This study aims to extract and characterize hydroxyapatite (HAp) nanoparticles from the exoskeleton of Portunus sanguinolentus (blood-spotted swimming crab) shells for potential biomedical applications, particularly in bone tissue engineering and periodontal regenerative dentistry.

Crab shells were cleaned, dried at 100 °C, and ground into powder. The powder was sintered at 1000 °C to obtain calcium carbonate (CaCO₃), which was then reacted with diammonium hydrogen phosphate [(NH₄)₂HPO₄]. in double-distilled water using a wet chemical method at pH >9. The precipitate was filtered, dried at 100 °C, and sintered at 800 °C to synthesize HAp nanoparticles. Characterization using FTIR, EDX, XRD, and SEM confirmed the nanoparticles' chemical composition, crystallinity, and nanoscale morphology. Biocompatibility was evaluated through MTT and live/dead cell assays on human gingival fibroblasts (HGF) and periodontal ligament fibroblasts (HPDLF). Osteogenic potential was assessed via real-time qPCR for ALP, BMP2, and RUNX2 gene expression and Alizarin Red S staining for calcium mineralization. Statistical analysis was conducted using ANOVA with Tukey's test.

Results demonstrated that crab shell-derived HAp nanoparticles exhibited excellent crystallinity, biocompatibility, and osteogenic potential. Enhanced cell viability and significant upregulation of osteogenic markers confirmed their role in periodontal bone regeneration. Increased calcium deposition further validated their extracellular matrix mineralization capability. These findings suggest that Portunus sanguinolentus-derived HAp nanoparticles are a promising, sustainable biomaterial for periodontal regenerative applications.

The use of Portunus sanguinolentus-derived hydroxyapatite presents a sustainable and cost-effective alternative to synthetic biomaterials in dental applications. With excellent biocompatibility and the ability to promote osteogenic differentiation, these nanoparticles hold promise for bone grafting, implant coatings, and periodontal regeneration, supporting eco-friendly and efficient solutions for clinical bone repair and regenerative dentistry.

Developing and utilizing effective local antimicrobial agents can help treat periodontitis while minimizing the risks associated with systemic antibiotic use. Recent studies have shown that the mucosal adhesion properties of hydrogels can play a potential role in the treatment of periodontitis. The hydrogel can improve the contact and retention time of drugs in the periodontal pocket. Through the adhesion of mucosa, it interacts with the mucin coating surface of epithelium and teeth to form a specific interface force. The hydrogel exhibits strong mucosal adhesion (adhesion strength: 5-6 N/cm2) and prolonged retention in periodontal pockets (≥6 h), enabling sustained drug release through dynamic sol-gel transitions triggered by pH and reactive oxygen species (ROS). This design overcomes the limitations of poor mechanical stability in conventional formulations. The dynamic balance of oral microbiota plays an important role in maintaining oral health. Probiotics, by colonizing the oral cavity, transform the infected site from an environment rich in inflammatory cytokines to a more benign environment, inhibit harmful pathogenic microorganisms, and contribute to overall health. Microenvironment sensitive hydrogels can perform dynamic sol gel transformation in situ, and can accurately control drug release when exposed to various stimuli (such as temperature change, light, pH change, reactive oxygen species, etc.). Oral probiotics and anti-inflammatory drugs are encapsulated in hydrogels to inhibit the proliferation and adhesion of oral pathogens by planting in the mouth and producing metabolites, effectively preventing and treating oral diseases.

BACKGROUND The assessment of alveolar bone loss and determining patterns of disease progression with respect to different etiologic or contributing factors plays a vital role in the diagnosis of periodontitis, prognosis of the disease, and better treatment planning. This study aimed to determine periodontal bone loss using cone beam computed tomography images obtained from various age groups and evaluate the effects of age, sex, jaw type, tooth type, and tooth surface width on periodontal destruction. MATERIAL AND METHODS In total, 200 cone beam computed tomography images obtained for any indication were randomly selected and analyzed. The distance between the alveolar crest and cemento-enamel junction was measured, and values exceeding 2 mm were considered as bone loss. Furthermore, the buccolingual and mesiodistal widths of all teeth at the cemento-enamel junction were measured to determine tooth surface width. RESULTS Among the patients included in the study, bone loss increased with age. The highest bone loss was observed in the maxillary molars, followed by the mandibular incisors. Although there was no significant difference in mean bone loss values between the jaws, distal surfaces in the maxilla showed greater bone loss than that in the mandible. Furthermore, the relationship between tooth surface width at the cemento-enamel junction and bone loss varied by tooth type. In mandibular incisors and premolars, bone loss increased as the buccolingual and mesiodistal widths decreased. CONCLUSIONS These findings indicate that periodontal bone loss is influenced by age, sex, tooth type, and tooth surface width.

Superhydrophobic antimicrobial photodynamic therapy (SH-aPDT) is advantageous wherein airborne singlet oxygen (1O2) is delivered from a device tip to kill a biofilm with no photosensitizer exposure and no bacterial selectivity (Gram + or Gram -). For effective treatment of periodontitis, the frequency of treatment as well as the optical light fluence required is not known. Thus, we sought to determine whether single or repeated SH-aPDT treatments would work best in vivo using two fluence values: 60 and 125 J/cm2. We assessed the efficacy of three protocols: single treatment; interval treatments (days 0, 2, and 7); and consecutive treatments (days 0, 1, and 2). After 30 days of evaluation, we found that, SH-aPDT in 3 consecutive treatments significantly decreased Porphyromonas gingivalis levels compared to single and interval SH-aPDT treatments, as well as SRP-chlorhexidine (CHX) controls (p < 0.05). Notably, clinical parameters also improved (p < 0.05), and histological and stereometric analyses revealed that consecutive SH-aPDT treatments were the most effective for promoting healing and reducing inflammation. Our study shows what works best for SH-aPDT, while also demonstrating SH-aPDT advantages to treatment of periodontitis including no bacterial selectivity (Gram + or Gram -) and preventing the development of bacterial resistance.

Growing evidence suggests that prediabetes may increase the risk of periodontitis, though the extent of this association remains unclear. To provide a clearer understanding, this meta-analysis focused on observational studies that utilized multivariate analyses to adjust for key confounding factors.

A comprehensive search of PubMed, Embase, and Web of Science was conducted to identify observational studies assessing the relationship between prediabetes and periodontitis. Only studies that utilized multivariate analyses were included to minimize confounding bias. The quality of the studies was evaluated with the Newcastle-Ottawa Scale (NOS). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using a random-effects model, with heterogeneity assessed by the I² statistic.

Ten observational studies with 38,727 participants were included. Overall, individuals with prediabetes had a significantly higher risk of periodontitis compared to normoglycemic individuals (OR: 1.27, 95% CI: 1.09 to 1.48, p < 0.001) with moderate heterogeneity (I² = 53%). Subgroup analyses revealed a stronger association in studies where the proportion of men was < 45% compared to those ≥ 45% (OR: 1.75 vs. 1.15, p for subgroup difference = 0.01). Studies with lower quality (NOS score = 7) showed a stronger association compared to higher-quality studies (NOS score = 8 or 9, p for subgroup difference = 0.003).

This meta-analysis found that prediabetes may be independently associated with an increased risk of periodontitis. Further research is needed to explore the mechanisms underlying this association and potential sex-specific effects.

Several studies have demonstrated an increased risk of periodontitis (PD) among patients diagnosed with systemic lupus erythematosus (SLE). However, the underlying common mechanism between them remains incompletely understood. Accordingly, the aim of this study is to examine diagnostic biomarkers and potential therapeutic targets for SLE and PD by leveraging publicly accessible microarray datasets and transcriptome analysis.

Datasets pertaining to SLE and PD were retrieved from the Gene Expression Omnibus (GEO) database, and subsequently analyzed for differentially expressed genes (DEGs). Key gene modules were identified through weighted gene co-expression network analysis (WGCNA), and shared genes were obtained by overlapping key genes between DEGs and WGCNA. These shared genes were subsequently subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, leading to the establishment of a Protein-Protein Interaction (PPI) network. Random forest (RF) and Least Absolute Shrinkage and Selection Operator (Lasso) regression were employed to identify key hub genes. Receiver operating characteristic (ROC) curves were generated using a new validation dataset to evaluate the performance of candidate genes. Finally, levels of immune cell infiltration in SLE and PD were assessed using CIBERSORTx.

A total of 50 core genes were identified between the genes screened by WGCNA and DEGs. Functional enrichment analysis revealed that these genes are primarily associated with the PI3K-Akt and B-cell receptor signaling pathways. Additionally, using machine learning algorithms and ROC curve analysis, a total of 8 key genes (PLEKHA1, CEACAM1, TNFAIP6, TCN2, GLDC, GNG7, LY96, VCAN) were identified Finally, immune infiltration analysis highlighted the significant roles of neutrophils, monocytes, plasma cells, and gammadelta T cells (γδ T cells) in the pathogenesis of both SLE and PD.

This study identifies 8 hub genes that could potentially serve as diagnostic markers for both SLE and PD, highlighting the importance of VCAN and LY96 in diagnosis. Moreover, the involvement of the PI3K-Akt signaling pathway in both diseases suggests its significant role. These identified key genes and signaling pathways lay the groundwork for deeper comprehension of the interplay between SLE and PD.

Bacterial infections continue to pose a major threat to public health, contributing to high mortality rates worldwide. The growing ineffectiveness of conventional antibiotics has created an urgent need for alternative solutions. Nanomaterials (NMs) have emerged as a promising approach to combating bacterial infections due to their unique physicochemical properties, and extensive research has been conducted to address this crisis, yielding notable results. However, challenges such as limited light absorption and inherent cytotoxicity remain significant concerns. Furthermore, the clinical adoption of single-mode phototherapy is often restricted by the shallow tissue penetration of traditional light sources. The second biological window (NIR-II, 950-1450 nm) offers a groundbreaking opportunity for therapeutic and diagnostic applications by enabling deeper tissue penetration. As a result, growing research efforts are dedicated to developing NIR-II activated photosensitizers and nanomaterials to overcome challenges such as poor light absorption, limited tissue penetration, and suboptimal activation. Despite significant advancements, a comprehensive review of antibacterial nanomaterials specifically designed for the NIR-II window is still lacking in literature. This review aims to fill that gap by discussing the latest advancements, challenges, and potential of light-activated antibacterial nanomaterials within the BW-II region. The goal is to enhance understanding and guide the development of more efficient nanomaterials for future biomedical and clinical applications.

To assist patients in maintaining oral health in patients with Parkinson's disease (PD), this review aims to search the literature on aspects related to oral health in PD patients. In contrast to other research, we included the involvement of microbes in PD patients' poor oral health. Finally, we conclude that, in comparison to healthy individuals, PD patients have poorer oral health and a higher incidence of oral ailments.

Oral diseases represent a significant global health and economic burden, necessitating the development of effective diagnostic tools. This study investigates the volatile organic compound (VOC) profiles of bacteria associated with dental caries and periodontal disease to explore their potential as diagnostic biomarkers. Four microbial strains-Streptococcus mutans (700610), Streptococcus sanguis (NCO 2863), Porphyromonas gingivalis (ATCC 33277), and Fusobacterium nucleatum (PK1594)-were cultured (N = 24), alongside intraoral samples (N = 60), from individuals with common oral diseases. Headspace VOCs were analyzed using gas chromatography-mass spectrometry (GC-MS), and statistical analyses were conducted by applying non-parametric Wilcoxon and Kruskal-Wallis tests. VOC identification was performed using the NIST14 database. Strain-specific VOC signatures were identified, with P. gingivalis and F. nucleatum exhibiting distinct profiles from each other and from Streptococcus strains. Comparative analysis of disease cohorts revealed statistically significant differences at multiple retention times between caries, gingivitis, and periodontitis. These findings suggest that VOC profiling enables differentiation between bacterial strains and disease phenotypes, supporting their potential application as diagnostic biomarkers for oral diseases. This study establishes a foundational framework for VOC-based diagnostic methodologies in dental pathology.

Background Selenomonas noxia is a putative periodontal pathogen in subgingival biofilm communities. This study compared the subgingival prevalence and levels of S. noxia in those with severe periodontitis and those with periodontal health and assessed the in vitro antibiotic susceptibility of the species. Methods Subgingival biofilm samples from 206 adults with stage III (severe) periodontitis and 48 adults with periodontal health were examined with an S. noxia-specific whole chromosomal nucleic acid probe. Minimum inhibitory concentration (MIC) values of six antibiotics against S. noxia were determined in vitro with antibiotic gradient strips. Results Selenomonas noxia was more frequently detected in patients with severe periodontitis (53.4%) than persons with periodontal health (20.8%) (2.6-fold more frequent, p = 0.0001, Fisher's exact test). Heavy subgingival colonization by S. noxia (≥106 cells/subject subgingival specimen) was also more frequent in persons with severe periodontitis (16.0%) than those with periodontal health (2.1%) (7.6-fold more frequent, p = 0.008, Fisher's exact test). Selenomonas noxia was susceptible in vitro to amoxicillin, azithromycin, clindamycin, doxycycline, and metronidazole (all MIC values ≤ 0.75 mg/L) but resistant to spiramycin (MIC > 32 mg/L). Conclusions Selenomonas noxia was significantly more prevalent at significantly higher subgingival levels in patients with severe periodontitis than adults with periodontal health. However, heavy S. noxia subgingival colonization was present in only a subset of severe periodontitis patients and rarely in those with periodontal health. Selenomonas noxia was susceptible in vitro to several antibiotics of potential therapeutic use in periodontitis therapy, with the exception of spiramycin. Selenomonas noxia may contribute to periodontitis in patients harboring high subgingival numbers of the organism.

Background/Objectives: The oral health disorder periodontal disease is widespread around the world and has a public health dimension. This study aimed to perform a systematic review and an appraised analysis that looks at both the prevalence and diversity of risk factors associated with periodontal disease in Saudi Arabia. It places a particular focus on subgroup analyses and pooled prevalence estimates to identify certain populations that could be described as high risk. Methods: Several databases, including PubMed, Scopus, and Google Scholar, were used to conduct the present systematic review. The search was designed to identify relevant studies published from 1980 to 2023. Both quantitative and qualitative studies were included. Subgroup analyses and meta-analyses were performed using a random-effects model to calculate pooled prevalence rates. The studies were evaluated using three criteria that focused on bias. Finally, the authors created a narrative synthesis of the review findings for ease of understanding. Results: The pooled overall prevalence of periodontal disease was 46.2% (95% CI: 40.5-51.8), with high heterogeneity (I2 = 85%). Subgroup analyses identified obese adults as having the highest prevalence of this condition (71.3%), and individuals diagnosed with diabetes also displayed a significantly high prevalence (52.1%). Adolescents aged 15-19 years had an age-specific prevalence of 8.6%, which was significantly lower than that of the other age groups analyzed. Poor oral hygiene, tobacco use, diabetes, and obesity have been recognized as risk factors for periodontal disease. Conclusions: The substantial burden of periodontal disease in Saudi Arabia, especially among high-risk groups, such as obese and diabetic adults, cannot be overstated. Our public health initiatives need to focus on these high-risk individuals, who are likely to be both periodontally and systemically compromised, to provide lifestyle modification counseling and oral hygiene education for them, as well as to routinize their dental care in a way that minimizes the chances of becoming periodontally compromised.

Periodontitis is a disease caused by a bacterial infection that causes chronic inflammation. The pathogenesis of periodontitis is mediated by several mediators, including chemokines, cytokines, metalloproteinases, and adipokines. Adiponectin is an adipokine that influences several metabolic processes and numerous immunological processes. In this study, we investigated the effect of adiponectin on the expression in the periodontal ligament of selected cytokines involved in the pathogenesis of periodontitis. Human periodontal ligament cells (hPDLCs) were stimulated with adiponectin and then analyzed for expression (TNF-α, IL-1, IL-6, IL-8, IL-10, IL-17, and IL-18) in cell cultures at the mRNA level and in supernatants at the protein level. The samples were analyzed after 12, 24, and 48 h of adiponectin stimulation. We found no significant effect of adipokine on TNF-α gene expression after 12, 24, and 48 h of stimulation. For IL-1, a statistically significant increase in IL-1 gene expression was found after 12 h of adiponectin stimulation, while the differences were not statistically significant after 24 and 48 h. Adiponectin caused a statistically significant increase in IL-6 gene expression after 12, 24, and 48 h of stimulation. Stimulating periodontal ligament cells with adiponectin significantly increased TNF-α, IL-6, and IL-8 protein levels in supernatants after 12, 24, and 48 h. The levels of IL-1 were statistically significantly increased after 12 and 24 h of adiponectin stimulation. There was no statistically significant effect of adiponectin on IL-10, IL-17, and IL-18 levels. The results of our study suggest that adiponectin may significantly increase the expression of selected cytokines in periodontal ligament cells.

Porphyromonas gingivalis (Pg) is a keystone pathogen in periodontitis, encoding a unique peptidyl arginine deiminase (PPAD) linked to protein citrullination, a process associated with rheumatoid arthritis (RA). Recently, we identified a super-active PPAD variant (T2) in Pg isolates. Here, we evaluated if the presence of the super-active T2 variant of PPAD affects the salivary microbiome, the severity of chronic periodontitis (CP), and subsequently CP's causative association with RA onset/progression.

We examined 56 CP patients and 36 healthy volunteers. Pg and Tannerella forsythia counts were measured via RT-PCR, and PPAD variant was typed via PCR. 16S rRNA from salivary DNA sequencing characterized microbiota composition, while CP severity was assessed through bleeding on probing (BoP), clinical attachment loss (CAL), and pocket depth (PD) parameters.

CP patients exhibited higher Pg and T. forsythia counts, with 30.7% harbouring the PPAD-T2 variant, compared to only one healthy volunteer. Clinical CP parameters were unaffected by the PPAD variant. However, PPAD-T2 influenced oral microbiota composition, enriching certain genera.

While the PPAD variant did not affect CP severity, it influenced oral microbiota composition. Further research is needed to understand citrullination's role in oral microbiota and chronic inflammatory disease development.

Multiple sclerosis (MS) is characterized by chronic inflammation and demyelination within the central nervous system (CNS), primarily driven by the abnormal activation of the peripheral immune system, notably Th1 cells. As the principal pathogen in periodontitis, Porphyromonas gingivalis (P. gingivalis) is linked to an increased risk of multiple sclerosis progression; however, its role in central nervous system inflammation remains unclear. In this study, we aimed to determine whether P. gingivalis promotes peripheral Th1 cell differentiation via the ZAP70/NF-κB signaling pathway, thereby exacerbating experimental autoimmune encephalomyelitis(EAE), a model of multiple sclerosis.

C57BL/6J mice were randomly divided into healthy control, periodontitis, EAE, and periodontitis with EAE group. Neurological function was assessed using Weaver's score. Histopathology (H&E, LFB staining) and Evans blue dye leakage evaluated inflammation, demyelination, and blood-brain barrier(BBB)permeability. Th1 and Th17 cells were quantified by flow cytometry, while immunofluorescence staining was performed to analyze Claudin-5, IFN-γ +CD4+ T -positive cell and IL-17+CD4+-positive cell expression. Western blotting measured NF-κB and related protein expression. Reference-based mRNA sequencing analysis and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment was conducted to identify differential gene expression and pathway enrichment.

In mice with experimental autoimmune encephalomyelitis, P. gingivalis infection significantly elevated Th1 cell proportions in the peripheral blood, increased interferon-gamma expression, and exacerbated central nervous system inflammation and demyelination by enhancing blood-brain barrier permeability. The infection also activated the ZAP70/NF-κB pathway, essential for peripheral Th1 differentiation, as evidenced by p65 nuclear translocation and significant upregulation of Th1-related genes, including those of the transcription factor Tbx21 and interleukin-12 receptors. In vitro, P. gingivalis lipopolysaccharide (LPS) stimulated Th1 differentiation via ZAP70/NF-κB, which was effectively blocked by pathway inhibitors, reducing Th1 cells and pro-inflammatory factors.

Our findings elucidate, for the first time, how P. gingivalis infection promotes central nervous system inflammation by driving Th1 cell differentiation via peripheral ZAP70/NF-κB pathway activation. This highlights P. gingivalis as a local periodontitis pathogen and significant contributor to neuroinflammation, providing new insights into the pathogenesis of multiple sclerosis and identifying promising targets for immunomodulatory therapeutic strategies.

The present study investigated the molecular presence of 4 species of pathogenic periodontal bacteria (Porphyromonas gulae, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola) using quantitative real-time polymerase chain reaction (PCR) in 230 household dogs with or without gingivitis, dental plaque and/or calculus. Overall, T. forsythia was most frequently present (77.8%), followed by P. gulae (50.9%), T. denticola (38.7%), and P. gingivalis (34.8%). A higher percentage of these bacteria was associated with factors such as age, grade of gingivitis, and an increase in dental plaque and/or calculus that indicated poor oral cleanliness. Even without a direct relation to gingivitis and plaque and/or calculus, these 4 species were consistently found not only in older dogs but also in younger ones. The results suggest that these bacteria are commonly present in household dogs, which puts them at risk of developing periodontal disease. Considering that 3 species of bacteria, excluding P. gulae, have zoonotic potential, it emphasizes the need for caution to prevent transmission between dogs and humans. Regarding overall bacterial DNA copy numbers, there was a wide range, with P. gulae having the most, followed by T. forsythia, P. gingivalis, and finally, T. denticola. The copy numbers did not always correlate with prevalence. The DNA copy numbers of T. forsythia were significantly lower in cases of higher-grade gingivitis and when there was poor oral cleanliness. These findings highlight the complexity of the interplay between bacterial type, prevalence, DNA copy numbers, and the oral health of household dogs.

Pterodon pubescens Benth is a Brazilian medicinal plant (sucupira, in Brazilian Portuguese). This paper aims to determine the volatile composition and antibacterial activities of hexane extract from P. pubescens seeds (HE-PP). Antibacterial activities were screened by the microdilution broth method in 96-well culture plates and MIC values were expressed as µg/mL. HE-PP was active against several oral bacteria whose MIC values ranged between 12.5 µg/mL and 50 µg/mL and against three mycobacterial strains (MIC = 125 µg/mL and 500 µg/mL). In addition, HE-PP was active against Xanthomonas citri strain (MIC = 100 µg/mL). Cytotoxic activity of the extract was evaluated in human tumour and non-tumour cell lines. HE-PP showed selective cytotoxicity to cervical adenocarcinoma (HeLa cells - IC50 = 53.47 µg/mL). Its major constituents were identified by GC-MS and GC-FID: E-caryophyllene, vouacapane, E-geranylgeraniol and dehydroabietol. Results reinforce the biological potential of HE-PP against a broad spectrum of pathogenic and phytopathogenic bacteria.

Alteration of the oral microbiome could potentially play a role in the etiology of certain patients with Autism Spectrum Disorder (ASD), similar to the established link between gut microbiota dysbiosis and ASD. Most studies have assessed oral microbiota in children only and few have explored the oral flora composition in adults with ASD.

In our study, periodontal and dental status was evaluated in 30 adults with ASD using appropriate indices. Oral microbiota samples were collected in crevicular fluid and supra-gingival plaque at inflamed sites in each patient and analyzed using PCR for bacteria and qPCR for protozoa. Demographic data, co-morbidities, medication and oral hygiene habits were also collected.

A total of 86.7% of the patients recruited suffering from severe ASD had periodontal disease and 67% had a high level of supra-gingival plaque. Two major periodontopathogens belonging to the red complex, Treponema denticola and Tannerella forsythia, were both detected in the supra-gingival plaque of 86.2% of patients and in the gingival crevicular fluid of 80 and 86.7% of patients, respectively. Certain microorganisms were statistically more frequently detected in patients with digestive disorders and taking certain medications.

The oral microbiota composition of the adults with ASD showed significant differences compared to neurotypical individuals, particularly in the prevalence of the specific microorganisms P. gingivalis, T. tenax and E. gingivalis ST1. The detection frequency of periodontitis and periodontopathogens may have been underestimated due to the lack of cooperation of the adults with ASD during clinical examination and microbiota sampling. Further studies on larger cohorts are needed to consolidate these results to gain a better understanding of variations in oral microbiota.

Aggressive Periodontitis (AP) and Feline Chronic Gingivostomatitis (FCGS) are two oral inflammatory diseases in cats with unknown etiology. Both conditions present with severe inflammation of the oral cavity and in FCGS it is found with additional deterioration of the non-keratinized mucosa. The oral microbiome is increasingly implicated in disease progression, but little is known about shifts in the microbial community during the AP and FCGS progression. To that end, we used deep metagenomic sequencing with total RNA on three longitudinal samples of the oral microbiome in a cat first diagnosed with AP that progressed to FCGS. This deep sequencing approach revealed that increased diversity at both the genus and species levels marked the shift from AP to FCGS, including increases in Porphyromonas and Treponema species, and decreased Streptobacillus species. The metatranscriptomes were then probed for expression of antimicrobial resistance genes and virulence factors. Disease-related genes that include cheY, and ompP5 were expressed in early AP and FCGS, while others like galU were only expressed in one or the other disease state. Both genus and species-level shifts were observed along the longitudinal microbiome samples with a noted increase in species diversity in the FCGS-associated microbiome. Corroborating that functional shifts accompany taxonomic changes, the AMR and virulence factor expression similarly changed between the sampling points. Together, these taxonomic and functional shifts indicate that AP and FCGS are potentially linked and may be marked by changes in the oral microbiome, which supports the development of microbial-based clinical diagnostics and therapeutics.

The copy number (CN) variant AMY1 encodes the salivary amylase enzyme which promotes starch digestion. Although this gene has been associated with dental caries and periodontal disease susceptibility, the impact of the interaction between AMY1 CN and starch on oral biofilms is unclear. We explored how oral microbiota communities shaped by AMY1 CN respond to starch by employing an in vitro model of biofilm formation. We cultured biofilms using saliva samples from 31 donors with a range of AMY1 CNs (between 2 and 20 copies) and self-reported gum disease states; we used media with and without starch. Many of the most prevalent genera in saliva were also prevalent in the derived biofilms. The presence of starch in the media was associated with lower biofilm alpha diversity. We found a significant interaction between AMY1 CN and the media carbohydrate content that influenced the proportions of Atopobium and Veillonella. Members of these genera have been associated with dental caries and periodontitis. These findings suggest that the effects of carbohydrates on oral microbiome composition depend on AMY1 CN and that human oral bacteria evolved in response to expansion of this host gene locus.

To evaluate the effects of Xianling Gubao Capsules (XGC) on alveolar bone and inflammatory mediators in the gingival crevicular fluid in patients with periodontitis.

A retrospective analysis was conducted on 90 periodontitis patients who received medication treatment at Daqing Longnan Hospital from September 2022 to June 2023. Patients were categorized into three groups: a control group (n=30, receiving basic periodontal treatment), a Caltrate group (n=30, receiving basic treatment plus Caltrate), and an XGC group (n=30, receiving basic treatment plus Xianling Gubao Capsules). Changes in alveolar bone defect height, alveolar bone density, plaque index (PI), probing depth (PD), gingival index (GI), gingival crevicular fluid volume, and inflammatory mediator levels were compared before and after treatment.

After 3 and 6 months of treatment, the XGC group exhibited significantly reduced alveolar bone defect height in incisors, canines, premolars, and molars and significantly increased alveolar bone density compared with the other two groups (all P<0.05). The XGC group also exhibited lower tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels and higher interleukin-17 (IL-17) levels than the Caltrate and control groups (all P<0.05). Additionally, PI, PD, GI, and gingival crevicular fluid volume were significantly lower in the XGC group at both time points (all P<0.05). The incidence of adverse reactions did not differ significantly among the three groups (P>0.05).

Xianling Gubao Capsules, when combined with conventional periodontal treatment, may enhance alveolar bone density, reduce alveolar bone defects, alleviate periodontal inflammation, and modulate inflammatory mediator levels in the gingival crevicular fluid. These findings suggest clinical benefits for periodontitis management.

Gingivitis and periodontitis are prevalent periodontal conditions associated with dysbiosis of the oral cavity, which leads to inflammation and bleeding of gums, loss of tooth attachment, and degradation of the underlying bone structure. The standard adjunctive treatment for periodontal conditions, chlorhexidine mouthwash, is effective but is associated with several side effects. Probiotics have been explored as an alternative solution that promotes oral health by restoring homeostasis in the oral cavity. This review presents a summary of clinical trials using the Darolac® (Oralis SB®) probiotic formulation (Lactobacillus acidophilus Rosell®-52, Lactobacillus rhamnosus Rosell®-11, Bifidobacterium longum Rosell®-175 and Saccharomyces boulardii CNCM I-1079) as a mouthwash to support the maintenance of oral health or the restoration of its balance. In reviewed studies, Darolac® is compared to a placebo or other common solutions for periodontal conditions, including chlorhexidine mouthwash. Studies show that Darolac® is as effective or even superior to other available solutions, which supports its use as an effective adjuvant to oral health. The effects of Darolac® on the reduction in oral pathogens and markers of oral dysbiosis are reviewed, and the association between periodontitis, inflammation, and systemic diseases, as well as their implications and the use of probiotics in the periodontal field, are discussed.

To examine the characteristics of the salivary microbiome in Type 2 diabetes mellitus (T2DM) patients with or without periodontitis.

Periodontitis has been identified as clear sequelae of T2DM. This chronic oral disease also impacts the management of the clinical features of diabetes. The oral microbiome characteristics in T2DM with and without periodontitis, as well as the response of this oral microbiome to nonsurgical therapy have not been well described. Knowledge of key oral biological features could help address the observed poorer clinical presentation of T2DM patients.

The oral microbiome in saliva of adult cohorts periodontally healthy/non-diabetic (non-periodontitis; NP; n = 31), T2DM without periodontitis (DWoP; n = 32), and T2DM with periodontitis (DWP; n = 29) were characterized by microbial molecular analysis using V3-V4 sequencing and Luminex or ELISA techniques for salivary host analytes.

Phyla distribution showed DWP with significantly lower levels of Firmicutes and Actinobacteria and higher levels of Fusobacteria and Spirochetes compared to the healthier groups. Approximately 10% of the detected microbial species showed significant differences in frequency and level of colonization among the DWP, DWoP, and NP samples. A subset of bacteria were significantly correlated with clinical disease features, as well as a specific repertoire of salivary analytes, in particular matrix metalloproteinase (MMP)8/MMP9, interleukin-1ß, B-cell activating factor, and resistin differed between the groups and were related to specific taxa. Principal component analysis that identified a majority of the DWP subjects microbiome was unique based upon an array of 27 taxa out of up to 255 detected in the saliva samples.

T2DM patients with periodontitis show unique oral microbiome and salivary analyte composition compared to diabetics or non-diabetic persons without periodontitis. Specific members of the oral microbiome relate directly to the clinical disease features and/or salivary biomolecules in T2DM individuals.

Background/Objectives: The 2017 Periodontal Classification offers a comprehensive framework for the diagnosis and management of periodontitis based on staging and grading criteria. Orthodontic therapy is increasingly incorporated into the management of periodontitis to rectify malocclusion, pathological tooth migration, and occlusal stability. Nonetheless, few data directly correspond with this revised classification scheme. The objective of this systematic review is to figure out the influence of orthodontic therapy on periodontal outcomes in patients with Stage III and IV periodontitis, as categorized by the 2017 framework. Methods: A systematic review was performed in accordance with the PRISMA 2020 principles. The databases examined were PubMed, Web of Science, Scopus, and Google Scholar. The evaluation focuses on research published from 2012 to 2024. Seventeen studies were assessed after the application of the inclusion criteria. Key outcomes included clinical attachment level (CAL) improvement, probing depth (PD) decrease, and radiographic bone fill. Results: The integration of orthodontic treatment with periodontal therapy markedly enhanced CAL (mean gain: 4.35-5.96 mm), decreased PD (mean reduction: 3.1-6.3 mm), and facilitated radiographic bone regeneration (mean vertical fill: 4.89 mm). Patients with Stage IV Grade C periodontitis had the most significant improvement, especially with early orthodontic intervention subsequent to regenerative treatment. Prolonged follow-ups (up to 10 years) validated consistent results. Conclusions: Orthodontic intervention, as a supplementary measure to periodontal therapy, improves results in severe periodontitis, especially in Stage III and IV patients. These results underscore the need for multidisciplinary teamwork and defined protocols for including orthodontics in periodontitis therapy.

Background: Poor oral health and periodontitis have been epidemiologically linked to cognitive decline and mild cognitive impairment (MCI) in older adults. However, specific metrics directly linking these clinical signs are exceedingly limited. Methods: To address this gap and develop novel tools to help clinicians identify individuals at risk of cognitive decline, we established the PerioMind Colombia Cohort, comprising elderly Colombian subjects who underwent comprehensive neurocognitive and periodontal evaluations. Results: The results revealed that subjects diagnosed with MCI exhibited significantly higher scores in specific periodontal indices, including gingival erythema and pocket depth parameters. The predictive model identified positive associations with MCI, with gingival erythema showing the strongest correlation, followed by the presence of periodontitis and variations in pocket depth measurements. Additionally, lower educational attainment was associated with a higher likelihood of being classified in the periodontitis-MCI group. Conclusions: Here, we show that specific altered periodontal metrics are associated with MCI diagnosis, and the generated results provide defined metric ranges for identifying individuals at risk. Upon validation in larger cohorts, the findings reported here could offer dental practitioners and clinicians innovative tools to identify individuals at risk of MCI and age-related dementias through routine oral health assessments, thereby enabling more accessible and highly sought-after early intervention strategies in both developing and developed countries.

Periodontitis (PD) is a polymicrobial dysbiotic immuno-inflammatory disease. Toll-like receptors (TLRs) are present on gingival epithelial cells and recognize pathogen-associated molecular patterns (PAMPs) on pathogenic bacteria, induce the secretion of proinflammatory cytokines, and initiate innate and adaptive antigen-specific immune responses to eradicate the invading microbes. Since PD is a chronic inflammatory disease, TLR2/TLR4 plays a vital role in disease pathogenesis and maintaining the periodontium during health. Many factors modulate the TLR-mediated signaling pathway, including specific miRNAs. The present study was designed to characterize the function of TLR2/4 signaling to the miRNA profile after polybacterial infection with Streptococcus gordonii, Fusobacterium nucleatum, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia in C57BL6/J wild-type, TLR2 -/- , and TLR4 -/- mice (n=16/group) using RT-qPCR. The selection of 15 dominant miRNAs for RT-qPCR analysis was based on prior NanoString global miRNA expression profiling in response to polymicrobial and monobacterial infection. Polybacterial infections established gingival colonization in wild-type, TLR2 -/- and TLR4 -/- mice with induction of bacterial-specific IgG. A significant reduction in alveolar bone resorption (ABR) and gingival inflammation was observed in the mandibles of TLR2/4 -/- mice compared to C57BL6/J wild-type mice ( p <0.0001). Periodontal bacteria disseminated from gingival tissue to the multiple organs in wild-type and TLR2 -/- mice (heart, lungs, brain, kidney) and limited to heart ( F. nucleatum ), lungs ( P. gingivalis ), kidney ( T. forsythia ) in TLR4 -/- mice. The diagnostic potential of miRNAs was assessed by receiver operating characteristic (ROC) curves. Among 15 miRNAs, three were upregulated in C57BL6/J wild-type mice, two in TLR2 -/- , and seven in TLR4 -/- mice. Notably, the anti-inflammatory miR-146a-5p was consistently upregulated in all the mice. Additionally, miR-15a-5p was upregulated in wild-type and TLR2 -/- mice. let-7c-5p was upregulated in TLR4 -/- mice and downregulated in the wild-type mice. Multi-species oral bacterial infection alters the TLR2/4 signaling pathways by modulating the expression of several potential biomarker miRNAs in periodontium.

Periodontitis is the most prevalent chronic immuno-infectious multispecies dysbiotic disease of the oral cavity. The Toll-like receptors (TLR) provide the first line of defense, one of the best-characterized pathogens-detection systems and play a vital role in recognizing multiple microbial products. Multispecies infection with periodontal bacteria S. gordonii, F. nucleatum, P. gingivalis, T. denticola, and T. forsythia induced gingival inflammation, alveolar bone resorption (ABR) and miRNA expression in the C57BL6/J wild-type mice and whereas infection did not increase significant ABR in the TLR2/4 deficient mice. Among the 15 miRNAs investigated, miR-146a - 5p, miR-15a-5p were upregulated in wild-type and TLR2 -/- mice and miR-146a-5p, miR-30c-5p, let-7c-5p were upregulated in the TLR4 -/- mice compared to sham-infected controls. Notably, inflammatory miRNA miR-146a-5p was upregulated uniquely among the three different infection groups. The upregulated miRNAs (miR-146a, miR-15-a-5p, let-7c-5p) and downregulated miRNAs could be markers for TLRs-mediated induction of periodontitis.

Alzheimer's disease (AD), the most common form of dementia, is a progressive neurodegenerative disorder that profoundly impacts cognitive function and the nervous system. Emerging evidence highlights the pivotal roles of iron homeostasis dysregulation and microbial inflammatory factors in the oral and gut microbiome as potential contributors to the pathogenesis of AD. Iron homeostasis disruption can result in excessive intracellular iron accumulation, promoting the generation of reactive oxygen species (ROS) and oxidative damage. Additionally, inflammatory agents produced by pathogenic bacteria may enter the body via two primary pathways: directly through the gut or indirectly via the oral cavity, entering the bloodstream and reaching the brain. This infiltration disrupts cellular homeostasis, induces neuroinflammation, and exacerbates AD-related pathology. Addressing these mechanisms through personalized treatment strategies that target the underlying causes of AD could play a critical role in preventing its onset and progression.

Periodontal diseases, if untreated, can cause gum recession and tooth root exposure, resulting in infection and irreversible damage. Traditional treatments using autologous grafts are painful and often result in postoperative complications. Scaffolds offer a less invasive alternative, promoting cell proliferation and healing without additional surgery, thus enhancing comfort for patients and doctors. This study developed Chitosan (Chit)/Collagen (Col) film surfaces and drug-loaded Polyvinyl Alcohol (PVA)/Amoxicillin (AMX) nanofibers using solvent casting and electrospinning methods, respectively. The surfaces are characterized by scanning electron microscopy (SEM), mechanical testing, Fourier Transform Infrared Spectroscopy (FTIR), and differential scanning calorimetry (DSC). Biocompatibility and antimicrobial properties are assessed using NIH/3T3 fibroblast cells and bacterial cultures. SEM images confirmed the structural integrity of AMX-loaded 13% PVA nanofibers, while FTIR analysis validated the compositional integrity of PVA/AMX nanofibers and Chit/Col film hybrid surfaces. Cell studies showed over 90% viability for Chit/Col film + PVA/AMX nanofiber hybrid bilayer membranes, confirming their biocompatibility. The antimicrobial assessment indicated that the Chit/Col film + PVA/AMX (0.2%) nanofiber hybrid bilayer membrane exhibited superior efficacy against Streptococcus mutans. These findings suggest that this hybrid bilayer membrane can enhance cell growth, promote proliferation, and enable controlled drug release, offering significant promise for regeneration of gingival tissues.

The current study aimed to: (1) systematically review the published literature regarding the proteomics analyses of saliva and gingival crevicular fluid (GCF) in healthy humans and gingivitis and/or periodontitis patients; and (2) to identify the differentially expressed proteins (DEPs) based on the systematic review, and comprehensively conduct meta-analyses and bioinformatics analyses.

An online search of Web of Science, Scopus, and PubMed was performed without any restriction on the year and language of publication. After the identification of the DEPs reported by the included human primary studies, gene ontology (GO), the Kyoto encyclopedia of genes and genomes pathway (KEGG), protein-protein interaction (PPI), and meta-analyses were conducted. The risk of bias among the included studies was evaluated using the modified Newcastle-Ottawa quality assessment scale.

The review identified significant differences in protein expression between healthy individuals and those with gingivitis and periodontitis. In GCF, 247 proteins were upregulated and 128 downregulated in periodontal diseases. Saliva analysis revealed 79 upregulated and 70 downregulated proteins. There were distinct protein profiles between gingivitis and periodontitis, with 159 and 31 unique upregulated proteins in GCF, respectively. Meta-analyses confirmed significant upregulation of various proteins in periodontitis, including ALB and MMP9, while CSTB and GSTP1 were downregulated. AMY1A and SERPINA1 were upregulated in periodontitis saliva. HBD was upregulated in gingivitis GCF, while DEFA3 was downregulated. PPI analysis revealed complex networks of interactions among DEPs. GO and KEGG pathway analyses provided insights into biological processes and pathways associated with periodontal diseases.

The ongoing MS-based proteomics studies emphasize the need for a highly sensitive and specific diagnostic tool for periodontal diseases. Clinician acceptance of the eventual diagnostic method relies on its ability to provide superior or complementary information to current clinical assessment procedures. Future research should prioritize the multiplex measurement of multiple biomarkers simultaneously to enhance diagnostic accuracy and large study cohorts are necessary to ensure the validity and reliability of research findings.

Periodontitis, one of the most common forms of periodontal disease, has been linked to several cardiovascular factors including metabolic syndrome and inflammatory processes. This study aimed to determine the association between type 2 diabetes mellitus (T2DM) and periodontitis in a representative sample of individuals in the north of Peru.

Secondary data analysis using information of a population-based survey, enrolling subjects aged 35 to 69 years. The outcome was periodontitis, evaluated using a self-reported and validated 8-item questionnaire (≥5 points compatible with severe periodontitis compared to those without severe periodontitis), whereas the exposure was the presence of T2DM, evaluated using results of oral glucose tolerance test and categorized into two different forms: (a) normoglycemic, prediabetes, and T2DM, and (b) without T2DM, with T2DM and <5 years of diagnosis, and with T2DM and ≥5 years of diagnosis. Poisson regression models were utilized to report prevalence ratios (PR) and 95% confidence intervals (95% CI).

Data from 1606 individuals were analyzed, with a mean age of 48.2 (SD: 10.6) years, and 50.3% were women. Of these, 272 (16.9%) had prediabetes and 176 (11.0%) had T2DM (71.6% with <5 years of disease). Overall, 97.0% presented at least one symptom compatible with periodontitis, 882 (55.0%) had mild, 643 (40.0%) had moderate, and 5% had severe periodontitis. In multivariable model, those with T2DM had a higher prevalence of severe periodontitis (PR = 1.99; 95% CI: 1.12 - 3.54). Similarly, those with <5 years of disease had a higher prevalence of severe periodontitis (PR = 2.48; 95% CI: 1.38 - 4.46).

Our research confirms the association between T2DM and severe periodontitis, especially among those with recent diagnosis (<5 years). Symptoms of periodontitis are quite common in our study population. Our results suggest a need to periodically assess oral health in patients with T2DM.

Oral health represents a public health problem due to its remarkable social impact and medical costs. Crenotherapy with sulfur water is shown to be a complementary, less toxic, and traumatizing therapy, but the number of studies that evaluate the effect of natural mineral waters effect on oral health are scarce. The aim of this pilot study is to evaluate the impact of thermal water therapy on the oral health of the participants, assessing parameters such as plaque index, gingival bleeding index and periodontal probing depth as well on the perception of symptoms of oral mucosa diseases (OMD).

An observational, longitudinal and comparative study was designed, and 90 thermalists were randomly allocated to two treatment groups for 14 days: Thermal sulfuric natural mineral water of the Amarante Thermal baths group (TW_TA group) (n = 45) or saline solution (control group) (n = 45), in May 2022. The study was based on clinical observation and application of a self-response questionnaire involving sociodemographic data and quality of life assessment. The evaluation was carried out in 2 different moments: before and at the end of treatment (14 days).

The study involved 90 thermal practitioners, evenly split between the TW_TA group and a control group. Most participants were women (70%), with a similar average age in both groups. Oral examination showed a high prevalence of filled and missing teeth, and around 25% of participants used removable prostheses, predominantly in the control group. Thermal treatment had a positive impact on oral health. In the TW_TA group, gingival bleeding significantly decreased from 68.9% to 40%, while it remained unchanged in the control group. Periodontal health improved, with no participants in the TW_TA group having pockets deeper than 5 mm by the end of the study, indicating reduced periodontal pathology. Also, plaque levels dropped in both groups after treatment, as assessed by the O'Leary index. Additionally, quality of life related to OMD improved, particularly in the TW_TA group. The overall reduction in symptoms was significant, although the differences between groups were not statistically significant.

This study demonstrates the positive effects of thermal water treatment on oral health, including reduced gingival bleeding and plaque levels, along with improved quality of life related to OMD. Further targeted research is needed to explore the benefits of thermal water effects and optimize oral health practices in Portugal using thermal waters.

Peri-implant and periodontal conditions share common underlying factors, including risk factors, microbiology, immunology, and treatment approaches.

This study aims to investigate the potential co-occurrence of peri-implant and periodontal conditions.

One hundred twenty-three implants were divided into three groups: peri-implantitis (41 implants), peri-implant mucositis (41 implants), and peri-implant health (41 implants). Peri-implant and periodontal statuses were assessed using the 2017 AAP/EFP World Workshop on Classification of Periodontal and Peri-implant Diseases and Conditions. All measurements were performed by a single clinician (T.Ş.). One-way analysis of variance was used to compare the study groups according to the data. An assessment was conducted regarding the coexistence of periodontal and peri-implant conditions.

Patients with peri-implant mucositis predominantly had gingivitis, whereas those with peri-implant health exhibited periodontal health. In contrast, patients with peri-implantitis mostly had gingivitis, with a lower occurrence of periodontitis. A significant difference was observed between the peri-implant and periodontal groups (p = 0.003). Significant differences were observed between peri-implant and periodontal evaluations for plaque indices, gingival indices, probing depth, gingival recession, and clinical attachment level (p = 0.001), (p = 0.006).

The findings of this study underscore the intricate influence of implant treatment on periodontal health. This observation emphasizes the importance of elucidating the underlying factors to improve clinical management and outcomes in patients with periodontal and peri-implant diseases, highlighting the relevance and potential impact of this research in the field.

Aim: This systematic review was aimed at addressing the focused question: What is the protective potential of biological agents against alveolar bone resorption during the progression of experimental periodontitis (EP)? Material and Methods: The study protocol was registered in the Open Science Framework database (doi:10.17605/OSF.IO/3P2HY). A comprehensive literature search was conducted across PubMed, Web of Science, Cochrane Library, Scopus, and Embase databases up to December 2023. Inclusion criteria consisted of preclinical studies in animal models of EP that examined the effects of biological agents on preventing periodontal bone loss and reducing tissue inflammation. Studies were excluded if they (i) used non-EP animal models; (ii) focused on antimicrobial agents; (iii) centered on prebiotics or probiotics; (iv) evaluated compounds not classified as biologicals; or (v) included randomized clinical trials, clinical studies, or reviews. Eligibility was determined based on the PI/ECOs framework, and study quality was assessed using the SYRCLE risk-of-bias tool. Results: After screening an initial pool of 5236 records from databases, registries, and hand searches, 39 studies met the inclusion criteria. A total of 23 biological agents were evaluated across these studies. The majority of studies employed the ligature-induced model of EP to test the effectiveness of biologicals as preventive or therapeutic interventions. The dosage of biological agents and the duration of disease induction varied depending on the EP model. In all studies, the main outcome-alveolar bone loss, a hallmark of EP-was significantly inhibited by biological agents, which also reduced proinflammatory mediators when compared to untreated controls. A key strength of this review is the high number of studies included, most of which were classified as having low risk of bias. However, a notable limitation is the absence of a meta-analysis, the short follow-up periods in the included studies, and the heterogeneity among the compound dosages and route of administration. Conclusion: This systematic review demonstrates that biological agents are effective in reducing bone loss and mitigating inflammation during EP progression. Randomized clinical trials are needed to confirm these findings in human populations.

To characterize the subgingival microbiota in subjects with stage I/II periodontitis (moderate periodontitis, MP), stage III/IV periodontitis (severe periodontitis, SP), and periodontal health (PH) at the same probing depth (PD) (shallow ≤ 3 mm, moderate 4-6 mm, or deep ≥ 7 mm), and to investigate the changes associated with probing depth progression.

100 subgingival plaque samples were collected from 50 subjects (16 MP, 17 SP and 17 PH), forming six groups: PHS (PH, shallow), MPS (MP, shallow), MPM (MP, moderate), SPS (SP, shallow), SPM (SP, moderate), and SPD (SP, deep). Samples were analyzed using high-throughput sequencing.

The subgingival microbiome showed significant differences associated with both PD and periodontitis stage (p < 0.05). With increasing PD, alpha diversity initially increased and then decreased. Pathogenic genera like Fusobacterium, Filifactor, and Porphyromonas increased, while health-associated genera like Streptococcus and Haemophilus decreased. At shallow sites, the PHS, MPS, and SPS groups showed similar community structure. At moderate and deep sites, the SPM and SPD groups exhibited significant differences in community structure compared to the MPM group, with the SPM and SPD groups showing decreased abundances of Actinomyces and increased abundances of Treponema. The microbial co-networks in the SPD and SPM groups exhibited greater complexity and connectivity and were more resilient to random microbial or node removal.

The subgingival microbiome shows strong associations with PD and periodontitis stage.

Once periodontitis progresses to stage III/IV, reconstructing a healthy subgingival microbiome may be challenging, emphasizing the importance of early prevention.

The human body hosts trillions of microorganisms throughout many diverse habitats with different physico-chemical characteristics. Among them, the oral cavity and the gut harbour some of the most dense and diverse microbial communities. Although these two sites are physiologically distinct, they are directly connected and can influence each other in several ways. For example, oral microorganisms can reach and colonize the gastrointestinal tract, particularly in the context of gut dysbiosis. However, the mechanisms of colonization and the role that the oral microbiome plays in causing or exacerbating diseases in other organs have not yet been fully elucidated. Here, we describe recent advances in our understanding of how the oral and intestinal microbiota interplay in relation to their impact on human health and disease.

Periodontitis, a non-communicable chronic inflammation disease resulting from dysbiosis of the oral microbiota, has been demonstrated to have a positive association with the risk of ischemic stroke (IS). The major periodontal pathogens contribute to the progression of stroke-related risk factors such as obesity, diabetes, atherosclerosis, and hypertension. Transcriptional changes in periodontitis pathogens have been detected in oral samples from stroke patients, suggesting a new conceptual framework involving microorganisms. The bidirectional regulation between the gut and the central nervous system (CNS) is mediated by interactions between intestinal microflora and brain cells. The connection between the oral cavity and gut through microbiota indicates that the oral microbial community may play a role in mediating complex communication between the oral cavity and the CNS; however, underlying mechanisms have yet to be fully understood. In this review, we present an overview of key concepts and potential mechanisms of interaction between the oral-gut-brain axis based on previous research, focusing on how the oral microbiome (especially the periodontal pathogens) impacts IS and its risk factors, as well as the mediating role of immune system homeostasis, and providing potential preventive and therapeutic approaches.

Chronic periodontitis is the sixth most prevalent disease worldwide and the leading cause of tooth loss in adults. With growing attention on the role of inflammatory and immune responses in its pathogenesis, there is an urgent need to evaluate host-modulatory agents. Non-steroidal anti-inflammatory drugs (NSAIDs) drugs play a crucial role in managing inflammatory conditions. This study examined the repercussions of long-term naproxen use in a periodontal inflammation model known for causing significant inflammation, disrupting epithelial and connective tissue attachment and leading to alveolar bone destruction.

Thirty BALB/c mice were treated with naproxen for 60 days or left untreated. From Day 30, an LPS solution was injected into gingival tissues three times per week for four weeks. This model enables LPS control over the inflammatory stimulus intensity throughout the experimental period, leading to chronic inflammation development involving both innate and adaptive immunity. The liver, stomach and maxillae were submitted to histological analysis. The oxidative damage was determined by measuring lipid peroxidation (LPO) in plasma and gingiva. The activities of myeloperoxidase (MPO), eosinophil peroxidase (EPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and levels of leukotriene B4, the interleukin (IL)-1β, TNF-α, IL-4, IL-5, IL-10, the chemokine CCL11 were also assessed in the gingival tissues.

The results indicated that none of the groups displayed any indications of liver damage or alterations; however, the NPx treatment led to severe gastric damage. In contrast, the treatment alleviated periodontal inflammation, resulting in a reduction of chronic and acute inflammatory cell infiltration and prevention of connective tissue loss in the gingival tissue. Additionally, the treatment increased the activities of endogenous antioxidant enzymes SOD, CAT and GPx, as well as the IL-10 cytokine, while decreasing the levels of leukotriene B4, TNF-α, IL-4 and IL-5. Furthermore, the activities of MPO, EPO and LPO were reduced in the treated groups.

These results suggest that NPx effectively inhibits periodontal inflammation in an inflammatory periodontal model. However, the harmful gastric effects dramatically limit its long-term use.

Background: Periodontal disease (PD) leads to the destruction of supportive tissues through an inflammatory response induced by biofilm accumulation. This low-grade systemic inflammation from PD increases the risk of comorbidities. Among potential therapeutic agents for PD, humic acids (HAs) are notable for their anti-inflammatory and immunomodulatory properties. This study aimed to evaluate the effects of varying HA doses on PD progression in an experimental model. Methods: Fifty-four Wistar rats were assigned to six groups (n = 8 each): control, PD, PD + 40 mg/kg HA, PD + 80 mg/kg HA, PD + 160 mg/kg HA, and PD + 320 mg/kg HA. HA from vermicompost was administered daily by gavage for 28 days, with PD induced by ligature on day 14. Post-euthanasia, mandibular samples were analyzed histomorphometrically for bone loss and osteocyte density. Alveolar bone topography and elemental composition were examined using Scanning Electron Microscopy (SEM) coupled with Energy Dispersive Spectroscopy (EDS). Renal and hepatic tissues were assessed histopathologically. Data were analyzed with Analysis of Variance (ANOVA) and Duncan's test. Results: HA-treated animals showed reduced epithelial attachment loss and alveolar bone loss, with improved bone quality parameters, such as reduced pore number and diameter and increased osteocyte density compared to the PD group. Renal lesions observed in PD animals were mitigated at 40 and 80 mg/kg HA doses. Conclusions: HA treatment improves alveolar bone integrity and, at lower doses, reduces PD-induced renal lesions.

Periodontitis, an oral disease initiated by a dysbiotic dental biofilm, has an unclear response to photobiomodulation (PBM) as an adjunctive treatment. This study investigates the effects of PBM on reactive oxygen species (ROS), apoptosis, oxidative stress, and inflammatory markers in a periodontitis model using C57BL/6 mice, divided into four groups: control (C), control + PBM (C + PBM), periodontitis (P), and periodontitis + PBM (P + PBM). An infrared diode laser (808 nm, 133.3 J/cm2, 4 J/session) was applied for three days. PBM reduced superoxide anions, hydrogen peroxide, and apoptosis in gingival cells, while decreasing systemic inflammation and protein oxidation. In the P + PBM group, pro-inflammatory cytokines IL-6 and IL-12p70 decreased, whereas IL-10 increased, suggesting improvements in oxidative stress and inflammation profiles.

Periodontal disease, initiated by dental biofilm and influenced by various local and systemic factors, includes stress as a potential contributor to its progression. Despite associations with severe forms like acute necrotizing ulcerative gingivitis, a comprehensive large-sample study linking stress to periodontal disease is lacking. This study aims to investigate the relationship between mental health and periodontal disease.

Leveraging data (secondary dataset) from the National Health and Nutrition Examination Survey (NHANES) from 2011-2012 and NHANES 2013-2014 cycles, relevant information was extracted. Mental health was the exposure variable, and periodontal disease, assessed through indices following Eke et al.'s definition, served as the outcome. Covariates (demographical characteristics) impacting periodontal disease were considered, and disease status analyses employed the Rao-Scott chi-squared test. A logistic regression model assessed mental health's impact on periodontal disease.

Among the 2764 Participants, more than a quarter (29.1%) were aged over 60 years, 52% were females. Logistic regression indicated higher odds of periodontal disease among individuals feeling bad about themselves for more than half of the day (OR 1.170, 95% CI 0.533-2.474), though statistical significance was not reached. Periodontitis prevalence significantly varied based on marital status, with 6.6% of married and 10.8% of unmarried Participants affected. Notably, a statistically significant difference in periodontitis prevalence existed between Participants with health insurance (8.3%) and those without (16.5%).

Our findings suggest trends in periodontal disease prevalence linked to mental health, marital status, and access to health insurance. However, the absence of statistically significant findings calls for caution in interpreting these relationships. We recommend that future studies further investigate these potential associations to provide a clearer understanding.

Periodontal diseases, a group of complex conditions marked by an excessive immune response and periodontal tissue destruction, are a global health concern. Since 1990, the incidence of these diseases has doubled, with Western sub-Saharan Africa experiencing the highest burden. Accurate diagnosis and case identification are crucial for understanding the etiology, features of disease, research, treatment and prevention. Modern perspectives on periodontal disease classification are based on commonality among those affected. However, current literature is often plagued by methodological inconsistencies and focused on disease mechanisms in European populations. Health inequalities in low- and middle-income countries (LMICs) are exacerbated by these challenges, with sub-Saharan Africa, and Nigeria specifically, facing unique difficulties such as clinical personnel shortages and limited research infrastructure. This review explored disparities in periodontal disease research, care and outcomes in African populations. We highlighted these disparities and identified the factors contributing to inequities in periodontal health outcomes. We further demonstrated the critical need for inclusive and equitable healthcare and research practices tailored to the unique challenges faced by diverse populations and regions with limited resources. Addressing these disparities is essential for ensuring that advancements in healthcare are accessible to all, thereby improving global oral health and general health.

Nonsurgical therapies have been recommended and employed as a less invasive and cost-effective modality in managing periodontitis. In this context, different therapeutic protocols have been tested in the last decades. Therefore, mapping the scientific trends and patterns provides critical insights into the state of research in the field, which has not been explored for overall nonsurgical periodontitis treatment studies. Articles from 2001 to 2020 were retrieved from the Web of Science database using appropriate terms and keywords. Article selection and data extraction were performed by calibrated examiners. All articles focusing on nonsurgical periodontitis treatment were included. Descriptive, bivariate, and multivariate logistic regression analyses were conducted. 1,519 articles were included. Randomized clinical trials (RCTs) were the most used design (44.1%), and professional biofilm control was the topic most studied (35.6%). Europe published the most significant number of articles (41.1%). The USA was the country that collaborated more with other countries. Asia (p<0.001), South America (p=0.004), and Oceania/Africa (p=0.016) showed a lower chance to have international collaboration. Studies from North America were more likely to be RCTs than studies from Europe (p=0.050); studies focusing on professional biofilm control (p<0.001) and other topics (p<0.001) were less likely to be evaluated by RCTs. The nonsurgical periodontitis treatment field mainly conducted RCTs, and the topic most explored by all studies was professional biofilm control. International collaboration and conduct of RCTs in this field occurred mainly among high-income countries. Decentralizing scientific resources, making integrative connections globally, and evaluating new topics may improve evidence-based periodontology.

Background/Objectives: Less often employed as a rinsing solution for controlling oral biofilms, NaOCL was used in oral rinses at various concentrations in steps 1 and 4 of periodontal therapy. The aim of this study was to quantitatively evaluate the biofilm-disruptive properties of a 0.2% NaOCl solution in standardized oral rinses using dedicated plaque-disclosing agents and 3D scanning methods in patients undergoing the regular Guided Biofilm Therapy® protocol. Methods: Eight patients with at least 20 teeth present evenly distributed between the two arches were included. After 24 h of refraining from oral hygiene, dental arches were stained with a disclosing agent, the subjects rinsed for 20 s, clinical photographs and 3D scans were performed, subjects rinsed again for 20 s, photographs and 3D scans were performed again, and then the GBT® protocol was resumed as usual. Data representing areas covered with dental plaque were acquired using the "Medit Scan for Clinics" software and then underwent a post-processing and rendering process. The outcome variable was the percent reduction in the plaque-covered areas. Results: For the upper jaw, the estimated mean percent reduction in the biofilm-covered area was 39.65%, while for the mandible, it was 38.26%. The analysis of individual photographs revealed changes in the plaque-covered areas and reductions in the color intensity of the residual plaque-covered areas under identical lighting conditions. Conclusions: When analyzed using 3D intraoral scanning, the 0.2% NaOCl rinsing solution seems to be a clinically efficient disruptor/dissolvent of the oral biofilm, both when integrated into modern protocols of periodontal therapy like GBT® and for home self-care.

Sugar is omnipresent in the current food environment and sugar consumption has drastically risen over the past century. Extensive evidence highlights the negative health consequences of consuming excess dietary sugars, leading the World Health Organization (WHO) and the American Heart Association (AHA) to devise guidelines to restrict sugar intake. According to the WHO's Global Oral Health Status Report of 2022, oral diseases and severe periodontitis are a massive public health problem, and dietary sugars are a modifiable risk factor.

We conducted a literature review using key databases to summarise the health effects of excessive sugar consumption and their potential role in periodontal inflammation.

Available evidence suggests that excess dietary fructose and sucrose can cause low-grade systemic inflammation; and induce dysbiosis in both gut and the oral microbiota. Also, dietary sugar is potentially addictive and hypercaloric and its overconsumption can lead to obesity, metabolic syndrome, and other risk factors for periodontal inflammation. Hence, an unbalanced diet with excess dietary sugars holds the potential to initiate and aggravate periodontal inflammation. In the modern food environment that enables and facilitates a high-sugar diet, adopting a diverse diet and restricting sugar intake according to WHO and AHA guidelines seem beneficial to systemic and periodontal health. Since clinical evidence is limited, future research should study the effectiveness of dietary interventions that control sugar consumption in preventing and managing the global public health problem of periodontal inflammation.