Mouth to whole body / An evidence pathway

A pathway.
Not a promise.

Source. Material. Route. Response. Decision.

Read what was tested, where it was tested, and what remains unproven. The dashed spaces matter as much as the findings.

Explore the map

The biological questions

Follow a question.
Inspect the bridge.

Five questions, not five proven causal links. Inspect the experimental evidence at each stage, then the missing bridge to an individual human claim.

Solid evidence markers: a reported finding in the stated study setting.

Dashed connections: open human attribution or validation questions.

What is missing between the stages?
  1. Source ecology to Released material

    Which source produced the material that was actually measured?

  2. Released material to Exposure route

    Does the characterized material reach a relevant compartment and remain active?

  3. Exposure route to Host response

    Can the response be linked to that exposure rather than an unmeasured alternative?

  4. Host response to Clinical translation

    Would this information improve a defined decision beyond ordinary clinical measures?

Research questions, not established human links.

Inspect the proposed validation gates

Stage 01 / Source ecology

Start with the source. Do not assume it.

Study setting: Mechanistic assays

The source question asks which organisms and local conditions belong in the record. Here, the published comparison is between vesicles from different periodontal organisms—not a personal oral-to-systemic source trace.

Evidence context: Cecil et al., 2016

Reported in the cited setting

Stage 02 / Released material

The preparation matters as much as the label.

Study setting: Cells + animal experiments

The cited experiments ask about particular vesicle preparations and cargo contributions. They do not justify treating every local activity signal as the same material or the same mechanism.

Evidence context: Farrugia et al., 2020 Evidence context: Han et al., 2019

Reported in the cited setting

Endothelial barrier
Cells + zebrafish

Wild-type and gingipain-deficient OMV comparisons supported a gingipain contribution to endothelial-barrier disruption, with PECAM-1 loss associated with the response. The zebrafish experiments used direct systemic injection, not oral exposure.

Original paper: Farrugia et al., 2020
The boundary

This does not calibrate an oral-rinse measurement to vascular leak, heart attack, or stroke risk in a person.

Read the study in context: Farrugia et al., 2020
Mechanism detail in the science spine Claim entry in the evidence ledger

Stage 03 / Exposure route

How it gets there changes the question.

Study setting: Cells + mouse delivery

Intracardiac injection and oral gavage are different experimental routes. The route and dose stay attached to the finding; neither can silently become an ordinary human oral exposure.

Evidence context: Han et al., 2019 Evidence context: Gong et al., 2022

Reported in the cited setting

Neuroinflammatory responses
Mouse experiment

Aged male mice given OMVs by oral gavage at 4 mg/kg every other day for eight weeks showed neuroinflammatory, tau-phosphorylation, and memory-task effects.

Original paper: Gong et al., 2022
The boundary

The experimental dose is not established as ordinary human exposure. This is not evidence for a personal Alzheimer’s risk meter or proof of human disease causation.

Read the study in context: Gong et al., 2022
Mechanism detail in the science spine Claim entry in the evidence ledger

Stage 04 / Host response

A specific response. Not a universal score.

Study setting: Cells + zebrafish + mice

The cited studies examine endothelial-barrier and hepatic insulin-signaling responses in their own experimental settings. These are distinct outcomes, not interchangeable measures of a person’s whole-body health.

Evidence context: Farrugia et al., 2020 Evidence context: Seyama et al., 2020

Reported in the cited setting

Endothelial barrier
Cells + zebrafish

Wild-type and gingipain-deficient OMV comparisons supported a gingipain contribution to endothelial-barrier disruption, with PECAM-1 loss associated with the response. The zebrafish experiments used direct systemic injection, not oral exposure.

Original paper: Farrugia et al., 2020
The boundary

This does not calibrate an oral-rinse measurement to vascular leak, heart attack, or stroke risk in a person.

Read the study in context: Farrugia et al., 2020
Mechanism detail in the science spine Claim entry in the evidence ledger
Hepatic insulin signaling
Mice + cells

Seyama and colleagues reported liver translocation and reduced insulin-responsive hepatic glycogen synthesis in mice. In HepG2 cells, OMVs attenuated insulin-stimulated Akt/GSK-3β signaling in a gingipain-dependent manner.

Original paper: Seyama et al., 2020
The boundary

This is not proof that a person’s glucose excursions are caused by oral vesicles, and it does not establish the same effect in muscle or adipose tissue.

Read the study in context: Seyama et al., 2020
Mechanism detail in the science spine Claim entry in the evidence ledger

Stage 05 / Clinical translation

A human observation is not yet a useful test.

Study setting: Human tissue + models

The tissue study below contains human observations and separate model experiments. Keep those evidence types apart before considering an oral-source claim, a prediction, or a clinical decision.

Evidence context: Zheng et al., 2024

Reported in the cited setting

Fusobacterium and tissue interactions
Human tissue + models

In five paired colorectal-cancer and adjacent-normal tissue samples, Zheng and colleagues found greater FomA signal in tumor-derived EV-enriched fractions, interpreted as F. nucleatum EV enrichment. Separate cell and mouse experiments supported FomA-transfer effects on adhesion, colonization, and tumor progression.

Original paper: Zheng et al., 2024
The boundary

FomA is not a vesicle-exclusive marker. Human tissue enrichment and model mechanisms are separate observations; they do not establish oral origin in an individual or validate an oral-rinse cancer predictor.

Marker-specificity discussion
Mechanism detail in the science spine Claim entry in the evidence ledger

Selected studies from the Fasolati science spine, not a systematic review. Model findings, human tissue observations, and proposed clinical uses remain separate. The map uses static, cited content. It accepts and stores no health information and makes no API or live-AI requests. Section links contain only public stage names.

From mechanism to interpretation

Keep the biology.
Keep the boundary.

The Life Board demonstration puts this discipline into a fictional record: oral, gut, and host observations stay distinct, even when they disagree.

Walk through the fictional Life Board Read the human evidence