Peri-implantitis and periodontitis are infectious inflammatory diseases driven by a dysbiotic shift in the dental plaque microbiome. The emergence of next-generation sequencing (NGS) technology enabled more precise understanding of the microbiome associated with these diseases. Despite clinical similarities and the presence of well-known periodontal pathogens, these two pathologies are characterized by distinct microbial structures and diversity. Most studies indicate that the peri-implantitis microbiome exhibits greater species diversity and complexity than the periodontitis microbiome, often showing significant enrichment of genera, such as Treponema. Furthermore, complex interspecific interactions drive disease progression, resulting in a pathogen-dominated state. The inorganic titanium surface of implants establishes a distinct ecological niche that differs from that of natural teeth. This distinction imposes unique selective pressures on microbial colonization, giving rise to a unique microbiome and host response.

  Treatment efficacy for peri-implantitis and periodontitis, whether non-surgical or surgical, is linked to the reconfiguration of the microbiome from a dysbiotic to a symbiont-rich profile. Although comprehensive monitoring, interpretation, and subsequent clinical application of full microbiome data remain challenging, simple indicators derived from these data, such as the Porphyromonas to Streptococcus ratio, potentially facilitate disease monitoring. In the future, integrated analysis of the oral microbiome, host immune response, and relevant clinical parameters, utilizing machine learning, holds the potential to significantly enhance risk stratification for peri-implantitis and facilitate the development of personalized treatment strategies. This review underscores the necessity of recognizing peri-implantitis as a pathology distinct from periodontitis and emphasizes the crucial role of microbiome analysis in its diagnosis and management.

  Introduction : Saliva plays a vital role in maintaining oral function and health ; however, many patients experience decreased salivary secretion for various reasons. Therefore, developing methods to preserve or enhance salivary gland function is highly desirable. The present study aimed to examine the effects of hyperbaric oxygen therapy (HBOT) on the expression of Aquaporin-1 and Aquaporin-5, key water channels in the salivary glands, specifically in the submandibular and parotid gland tissues. In addition, the expression of hypoxia-inducible factor 1-alpha (HIF-1α) and vascular endothelial growth factor (VEGF), which are associated with aquaporin regulation, was also investigated.

  Materials and Methods : Rats were randomly assigned to experimental groups (HBOT group) based on the duration of exposure (30 or 60min) and intervention period (1 day, 5 days, and 14 days) under 2.5 ATA with 100% oxygen (no treatment as control). Aquaporin-1, Aquaporin 5, HIF-1α, and VEGF expression levels in the submandibular and parotid glands were evaluated using enzyme-linked immunosorbent assay (ELISA).

  Results : Aquaporin-1, HIF-1α, and VEGF were significantly upregulated in the submandibular glands by 60min HBOT (P＜0.05), while no significant effect was observed in the parotid glands. The time-course showed Aquaporin-1 and Aquaporin-5 elevation on Day 14 only submandibular glands.

  Conclusion : These findings suggest that HBOT modulates the expression levels of Aquaporin-1 and Aquaporin-5 in rat salivary glands. This modulation was associated with the activation of the HIF-1α and VEGF signaling pathway.

  Introduction : Pregnancy and lactation are accompanied by profound physiological and hormonal changes that strongly influence the maternal microbiome. However, the transition of microbial communities from pre-pregnancy to postpartum state remains poorly understood. This study aimed to investigate the compositional and structural changes in the maternal oral and gut microbiomes before pregnancy and during the postpartum period.

  Materials and Methods : Wild-type female 15-16-week-old C57BL/6J mice were analyzed before pregnancy and during lactation. Ligatures ligated for 3 h at the maxillary second molars and feces were collected for evaluation of the oral and gut microbiomes, respectively, using 16S rRNA gene sequencing. “Before pregnancy” was defined as the day before mating with male mice. Ligature and fecal samples were collected before pregnancy and 3 weeks after delivery during breastfeeding.

  Results : Principal component analysis revealed significant differences in β-diversity in both the oral and gut microbiomes between the two stages. During lactation, the oral microbiome exhibited higher α-diversity, with higher class Actinobacteria and lower genus Lactobacillus and genus Bacteroides. The reduction in Bacteroides is typically associated with inflammation, suggests a shift toward an anti-inflammatory and restorative state after delivery. In contrast, the gut microbiome showed lower α-diversity, with higher genus Gordonibacter and Candidatus_Stoquefichus, and lower order/family Clostridia_vadinBB60_group and genus Tyzzerella during breastfeeding.

  Conclusion : Delivery and lactation are associated with site-specific yet coordinated remodeling of the maternal microbiome, contributing to systemic recovery and physiological adaptation during the postpartum period.

  Introduction : Dentin undergoes progressive mineralization by external stimuli. Orthodontic tooth movement (OTM) applies continuous mechanical forces to teeth, yet its biological effects on dentin mineralization remain unclear. We aimed to investigate the influence of OTM on dentin mineralization and the associated molecular responses using a rat model.

  Materials and Methods : Twelve-week-old male Wistar rats were assigned to OTM (10gf, an appropriate load for OTM, was applied to the maxillary first molar using nickel-titanium coil spring) or non-OTM groups (n=5 per group). The dental pulp volume, and root mineral density (RMD) were assessed using micro-computed tomography on days 0, 7, 14, and 21. Histological and immunohistochemical analyses were conducted on days 0, 14, and 21 to evaluate tertiary dentin and dentin matrix protein-1 (DMP1) expression. Statistical analysis was performed using Wilcoxon rank-sum testing (p＜0.05).

  Results : Comparing with controls, on day 21 in the OTM group, dental pulp volume was significantly reduced (p＜0.01) and RMD was significantly increased (p＜0.01). Histologically, the OTM group demonstrated clear tertiary dentin deposition along the pulp-dentin border after day 14. DMP1 expression increased over time in the OTM group, with a significantly greater staining area on the compression side at day 14 (p＜0.01) and 21 (p＜0.05).

  Conclusion : OTM induced tertiary dentin formation and enhanced root dentin mineralization in a time-dependent manner. Increased DMP1 expression, particularly on the compression side of OTM, preceded mineral deposition, suggesting a mechanobiological pathway linking mechanical load to dentin mineralization.

  Neuropathic pain is a refractory pain syndrome resulting from lesions or dysfunction of the somatosensory nervous system. Schwann cells, the glial cells of the peripheral nervous system, have been shown to contribute to neuropathic pain through the release of inflammatory mediators. However, the molecular mechanisms that regulate the expression of inflammatory genes in Schwann cells are poorly understood. Long non-coding RNAs (lncRNAs) play a key role in regulating a variety of gene expression processes. Among them, the lncRNA H19 is upregulated in Schwann cells following nerve injury and contributes to neuropathic pain. Therefore, this study aimed to elucidate the function of H19 in Schwann cells. In the rat Schwann cell line, H19 induced the expression of chemokine C-X-C motif chemokine ligand 1 (CXCL1). Consistent with these findings, both H19 and CXCL1 expression were persistently elevated in the injured spinal nerves of rats with neuropathic pain. These findings suggest that H19 upregulation in Schwann cells may contribute to neuropathic pain through the induction of CXCL1 expression.

  This retrospective, single-center study evaluated the analgesic effects and tolerability of mirogabalin in patients aged 18 years or older who were diagnosed with post-traumatic trigeminal neuropathic pain (PTNP). All the participants received mirogabalin between April 2022 and March 2024. Pain intensity was assessed using a visual analog scale (VAS) before and after treatment. Treatment effectiveness was defined as a ≥30% reduction in VAS score or voluntary discontinuation of dose escalation due to sufficient pain relief. Adverse reactions (ARs) were documented at each visit and potential predictors of treatment efficacy, including age, sex, disease duration, dose, and the presence of ARs, were analyzed.

  Of the 90 screened patients, 47 met the inclusion criteria. The mean VAS score significantly decreased from 64.4±16.6mm to 31.1±29.5mm (p＜0.01), and 63.8% of patients were classified as responders. The most frequently observed ARs were somnolence (44.7%) and dizziness (14.9%), none of which was serious. In 39 patients who did not reach the maximum approved dose of 30mg/day, 25 patients achieved pain relief with mild or no ARs at an average dose of 11.54±6.25mg/day. Logistic regression showed that ARs significantly reduced treatment success.

  These findings indicate that mirogabalin effectively alleviates PTNP in approximately 60% of patients. However, the development of ARs may compromise treatment success. Careful titration appears to be essential for achieving optimal outcomes while minimizing ARs. These results support the clinical utility of mirogabalin in the management of PTNP patients.