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International Journal of Molecular... Feb 2024Periodontitis is an inflammatory condition affecting the supporting structures of the teeth. Periodontal conditions may increase the susceptibility of individuals to... (Review)
Review
Periodontitis is an inflammatory condition affecting the supporting structures of the teeth. Periodontal conditions may increase the susceptibility of individuals to various systemic illnesses, including Alzheimer's disease. Alzheimer's disease is a neurodegenerative condition characterized by a gradual onset and progressive deterioration, making it the primary cause of dementia, although the exact cause of the disease remains elusive. Both Alzheimer's disease and periodontitis share risk factors and clinical studies comparing the associations and occurrence of periodontitis among individuals with Alzheimer's disease have suggested a potential correlation between these conditions. Brains of individuals with Alzheimer's disease have substantiated the existence of microorganisms related to periodontitis, especially , which produces neurotoxic gingipains and may present the capability to breach the blood-brain barrier. may induce tau hyperphosphorylation and lead to neuronal apoptosis. Lipopolysaccharides-components of bacterial cell membranes and mediators of inflammation-also have an impact on brain function. Further research could unveil therapeutic approaches targeting periodontal pathogens to potentially alleviate AD progression.
Topics: Humans; Alzheimer Disease; Periodontitis; Inflammation; Porphyromonas gingivalis; Risk Factors
PubMed: 38473858
DOI: 10.3390/ijms25052612 -
Oral Diseases Apr 2024Non-alcoholic fatty liver disease (NAFLD) is a clinicopathological syndrome characterized by excessive fat deposition in hepatocytes caused by non-alcoholic liver...
OBJECTIVE
Non-alcoholic fatty liver disease (NAFLD) is a clinicopathological syndrome characterized by excessive fat deposition in hepatocytes caused by non-alcoholic liver injury. Porphyromonas gingivalis (P.g) is the main pathogen causing periodontitis, which can aggravate the progression of NAFLD in our previously study. The objective of this study was to further investigate the pathogenesis and moleculer michanisma of NAFLD aggravated by P.g.
METHODS
A mouse model of NAFLD was established, and the changes of inflammatory factors and NF-κB signaling pathway in liver tissue and L-02 cells were analyzed by transcriptome sequencing, Western blot, IHC and RT-PCR. In addition, the NF-κB signaling pathway inhibitor QNZ and ferroptosis inhibitor Fer-1 were used to analyze the relationship between NF-κB signaling pathway and ferroptosis in vitro.
RESULTS
In vivo and in vitro experiments, P.g can induce liver inflammation and activate NF-κB signaling pathway. At the same time, P.g promotes ferroptosis and inflammation in L-02 in vitro. QNZ alleviates ferroptosis and inflammatory activation in L-02. Fer-1 can relieve the L-02 inflammation caused by P.g products.
CONCLUSION
Porphyromonas gingivalis can induce ferroptosis and inflammation in hepatocytes and further worsen liver lesions. The mechanism of ferroptosis in hepatocytes depends on NF-κB signaling pathway, which provides a new strategy for clinical treatment and prevention of NAFLD.
Topics: Porphyromonas gingivalis; Animals; NF-kappa B; Hepatocytes; Non-alcoholic Fatty Liver Disease; Signal Transduction; Mice; Ferroptosis; Inflammation; Male; Mice, Inbred C57BL; Humans; Disease Models, Animal; Bacteroidaceae Infections; Cell Line
PubMed: 36939447
DOI: 10.1111/odi.14537 -
Annals of Surgical Oncology Dec 2023The association between oral microbiota and pancreatic cancer (PC) is increasingly recognized and studied. Yet, contrasting results are seen in current studies. This... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
The association between oral microbiota and pancreatic cancer (PC) is increasingly recognized and studied. Yet, contrasting results are seen in current studies. This study aimed to provide systematic review and meta-analysis comparing PC and oral microbiota.
METHODS
Studies related to the association between oral microbiota and PC were identified through digital databases including PubMed, Medline, EMBASE, COCHRANE, and SCOPUS without limitations on language or publication period. The last identification date was 10 March 2023. Three case-control studies concerning the issue were included. For the meta-analyses, RevMan software version 5.4 was used. The Newcastle-Ottawa scale was used to evaluate articles and measurement of study differences, and publication bias was shown.
RESULTS
Porphyromonas gingivalis in oral bacteria was detected at a comparatively high detection rate in PC patients compared with healthy controls (odds ratio [OR], 1.38; 95 % confidence interval [CI], 1.09-1.74; P = 0.007; I = 34 %). The detection rate did not differ significantly between PC patients and healthy control patients for Aggregatibacter actinomycetemcomitans (OR 0.98; 95 % CI 0.75-1.29; P = 0.90; I = 76 %); Tannerella forsythiaand (OR 1.12; 95 % CI 0.89-1.42; P = 0.33; I = 0 %), or Prevotella intermedia (OR 1.08; 95 % CI 0.84-1.39; P = 0.55; I = 0 %).
CONCLUSION
Oral microbiota were closely related to PC, whereas P. gingivalis was more commonly found in the PC patients than in the healthy controls. For patients with PC, P. gingivalis may play a role in early diagnosis.
Topics: Humans; Porphyromonas gingivalis; Prevotella intermedia; Pancreatic Neoplasms; Microbiota
PubMed: 37787951
DOI: 10.1245/s10434-023-14366-7 -
Cureus Aug 2023The aim of the study is to prepare the dual gel using nutmeg and Tulsi and then the evaluation of the antimicrobial properties and cytotoxic potential.
AIM
The aim of the study is to prepare the dual gel using nutmeg and Tulsi and then the evaluation of the antimicrobial properties and cytotoxic potential.
MATERIALS AND METHODS
The Nutmeg Tulsi gel preparation has been done with a mixture of equal amounts of nutmeg and Tulsi powder. To the above-mentioned mixture, 5 mL of the concentrate is added and mixed thoroughly until the gel formation is done. The antimicrobial property is checked in the organism (p>0.05). The cytotoxic potential is checked in the Brine variety of the shrimp. The statistical analysis is done using a Paired t-test.
RESULTS
The results stated that the Nutmeg Tulsi gel at a concentration of 100 microgram/mL showed a greater zone of inhibition (4.1±0.09 mm) when compared with doxycycline and has high antimicrobial potential in both and Conclusion: The antimicrobial property of Nutmeg Tulsi gel has been demonstrated to be effective against and . This suggests that it could be used as an affordable and effective "adjunct" alongside standard care for managing periodontal conditions.
PubMed: 37753020
DOI: 10.7759/cureus.44140 -
American Journal of Cancer Research 2023Maintaining and transferring intact genomes from one generation to another plays a pivotal role in all living organisms. DNA damage caused by numerous endogenous and... (Review)
Review
Maintaining and transferring intact genomes from one generation to another plays a pivotal role in all living organisms. DNA damage caused by numerous endogenous and exogenous factors must be adequately repaired, as unrepaired and accumulated DNA mutations can cause severe deleterious effects, such as cell death and cancer. To prevent adverse consequences, cells have established DNA damage response mechanisms that address different forms of DNA damage, including DNA double-strand breaks, mismatches, nucleotide excision, and base excision. Among several sources of exogenous DNA damage, bacterial infections cause inflammation in the host, generating reactive oxygen species (ROS) and causing oxidative DNA damage. Recent studies have revealed the importance of the oral microbiome in inflammation and several systemic host diseases. Dysbiosis of oral bacteria can induce chronic inflammation, which enhances ROS-induced DNA damage, and improperly repaired damage can lead to carcinogenesis. This review describes the various DNA repair pathways that are affected by chronic inflammation and the discovery of the DNA damage response induced by oral bacteria such as and .
PubMed: 37559975
DOI: No ID Found -
Journal of Periodontal Research Apr 2024As a chronic inflammatory disease, periodontitis threatens oral health and is a risk factor for Alzheimer's disease (AD). There is growing evidence that these two...
BACKGROUND AND OBJECTIVE
As a chronic inflammatory disease, periodontitis threatens oral health and is a risk factor for Alzheimer's disease (AD). There is growing evidence that these two diseases are closely related. However, current research is still incomplete in understanding the common genes and common mechanisms between periodontitis and AD. In this study, we aimed to identify common genes in periodontitis and AD and analyze the relationship between crucial genes and immune cells to provide new therapeutic targets for clinical treatment.
MATERIALS AND METHODS
We evaluated differentially expressed genes (DEGs) specific to periodontitis and AD. Co-expressed genes were identified by obtaining gene expression profile data from the Gene Expression Omnibus (GEO) database. Using the STRING database, protein-protein interaction (PPI) networks were constructed, and essential genes were identified. We also used four algorithms to identify critical genes and constructed regulatory networks. The association of crucial genes with immune cells and potential therapeutic effects was also assessed.
RESULTS
PDGFRB, VCAN, TIMP1, CHL1, EFEMP2, and IGFBP5 were obtained as crucial common genes. Immune infiltration analysis showed that Natural killer cells and Myeloid-derived suppressor cells were significantly differentially expressed in patients with PD and AD compared with the normal group. FOXC1 and GATA2 are important TFs for PD and AD. MiR-23a, miR-23b, miR-23a, and miR-23b were associated with AD and PD. Finally, the hub genes retrieved from the DSigDB database indicate multiple drug molecule and drug-target interactions.
CONCLUSION
This study reveals commonalities in common hub genes and immune infiltration between periodontitis and AD, and the analysis of six hub genes and immune cells may provide new insights into potential therapeutic directions for the pathogenesis of periodontitis complicated by AD.
Topics: Humans; Alzheimer Disease; Periodontitis; Computational Biology; Databases, Factual; MicroRNAs; Gene Expression Profiling
PubMed: 38189472
DOI: 10.1111/jre.13220 -
BMC Microbiology Apr 2024Oral microbiota imbalance is associated with the progression of various lung diseases, including lung cancer. Pulmonary nodules (PNs) are often considered a critical...
BACKGROUND
Oral microbiota imbalance is associated with the progression of various lung diseases, including lung cancer. Pulmonary nodules (PNs) are often considered a critical stage for the early detection of lung cancer; however, the relationship between oral microbiota and PNs remains unknown.
METHODS
We conducted a 'Microbiome with pulmonary nodule series study 1' (MCEPN-1) where we compared PN patients and healthy controls (HCs), aiming to identify differences in oral microbiota characteristics and discover potential microbiota biomarkers for non-invasive, radiation-free PNs diagnosis and warning in the future. We performed 16 S rRNA amplicon sequencing on saliva samples from 173 PN patients and 40 HCs to compare the characteristics and functional changes in oral microbiota between the two groups. The random forest algorithm was used to identify PN salivary microbial markers. Biological functions and potential mechanisms of differential genes in saliva samples were preliminarily explored using the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Cluster of Orthologous Groups (COG) analyses.
RESULTS
The diversity of salivary microorganisms was higher in the PN group than in the HC group. Significant differences were noted in community composition and abundance of oral microorganisms between the two groups. Neisseria, Prevotella, Haemophilus and Actinomyces, Porphyromonas, Fusobacterium, 7M7x, Granulicatella and Selenomonas were the main differential genera between the PN and HC groups. Fusobacterium, Porphyromonas, Parvimonas, Peptostreptococcus and Haemophilus constituted the optimal marker sets (area under curve, AUC = 0.80), which can distinguish between patients with PNs and HCs. Further, the salivary microbiota composition was significantly correlated with age, sex, and smoking history (P < 0.001), but not with personal history of cancer (P > 0.05). Bioinformatics analysis of differential genes showed that patients with PN showed significant enrichment in protein/molecular functions related to immune deficiency and energy metabolisms, such as the cytoskeleton protein RodZ, nicotinamide adenine dinucleotide phosphate dehydrogenase (NADPH) dehydrogenase, major facilitator superfamily transporters and AraC family transcription regulators.
CONCLUSIONS
Our study provides the first evidence that the salivary microbiota can serve as potential biomarkers for identifying PN. We observed a significant association between changes in the oral microbiota and PNs, indicating the potential of salivary microbiota as a new non-invasive biomarker for PNs.
TRIAL REGISTRATION
Clinical trial registration number: ChiCTR2200062140; Date of registration: 07/25/2022.
Topics: Humans; Saliva; RNA, Ribosomal, 16S; Microbiota; Biomarkers; Lung Neoplasms; Oxidoreductases
PubMed: 38643115
DOI: 10.1186/s12866-024-03280-x -
P. gingivalis in oral-prostate axis exacerbates benign prostatic hyperplasia via IL-6/IL-6R pathway.Military Medical Research May 2024Benign prostatic hyperplasia (BPH) is the most common disease in elderly men. There is increasing evidence that periodontitis increases the risk of BPH, but the specific...
BACKGROUND
Benign prostatic hyperplasia (BPH) is the most common disease in elderly men. There is increasing evidence that periodontitis increases the risk of BPH, but the specific mechanism remains unclear. This study aimed to explore the role and mechanism of the key periodontal pathogen Porphyromonas gingivalis (P. gingivalis) in the development of BPH.
METHODS
The subgingival plaque (Sp) and prostatic fluid (Pf) of patients with BPH concurrent periodontitis were extracted and cultured for 16S rDNA sequencing. Ligature-induced periodontitis, testosterone-induced BPH and the composite models in rats were established. The P. gingivalis and its toxic factor P. gingivalis lipopolysaccharide (P.g-LPS) were injected into the ventral lobe of prostate in rats to simulate its colonization of prostate. P.g-LPS was used to construct the prostate cell infection model for mechanism exploration.
RESULTS
P. gingivalis, Streptococcus oralis, Capnocytophaga ochracea and other oral pathogens were simultaneously detected in the Pf and Sp of patients with BPH concurrent periodontitis, and the average relative abundance of P. gingivalis was found to be the highest. P. gingivalis was detected in both Pf and Sp in 62.5% of patients. Simultaneous periodontitis and BPH synergistically aggravated prostate histological changes. P. gingivalis and P.g-LPS infection could induce obvious hyperplasia of the prostate epithelium and stroma (epithelial thickness was 2.97- and 3.08-fold that of control group, respectively), and increase of collagen fibrosis (3.81- and 5.02-fold that of control group, respectively). P. gingivalis infection promoted prostate cell proliferation, inhibited apoptosis, and upregulated the expression of inflammatory cytokines interleukin-6 (IL-6; 4.47-fold), interleukin-6 receptor-α (IL-6Rα; 5.74-fold) and glycoprotein 130 (gp130; 4.47-fold) in prostatic tissue. P.g-LPS could significantly inhibit cell apoptosis, promote mitosis and proliferation of cells. P.g-LPS activates the Akt pathway through IL-6/IL-6Rα/gp130 complex, which destroys the imbalance between proliferation and apoptosis of prostate cells, induces BPH.
CONCLUSION
P. gingivalis was abundant in the Pf of patients with BPH concurrent periodontitis. P. gingivalis infection can promote BPH, which may affect the progression of BPH via inflammation and the Akt signaling pathway.
Topics: Male; Prostatic Hyperplasia; Porphyromonas gingivalis; Rats; Humans; Animals; Interleukin-6; Receptors, Interleukin-6; Prostate; Periodontitis; Aged; Middle Aged; Rats, Sprague-Dawley; Disease Models, Animal; Signal Transduction
PubMed: 38764065
DOI: 10.1186/s40779-024-00533-8 -
Inflammation Oct 2023As a chronic inflammatory disease, periodontitis involves many biological processes including autophagy. At the same time, casein kinase 2 interacting protein-1 (CKIP-1)...
As a chronic inflammatory disease, periodontitis involves many biological processes including autophagy. At the same time, casein kinase 2 interacting protein-1 (CKIP-1) was reported to play a role in regulation of inflammation. But whether CKIP-1 and autophagy interact in periodontitis remains unclear. In this paper, our research team verified the levels of CKIP-1 expression and autophagy increase in the periodontal tissues of a ligature-induced periodontitis mouse model. And this result was also confirmed in Porphyromonas gingivalis (Pg)-induced human gingival fibroblasts (HGF) and human periodontal ligament cells (PDLC). We also showed the autophagy level in periodontal tissues is higher in Ckip-1 knockout (KO) mice than wild type (WT). At the same time, CKIP-1 knockdown lentivirus was used in PDLC and HGF, and it was found that silencing CKIP-1 significantly activated autophagy. Unfortunately, the regulatory role of autophagy in periodontitis is still unclear. Then, the autophagy agonist Rapamycin and inhibitor 3-MA were used in a periodontitis mouse model to investigate periodontal tissue destruction. We found the inflammation in periodontal tissue was reduced when autophagy activated. All these conclusions have been verified both in vivo and in vitro experiments. Finally, our research proved that silencing CKIP-1 reduces the expression of inflammatory cytokines in Pg-induced PDLC and HGF by regulating autophagy. Overall, a new role for CKIP-1 in regulating periodontal tissue inflammation was demonstrated in our study, and it is possible to treat periodontitis by targeting the CKIP-1 gene.
Topics: Mice; Animals; Humans; Inflammation; Periodontitis; Gingiva; Cytokines; Porphyromonas gingivalis; Autophagy; Carrier Proteins
PubMed: 37351817
DOI: 10.1007/s10753-023-01856-9 -
Journal of Clinical Periodontology Sep 2023Porphyromonas gingivalis (P. gingivalis), a major periodontal pathogen, increases the risk of systemic diseases. P. gingivalis infection is closely associated with...
AIM
Porphyromonas gingivalis (P. gingivalis), a major periodontal pathogen, increases the risk of systemic diseases. P. gingivalis infection is closely associated with alcoholic liver disease (ALD), but the underlying mechanism remains unclear. We aimed to investigate the role of P. gingivalis in the pathogenesis of ALD.
MATERIALS AND METHODS
An ALD mouse model was established using a Lieber-DeCarli liquid diet, and C57BL/6 mice were treated with P. gingivalis to detect the pathological indicators of ALD.
RESULTS
Oral administration of P. gingivalis exacerbated alcohol-induced alterations in the gut microbiota, leading to gut barrier dysfunction and inflammatory response and disruption of the T-helper 17 cell/T-regulatory cell ratio in the colon of ALD mice. Furthermore, P. gingivalis worsened liver inflammation in ALD mice by increasing the protein expression of toll-like receptor 4 (TLR4) and p65, increasing the mRNA expression of interleukins-6 (IL-6) and tumour necrosis factor-alpha (TNF-α) and up-regulating the transforming growth factor-beta 1 (TGF-β1) and galectin-3 (Gal-3) production.
CONCLUSIONS
These results indicate that P. gingivalis accelerates the pathogenesis of ALD via the oral-gut-liver axis, necessitating a new treatment strategy for patients with ALD complicated by periodontitis.
Topics: Animals; Mice; Porphyromonas gingivalis; Gastrointestinal Microbiome; Mice, Inbred C57BL; Liver Diseases, Alcoholic; Immunity
PubMed: 37381658
DOI: 10.1111/jcpe.13833