Unavoidable Exposures · Part 3
This series covers the modern toxic background that conventional medicine isn't measuring. Part 1 covered synthetic fragrance. Part 2 covered vaping. This post covers dental procedures and oral health — an exposure most people never think about because it happens in a clinical setting that implies safety.
There is a particular category of toxic exposure that gets very little attention in functional health circles — not because it's rare or minor, but because it happens in a clinical environment and is therefore assumed to be safe by association.
Dental treatment is that exposure.
I am not making the argument that dentistry is inherently dangerous or that people should avoid dental care. The opposite is true — dental disease, untreated, has serious and well-documented systemic health consequences. The tooth-cardiovascular connection alone is sufficient reason to take oral health seriously as a systemic health issue.
What I am making the argument for is awareness — understanding what goes into your body during a dental appointment, which aspects are genuinely concerning and which are overstated, and what is worth asking your dentist about.
The exposures — what's actually happening
Mercury Amalgam
Dental fillings · Ongoing vapour release
Dental amalgam is approximately 50% mercury by weight — the remainder being silver, tin, copper, and zinc. It has been used in dentistry for over 150 years. The controversy is not about whether amalgam releases mercury — it does, continuously, particularly during chewing, grinding, and temperature changes. The controversy is about whether the dose is clinically significant at the individual level.
The World Health Organisation states that dental amalgam is the largest source of mercury exposure for people in developed countries who have multiple fillings. The vapour released is inorganic mercury, which is absorbed through the lungs and distributed to organs — with particular affinity for the kidneys, liver, and brain. Mercury is a potent neurotoxin and nephrotoxin. It inhibits multiple enzyme systems, depletes glutathione, and interferes with selenium metabolism (selenium binds mercury in a 1:1 ratio, effectively sequestering it — which is why selenium status matters for those with amalgam fillings).
The significant exposure events are amalgam placement and removal — both involve drilling which generates mercury vapour and particles. Removal of amalgam fillings without appropriate protective protocol (rubber dam, high-volume suction, protective supplements) is potentially more hazardous than leaving them in place. This is one of the most important pieces of information anyone with amalgam fillings should have before agreeing to have them removed.
Clinical relevance: highest for people with multiple fillings, kidney dysfunction, high fish consumption (cumulative mercury load), and anyone with a confirmed mercury allergy
BPA and Composite Resins
White fillings · Dental sealants · Bonding agents
Composite resins — the tooth-coloured materials used in white fillings and sealants — were introduced largely as a mercury-free alternative to amalgam. The irony is that many contain bisphenol-A (BPA) or BPA-releasing compounds including bis-GMA (bisphenol A glycidyl methacrylate) and bis-DMA (bisphenol A dimethacrylate).
BPA is a well-characterised endocrine disruptor — it binds oestrogen receptors and disrupts hormonal signalling at nanogram concentrations. Studies have detected BPA in saliva for up to 24 hours after composite placement. Dental sealants in children are a particular concern given the oestrogenic effects of BPA on developing endocrine systems.
Not all composites contain BPA — BPA-free formulations exist and a dentist who is asked specifically about BPA content should be able to specify what they're using. The problem is that this question is almost never asked, and the information is almost never volunteered.
Clinical relevance: highest for women with oestrogen-sensitive conditions (endometriosis, fibroids, hormonal cancers), children receiving sealants
Local Anaesthetic — Articaine and Epinephrine
Injected during most dental procedures
The most commonly used dental local anaesthetic in the UK is articaine with epinephrine (adrenaline). The epinephrine serves as a vasoconstrictor — it narrows blood vessels at the injection site, reducing bleeding and extending the duration of anaesthesia by slowing the absorption of articaine into systemic circulation.
The systemic epinephrine load from a standard dental injection is small and is generally well tolerated. However, in people with cardiovascular disease, arrhythmias, thyroid conditions (particularly hyperthyroidism), or anxiety disorders, even small doses of systemic epinephrine can trigger palpitations, tachycardia, elevated blood pressure, and anxiety responses. People who notice their heart racing, feel shaky, or feel intensely anxious after dental injections are likely responding to the epinephrine component, not the articaine itself.
Epinephrine-free local anaesthetics are available (mepivacaine, prilocaine) and are appropriate for people with relevant cardiovascular conditions. Asking your dentist specifically for epinephrine-free anaesthetic is a reasonable and achievable request.
Clinical relevance: cardiovascular conditions, arrhythmias, hyperthyroidism, anxiety disorders, adrenal insufficiency, those on monoamine oxidase inhibitors or tricyclic antidepressants
Chlorhexidine Mouthwash
Routinely prescribed post-extraction and for gum disease
Chlorhexidine is a broad-spectrum antiseptic mouthwash routinely prescribed after dental extractions and for the management of periodontal disease. It is effective at reducing oral bacterial load. It is also indiscriminate — it kills beneficial bacteria alongside pathogens, including the nitrate-reducing bacteria in the oral cavity that are essential for nitric oxide production.
This is the most clinically striking dental toxicity story that almost nobody knows. Nitric oxide — produced when oral bacteria convert dietary nitrate (from green leafy vegetables, beetroot) to nitrite, which is then reduced to NO — is a potent vasodilator that regulates blood pressure, endothelial function, and cardiovascular health. The oral nitrate-to-nitrite-to-nitric oxide pathway is a significant contributor to systemic NO bioavailability.
A landmark study published in
Free Radical Biology and Medicine (Joshipura et al., 2013) showed that twice-daily chlorhexidine mouthwash use significantly increased systolic blood pressure — by an average of 2–3.5 mmHg — in 19 healthy volunteers, compared with a week without it, as oral nitrite production fell by 90% (
Kapil 2013). A small, short study, but a measurable effect from a commonly prescribed mouthwash.
Short-term use for specific indications is clinically appropriate. Routine long-term use — which many patients are effectively encouraged toward — carries genuine cardiovascular cost.
Clinical relevance: anyone with elevated blood pressure, cardiovascular disease risk, or regular mouthwash use.
Fluoride
Treatment gels · Toothpastes · Water supply in some areas
Fluoride's role in dental health — reducing caries by incorporating into the hydroxyapatite crystal structure of tooth enamel — is well established and represents one of public health's genuine successes. The controversy is not about topical fluoride at appropriate concentrations. It is about systemic fluoride accumulation from multiple simultaneous sources — water, toothpaste, dental treatments, fluoridated salt, some foods — and the evidence for effects on thyroid function and neurological development at higher cumulative exposures.
Fluoride is a competitive inhibitor of iodine uptake in the thyroid — iodine and fluoride both use the sodium-iodide symporter. At sufficient concentrations, fluoride reduces thyroid hormone synthesis. A systematic review of studies from high-fluoride areas found consistent associations with lower IQ in children — the mechanism likely involves fluoride's effects on neurological development and thyroid function. These studies were from areas with naturally high water fluoride concentrations above those used in UK water fluoridation, but they raise legitimate questions about cumulative exposures.
The precautionary principle for thyroid-compromised individuals — particularly those with Hashimoto's or hypothyroidism already on the borderline of adequate function — is to minimise unnecessary systemic fluoride exposure while maintaining appropriate topical dental fluoride use.
Clinical relevance: highest for those with thyroid conditions, iodine insufficiency, and children during neurological development periods
Dental X-Ray Radiation
Diagnostic imaging · Routine check-ups
Modern digital dental X-rays deliver a fraction of the radiation dose of older film X-rays — a bitewing X-ray delivers approximately 5 microsieverts, comparable to a few hours of background radiation. For most people, this represents a negligible risk. The concern arises with frequency — annual full-mouth X-ray series for patients who may not clinically require them, and the cumulative effect across a lifetime of dental care.
The thyroid gland sits directly in the field of panoramic dental X-rays. Lead thyroid collars should be standard practice during dental X-rays — they are not always offered or used. For patients with thyroid conditions, requesting a thyroid collar explicitly is a reasonable precaution. The clinical question of whether X-ray frequency matches clinical need is a legitimate conversation to have with your dentist.
Clinical relevance: thyroid conditions, pregnancy, children, those receiving frequent X-rays for ongoing dental work
The tooth-heart connection — what the evidence actually shows
The relationship between oral health and cardiovascular disease is one of the most well-documented but least-discussed connections in medicine.
Oral Health and Cardiovascular Disease — The Evidence
Porphyromonas gingivalis — the primary pathogen in periodontal disease — has been detected in atherosclerotic plaques. It produces enzymes that degrade vessel wall components and drives local inflammation.
Streptococcus mutans — the primary caries-causing bacterium — can enter the bloodstream during dental procedures and colonise damaged heart valves. Infective endocarditis is a serious and potentially fatal consequence.
People with periodontal disease have significantly higher rates of cardiovascular disease, stroke, and diabetes — independent of shared risk factors like smoking. An American Heart Association review found that observational studies support a link between gum disease and heart and artery disease independent of known confounders, but not that one causes the other, and no evidence yet that treating gum disease prevents heart disease (
Lockhart 2012).
The mechanism is dual — direct bacterial translocation into circulation AND chronic systemic inflammation from periodontal disease driving CRP elevation, endothelial dysfunction, and accelerated atherosclerosis.
The chlorhexidine-blood pressure connection (described above) represents a third pathway — oral microbiome disruption impairs the nitrate-nitric oxide pathway that regulates vascular tone.
People with missing teeth — a surrogate marker for historical dental disease — have higher all-cause mortality. This is not fully explained by shared lifestyle factors.
The clinical implication is that oral health is not a separate department from systemic health. It is part of the same system — and the microorganisms, inflammatory signals, and chemicals that enter circulation at the gum-tooth interface affect the whole body in ways that dentistry as a discipline has been slow to communicate and medicine has been slow to integrate.
The oral microbiome — more important than you think
The mouth contains approximately 700 bacterial species in a biofilm ecosystem that has evolved alongside the human body for millions of years. This ecosystem performs functions that are only now being properly mapped — nitric oxide production, immune modulation, digestion of dietary nitrates, and protection against pathogenic organisms.
The oral microbiome is the gateway to the gut microbiome — the bacteria you swallow continuously from your oral cavity seed and influence the gut microbial community. Oral dysbiosis — a pathogenic shift in oral microbial populations — is associated with dysbiotic changes in the gut. The oral-gut microbiome connection is real and runs in both directions.
Chlorhexidine, antibiotics prescribed for dental infections, and repeated dental antiseptic treatments all disrupt the oral microbiome. The consequences extend beyond the mouth — into gut health, cardiovascular function, and systemic immune regulation.
Oral probiotics — particularly Lactobacillus reuteri, Lactobacillus salivarius, and Streptococcus salivarius K12 — have emerging evidence for supporting oral microbiome health, reducing periodontal pathogen burden, and reducing gum inflammation. They represent a restorative intervention after any antimicrobial dental treatment.
Around a dental procedure: what’s worth doing
This section used to be a supplement protocol: chlorella, vitamin C, NAC, selenium and modified citrus pectin, with doses, to “bind” and “clear” mercury before and after dental work. I couldn’t find a trial testing any of them for reducing harm from a dental procedure, and binders can’t pull anything out of your tissues (what binders can and can’t do). Grade: untested. I’ve taken it down. This is what has a reason behind it.
Around a dental procedure
Things to ask your dentist
→If old amalgam is being drilled or removed: will they use a rubber dam and high-volume suction? These are the standard ways to cut how much you breathe in or swallow during removal.
→If you’re concerned about BPA: ask whether the composite is BPA-free. Some practices use BPA-free materials as standard.
→If you have a heart rhythm problem, or reacted badly to dental anaesthetic before: tell your dentist. Adrenaline-free options (such as mepivacaine) exist; for most people the adrenaline in dental anaesthetic is well tolerated.
Mouthwash
→Chlorhexidine: if it’s prescribed for an infection or after surgery, use it as prescribed. For routine everyday use, ask whether you need it: a week of it raised blood pressure slightly in healthy volunteers (Kapil 2013, above). Don’t stop a prescribed rinse without asking.
Food and recovery
→Nitrate-rich vegetables (rocket, spinach, beetroot) are part of eating well anyway and feed the oral nitrate pathway. Grade: mechanistic.
→Oral probiotics (such as L. reuteri or S. salivarius K12) have small trials in gum disease with mixed results. Reasonable to try after antibiotics; not essential. Grade: mixed.
→Routine check-ups and a scale and polish need nothing extra.
The underlying oral health foundation
The most effective pre-dental protocol is the one that reduces the need for significant dental intervention in the first place. Oral health is substantially nutritionally determined — and the nutritional factors that drive dental disease are the same ones that drive systemic disease.
Vitamin K2 is essential for the proper mineralisation of tooth enamel — via the same osteocalcin-activation mechanism relevant to bone health. Weston A Price's observation, documented in the 1930s, that traditional populations eating nutrient-dense traditional diets had remarkably low rates of dental caries while industrially-fed populations showed dramatic increases — is supported by the modern understanding of fat-soluble vitamin K2's role in dental mineralisation.
Vitamin D supports tooth mineralisation and the immune defence of the oral mucosa. Low vitamin D is associated with higher rates of periodontal disease and caries.
Magnesium is incorporated into tooth enamel alongside calcium. Low magnesium produces structurally inferior enamel that is more susceptible to decay.
Sugar and refined carbohydrates feed Streptococcus mutans — the acid-producing caries bacterium. The frequency of sugar exposure matters as much as the quantity — continuous snacking on sugary foods maintains the acidic oral environment that drives enamel erosion, while eating sweets as part of a meal followed by saliva flow is significantly less damaging.
Xylitol is worth a specific mention — it actively inhibits Streptococcus mutans growth (the bacterium cannot metabolise it and it competitively occupies the receptor sites the bacterium uses for adhesion). Xylitol chewing gum after meals has genuine clinical evidence for caries reduction and is one of the few genuinely evidence-based dental interventions that doesn't involve a pharmaceutical or a drill.
The mouth is not a separate organ that the dentist manages twice a year. It is the beginning of the digestive tract, the first point of immune contact with the external environment, and a continuous source of bacterial and inflammatory signals that enter systemic circulation. Oral health is systemic health — the research has been saying this for decades. The clinical silos haven't caught up.
A note on amalgam removal decisions
The question of whether to remove existing amalgam fillings is one I am asked regularly, and I want to answer it carefully.
Amalgam in stable, intact fillings releases mercury at a low, continuous rate. Drilling it out releases a significant pulse of mercury vapour and particles — far exceeding the chronic low-level release of the intact filling. Removing amalgam fillings without appropriate precautions (rubber dam, high-volume suction, a dentist experienced in safe removal) can produce a worse acute exposure than leaving the fillings in place.
Reasons dentists replace amalgam include fillings that are fractured, decayed underneath or failing; a confirmed allergy or a reaction in the gum next to a filling; and, for some people, planning a pregnancy, which is worth discussing with your dentist. A urine or hair “mercury burden” result isn’t a validated reason (see below).
For people without these specific indications, the decision to remove intact amalgam fillings is not straightforward and should not be made on aesthetic grounds alone without understanding the procedural exposure risk. If you decide to remove them, do it with a dentist trained in SMART protocol, don't rush the process — one or two fillings per session with adequate recovery between.
Testing for mercury
Blood mercury mostly reflects recent intake, much of it methylmercury from fish. Urine mercury, collected normally, reflects inorganic mercury, including from amalgam. “Provoked” testing, where a chelating drug (DMSA or DMPS) is given first, makes anyone’s urine metals rise, and there are no valid reference ranges for it. The American College of Medical Toxicology recommends against it (ACMT 2017). I don’t use it. If you’re worried about mercury, start with your history and a normal blood or urine test through your GP or a practitioner.
Tracking the nitrate pathway
Saliva test strips that read nitrate and nitrite can show whether your mouth is converting dietary nitrate, for example before and after a course of mouthwash. They’re fine for self-tracking. They aren’t validated for clinical decisions, and a single reading means little. Grade: untested for outcomes.
Questions about dental exposures and your health?
The DH Clinical Concierge can help you understand the clinical picture behind dental toxicity and whether a pre or post dental protocol is relevant for your situation.
Talk to the Concierge
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