Search Results (88)

Background: Understanding the mechanisms underlying dental pain caused by pulpitis in humans has led to the development of animal models, such as the rat, which enable the study of the mechanisms underlying inflammation; the use of these models is considered ethically justified when the anticipated scientific benefits outweigh the potential impacts on animals in the harm/benefit balance. Objective: To develop a rat model of mechanically induced pulpitis and to evaluate the potential impact on animal well-being. Methods: Pulpitis was mechanically induced in male Lewis rats (13–16 weeks, 350–400 g) which were anesthetized and endotracheally intubated. Following pulp exposure, the cavity was sealed with either amalgam (n = 10) or zinc phosphate cement (n = 10). Following recovery and return to their housing, behavioral assessments and histological evaluations using Hematoxylin and Eosin (H&E) staining were conducted in separate cohorts at two time points: 3 h and 5 days following the procedure. Results: A standardized model of mechanically induced pulpitis was established and verified clinically and by histopathological analysis, which showed evidence of the inflammatory process and revealed no statistically significant differences in the scoring of pain, discomfort, or distress, nor in the measurements of food and water consumption or body weight. Conclusions: The behavioral assessments conducted in this study supported the implementation of a safe and easily reproducible model for future research aimed at elucidating the mechanisms underlying pulp inflammation. Full article

Background/Objectives: Pulp inflammation impairs healing, yet the underlying vascular and neural mechanisms remain poorly understood. This study investigated the differential regulation of lymphatic vessels, blood vessels, and neural tissue in pulpitis to elucidate healing limitations in inflamed dental pulp. Methods: This study evaluated 38 pulp samples (14 symptomatic irreversible pulpitis, 13 asymptomatic irreversible pulpitis, and 11 healthy controls) via immunohistochemistry, using D2-40 to identify lymphatic vessels, CD31 to mark blood vessels, and PGP9.5 to detect neural tissue. Vessel counts and neural tissue scoring were performed by blinded examiners and analyzed using appropriate statistical tests. Results: Dental pulp with symptomatic irreversible pulpitis exhibited significantly increased blood vessel density (50.3 vs. 39.2 in asymptomatic irreversible pulpitis and 25.8 in controls, p = 0.001, Cohen’s d = 1.82), while lymphatic vessel density remained unchanged across all groups (p ≥ 0.05), indicating impaired lymphangiogenesis despite inflammation. Neural tissue density was consistent across conditions, with a significant negative correlation between PGP9.5 expression and age (r = −0.5, p = 0.001). CD31 and D2-40 expression showed a positive correlation (r = 0.389, p = 0.016), suggesting coordinated vascular development. Conclusions: Our findings reveal a critical imbalance between enhanced angiogenesis and impaired lymphangiogenesis during pulpitis, potentially explaining the compromised healing capacity of inflamed dental pulp. This vascular dysregulation, combined with persistent neural tissue density, creates an environment in which inflammatory exudates accumulate with limited clearance. These insights indicate a need for new therapeutic strategies aimed at enhancing lymphangiogenesis to improve endodontic outcomes. Full article

MicroRNA (miR)-200c enhances osteogenesis, modulates inflammation, and participates in dentin development. This study was to investigate the beneficial potential of miR-200c in vital pulp therapy (VPT) by mitigating pulpitis and promoting dentin regeneration. We explored the miR-200c variations in inflamed pulp tissues from patients with symptomatic irreversible pulpitis and primary human dental pulp-derived cells (DPCs) challenged with P.g. lipopolysaccharide (Pg-LPS). We further assessed the functions of overexpression of miR-200c on odontogenic differentiation, pulpal inflammation, and dentin regeneration in vitro and in vivo. Our findings revealed a noteworthy downregulation of miR-200c expression in inflamed pulp tissues and primary human DPCs. Through the overexpression of miR-200c via transfecting plasmid DNA (pDNA), we observed a substantial downregulation of proinflammatory cytokines interleukin (IL)-6 and IL-8 in human DPCs. Furthermore, this overexpression significantly enhanced the transcript and protein levels of odontogenic differentiation markers, including Runt-related transcription factor (Runx)2, osteocalcin (OCN), dentin matrix protein (DMP)1, and dentin sialophosphoprotein (DSPP). In a rat model of pulpitis induced by Pg-LPS, we demonstrated notable benefits by local application of pDNA encoding miR-200c delivered by CaCO₃-based nanoparticles to reduce pulpal inflammation and promote dentin formation. These results underscore the significant impact of locally applied miR-200c in modulating pulpal inflammation and facilitating dentin repair, showcasing its ability to improve VPT outcomes. Full article

Severe dental pulp inflammation can lead to tissue lysis and destruction, underscoring the necessity for effective treatment of pulpitis. N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac⁴C) modification has recently emerged as a key regulator in inflammatory processes. However, whether NAT10 affects the inflammatory response in human dental pulp stem cells (hDPSCs) remains unelucidated. In this study, elevated NAT10 expression was observed in pulpitis tissues and LPS-stimulated hDPSCs. Knockdown of NAT10 led to reduced inflammatory gene expression and lower reactive oxygen species (ROS) production in LPS-stimulated hDPSCs, while the chemotactic migration of macrophages was also suppressed. Similar results were observed when hDPSCs were treated with Remodelin, an inhibitor of NAT10. Differentially expressed genes identified through RNA sequencing were significantly enriched in inflammatory signaling pathways after NAT10 depletion. Among the differential genes, pentraxins 3 (PTX3) was identified as the potential target gene due to the presence of the ac⁴C modification site and its known ability to regulate dental pulp inflammation. The mRNA and protein levels of PTX3 were reduced in NAT10-deficient cells, along with a decrease in its mRNA stability. Exogenous PTX3 supplementation partially reversed the inflammatory inhibition induced by NAT10 knockdown. Further evidence in vivo revealed that Remodelin treatment attenuated the severity of dental pulp inflammation in rats with pulpitis. In summary, these data indicated that NAT10 deficiency inhibited the stability of PTX3 mRNA and further inhibited hDPSC inflammation, while Remodelin might be a potential therapeutic agent for pulp capping. Full article

Idiopathic nephrotic syndrome (NS) is associated with immune dysfunction and increased susceptibility to infections. Oral health may influence systemic inflammation and disease progression. This study aimed to evaluate the salivary levels of interleukin-6 (IL-6) and interleukin-18 (IL-18) in children with NS and their association with dental health, particularly caries prevalence and the consequences of untreated caries. A cross-sectional study was conducted on 86 children aged 5–17 years, including 40 NS patients and 46 healthy controls. Clinical dental examinations assessed caries prevalence using the dmft/DMFT index and the impact of untreated caries using the pufa/PUFA index. Unstimulated saliva samples were collected, and IL-6 and IL-18 concentrations were measured using enzyme-linked immunosorbent assay. NS patients exhibited a significantly lower prevalence of active carious lesions than controls (50% vs. 72%, p = 0.039). The DMFT index was lower in the NS group (p = 0.003). Salivary IL-6 levels were significantly reduced in NS patients compared to controls (p = 0.015), while IL-18 levels showed no significant difference. IL-6 positively correlated with decayed permanent teeth and pulp/periapical tissue diseases, whereas IL-18 correlated with white spot lesions and pulp infections. IL-6 and IL-18 could serve as potential non-invasive indicators of disease progression in NS patients. Full article

Background: Irreversible pulpitis is a severe inflammation of the dental pulp. The purpose of this clinical trial was to evaluate the effectiveness of an inferior alveolar nerve block (IANB) injection followed by oral dexamethasone administration in reducing the pain associated with symptomatic irreversible pulpitis (SIP) in mandibular molars, without performing conventional pulpotomy. Methods: A sample of 80 subjects suffering from acute pain due to SIP on a mandibular molar were assigned to the dexamethasone group, who received an IANB injection followed by one oral dose of 4 mg of dexamethasone during the emergency visit followed by one dose of 4 mg after 8 h, or the control group, who received a conventional pulpotomy. Both groups received complete endodontic treatment after five to six days. The intensity of the preoperative pain and pain levels were measured in both groups at different times after each intervention. The Mann–Whitney U test was used to compare the pain scores between the groups at the same time point, while Friedman’s test was used to compare the pain scores between the four time points within the same intervention group, followed by the Bonferroni correction for multiple pairwise comparisons. Success was determined when the pain score on the visual analogue scale (VAS) was 20 or lower. Results: A survival analysis was conducted, where the event was considered as the disappearance of symptoms (or success: pain score ≤ 20). For both groups, the pain significantly decreased 8 h postoperatively (p < 0.05). The success rates at 8 and 12 h were significantly higher in the dexamethasone group compared to the control group (p = 0.05). However, the pain scores at 24 h remained comparable. Conclusions: An IANB injection followed by 8 mg of oral dexamethasone could reduce pain significantly in patients with SIP without performing conventional pulpotomy. The oral administration of dexamethasone could therefore be a valuable strategy to temporarily alleviate SIP symptoms until definitive treatment becomes feasible. Dexamethasone is a temporary pain management strategy rather than a replacement for pulpotomy. Full article

With increasing life expectancy and an aging population, the demand for dental treatments that preserve natural teeth has grown significantly. Among these treatments, endodontic therapies for pulpitis and apical periodontitis play a vital role, not only in keeping occlusal function, but also in preventing the exacerbation of systemic diseases. Both pulpitis and apical periodontitis are primarily caused by infections of the oral pathobiont within the root canal, leading to inflammation and destruction of the pulp, apical periodontal tissue, and bone. Standard root canal therapy aims to remove the infection source and facilitate natural tissue healing through the body’s regenerative capacity. However, challenges remain, including limited tooth functionality after complete pulp removal in pulpitis and insufficient recovery of the large bone defect in apical periodontitis. To address these limitations, endodontic regenerative therapies have emerged as promising alternatives. Pulp regeneration therapy seeks to restore the functionality of dental pulp, while bone regeneration therapy aims to repair and regenerate large bone defects affected by apical periodontal tissue. Full article

With the paradigm shift towards minimally invasive biologic therapies, vital pulp therapy (VPT) has been receiving increasing attention. Currently, bioactive materials (BMs), including MTAs, Biodentine, Bioaggregate, and iRoot BP Plus, are clinically widely used for the repair of damaged pulp tissue. Emerging evidence highlights the crucial role of inflammation in pulp repair, with mild to moderate inflammation serving as a prerequisite for promoting pulp repair. BMs play a pivotal role in regulating the balance between inflammatory response and reparative events for dentine repair. Despite their widespread application as pulp-capping agents, the precise mechanisms underlying the actions of BMs remain poorly understood. A comprehensive literature review was conducted, covering studies on the inflammatory responses induced by BMs published up to December 2023. Sources were identified through searches of PubMed and MEDLINE databases, supplemented by manual review of cross-references from relevant studies. The purpose of this article is to discuss diverse mechanisms by which BMs may regulate the balance between tissue inflammation and repair. A deeper understanding of these regulatory mechanisms will facilitate the optimization of current pulp-capping agents, enabling the development of targeted regenerative strategies to achieve superior clinical outcomes. Full article

Background: Chemotherapy (CMT) in children can disrupt dental development and calcification, causing long-term dental issues, but good dental care and habits can help improve quality of life. This case report examines permanent dental disturbances in a 7-year, 4-month-old girl undergoing CMT, explores the histology of microdontia, and outlines an oral treatment plan for CMT management. Methods: Clinical examination revealed microdontia and a groove crossing the cervical area (chronological hypoplasia), which were assessed using panoramic radiographs and histological analysis. The patient was monitored for five years, and microdontia was extracted for orthodontic reasons. A tailored treatment plan was implemented to maintain oral health during CMT. Results: Clinical and radiographic findings indicated tooth agenesis, rudimentary form, chronological hypoplasia, and microdontia. Histological analysis showed reduced odontoblast counts, abnormal dentinal tubules, thinner pre-dentin, and interglobular dentin (hypocalcification) surrounded by globular dentin (normal calcification). CMT-related microdontia caused inflammation with dilated blood vessels in the pulp. A high fever during CMT led to a groove in the enamel of all teeth, presenting as chronological hypoplasia. No new dental caries was observed over the follow-up. Conclusions: This report highlights long-term dental disturbances from CMT in permanent dentition and associated histopathological changes. It proposes an oral care protocol for managing these issues. Maintaining oral hygiene and preventing caries during the five-year follow-up reduced CMT side effects and improved the quality of the patient’s life. Full article

Dental inflammatory diseases remain a challenging clinical issue, whose causes and development are still not fully understood. During dental caries, bacteria penetrate the tooth pulp, causing pulpitis. To prevent pulp necrosis, it is crucial to promote tissue repair by recruiting immune cells, such as macrophages, able to secrete signal molecules for the pulp microenvironment and thus to recruit dental pulp stem cells (DPSCs) in the damaged site. To date, root canal therapy is the standard for dental caries, but alternative regenerative treatments are gaining attention. Complex Multifrequency Magnetoelectric Fields (CMFs) represent an interesting tool due to their potential anti-inflammatory activity. Against this background, the present work aims at investigating whether the CMF treatment might restore redox balance in a co-culture model of DPSCs and inflamed macrophages mimicking an inflammatory condition, like pulpitis. Results show that superoxide anion levels and markers related to the polarization of macrophages are modulated by the CMF treatment. In parallel, the use of CMFs discloses an impact on the odontogenic commitment of DPSCs, their immunophenotype being considerably modified. In conclusion, CMFs, by modulating the odontogenic commitment and the anti-inflammatory response of DPSCs, might represent a suitable therapeutic tool against pulpitis and, in general, towards dental inflammatory diseases. Full article

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. Full article

Dental caries is a highly prevalent chronic disease that leads to dental pulp inflammation. It is treated by removing the damaged tooth structure and applying a material that promotes resolution of pulpal inflammation. Tumor necrosis factor superfamily 14 (TNFSF14) is an immunomodulatory cytokine and a member of the TNF superfamily. This study aimed to evaluate the effect of TNFSF14 on the levels of inflammatory cytokines involved in pulpal inflammation using lipoteichoic acid (LTA)-induced human dental pulp stem cells (hDPSCs). hDPSCs were cultured and induced with LTA, followed by treatment with TNFSF14 at 25 and 50 ng/mL. Cellular viability was evaluated using the Alamar Blue assay. The levels of inflammatory cytokines IL-6, IL-8, IL-10, and TNF-α were quantified using reverse transcription–quantitative polymerase chain reaction (RT–qPCR) and enzyme-linked immunosorbent assay (ELISA). TNFSF14 at 25 and 50 ng/mL significantly reduced the mRNA and protein levels of pro-inflammatory cytokines TNF-α, IL-6, and IL-8, and increased the anti-inflammatory cytokine IL-10. In addition, TNFSF14-treated groups enhanced cell viability. Adding TNFSF14 to LTA-induced hDPSCs regulated the production of inflammatory cytokines by lowering the levels of IL-6, IL-8, and TNF-α and elevating IL-10 levels. Full article

Regenerative medicine in dentistry focuses on repairing damaged oral tissues using advanced tools like stem cells, biomaterials, and tissue engineering (TE). Mesenchymal stem cells (MSCs) from dental sources, such as dental pulp and periodontal ligament, show significant potential for tissue regeneration due to their proliferative and differentiative abilities. This systematic review, following PRISMA guidelines, evaluated fifteen studies and identified effective strategies for improving dental, periodontal, and bone tissue regeneration through scaffolds, secretomes, and bioengineering methods. Key advancements include the use of dental pulp stem cells (DPSCs) and periodontal ligament stem cells (PDLSCs) to boost cell viability and manage inflammation. Additionally, pharmacological agents like matrine and surface modifications on biomaterials improve stem cell adhesion and promote osteogenic differentiation. By integrating these approaches, regenerative medicine and TE can optimize dental therapies and enhance patient outcomes. This review highlights the potential and challenges in this field, providing a critical assessment of current research and future directions. Full article

Implant stability can be compromised by factors such as inadequate bone quality and infection, leading to potential implant failure. Ensuring implant stability and longevity is crucial for patient satisfaction and quality of life. In this multicenter, randomized, double-blind clinical trial, we assessed the impact of a bone bioactive liquid (BBL) on the Galaxy TS implant’s performance, stability, and osseointegration. We evaluated the impact stability, osseointegration, and pain levels using initial stability quotient (ISQ) measurements, CBCT scans, and pain assessment post-surgery. Surface analysis was performed using scanning electron microscopy (SEM) and atomic force microscopy (AFM). In vitro studies examined the BBL’s effects on dental pulp pluripotent stem cells’ (DPPSCs’) osteogenesis and inflammation modulation in human macrophages. All implants successfully osseointegrated, as demonstrated by the results of our clinical and histological studies. The BBL-treated implants showed significantly lower pain scores by day 7 (p < 0.00001) and improved stability by day 30 (ISQ > 62.00 ± 0.59, p < 8 × 10⁻⁷). By day 60, CBCT scans revealed an increased bone area ratio in BBL-treated implants. AFM images demonstrated the BBL’s softening and wettability effect on implant surfaces. Furthermore, the BBL promoted DPPSCs’ osteogenesis and modulated inflammatory markers in human primary macrophages. This study presents compelling clinical and biological evidence that BBL treatment improves Galaxy TS implant stability, reduces pain, and enhances bone formation, possibly through surface tension modulation and immunomodulatory effects. This advancement holds promise for enhancing patient outcomes and implant longevity. Full article

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. Full article