Research Article

P. gingivalis/F. nucleatum in Chronic Apical Periodontitis are Associated with Gestational Shortening via the TLR4/MyD88/NF-κB Pathway

DOI:

10.3791/70793

May 15th, 2026

In This Article

Summary

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Chronic apical periodontitis–associated oral pathogens (P. gingivalis, F. nucleatum) are evaluated using murine CAP models and human trophoblast infection assays. Gestational shortening is observed alongside placental inflammatory activation consistent with TLR4/MyD88/NF-κB signaling. Bacterial DNA is detectable in placental/vascular tissues, supporting a hematogenous link and potential intervention targets.

Abstract

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Spontaneous preterm birth (sPTB; delivery before 37 weeks) remains a leading cause of neonatal mortality, and intrauterine infection is implicated in a substantial proportion of cases. Emerging evidence links oral pathogens such as Porphyromonas gingivalis and Fusobacterium nucleatum to adverse gestational outcomes; however, the mechanistic pathways connecting chronic apical periodontitis (CAP) with gestational risk remain incompletely defined. In pregnant C57BL/6J mice, CAP was established by root canal inoculation and complemented by a tail-vein challenge model using bacterial suspensions (1 × 108 CFU/mL). Gestational length, placental histopathology, inflammatory markers, and bacterial DNA signals were assessed by qPCR. In parallel, human trophoblasts were exposed to P. gingivalis or F. nucleatum (MOI = 50, 24 h) to examine inflammatory signaling consistent with activation of the TLR4/MyD88/NF-κB axis. Relative to controls, CAP-associated groups showed gestational shortening (median 19.5 vs 20.5 days), accompanied by increased placental inflammatory readouts (including elevated IL-1β and TNF-α) and histopathological features consistent with inflammatory injury. qPCR further indicated the presence of bacterial DNA signals in placental and vascular tissues. In trophoblast assays, F. nucleatum elicited stronger proinflammatory responses than P. gingivalis, in association with increased NF-κB phosphorylation. Collectively, these findings suggest that CAP-associated oral pathogens may contribute to gestational shortening by driving placental inflammation via TLR4/MyD88/NF-κB signaling, supporting an oral–placental microbial axis as a potential target for mitigating infection-related gestational risk.

Introduction

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Spontaneous preterm birth (sPTB) is defined as delivery occurring between 20–37 weeks of gestation without medical intervention1. As a critical global public health concern, the incidence of sPTB ranges from approximately 5%–9% in developed countries to 12%–18% in resource-limited regions2,3. Preterm birth and its complications remain a leading cause of mortality in children under 5 years of age, accounting for approximately one million neonatal deaths annually4. Survivors often experience both immediate complications, such as respiratory distress syndrome, and long-term sequelae, including cerebral palsy and developmental delays5,6, thereby imposing substantial economic burdens on families and society7,8.

The etiology of sPTB is multifactorial, reflecting interactions among maternal, fetal, and environmental factors, including uterine contractile dysfunction, cervical insufficiency, endocrine disturbances, placental disorders, and intrauterine infection9. Intrauterine infection is recognized as a major contributor and is estimated to account for approximately 30%–40% of preterm birth cases10,11. Pathogens may access the amniotic cavity through ascending (e.g., cervicovaginal) or hematogenous routes, activating host immune responses and promoting the release of proinflammatory cytokines (e.g., IL-6, TNF-α) and prostaglandins that can precipitate parturition12. Trophoblasts, as key cellular components of the maternal–fetal interface, contribute to immune tolerance as well as antimicrobial defense13.

Oral microorganisms, including Porphyromonas gingivalis and Fusobacterium nucleatum, have been implicated in sPTB-related inflammatory processes, potentially through bacteremia and/or dissemination of inflammatory mediators14. These species are established periodontal pathogens, and associations between periodontitis and sPTB have been reported in epidemiological and clinical studies15,16,17. Notably, P. gingivalis and F. nucleatum are also frequently detected in chronic apical periodontitis (CAP)18,19, yet the relationship between CAP and adverse gestational outcomes remains comparatively understudied, and the relevant biological pathways are not fully defined20. Harjunmaa et al. first reported an association between apical periodontitis and reduced gestational length and low birth weight in 201521. A follow-up study of the same cohort did not support direct bacterial transfer to the placenta, suggesting that systemic inflammation may represent a plausible link between apical periodontitis and pregnancy outcomes22. Consistent with this interpretation, radiographically confirmed apical periodontitis has been associated with an elevated risk of preterm low birth weight deliveries23. As a persistent occult infection, CAP may contribute to gestational risk through chronic low-grade systemic inflammation and/or hematogenous exposure to microbial components24,25. Further clarification of the CAP–gestation relationship is therefore needed to refine the understanding of oral–placental inflammatory pathways and to inform prevention strategies for infection-related gestational risk.

Recent studies have highlighted the relevance of the TLR4/MyD88/NF-κB signaling axis in inflammation-associated preterm birth. Robertson et al. identified TLR4 as a potential therapeutic target in inflammation-induced preterm labor and reported preventive effects in animal models26. Peng et al. further showed that miR-199a-3p attenuates cervical epithelial inflammation through suppression of the HMGB1/TLR4/NF-κB pathway27. In addition, Shen et al. described antioxidative and anti-inflammatory effects of syringin in diabetic pregnant rats, with modulation of the TLR4/MyD88/NF-κB pathway implicated in the observed improvements28. Together, these findings support a mechanistic framework in which TLR4/MyD88/NF-κB–linked inflammatory signaling contributes to infection-associated pathways that influence parturition, while acknowledging that multiple innate immune receptors may act in parallel depending on pathogen context.

The present study evaluates CAP-associated gestational effects using complementary in vitro trophoblast assays and in vivo murine models. The trophoblast model enables controlled interrogation of pathogen-induced inflammatory signaling, whereas the pregnant murine CAP model connects cellular responses to organism-level pregnancy phenotypes under physiologic gestational conditions. A tail-vein challenge model is included to provide a complementary hematogenous exposure route and to assess whether inflammatory activation patterns observed in the oral-infection setting are recapitulated when bacterial components access the maternal circulation. Specifically, trophoblast exposure to P. gingivalis and F. nucleatum is used to profile cytokine responses and activation of the TLR4/MyD88/NF-κB axis, while animal experiments assess gestational length, placental inflammation, and qPCR-based detection of bacterial DNA signals in carotid bifurcation and placental tissues. Because qPCR indicates the presence of bacterial DNA rather than viability or cellular localization, interpretations regarding microbial presence at the maternal–fetal interface remain cautious. In addition, species differences and controlled experimental exposure may limit direct clinical translation, underscoring the need for subsequent validation in human-relevant settings.

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Protocol

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All animal experiments were conducted in strict compliance with the ethical guidelines established by the Animal Research Ethics Committee of the First Affiliated Hospital of Xinjiang Medical University (Approval No.: IACUC-20231121-13) and in accordance with the National Institutes of Health (NIH) guide for the care and use of laboratory animals (2011 edition). Furthermore, this study was performed in accordance with ARRIVE guidelines. All supplies (reagents, consumables, equipment, and software) and their corresponding manufacturer information and catalog numbers are provided in the Table of Materials to facilitate reproducibility.

1. Bacterial culture 

Reference strains of Porphyromonas gingivalis and Fusobacterium nucleatum (strain identifiers provided in the Table of Materials) were handled under anaerobic conditions. Primary cultures were established on pre-reduced Columbia blood agar plates and incubated anaerobically (85% N₂, 10% H₂, and 5% CO₂) at 37 °C for 48 h. For experimental preparations, a single well-isolated colony was inoculated into 40 mL brain heart infusion broth and incubated under identical anaerobic conditions until mid-log phase growth (OD660 = 0.6–0.8). To minimize oxygen exposure, inoculation and transfer steps were performed inside an anaerobic workstation using pre-reduced media and tools. Bacterial concentrations were standardized to 1 × 108 CFU/mL for animal exposure using OD660-based quantification with a strain-specific OD–CFU standard curve generated under the same culture conditions; the calibration curve was established by serial dilution and colony counting on anaerobic agar plates with at least three independent calibrations. For trophoblast infection studies, bacterial suspensions were quantified using a validated enumeration method and diluted in antibiotic-free complete culture medium to achieve the specified multiplicity of infection (MOI) immediately before co-culture.

2. Animal housing and grouping 

Specific pathogen-free C57BL/6J mice (n = 90; 60 females, 30 males) aged 6–7 weeks were housed under controlled conditions (22 °C ± 2 °C, 60% ± 10% humidity, 12 h light cycle) with ad libitum access to food and water. After 1 week of acclimatization, mice were randomly allocated into six experimental groups (n = 15/group): Normal control (NC), CAP with P. gingivalis (AP), CAP with F. nucleatum (AF), normal saline tail vein injection (VN), P. gingivalis tail vein injection (VP), and F. nucleatum tail vein injection (VF). Randomization and cage allocation were recorded to minimize allocation bias and potential cage effects.

3. Establishment of the CAP model

All surgical procedures were performed under aseptic conditions. Anesthesia was induced by intraperitoneal administration of pentobarbital sodium (1.62 mg/30 g body weight) combined with atropine sulfate (12.5 µg/30 g body weight), and adequate anesthetic depth was confirmed by the absence of pedal withdrawal reflex. Mice were positioned supine on a warming pad to maintain body temperature, and the mouth was gently opened to enable stable visualization of the bilateral maxillary first molars. Under magnification, the pulp chambers of the bilateral maxillary first molars were opened using a sterile round bur, followed by removal of coronal pulp tissue with sterile micro-instruments. Root canal orifices were identified using a small endodontic file (size 06–10), and canals were gently negotiated to achieve patency while avoiding excessive force to minimize the risk of perforation. The chamber was rinsed with sterile saline (or sterile PBS) and dried with sterile paper points prior to inoculation.

Bacterial inoculation was performed using a standardized suspension at 1 × 108 CFU/mL. To make dosing reproducible, the delivered volume was operationally fixed at 2 µL per tooth (approximately 2 × 105 CFU per tooth), delivered using a calibrated micropipette tip positioned at the chamber entrance. A sterile absorbent paper point pre-soaked with the same suspension was then placed into the pulp chamber to maintain localized exposure. Successful delivery was confirmed by visible wetting of the paper point and absence of leakage into the oral cavity. After inoculation, the chamber was air-dried until no visible liquid remained, then sealed with a light-cured dental adhesive (20 s), followed by restoration using a light-cured flowable resin composite (20 s). Seal integrity was confirmed by visual inspection and gentle probing; restorations showing gaps or early loss were re-sealed immediately. Post-procedural analgesia and monitoring were provided according to institutional animal care guidance.

Two weeks later, periapical radiographs were obtained to confirm CAP establishment. Successful establishment was defined by a clear periapical radiolucency with surrounding bone changes consistent with chronic periapical inflammation and bone destruction. Mating was initiated two weeks after infection/model establishment.

4. Establishment of tail vein injection model

Bacterial suspensions were prepared at a concentration of 1 × 108 CFU/mL in sterile saline. Mice were restrained, and the tail was warmed for 1–2 min to dilate the lateral tail veins. Injections were performed using a fine-gauge needle (typically 29–30 G) inserted bevel-up into the lateral tail vein at a shallow angle (approximately 10–15°). Correct intravenous placement was confirmed by a flash of blood in the hub and smooth infusion with low resistance; unsuccessful placement was indicated by increased resistance and/or formation of a subcutaneous bleb, in which case infusion was stopped and repeated at a more proximal site after brief re-warming. Mice received daily injections for three consecutive days (100 µL per mouse each time). After three days, females were co-housed with males, and vaginal plugs were checked the following morning. Following confirmation of vaginal plugs (GD 0.5), injections were administered every three days (100 µL per mouse each time) until gestational day 15.

5. Establishment of pregnant mouse model

Female and male mice were co-housed at a 2:1 ratio (female:male) overnight starting at 20:00 each day. The presence of a vaginal plug or a sperm-positive vaginal smear at 08:00 the next morning was designated as gestational day (GD) 0.5. For each mouse, initial body weight, prepartum weight, postpartum weight, gestational length, neonatal birth weight, litter size, and number of stillbirths were recorded. Based on previous studies29,30, delivery occurring before GD 18.5 was operationally defined as preterm birth in mice. Because gestational shortening may occur within the term range, pregnancy outcomes were interpreted with attention to the distinction between true preterm delivery and gestational shortening phenotypes.

6. Sample collection and processing

At gestational day 15, three pregnant mice per group were randomly selected for placental and vascular sampling (NC/AP/AF and VN/VP/VF). Following anesthesia induced by intraperitoneal injection of pentobarbital sodium (1.62 mg per 30 g body weight) and atropine sulfate (12.5 µg per 30 g body weight), blood samples were obtained via retro-orbital bleeding. Mice were euthanized in a carbon dioxide chamber until death was confirmed by absence of respiration, heartbeat, and corneal reflex; carbon dioxide delivery followed a gradual-fill approach consistent with institutional animal welfare guidance. Carotid artery bifurcation and placental tissues were collected promptly using sterile instruments to reduce cross-sample contamination. Placental tissue was divided into two portions: one portion was stored at −80 °C, and the other portion was fixed in 10% neutral buffered formalin for 24 h, followed by graded ethanol dehydration and paraffin embedding. The remaining mice were monitored for daily body weight, gestational length, litter size, and neonatal birth weight.

7. Cell culture and treatment 

The human trophoblast cell line HTR-8/SVneo was cultured in RPMI 1640 medium supplemented with 10% heat-inactivated fetal bovine serum at 37 °C with 5% CO₂. For infection experiments, HTR-8/SVneo cells (1 × 106 cells) in logarithmic growth phase were seeded into 6-well plates and allowed to adhere overnight. Prior to bacterial challenge, the medium was replaced with antibiotic-free complete medium to avoid antibacterial carryover effects during co-culture. Bacterial suspensions of P. gingivalis or F. nucleatum were added at MOI = 50, and each well was adjusted to a final volume of 2.5 mL using complete culture medium. Plates were incubated for 24 h. Supernatants were collected at 24 h and clarified by brief centrifugation to remove debris prior to cytokine measurement. Adherent cells were washed twice with sterile PBS to remove non-adherent bacteria and then processed immediately for RNA or protein extraction according to the workflows described below.

8. Histological analysis of the mouse placenta

Placental tissues were fixed in 10% neutral buffered formalin for 24 h, paraffin-embedded, and sectioned at 4.5 µm thickness. Routine hematoxylin and eosin (H&E) staining was performed to examine placental morphology. For immunohistochemical staining, antigen localization was visualized using a chromogenic peroxidase substrate producing brown deposits at positive sites, followed by counterstaining with hematoxylin. Negative controls were run by replacing primary antibodies with non-immune serum.

To enhance reproducibility and transparency, immunohistochemical evaluation used a prespecified semi-quantitative scoring approach. Staining intensity was graded as 0 (none), 1 (weak), 2 (moderate), or 3 (strong), and the percentage of positive cells was scored as 0 (<5%), 1 (5–25%), 2 (26–50%), 3 (51–75%), or 4 (>75%). An immunoreactivity score was calculated by multiplying intensity and percentage scores for each field. For each placenta, at least five non-overlapping high-power fields from comparable anatomical regions were scored. Scoring was conducted independently by two observers blinded to group allocation, and disagreements were resolved by joint review.

9. Quantitative real-time PCR detection of bacterial DNA signals in the mouse carotid bifurcation and placenta

Tissue DNA was extracted using a silica column-based tissue DNA extraction workflow. Tissue lysates were clarified by centrifugation at 12,000 × g for 5 min at 20–25 °C, and supernatants were applied to silica columns for DNA binding by centrifugation at 12,000 × g for 1 min at 20–25 °C. Wash steps were performed according to the workflow, with each wash followed by centrifugation at 12,000 × g for 1 min at 20–25 °C. A final dry spin was performed at 12,000 × g for 2 min at 20–25 °C to remove residual ethanol. DNA was eluted in 50 µL elution buffer after a 2-min incubation at 20–25 °C and collected by centrifugation at 12,000 × g for 1 min at 20–25 °C. Bacterial genomic DNA was extracted using a silica column-based bacterial DNA extraction workflow using the same binding/wash/dry spin/elution centrifugation parameters unless otherwise required by the workflow.

DNA concentration and purity were measured using a microvolume nucleic acid quantifier, and integrity was assessed by agarose gel electrophoresis. Qualified DNA samples were stored at –20 °C for subsequent analysis. Target bacterial genes were amplified and cloned using primers listed in Supplementary Table 1, with PCR conditions detailed in Supplementary Table 2 and Supplementary Table 3. Amplified target bands were purified, cloned according to Supplementary Table 4 specifications, and transformed into competent Escherichia coli DH5α cells. Recombinant plasmid-containing strains were verified to ensure correct insert sequences, and plasmid DNA was extracted for standard preparation. Standard curves were generated by performing qPCR on serially diluted plasmid standards containing target bacterial gene fragments. The P. gingivalis 16S and F. nucleatum 16S bacterial DNA signals in carotid bifurcation and placental samples were quantitatively detected by real-time PCR, with DNA copy numbers calculated from Ct values using the standard curve. Reaction systems and programs are detailed in Supplementary Table 5 and Supplementary Table 6, respectively. Because qPCR indicates bacterial DNA signals rather than viability or cellular localization, interpretations regarding microbial presence at the maternal-fetal interface remain cautious.

10. ELISA detection of inflammatory factors in mouse serum samples and cell culture supernatants 

All reagents and samples were equilibrated to room temperature prior to testing. Serum levels of TNF-α and IL-1β were measured using mouse ELISA workflows, and TNF-α and IL-1β levels in cell culture supernatants were determined using human ELISA workflows, following the kit procedures. Standards and samples were measured in duplicate wells, and standard curves were generated for each plate. Technical duplicates were averaged to yield one value per biological replicate.

11. Other molecular biology analyses 

For qRT-PCR, total RNA was extracted from cultured cells using a phenol-chloroform-based RNA extraction workflow. After phase separation, the aqueous phase was clarified by centrifugation at 12,000 × g for 10 min at 4 °C, and RNA was precipitated, washed, and resuspended according to the workflow. RNA concentration was measured using a nucleic acid analyzer, and RNA integrity was assessed by agarose gel electrophoresis. Reverse transcription was performed to generate cDNA, and quantitative real-time PCR was used to quantify TNF-α and IL-1β mRNA levels. Primer sequences are listed in Supplementary Table 7, reaction mixtures in Supplementary Table 8, and reaction programs in Supplementary Table 9.

For Western blotting, protein lysates from mouse placental tissues or trophoblast cells were clarified by centrifugation at 12,000 × g for 15 min at 4 °C, quantified, and subjected to SDS-PAGE followed by membrane transfer and antibody-based detection using a fluorescence imaging workflow. Equal protein loading was set at 30 µg per lane. Original, uncropped membrane images, including molecular weight markers, were retained for all blots presented in the figures and are available DOI: 10.57760/sciencedb.28254. Unless otherwise specified, “n” refers to biological replicates (individual animals or independent cell cultures), while technical repeats are used for quality control and do not replace biological replication.

12. Statistical analysis 

Statistical analyses were performed using statistical analysis software, and figures were generated using graphing software (listed in the Table of Materials). Normally distributed continuous data were presented as mean ± standard deviation and analyzed by one-way ANOVA with appropriate post hoc tests, while non-normally distributed data were expressed as median (interquartile range) and analyzed using the Kruskal–Wallis test with appropriate pairwise comparisons. Statistical significance thresholds were set at P < 0.05, P < 0.01, and P < 0.001. Unless otherwise specified, “n” denotes biological replicates, and technical replicates (e.g., duplicate ELISA wells) were averaged to yield a single value per biological replicate.

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Results

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Infection with P. gingivalis or F. nucleatum is associated with gestational shortening and elevated serum proinflammatory cytokines in mice
The basic statistics for maternal weight changes, neonatal outcomes, and gestational length are summarized in Table 1 and Figure 1. Maternal weight trajectories and neonatal conditions did not differ significantly among groups (one-way ANOVA, P > 0.05; Figure 1A

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Discussion

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In recent years, accumulating evidence has suggested close links between oral health and pregnancy outcomes, prompting increasing attention to potential associations between chronic apical periodontitis (CAP) and adverse pregnancy outcomes, including preterm birth-related phenotypes31 . A systematic review indicates that the current clinical evidence base remains limited and heterogeneous, but overall supports a positive association between maternal apical periodontitis and adverse pregnancy outco...

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Disclosures

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The authors have no competing interests to declare.

Acknowledgements

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This work was supported by the Foundation of Development and Related Diseases of Women and Children Key Laboratory of Sichuan Province (Grant No. FYYFEJB2025002).

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Materials

List of materials used in this article
NameCompanyCatalog NumberComments
Chromogenic Peroxidase SubstrateAgilent DakoK3468Chromogenic peroxidase substrate for IHC
Defibrinated sheep blood, sterileThermo Fisher (Remel)R54012Additive for blood agar (5%)
Dental X-ray unit / radiography systemPlanmecaIntra (model)Periapical radiographs for CAP confirmation
DNeasy Blood & Tissue KitQIAGEN69504Silica-column DNA extraction from tissues/bacteria
E. coli DH5α Competent CellsTaKaRa9057Transformation for plasmid standard construction
Eosin Y solution, alcoholicSigma-Aldrich (Merck)HT110132H&E stain
Fetal Bovine Serum (FBS), qualified, AustraliaGibco (Thermo Fisher Scientific)10099-141Supplement to complete medium 
Flowable resin composite3MFiltek Supreme Flowable 6010Restoration after sealing; light-cure
Fusobacterium nucleatum subsp. nucleatum reference strainATCC25586Anaerobic culture; CAP and tail-vein exposure
GraphPad PrismGraphPad SoftwarePrism 9 (version)Statistical analysis and figure generation
Hematoxylin solutionSigma-Aldrich (Merck)HHS32H&E counterstain
HTR-8/SVneo human trophoblast cell lineATCCCRL-3271In vitro infection assays 
Human IL-1β/IL-1F2 Quantikine ELISA KitR&D Systems (Bio-Techne)DLB50Cell supernatant IL-1β measurement
Human TNF-α Quantikine ELISA KitR&D Systems (Bio-Techne)DTA00DCell supernatant TNF-α measurement
Immobilon-FL PVDF membrane, 0.45 µmMillipore (Merck)IPFL00010Fluorescent Western blot transfer
IRDye 680RD Goat anti-Rabbit IgG (H+L)LI-COR925-68071Fluorescent secondary antibody
IRDye 800CW Goat anti-Rabbit IgG (H+L)LI-COR926-32211Fluorescent secondary antibody
IκBα (44D4) Rabbit mAbCell Signaling Technology4812Primary antibody (WB)
K-File (endodontic file)Dentsply Sirona (Maillefer)A012D015Canal instrumentation (example size 15)
LED dental curing light3MElipar DeepCure-S (model)20 s curing (per protocol)
Mouse IL-1β/IL-1F2 Quantikine ELISA KitR&D Systems (Bio-Techne)MLB00CSerum IL-1β measurement
Mouse TNF-α Quantikine ELISA KitR&D Systems (Bio-Techne)MTA00BSerum TNF-α measurement
MyD88 (D80F5) Rabbit mAbCell Signaling Technology4283Primary antibody (WB)
NanoDrop One Microvolume UV-Vis SpectrophotometerThermo Fisher ScientificND-ONE-WDNA/RNA quantification
Near-infrared imaging systemLI-COROdyssey CLx (model)Fluorescent Western blot imaging
NF-κB p65 (D14E12) Rabbit mAbCell Signaling Technology8242Primary antibody (WB)
PBS, pH 7.4, without Ca2+/Mg2+Gibco (Thermo Fisher Scientific)10010-023Cell washing and reagent preparation
Penicillin-Streptomycin Gibco (Thermo Fisher Scientific)15140-122Antibiotics 
Pentobarbital sodium saltSigma-Aldrich (Merck)P3761Anesthesia induction (per protocol dosing)
Peroxidase blocking solutionAgilent DakoS2023Block endogenous peroxidase for IHC
Phospho-NF-κB p65 (Ser536) (93H1) Rabbit mAbCell Signaling Technology3033Primary antibody (WB)
Porphyromonas gingivalis reference strainATCC33277Anaerobic culture; CAP and tail-vein exposure
PrimeScript RT Reagent Kit (Perfect Real Time)TaKaRaRR037AcDNA synthesis
Real-time PCR systemApplied BiosystemsQuantStudio 5 (model)qPCR quantification of 16S targets
Round bur (sterile)Dentsply SironaH1-010Access opening for maxillary first molar pulp chamber
RPMI 1640 MediumGibco (Thermo Fisher Scientific)11875-093HTR-8/SVneo culture medium base
SYBR-safe DNA gel stainInvitrogenS33102DNA visualization
TaKaRa MiniBEST Plasmid Purification Kit Ver.4.0TaKaRa9760Plasmid miniprep for standards
TB Green Premix Ex Taq II (Tli RNaseH Plus)TaKaRaRR820AqPCR master mix (dye-based)
TLR4 (D8L5W) Rabbit mAbCell Signaling Technology14358Primary antibody (WB)
TRIzol ReagentInvitrogen15596-026Phenol–chloroform RNA extraction
Trypsin-EDTA (0.25%), phenol redGibco (Thermo Fisher Scientific)25200-056Cell detachment
T-Vector pMD19 (Simple)TaKaRa3271PCR product cloning for standard curves
Universal dental adhesive3MScotchbond Universal Adhesive 26200Seal pulp chamber after inoculation

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Tags

Chronic Apical PeriodontitisGestational ShorteningPorphyromonas GingivalisFusobacterium NucleatumTLR4 PathwayMyD88 SignalingNF KappaB ActivationPlacental InflammationPreterm BirthOral Pathogens

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