Mouth, saliva and swallowing
The mouth wets, breaks up and packages food, then hands it over in a one-second reflex that has to shut the nose, shut the larynx and open the top of the oesophagus in the right order. Saliva keeps the mouth alive and the teeth intact; the swallow keeps food out of the lungs. When either fails, the damage is fast — teeth rot in months, lungs get infected in days.
What it normally does
Three paired major glands, plus several hundred minor glands scattered through the lips, cheeks and palate, make 0.5 to 1.5 litres of saliva a day. At rest most of the volume comes from the submandibular glands (a mixed, sero-mucous, slightly stringy secretion); when you eat or smell food the parotids take over with a thin watery fluid rich in amylase. The minor glands add little volume but much of the mucin. Production is unusual in being driven almost entirely by the parasympathetic nervous system — acetylcholine on M3 muscarinic receptors on the acinar cells (via the chorda tympani from the facial nerve, relaying in the submandibular ganglion, to the submandibular and sublingual glands; and via the lesser petrosal nerve from the glossopharyngeal nerve, relaying in the otic ganglion, to the parotid). There is no meaningful sympathetic 'off switch' for volume: sympathetic firing adds protein and mucus but very little water, which is why a frightened mouth feels dry and sticky rather than simply empty. The acinus makes a plasma-like fluid; the duct then pulls sodium and chloride back out and adds potassium and bicarbonate, and because the duct wall will not let water follow, saliva arrives in the mouth dilute (hypotonic). Resting saliva sits close to neutral, around pH 6.5 to 7; as flow rises the duct has less time to strip it, bicarbonate climbs and saliva becomes alkaline — so buffering power is a function of flow rate. It carries mucins for lubrication, bicarbonate to neutralise acid, calcium and phosphate to rebuild enamel, and antimicrobials — IgA, lysozyme, lactoferrin.
Every one of those jobs fails at once when flow stops, and any drug that blocks M3 receptors anywhere in the body turns the tap off here — xerostomia.
The first phase of swallowing is voluntary and is mostly the tongue. Teeth and the muscles of mastication (trigeminal nerve, V3) cut and grind; the tongue (hypoglossal nerve, XII) mixes the food with saliva, gathers it into a single ball on its upper surface (the bolus) and holds it against the hard palate, sealed at the back by the tongue base against the soft palate. The lips and cheeks (facial nerve, VII) keep it in. Then the tongue strips backwards against the palate like a squeegee and throws the bolus into the oropharynx. Nothing further happens until sensation from the back of the mouth and pharynx reaches the brainstem and triggers the reflex.
A weak tongue, a weak face, no teeth or no saliva means the bolus is never properly formed or properly delivered — food is drooled, pocketed in the cheek, or arrives at the pharynx in an uncontrolled dribble.
The second phase is a reflex and takes about one second. Sensory fibres from the oropharynx and the entrance to the larynx (glossopharyngeal nerve, and the internal branch of the superior laryngeal nerve from the vagus) reach a pattern generator in the medulla (nucleus tractus solitarius feeding nucleus ambiguus), which fires a fixed motor sequence out through V, VII, IX, X and XII. Five things happen almost together: the soft palate lifts and shuts off the nose; the larynx is pulled upwards and forwards under the tongue base; the epiglottis tips backwards over the laryngeal inlet; the vocal cords close; and breathing stops for the duration (deglutitive apnoea, normally interrupting expiration, so the next breath out helps clear the entrance). The same forward-and-up movement of the larynx physically pulls open the upper oesophageal sphincter (cricopharyngeus), which relaxes at the same moment. If food does get past the cords, sensation from the larynx triggers a cough — the last line of defence.
Break any step and the food goes somewhere it should not: back up the nose, into the larynx, or nowhere at all — and if laryngeal sensation is lost, it goes in with no cough at all (silent aspiration).
The mouth is not sterile and is not meant to be. Several hundred bacterial species live in a biofilm on the teeth, tongue and gums, and roughly a litre of that contaminated saliva is swallowed every day, with most of the organisms killed by stomach acid. Saliva flow, IgA and the flushing action of chewing hold the population in balance; between meals, salivary bicarbonate lifts a fallen pH back up and calcium and phosphate put mineral back into the enamel surface. Around half of healthy adults aspirate small amounts of oral secretion during sleep and clear it with cilia and cough without ever knowing. What decides whether that becomes pneumonia is the volume aspirated, how many bacteria are in it, and whether the lung can clear them.
Caries, thrush and aspiration pneumonia are all failures of that balance, not of hygiene alone — which is why a dirty mouth in a person who cannot swallow is a lung problem.
What goes wrong
- Dry mouth (xerostomia)← from “Three paired major glands, plus several hundre…”
Salivary flow falls below what the mouth needs. Three routes get you there. Drugs are the commonest by far: anything that blocks M3 muscarinic receptors on the acinar cell stops the water — tricyclics such as amitriptyline, oxybutynin and solifenacin for bladder, older sedating antihistamines, antipsychotics such as olanzapine and quetiapine, and less directly opioids (which suppress salivary secretion centrally rather than by blocking the acinar receptor) and diuretics (which dry the mouth by reducing the water available). Clozapine is the exception that catches people out: despite being strongly antimuscarinic it characteristically causes hypersalivation and night-time drooling, not dryness. Autoimmune destruction is the second: in Sjogren syndrome lymphocytes infiltrate and destroy the acini in salivary and lacrimal glands, so the mouth and the eyes dry together and the loss is permanent. The third is radiotherapy to the head and neck — serous acinar cells are unusually radiosensitive for a non-dividing tissue, so parotid function falls within weeks; recovery is dose-dependent and largely does not happen once the mean parotid dose is high, which is why sparing at least one parotid is a planning priority. Whatever the cause, the consequences follow the list of things saliva was doing: no lubrication (a dry bolus that will not go down), no buffering or remineralisation (caries), no antimicrobials or flushing (thrush), no clearance and no wetting of taste receptors.
The commonest cause is the medication list, so read it before ordering anything. Anticholinergic burden is cumulative — three weakly antimuscarinic drugs will do it. Sjogren is around 10 times more common in women and usually presents in middle age; the reason it matters beyond dryness is a many-fold increase in non-Hodgkin lymphoma risk (commonly quoted at roughly 10 to 20 times, typically parotid MALT lymphoma), so persistent unilateral parotid swelling in Sjogren gets investigated, not reassured.
You would find: A tongue depressor or dental mirror sticks to the buccal mucosa. No pool of saliva in the floor of the mouth when the tongue is lifted. Dry, fissured, lobulated tongue; lipstick sticking to the teeth. Ask about needing water to swallow dry biscuits or bread, waking at night to sip, and difficulty speaking for long. Look specifically at the necks of the teeth at the gum line and the incisal edges — decay there is the saliva-loss pattern. Dry eyes and gritty sensation alongside points to Sjogren; check for parotid swelling and order anti-Ro (SSA) and anti-La (SSB) antibodies.
Bacteria in the plaque biofilm, mainly Streptococcus mutans and lactobacilli, ferment dietary sugar to acid. When the pH at the enamel surface falls below about 5.5 the crystal starts to dissolve (demineralisation). Between acid attacks, saliva's bicarbonate lifts the pH back and its calcium and phosphate drive mineral back in (remineralisation). Caries is not one event, it is that balance tipping — many sugar exposures a day, or too little saliva, and demineralisation wins. The white spot lesion is the reversible stage; once the surface collapses into a cavity the mineral cannot be replaced. Grazing on sugar, sipping soft drink through the day, or a bottle of milk or juice in bed is worse than the same total sugar eaten at once, because each exposure buys 20 to 30 minutes below the critical pH — and salivary flow drops to almost nothing during sleep.
Caries is the most common chronic disease in Australia and dental conditions are a leading cause of potentially preventable hospitalisation, with the highest rates in young children, many of whom need extractions under general anaesthetic. The burden is starkly unequal: Aboriginal and Torres Strait Islander children have roughly twice the decay experience of other Australian children, and in some remote communities early childhood caries is close to universal, driven by expensive fresh food, cheap sugary drinks, no fluoridated water supply and no local dentist. Fluoridation reaches around 89% of the Australian population but coverage is patchiest in regional Queensland. Treat this as a social determinant problem with a chemical adjunct, not the other way round.
You would find: White or brown spots along the gum margin, cavitation, and pain that goes from cold-sensitive and brief (reversible pulpitis) to spontaneous, throbbing and keeping the patient awake (irreversible pulpitis), then to a tender-to-percuss tooth with facial swelling once the pulp dies and infection reaches the bone. Swelling that crosses to the floor of the mouth, a raised tongue, drooling or difficulty swallowing is Ludwig angina and is an airway emergency.
- Oropharyngeal dysphagia (difficulty starting the swallow)← from “The first phase of swallowing is voluntary and…”
The voluntary phase or the trigger fails. After a stroke, weakness of the tongue and face means the bolus is never gathered or propelled, and the reflex is triggered late — the bolus is already sitting at an open laryngeal inlet when the sequence finally starts. In Parkinson disease the tongue movements are slow and repetitive (lingual pumping) and the whole sequence is bradykinetic. In motor neurone disease the bulbar muscles waste. In advanced dementia the voluntary phase is simply not initiated — food is held in the mouth. Head and neck cancer or its radiotherapy stiffens and scars the moving parts. The clinical point is that the problem sits at the mouth and throat, so the trouble appears within a second of starting to swallow, not a minute later.
Around half of acute stroke patients have dysphagia; most recover within weeks, but they are at their most vulnerable in the first days, which is exactly when someone offers them a cup of tea. Aboriginal and Torres Strait Islander Australians have stroke at roughly twice the rate and at a substantially younger age, so this is not only a geriatric problem. No drug treats the swallow. The interventions are a speech pathology assessment, positioning, texture modification, mouth care, and reviewing the drug chart for sedatives and antimuscarinics that make it worse.
You would find: Coughing or choking on food or drink — thin fluids are the hardest, because they move fastest. A wet, gurgly voice after swallowing. Food or drink coming back down the nose. Drooling, food pocketed in the cheek, multiple swallows for one mouthful, or a meal that takes 40 minutes. Weight loss and recurrent chest infections. The patient points to the throat, not the chest. Contrast with oesophageal dysphagia: food sticks seconds later, the patient points to the sternum, and solids give trouble before liquids when the cause is a narrowing — though achalasia and other motility disorders trouble solids and liquids together from the start. Every acute stroke gets a swallow screen before any food, drink or oral medication.
- Aspiration pneumonia and aspiration pneumonitis← from “The second phase is a reflex and takes about o…”
Material gets past a larynx that failed to close or failed to feel it. Two different things follow, and they are managed differently. Aspiration pneumonitis is a chemical burn: a large volume of acidic gastric content injures the alveolar epithelium within minutes, giving hypoxia and infiltrates within hours — sterile at first, so antibiotics on day one are usually not the answer. Aspiration pneumonia is infection: repeated small volumes of bacteria-laden oral secretions, so the load of organisms in the mouth matters as much as the swallow. Gravity decides the site — sitting up, it lands in the basal segments of the right lower lobe; lying flat, in the posterior segment of the right upper lobe or the superior segment of the right lower lobe. Right more than left, because the right main bronchus is wider, shorter and more vertical. If laryngeal sensation is impaired, none of this is announced by a cough.
Twice daily mouth care and keeping the patient upright to eat prevent more aspiration pneumonia than any antibiotic. In advanced dementia, thickened fluids and PEG feeding have not been shown to prevent aspiration pneumonia or prolong life — careful hand feeding is the standard, and a feeding tube is not the safety net families are often told it is.
You would find: Fever, new cough and hypoxia a day or two after a choking episode, or recurrent right-sided pneumonia in someone with a stroke, dementia, Parkinson disease, or reduced consciousness from alcohol, opioids or seizures. Chest x-ray consolidation in the dependent segments. Suspect it silently in a frail patient with unexplained fever and no cough at all — a large proportion of stroke patients who aspirate, at least a third and in some series more than half, do so silently. Look in the mouth: dirty teeth and gum disease raise the bacterial load being inhaled.
- Oral candidiasis (thrush)← from “The mouth is not sterile and is not meant to b…”
Candida albicans is carried harmlessly in about half of healthy mouths, held in check by saliva flow, IgA, and competition from bacteria. Remove any of those and it overgrows and invades the surface epithelium: dry mouth, broad-spectrum antibiotics wiping out the competing bacteria, corticosteroids and other immunosuppression, poorly controlled diabetes with high glucose in the saliva, dentures that provide a warm covered surface that saliva never washes, and infancy or old age. Inhaled corticosteroid thrush is the same mechanism in a specific place — drug deposits in the oropharynx and locally suppresses mucosal immunity, which is why rinsing and spitting after the puffer, or a spacer, prevents it.
Thrush in a healthy-looking adult with no dentures, no inhaler and no antibiotics is a reason to look for the cause — undiagnosed diabetes or HIV. Oesophageal candidiasis (thrush plus pain on swallowing) is an AIDS-defining illness. In breastfed babies, the mother's nipples are treated at the same time or it ping-pongs back.
You would find: White curd-like plaques on the tongue, palate and buccal mucosa that scrape off leaving a raw, sometimes bleeding base — that scraping is what separates it from leukoplakia, which does not budge. Other patterns: red, sore, shiny mucosa under a denture (denture stomatitis), and cracked sore corners of the mouth (angular cheilitis). Ask about burning and altered taste.
What we give, and how it works
Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.
- Binds
- Muscarinic acetylcholine receptors, mainly M3, on salivary and lacrimal acinar cells. Pilocarpine is a non-selective muscarinic agonist, so every muscarinic receptor in the body is fair game.
- Which does
- M3 is Gq coupled: phospholipase C, IP3, a rise in intracellular calcium. Calcium opens chloride channels on the apical membrane, chloride moves into the lumen, sodium follows through the tight junctions, and water follows both through aquaporin-5 channels. The acinus makes fluid.
- So you see
- Saliva flow rises within about 20 to 30 minutes and lasts a few hours, so it is taken several times through the day. Tear production increases too, for the same reason.
- And the same mechanism causes
- There is nothing selective about it — the drug reaches muscarinic receptors everywhere. The commonest adverse effect is sweating, because eccrine sweat glands are the one sympathetically innervated tissue that uses acetylcholine on muscarinic (mainly M3) receptors, and patients can sweat drenchingly. Then flushing, urinary frequency (M3 on the detrusor), abdominal cramping and increased gut motility, increased gastric acid secretion, and bronchial narrowing with increased bronchial secretion — which is why it is avoided in poorly controlled asthma and COPD. In the eye, ciliary muscle contraction causes accommodative spasm, so the eye is pulled towards near focus and distance vision blurs, and sphincter pupillae contraction gives a small pupil and poor vision in dim light — a driving hazard at night. Slowing of the heart is an M2 effect at the sinoatrial node.
- Handling
- Contraindicated in uncontrolled asthma, acute iritis and narrow-angle glaucoma (note the apparent paradox: topical pilocarpine is used to break acute angle closure, but systemic pilocarpine is not the way to treat it). Use cautiously in bradycardia and other significant cardiac disease, and in peptic ulcer disease. Effects wear off with the dose, so it does not protect the teeth overnight when flow is lowest.
Catches people out: Reversing the cause beats adding pilocarpine. Every dry mouth deserves an anticholinergic burden count first, plus fluoride and dental review, because these patients lose teeth fast.
- Binds
- The hydroxyapatite crystal surface of enamel, and bacterial enolase and the proton-pumping (F-type) ATPase in plaque organisms.
- Which does
- Fluoride substitutes for hydroxyl in the crystal, forming fluorapatite, which needs a lower pH (about 4.5 rather than 5.5) before it will dissolve. It also sits in the plaque fluid and catalyses the redeposition of calcium and phosphate from saliva onto a partly demineralised surface. At the higher concentrations of a varnish it inhibits bacterial glycolysis and acid tolerance, so the plaque makes less acid.
- So you see
- Fewer new cavities, and white spot lesions that harden and stop progressing instead of collapsing. The benefit tracks how often fluoride is present, not how much is used at once — hence twice-daily brushing, and spitting rather than rinsing so a low concentration lingers.
- And the same mechanism causes
- The same incorporation into forming crystal is the adverse effect. Fluoride swallowed while the permanent teeth are still mineralising is built into that enamel and produces dental fluorosis; the window that matters cosmetically is roughly the first six years of life, when the permanent front teeth are forming. It is faint white flecks at worst in most cases, mottling and brown staining with heavy exposure. That is why Australian guidance is no toothpaste under 18 months; a pea-sized amount of low-fluoride children's toothpaste from 18 months to 5 years, spat out and not swallowed and with brushing supervised; and standard fluoride toothpaste from 6 years. In acute overdose fluoride binds calcium in the blood and forms hydrofluoric acid in the stomach, so a child who eats a tube of toothpaste can get vomiting and hypocalcaemia — give milk or another calcium-containing drink and ring the Poisons Information Centre on 13 11 26.
- Handling
- Varnish is applied by a clinician a few times a year in high-risk children and can be used from the eruption of the first tooth.
Catches people out: Fluoride will not out-run the diet. A child sipping soft drink or juice through the day, or going to bed with a bottle, keeps the enamel below its critical pH for hours and will decay through any toothpaste.
- Binds
- Nystatin binds ergosterol, the sterol in the fungal membrane. The azoles (miconazole, fluconazole) inhibit the fungal enzyme lanosterol 14-alpha-demethylase (CYP51), which the fungus needs to make ergosterol.
- Which does
- Nystatin inserts into the membrane and forms pores, so potassium and other ions leak out and the cell dies — the reason it kills rather than merely inhibits, and the reason resistance is rare. The azoles starve the membrane of ergosterol and let toxic sterol precursors accumulate, so growth stops.
- So you see
- Plaques clear over about 7 to 14 days. Treatment continues a few days past the visible clearing, because the organism is still in the biofilm.
- And the same mechanism causes
- Ergosterol is a fungal sterol, so nystatin barely touches human cells and, being unabsorbed, causes little more than a bad taste and nausea. The azoles are the opposite problem: CYP51 is a cytochrome P450, and these drugs are not tidy about which human P450s they also inhibit. Fluconazole blocks CYP2C9 and, less potently, CYP3A4 — so warfarin is not metabolised, the INR climbs, and the patient bleeds; phenytoin and statin levels rise the same way. It also prolongs the QT interval. Ketoconazole in particular, and other azoles at high dose, inhibit the P450s of adrenal steroid synthesis. The trap for students is that miconazole oral gel is 'topical': enough is swallowed and absorbed to inhibit CYP2C9, and it has caused serious bleeding in patients on warfarin.
- Handling
- Fluconazole is renally cleared, so the dose is reduced in significant renal impairment; it crosses the placenta, and high-dose or prolonged use in the first trimester is associated with fetal malformations. Miconazole oral gel carries a choking risk in young infants and should not be applied as a bolus to the back of the mouth of a baby under 6 months — smear a small amount on the front of the tongue and inside the cheeks, or use nystatin drops.
Catches people out: Any oral antifungal in a patient on warfarin is a warfarin problem until proven otherwise, including the gel.
- Binds
- Penicillin-binding proteins — the transpeptidase enzymes bacteria use to cross-link peptidoglycan in the cell wall. Clavulanate binds and inactivates bacterial beta-lactamase, protecting the amoxicillin rather than killing anything itself.
- Which does
- The beta-lactam ring mimics the D-Ala-D-Ala end of the peptidoglycan chain and acylates the enzyme's active site. Cross-linking stops, the wall weakens as the bacterium keeps growing, autolysins are unleashed and the cell bursts under its own osmotic pressure. Bactericidal, and time-dependent — what matters is how long the concentration stays above the minimum inhibitory concentration, which is why these drugs are given several times a day.
- So you see
- Fever and hypoxia settle over 48 to 72 hours in a straightforward aspiration pneumonia.
- And the same mechanism causes
- The same wall-directed killing hits commensal bacteria in the gut, so diarrhoea is common and Clostridioides difficile colitis follows loss of colonisation resistance — clavulanate broadens the spectrum and raises both risks, and it is also the component behind cholestatic hepatitis. Killing the mouth's bacteria removes Candida's competition, which is why a course of antibiotics is a standard cause of thrush. The beta-lactam ring itself is chemically reactive: it haptenates host proteins, and that is the basis of true IgE-mediated penicillin allergy. Ampicillin or amoxicillin given during Epstein-Barr virus infection produces a widespread maculopapular rash which is not an allergy.
- Handling
- Amoxicillin is renally cleared, so the dose is reduced in significant renal impairment.
Catches people out: The old teaching that every aspiration needs anaerobic cover with metronidazole or clindamycin is out of date in Australian guidelines. Treat it as community-acquired pneumonia; reserve anaerobic cover for lung abscess, empyema or necrotising pneumonia.
Three things carry the page. First, dry mouth is usually a prescription, not a disease — count the antimuscarinic load before you reach for pilocarpine, and remember that the mouth dries at the same M3 receptor a bladder antimuscarinic is aimed at, which a tricyclic or antipsychotic blocks off-target (clozapine is the famous exception, causing drooling instead). Second, the level of dysphagia is a history question, not an imaging one: coughing within a second and pointing to the throat is oropharyngeal, food sticking seconds later behind the sternum is oesophageal. Third, no drug treats the swallow — after a stroke, the interventions that matter are a swallow screen before anything by mouth, sitting the patient upright, twice-daily mouth care, and stopping the sedatives. And a cough is not required for aspiration: a large share of stroke patients who aspirate do it silently, so the first sign is a fever and a right lower lobe on the film.
Now test whether it stuck
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