Mind & body, in brief

Treating without cutting

A protein coating grew new crystals on eroded human teeth and took their hardness from 1.1 back to 3.1 gigapascals. [1] Silver fluoride painted on children's first adult molars left 88.1% of them with no visible decay after six months. [10] Antibiotics let 73% of appendicitis patients avoid an operation in the first year. [11]

Gum trouble reaching the heart

Treating gum disease lowered the upper blood pressure number by about 4.6 points across randomised trials. [12] Across 17 studies covering 146,001 people, those with gum disease had 84% higher odds of a heart attack. [13] A review by the American Heart Association, a US doctors' body, found no link with heart events at all. [14]

Protection that wears off

The World Health Organization found two applications of fluoride varnish a year beat one, and silver fluoride is usually painted on twice a year too. [15] In a meta-analysis of 4,784 children, the largest reduction, 54%, came where varnish was applied quarterly. [7] Most people never put on or renew enough sunscreen to get the protection printed on the bottle. [16]

Labels ahead of the tests

Sixteen of 20 Australian sunscreens sold as SPF 50 or above came in below their label. [9] Fewer than 2% of the extra ingredients added to sunscreens have been tested in people, and only 18 are approved. [16] A fluoride-free toothpaste sold on rebuilding enamel matched an ordinary fluoride paste over 27 months in 1,063 children, with no untreated group in the trial at all. [17]

One pressure seen across the day runs through Mind & body too.

• Proof that measures something elseBuilding ↑ · seen in 2 beats→

1. 1Your enamel has no living cells, so it cannot heal a hole - but before the hole it can be rebuilt from the outside
2. 2Fluoride makes a tougher mineral, not new tissue
3. 3Hydroxyapatite pastes matched fluoride in a dish
4. 4Two minerals together beat either alone
5. 5A peptide that gets under the surface

Tooth enamel is the hardest and most mineralised tissue in the body, and it cannot regenerate, because there is nothing living inside it to do the rebuilding. [1]

No one has yet tested the coating on a tooth inside a living mouth.

Every result so far comes from extracted human teeth in a laboratory, and the team says it hopes for a first product within about a year. [1][6]

Ordinary enamel is hydroxyapatite, which starts dissolving when the liquid around it falls to about pH 5.5.

When fluoride is present, some of it swaps into the crystal and makes fluorapatite, which holds out until about pH 4.5. [5]

Fluoride also slows the bacteria down: inside them it blocks enolase, an enzyme they need to make energy and acid. [5]

So fluoride works from outside the tooth, on the mineral and on the microbes, never on any living part of the tooth. [2]

It explains why fluoride is painted on rather than taken as a course, and why stopping it moves the balance straight back.

Researchers made early decay on 105 blocks of cattle enamel by feeding a bacterial model 10% sucrose three times a day for four days.

They then brushed the blocks with pastes containing natural hydroxyapatite, synthetic hydroxyapatite or fluoride.

Mineral recovery was 29.2% for the natural hydroxyapatite paste and 27.1% for fluoride, against 9.6% for artificial saliva alone. [18] These are blocks in a rig, not teeth in children.

Fluoride-free pastes are sold on exactly this comparison, and the comparison has so far been made outside the mouth.

A second laboratory study put cattle enamel through 14 days of acid and recovery cycles with four toothpastes.

A paste holding both calcium hypophosphite and hydroxyapatite restored 89.7% of the lost hardness. Calcium hypophosphite alone managed 75.4%, hydroxyapatite alone 62.4% and standard 1,450 ppm fluoride 60.3%. [19]

Each group improved from its own starting point; the differences are between the groups.

It points at combinations rather than single ingredients, and at the same time shows how far these results still are from a child's mouth.

A white spot on a tooth is decay that has taken mineral from beneath a surface that is still unbroken.

A self-assembling peptide called P11-4 is designed to soak into that space and give new crystal somewhere to form.

A review of seven controlled clinical studies found P11-4 did better than fluoride on subsurface repair in every one, with laser readings of lesion depth falling by 23% to 41%. [20]

The studies were small and mostly in people wearing braces.

This is one of the few places where the new materials have been compared in actual patients rather than in extracted teeth.

A double-blind trial enrolled 1,063 children aged three and four from 12 kindergartens in Hubei province, China.

Half were given a fluoride-free toothpaste containing 7.5% bioactive glass; half got a normal paste with 800 parts per million of fluoride.

After 27 months there was no significant difference in how much new decay appeared, and the same was true at 12 months. [17] There was no group using nothing.

A tie can mean both worked or neither did, and without an untreated arm the trial cannot tell those apart.

A clinical study followed white spots on children's primary teeth for a year, checking them by eye and with a laser fluorescence meter at three, six, nine and twelve months.

An intensive protocol using Curodont Repair Fluoride Plus had 6.5 times the odds of arresting decay compared with a standard Duraphat varnish, and nearly 20 times the odds of turning active lesions inactive. [21]

A third product, MI varnish, was no better than Duraphat.

It is one of the clearer patient results in this field, and it still measures lesions rather than teeth saved.

Fixed braces trap plaque where a brush cannot easily reach, and white spots are the common result.

A review of human trials found that after six months, 9.5% of teeth developed a white spot among people using a nanosilver mouthwash, against 24.4% for both fluoride and chlorhexidine rinses. [22]

The upper right lateral incisor was the worst-affected tooth, at 38.1%.

Orthodontic patients are the group where prevention and damage run on the same two-year clock.

Erosion is the chemical loss of tooth surface to acid that never passed through a microbe, and it is common: roughly 30% to 50% of children and 20% to 40% of adults. [4]

The acid comes from fizzy drinks, fruit juice and energy drinks, or from stomach contents in reflux. [4]

In one laboratory comparison, carbonated drinks roughened enamel the most, and brushing straight after an acid exposure made the loss worse. [23]

It is a separate route to the same damage, and it does not respond to anything aimed at bacteria.

Researchers took 80 baby second molars and 80 adult premolars and soaked them for 72 hours in gastric acid at pH 1.2 or in kefir at pH 4.5.

They then treated the samples with three commercial repair agents for 14 days, with artificial saliva alone as the control. [24]

Reflux disease, which sends stomach contents back up the gullet, affects an estimated 10% to 30% of people worldwide. [24]

It sets the size of the problem for anyone whose acid comes from inside rather than from a bottle.

A blinded trial randomised 165 children aged six to twelve by school.

One group had 38% silver diamine fluoride with potassium iodide painted on early decay in their first adult molars; the other had a 5% fluoride varnish.

After six months, 88.1% of the silver-treated teeth scored as sound, against 65.6% of the varnish ones. [10] How far the molar had erupted made no difference either way.

Silver fluoride stains the treated spot black, which is why it is used most where a filling is not available.

Enamel has no living cells, so nothing inside the tooth rebuilds it; the minerals come from the saliva and paste outside.

The calcium and phosphate come from the saliva and the toothpaste outside, because nothing inside the tooth can supply them.

the tooth does nothing; a liquid is painted on the surface, and it has to be painted on again about every six months

skin can repair its own DNA and cannot keep up, so the protection that worked was a layer applied on top and renewed daily

nothing is removed and the conditions inside are changed instead, and the same repeat-it problem shows up as 44.3% coming back for the operation

the work is done on the outside of a tooth root and the change appears in a blood vessel, which is the same outside-in route

Once it caves in and leaves a hole, no amount of mineral in the saliva puts it back, and the tooth needs a filling.

What happened in between was thousands of small swings in one direction and then the other, and nobody watched any of them, including the person the tooth belongs to.

An updated review pooled randomised trials comparing silver diamine fluoride with plain sodium fluoride in children under six.

Silver had higher odds of stopping a lesion, at 1.41, but no measurable advantage on the count of decayed, missing and filled surfaces. [25]

Untreated decay in baby teeth affected about 532 million children in 2017, the tenth most common condition in the world. [25]

Stopping a lesion that already exists and preventing the next one are two different jobs. Silver did better on the first and no better on the second.

A meta-analysis screened 2,315 records and analysed 13 randomised trials covering 4,784 participants. Fluoride varnish cut decay across the pooled group.

The largest effect was in younger children and in those with a dry mouth, where quarterly applications were associated with a 54% reduction and unwanted effects stayed below 5%. [7]

Variation between the trials was high, which the authors put down to inconsistent application protocols. [7]

The dose here is a schedule, not a quantity, and the benefit is counted per visit.

The World Health Organization's guidance on mercury-free dental products reviewed ten systematic reviews of fluoride varnish.

It reports that twice a year beat once a year for preventing early childhood decay, with a mean caries increment 3.57 surfaces lower after a year in one study. [15]

It found no treatment-related adverse events in the varnish trials, though few of them collected that information. [15] Varnish is on the agency's model list of essential medicines. [15]

Being on that list is what makes a treatment something health ministries are expected to stock rather than something patients buy.

An economic model followed Brazilian preschoolers over four years in six-month cycles.

Adding fluoride varnish to standard care prevented cavities in four children out of every 100, at an average cost of 33 Brazilian reais a child a year. [26]

The full incremental cost came to R$6,929 per cavitated lesion prevented. [26] The model assumed each child who developed decay developed only one lesion.

It is the number a health ministry actually decides on, and it is a different number from the trial result.

A review of 14 randomised trials across different countries and income levels pooled data from more than 13,000 children given fluoride varnish.

Its background section sets the scale: decay affects around 40% of seven-year-olds and about 85% of people by the age of 17. [27]

The review cites reductions of roughly 37% in baby teeth and 47% in adult teeth. [27]

Decay reaches almost everyone, so the practical argument is about getting varnish to children rather than about finding a new treatment.

Streptococcus mutans lives on tooth surfaces and ferments dietary sugar into lactic acid.

It also builds sticky sugar chains called glucans that glue it to enamel and hold the film together, and it can keep working at a low pH that silences its neighbours. [5][28]

Sucrose matters most, because the glue is made from it. [28] A healthy film contains species that buffer acid instead of making it. [29]

The film is not a dirt layer to be scrubbed off but a community, and which members dominate it is decided partly by what arrives.

Researchers built a test platform to measure how cariogenic a sugar is, then compared allulose, a rare sugar used as a sweetener, against sucrose.

Habitual refined sugar reduces the variety of microbes in the mouth and favours the acid-makers. [28] Allulose did not support the same biofilm growth. [28]

The work was done in a laboratory model of the mouth, not in people.

Sugar substitutes are usually sold on calories; this is the other thing they change.

Stevioside, the sweet compound from the stevia plant, was tested against Streptococcus mutans.

The bacterium builds its film using an enzyme, glucosyltransferase, that turns sucrose into glue, and it defends itself against acid with a tolerance response. [30]

The extract interfered with biofilm formation and with those virulence traits. [30] Non-sugar sweeteners are being looked at for this second job rather than for sweetness.

If a sweetener cannot be turned into glue, the film has less to hold on with.

Sialyllactose is one of the complex sugars in human milk that babies cannot digest.

Researchers grew Streptococcus mutans and mixed streptococcal species in the laboratory and tested those milk sugars and a fragment of them against biofilm formation. [31]

The mouth holds more than 700 bacterial species and about 100 million to a billion cells in every millilitre of saliva. [31]

Inside a film, bacteria are shielded from antibacterial agents and from immune cells. [31]

It is one reason the film is hard to treat once formed, and why the work keeps returning to stopping it forming.

Forensic scientists sampled 50 bodies aged from newborn to 94 and looked for Streptococcus mutans along the gut.

They found it in the mouth in 14 cases, 28%, in the gullet in three, in the stomach in one, in the small intestine in one and in the large intestine in four, 8%. [32]

Oral bacteria are swallowed constantly with saliva and food. [32] The study reports where the organism was, not what it did there.

Finding a bacterium somewhere does not show it does anything there. Most claims linking mouth microbes to the rest of the body still rest on where organisms were found.

The mouth's microbes divide the territory: some prefer tooth surfaces, some the tongue, some the pocket between tooth and gum. [33]

Helpful species such as Veillonella, Actinomyces and Neisseria can crowd out the harmful ones, and some produce their own antibacterial proteins. [33]

A systematic review of 22 studies, eight of them randomised trials, found diet is a major determinant of which species dominate. [34]

More than 80% of Americans have had a cavity by their mid-thirties. [33]

The tooth surface is the one part of the body where the resident population and the mineral balance are the same story.

A meta-analysis of randomised trials measured what happens elsewhere in the body after gum disease is treated.

Systolic blood pressure fell by an average of 4.64 millimetres of mercury and diastolic by 1.84.

C-reactive protein, a general marker of inflammation in the blood, fell by 0.58 milligrams per litre. [12] The treatment is mechanical cleaning of the tooth root below the gum line.

The change is made on a tooth surface and shows up in a blood vessel, which is what makes this a whole-body finding rather than a dental one.

A meta-analysis pooled 17 studies covering 146,001 participants and 3,199 heart attacks. People with periodontitis had 84% higher odds of a heart attack, an odds ratio of 1.84. [13]

Publication bias was detected; correcting for it brought the figure down to 1.26, still above one. [13]

Bleeding when the gum is probed carried an odds ratio of 2.90 on its own. [13]

The authors' own correction moves the number a long way, which is the honest size of what is known.

A separate review pooled long-running cohorts with follow-up between 5.4 and 13 years and mean ages from 43 to 65.

Gum disease was associated with a 58% higher risk of heart failure, a crude relative risk of 1.58. [35]

Heart failure affects about 1% to 2% of people and more than 10% of those over 70. [35]

The proposed route is bacteria and inflammatory signals entering the bloodstream from the gum. [35]

It is the same suspected mechanism as the heart attack finding, measured on a different outcome.

A review of cohort studies found gum disease associated with irregular heart rhythm, with adjusted hazard ratios from 1.03 to 1.31. Severe disease carried the top of that range. [36]

In people whose gum disease had recovered, the extra risk disappeared, with a hazard ratio of 1.00. [36]

Gum disease affected about 951 million people in 2021 and accounted for 6.2 million years of healthy life lost. [36]

The extra risk disappeared in people whose gum disease had cleared up. That is as close to a test as an observational study gets.

Meta-analyses of epidemiological work put the extra relative risk of a cardiovascular event at between 12% and 59% after adjusting for the usual risk factors. [14]

A review by the American Heart Association, a US doctors' body, found no association between gum disease and cardiovascular events. [14]

The authors state plainly that there is no conclusive evidence either way on whether gum disease is an independent risk factor. [14]

More than 40% of adults over 30 in the United States have gum disease. [37]

Two sets of experts read the same studies and came to opposite conclusions. Nobody has run the trial that would settle it.

Porphyromonas gingivalis is the organism treated as the keystone of chronic gum disease, because it tips the whole microbial community out of balance. [38]

Its outer coat contains lipopolysaccharide, which can enter the bloodstream, bind receptors on the cells lining brain blood vessels and make that barrier leakier. [38]

Chronically raised inflammatory signals are proposed as the route to nerve damage in older people. [38] This is a proposed mechanism, not a demonstrated cause.

It is the same inflammation argument as the heart work, aimed at a different organ and standing on weaker evidence.

A clinical review screened studies and kept 110 covering diabetes, gum disease and heart disease together.

High blood sugar produces advanced glycation end-products, which bind receptors on immune cells and raise inflammatory signalling. [39]

People with poorly controlled diabetes have more and worse gum disease, and people with gum disease tend to have worse blood sugar control. [39]

Treating the gums produced modest gains in blood sugar control. [39]

High blood sugar makes gum disease worse, and gum disease makes blood sugar harder to control. Each one keeps feeding the other.

The APPAC trial in Finland randomised adults with appendicitis confirmed on a scan to surgery or to antibiotics, and has now reported ten-year results.

Of 257 patients given antibiotics, 253 were still being followed. Appendicitis came back, confirmed on tissue, in 37.8% of them, and 44.3% had had the appendix removed by ten years. [8]

The treatment was three days of intravenous ertapenem then a week of tablets. [8]

It is the longest randomised follow-up available on treating an organ rather than removing it, and the recurrence keeps accumulating.

In APPAC's first year, 73% of patients with scan-confirmed uncomplicated appendicitis avoided an operation on antibiotics alone. [11]

By five years the cumulative operation rate was 39.1%, with no rise in burst appendixes or serious complications among those who went on to surgery. [11]

Complications overall were lower in the antibiotic group, 6.5% against 24.4% in the surgical group. [11]

The trade is fewer complications now against a running chance of the operation later, and the trial reports both halves.

A network meta-analysis compared surgery, antibiotics and a newer keyhole technique that clears the appendix from the inside through a colonoscope.

On complications the endoscopic route came out best and surgery worst. On recurrence surgery came out best and antibiotics worst, with an odds ratio of 0.06 for surgery against antibiotics. [40]

A separate review of ten studies in 1,372 children found no significant difference in recurrence between the endoscopic route and the comparison groups. [41]

Each option wins on a different measure, so the choice depends on which failure a patient and a surgeon mind most.

A meta-analysis of six randomised trials covering 2,101 adults found 34% of antibiotic-treated patients needed an operation within a year, and a quarter of those turned out to have complicated appendicitis. [42]

Patients with an appendicolith, a hardened lump blocking the appendix, did much worse: 49% needed surgery, with significantly higher complication rates. [42]

It is the closest thing in this cluster to a rule for who the antibiotic route suits.

A single hospital reviewed every patient diagnosed with uncomplicated appendicitis between 2020 and 2022 who was discharged from the emergency department on oral antibiotics with no admission.

Of 99 patients, 76% were still free of surgery at one year, and 70% at a median follow-up of 34 months. [43]

Four in five of the operations that did happen came within the first ten months. [43] A separate cohort followed for a mean of 64 months reported a 95.7% success rate. [44]

The two cohorts disagree by a wide margin, and neither was randomised.

The US Food and Drug Administration has approved bemotrizinol, the first new active sunscreen ingredient cleared there in more than 25 years.

It was first proposed more than 20 years ago.

The United States regulates sunscreen as an over-the-counter drug, while the European Union treats it as a cosmetic, which is why filters available elsewhere have not been sold there. [9]

What kept those filters out was the legal category sunscreen sits in, not a finding about the filters themselves. It decides which bottles reach which shelves.