, has demonstrated pharmacological properties, including anti-inflammatory and antioxidant effects, making it a potential candidate for mitigating LPS-induced pulp inflammation. This in vivo study aims to investigate the impact of Asiatic acid on the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in Rattus norvegicus with LPS-induced pulp inflammation. Methods: This quasi-laboratory experimental in vivo study employed a post-test-only control group design to investigate the effects of Asiatic acid on LPS-induced pulp inflammation in Wistar rats. Thirty rats were randomly divided into six groups subjected to various interventions. LPS was administered to all groups for 6 h except the standard control group (CG, n = 5). The negative control group (NCG, n = 5) received only glass ionomer cement. The positive control group (PCG, n = 5) received Eugenol with glass ionomer cement. Intervention groups 1, 2, and 3 (IG1, IG2, IG3; n = 5 each) received Asiatic acid at concentrations of 0.5%, 1%, and 2%, respectively, with glass ionomer cement. Dental pulp inflammation was confirmed through immunological (tumor necrosis factor alpha (TNF-α) levels), histopathological (inflammatory parameters), and physiological (pain assessment using the rat grimace scale) analyses. Additionally, Nrf2 levels were examined using enzyme-linked immunosorbent assay (ELISA). Results: Asiatic acid administration significantly influenced Nrf2 levels in rats with LPS-induced pulp inflammation. Nrf2 levels were significantly higher in groups treated with 0.5% (IG1) (8.810 ± 1.092 ng/mL; p = 0.047), 1.0% (IG2) (9.132 ± 1.285 ng/mL; p = 0.020), and 2.0% (IG3) (11.972 ± 1.888 ng/mL; p = 0.000) Asiatic acid compared to NCG (7.146 ± 0.706). Notably, Nrf2 levels were also significantly higher in the 2.0% Asiatic acid group (IG3) compared to the PCG treated with Eugenol (8.846 ± 0.888 ng/mL; p = 0.001), as well as IG1 (p = 0.001) and IG2 (p = 0.002). However, no significant difference was observed between administering 0.5% Asiatic acid (IG1), 1.0% Asiatic acid (IG2), and Eugenol (PCG). Conclusion: This research showed that Asiatic acid significantly impacted the Nrf2 levels in rats with LPS-induced pulp inflammation. This suggests that it has the potential to be used as a therapeutic agent for reducing dental pulp inflammation. These findings support the need to further explore Asiatic acid as a promising intervention for maintaining dental pulp health.

GREM1 Negatively Regulates Osteo-/Dentinogenic Differentiation of Dental Pulp Stem Cells via Association with YWHAH.

OBJECTIVE: To investigate the biological regulatory function of Gremlin1 (GREM1) and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein eta (YWHAH) in dental pulp stem cells (DPSCs), and determine the underlying molecular mechanism involved. METHODS: Alkaline phosphatase (ALP) activity, alizarin red staining, scratch migration assays and in vitro and in vivo osteo-/dentinogenic marker detection of bone-like tissue generation in nude mice were used to assess osteo-/dentinogenic differentiation. Coimmunoprecipitation and polypeptide microarray assays were employed to detect the molecular mechanisms involved. RESULTS: The data revealed that knockdown of GREM1 promoted ALP activity, mineralisation in vitro and the expression of osteo-/dentinogenic differentiation markers and enhanced osteo-/ dentinogenesis of DPSCs in vivo. GREM1 bound to YWHAH in DPSCs, and the binding site was also identified. Knockdown of YWHAH suppressed the osteo-/dentinogenesis of DPSCs in vitro, and overexpression of YWHAH promoted the osteo-/dentinogenesis of DPSCs in vitro and in vivo. CONCLUSION: Taken together, the findings highlight the critical roles of GREM1-YWHAH in the osteo-/dentinogenesis of DPSCs.

Evaluation of pulp tissue dissolving efficiency of sodium and calcium hypochlorite solutions activated by ultrasonics and laser: an in vitro study.

OBJECTIVES: This study aimed to compare the tissue dissolving capacities of sodium and calcium hypochlorite [NaOCl and Ca(OCl)2] solutions applied without activation or with two irrigant activation methods. MATERIALS AND METHODS: One hundred and eight dentin cavities were prepared. Preweighed tissue pieces were placed in these dentin cavities, and samples were divided into nine groups of twelve. In groups 1, 2, and 3, NaOCl was used with non-activation (NA), passive ultrasonic (PUA), and laser activation (LA). With the same techniques, Ca(OCl)2 was used in groups 4, 5, and 6, and distilled water was used in groups 7, 8, and 9. The weight loss of tissue samples was calculated and analyzed using Two-way ANOVA and Duncan tests. RESULTS: Distilled water groups showed no tissue dissolution in any conditions. NaOCI and Ca(OCI)2 showed statistically similar dissolving effectiveness when used with the same technique. Activated groups dissolved significantly greater tissue than non-activated ones, the highest in LA. CONCLUSIONS: Ca(OCI)2 can be an alternative to NaOCl; for both, the first choice of activation may be the LA.

Assessment of the onset of analgesia and length of analgesia following the use of PBM with different wavelengths: a clinical study.

This clinical study assessed photobiomodulation (PBM) induced analgesic effects of diode lasers and an LED light source on the dental pulp. Baseline responses to electric pulp testing (EPT) were recorded in 93 healthy unrestored premolar teeth in 26 adults (age range 22-63 years) attending a private dental practice. The teeth were irradiated on buccal and lingual aspects of the crown, by placing the tips on the middle third of the crown of the teeth, on separate days for each of 4 different light sources (660, 808, or 904 nm diode lasers, or a novel multi-wavelength LED light source (700-1100 nm)) using comparable parameters (100 mW, 30 s, 6 J). EPT scores were measured after a further 1-, 2-, 5- and 20-min. Discomfort caused by PBM therapy was recorded using the Wong-Baker scale. EPT changes were tracked over time using repeated measures analysis of variance. Baseline EPT scores were very consistent between different days (linear regression r2 0.9422-0.9648). All PBM devices caused a significant elevation in EPT at 5 min, with an earlier onset at 2 mins for 904 nm and LED. The LED was the only light source that elevated scores at 20 min. Across 2-20 min, when ranked by effectiveness, the greatest EPT elevations were seen for LED, followed by 904 nm, then 660 nm and finally 808 nm. Discomfort during PBM was most common with 904 nm, followed by 808 nm. No discomfort occurred from the LED. Among the light sources utilized, the LED multi-wavelength system demonstrated the largest increase in EPT readings, suggesting its potential as a non-pharmacological alternative for achieving dental analgesia compared to diode lasers.

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

OBJECTIVE: 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. METHODS: 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. RESULTS: 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-1ß, and IL-6. miR-32-5p was identified as a downstream miRNA of TFAP2A-AS1. CONCLUSION: 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.

Biocompatibility and pro-mineralization effects of premixed calcium silicate-based materials on human dental pulp stem cells: An in vitro and in vivo study.

Premixed calcium silicate-based materials have recently been developed and are recommended for a wide range of endodontic procedures, including vital pulp therapy. This study investigated the in vitro biocompatibility and pro-mineralization effect and in vivo reparative dentin formation of EndoSequence Root Repair Material, EndoSequence BCRRM, Bio-C Repair, and Well-pulp PT. Both fresh and set extracts had no detrimental effect on the growth of human dental pulp stem cells. The fresh extracts had a higher calcium concentration than the set extracts and induced considerably greater mineralized nodule formation. EndoSequence Root Repair Material had the longest setting time, whereas Bio-C Repair had the shortest. When these materials were applied to exposed rat molar pulps, mineralized tissue deposition was found at the exposure sites after 2 weeks. These results indicate that the premixed calcium silicate-based materials tested could have positive benefits for direct pulp capping procedures.

Comparative Analysis of Calcium and Hydroxyl Ion Release from Pulp Dressing Materials in Pulpotomized Premolars.

BACKGROUND The aim of this study was to evaluate the time-dependent release of calcium (Ca⁺⁺) and hydroxyl (OH⁻) ions from 3 different pulp dressing materials used to cap root canal orifices in pulpotomized premolars. MATERIAL AND METHODS Freshly extracted (n=40) premolars were subjected to standardized pulpotomy procedure and finally restored in 5 groups using resin-modified glass ionmmer liner (RMGI) and bonded resin composite directly against the pulp chamber's floor (Control, G2) and over 3 different orifices' capping materials - Dycal (G3), Endo Sequence root repair material (ESRRM, G4), and mineral trioxide aggregate (MTA) Angelus (G5). Another 10 sound premolars served as the Reference group (G1). The restored teeth were incubated at 37±1°C in sealed containers filled with deionized water to assess Ca⁺⁺ and OH⁻ ions release after 24 h and at 1, 4, and 8 weeks. Two-way ANOVA and Tukey's comparisons at alpha=0.05 were used to statistically analyze the collected data. RESULTS Two-way ANOVA revealed significant differences in Ca⁺⁺ ions between test groups at different testing time intervals (P<0.05). Despite the constant (Tukey's, P<0.05) pH levels (OH⁻ release), Group 5 specimens exhibited higher Ca⁺⁺ ion release in comparison to Groups 4 and 3 at different testing timepoints (Tukey's, P<0.05). CONCLUSIONS Although all the assessed pulp dressing materials had equivalent and stable pH levels, ESRRM and MTA-Angelus had the highest Ca⁺⁺ ion release at the assessment intervals.

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

BACKGROUND: Previous 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. METHODS: HIF-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. RESULTS: The 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. CONCLUSIONS: HIF-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.

Apoptosis Regulation in Dental Pulp Cells and PD-1/PD-L1 Expression Dynamics Under Ozone Exposure - A Pilot Approach.

This study aimed to determine the effect of ozone on the expression of Bax and Bcl-2 genes in dental pulp cells. Additionally, the programmed cell death protein 1, programmed death-ligand 1, and CD200 antigens were determined in lymphocytes to assess their surface expression. Dental pulp cells were cultured from extracted healthy third molars and characterized as dental pulp stromal cells. Gene expression of Bcl-2 and Bax was analyzed at 0 s, 6 s, and 12 s of ozone exposure using real-time PCR. Lymphocytes from dental pulp were subjected to ozone exposure for 12 s and PD-1, PD-L1, and CD200/CD200R expression was analyzed by flow cytometry. Upon exposure to ozone for 6 s, the Bcl-2 expression decreased significantly to -0.09, and at 12 s, it increased significantly to 0.3. Bax gene expression level increased significantly to 0.188 after 6 s exposure, and at 12 s, to 0.16. Lymphocytes exposed to ozone for 12 s showed minimal changes in PD-1, PD-L1, and CD200/CD200R expression levels, indicating that oxidative stress does not impact the signaling pathways regulating these molecules. The significant upregulation of Bcl-2 at 12 s highlights the cells' effort to protect themselves from prolonged oxidative stress, possibly tipping the balance toward cell survival and tissue repair. However, the absence of changes in PD-1 and PD-L1 expression on lymphocytes under oxidative stress suggests that these molecules are not sensitive to oxidative stress in this context.

[Immune responses of pulpodentinal complex during caries progression].

Caries is an infectious disease in which the invasion of pathogens and their metabolites can activate the recognition and defense system of the pulpodentinal complex. In-depth understanding of the immune responses mediated by the pulpodentinal complex will help to estimate the real state of the dental pulp during the progression of caries and to take reasonable clinical treatment strategies, which can be more targeted and less invasive. Based on the physiology of the pulpodentinal complex, the present article introduce its immunocompetence and mechanism, reactive changes, clinical intervention and its significance during the caries progression, as to improve diagnostics as well as treatment strategies for caries.

NQO1 promotes osteogenesis and suppresses angiogenesis in DPSCs via MAPK pathway modulation.

BACKGROUND: Influence on stem cells' angiogenesis and osteogenesis of NAD(P)H Quinone Dehydrogenase 1(NQO1) has been established, but its impact on dental pulp stem cells (DPSCs) is unexplored. An important strategy for the treatment of arteriosclerosis is to inhibit calcium deposition and to promote vascular repair and angiogenesis. This study investigated the function and mechanism of NQO1 on angiogenesis and osteogenesis of DPSCs, so as to provide a new ideal for the treatment of arteriosclerosis. METHODS: Co-culture of human DPSCs and human umbilical vein endothelial cells (HUVECs) was used to detect the angiogenesis ability. Alkaline phosphatase (ALP) activity, alizarin red staining (ARS), and transplantation of HA/tricalcium phosphate with DPSCs were used to detect osteogenesis. RESULTS: NQO1 suppressed in vitro tubule formation, migration, chemotaxis, and in vivo angiogenesis, as evidenced by reduced CD31 expression. It also enhanced ALP activity, ARS, DSPP expression and osteogenesis and boosted mitochondrial function in DPSCs. CoQ10, an electron transport chain activator, counteracted the effects of NQO1 knockdown on these processes. Additionally, NQO1 downregulated MAPK signaling, which was reversed by CoQ10 supplementation in DPSCs-NQO1sh. CONCLUSIONS: NQO1 inhibited angiogenesis and promoted the osteogenesis of DPSCs by suppressing MAPK signaling pathways and enhancing mitochondrial respiration.

The orthodontic-endodontic interface: trauma and pulpal considerations.

The interpretation of the clinical signs and symptoms arising from the interdisciplinary relationship between orthodontics and endodontics becomes more complicated when superimposed by dental trauma. A history of dental trauma before or during orthodontic tooth movement may have implications for pulpal health and clinical outcomes. An understanding of the biology is essential for appropriate treatment planning. This review and treatment recommendations will assist dental practitioners in managing orthodontic-endodontic interactions.

The Effect of Tideglusib Application on Type 1 and Type 3 Collagen Expressions by Human Dental-Pulp Derived Stem Cells: A Preliminary Study.

BACKGROUND: Although Tideglusib cytotoxicity studies and its effects on human dental pulp-derived stem cells (DPSCs) have been examined in previous studies, there is no study investigating the expression of type 1 collagen and type 3 collagen by Tideglusib. AIM: The purpose of this study is to examine the effect of Wnt signaling activation using Tideglusib execution on human DPSC to determine its potential efficacy in collagen expression. METHODS: Stem cell isolation was performed from five human third molar wisdom tooth pulps. DPSCs identified in only one sample were treated with 50 nM Tideglusib for 24 h and 1 week. Axin-2, type 1 and type 3 collagen expressions were evaluated by Western blot analysis. DPSCs without treatment served as a negative control. The Mann-Whitney U test was used for statistical analysis. RESULTS: The levels of type 1 collagen and Axin-2 in the test group were significantly higher than those in the control group at 24 h (P = 0.000, P = 0.001, respectively). Compared to the control group, a slight increase in type 3 collagen expression was observed in the test group at 24 h (P value = 0.063). Application of 50 nM Tideglusib for 1 week revealed marked decreases in type 1 and type 3 collagen expressions (P = 0.029, P = 0.038, respectively). In contrast, there was a significant increase in the level of Axin-2 (P = 0.000) compared to the control group. CONCLUSION: The fact that Wnt signaling pathway activation obtained by Tideglusib application on DPSCs confirmed by the finding in the increase of Axin-2 at short and long-term evaluation periods which is resulted in the increase in the type 1 collagen expression at 24 h and decrease at 1 week together with the decrease in type 3 collagen expression at 1 week warrants further studies to evaluate the effect of Tideglusib on extracellular matrix expression.

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-1ß-stimulated human dental pulp fibroblasts.

In response to pro-inflammatory cytokines such as interleukin (IL)-1ß, 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 100 ng/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-1ß synergistically enhanced the production of IL-6, CCL20, IL-8 and CXCL10. IL-1ß 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-1ß. These findings suggest that IL-17A participates in the progression of dental pulp inflammation through the enhanced production of inflammatory mediators in HDPFs.

Research progress of dental pulp regeneration treatment. / å†ç”Ÿæ€§ç‰™é«“æ²»ç–—çš„ç ”ç©¶è¿›å±•.

The dental pulp is the only soft tissue structure within the tooth, serving functions such as sensation and nutrition. However, the dental pulp is highly susceptible to necrosis due to external factors. Currently, root canal therapy is the most commonly used treatment for pulp necrosis. Nevertheless, teeth treated with root canal therapy are prone to secondary infections and adverse outcomes like vertical root fractures. Regenerative endodontic therapy has emerged as a solution, aiming to replace damaged tooth structures, including dentin, root structure, and the pulp-dentin complex cells. This approach demonstrates significant advantages in addressing clinical symptoms and achieving regeneration of the root and even the pulp. Since the discovery of dental pulp stem cells, regenerative endodontic therapy has gained new momentum. Advances in cell transplantation and cell homing techniques have rapidly developed, showing promising potential for clinical applications.

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-1ß, 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.