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Surfactants in Toothpastes: Effects on Oral Health
Explore the role of surfactants in toothpastes, their ability to produce foam, and their interaction with mucosa and saliva. Learn about their significance for oral hygiene and the impacts they have on overall oral health.
SCIENCE
Luigi Cellini
9/28/202610 min read
Surfactants and foam in toothpaste: what role do they really play?
We brush our teeth and expect foam to appear.
It is such a habitual association that it is easy to interpret foam as a sign of cleaning: the more foam a toothpaste produces, the more it seems to be working.
But foam and cleaning are not exactly the same thing.
Foam is, above all, a consequence of the presence of surfactants. And understanding why these substances are added to a toothpaste allows us to separate three concepts that we frequently confuse: cleaning, producing foam and generating a particular sensation during brushing.
What is a surfactant?
A surfactant is a substance capable of reducing the surface tension between different media.
In a toothpaste it facilitates the dispersion of its components, helps to loosen and keep certain residues in suspension, and encourages the product to spread throughout the mouth.
One of the surfactants most used historically in toothpastes is sodium lauryl sulphate, known by the abbreviation SLS (Sodium Lauryl Sulphate).
In addition to its detergent properties, SLS produces something immediately perceptible to the consumer:
foam.
And that foam has ended up forming part of our idea of what it means to "clean one's teeth".
Does foam clean teeth?
We should not use foam and cleaning as synonyms.
The removal of dental plaque depends to a large extent on the mechanical action of brushing. Toothpastes also incorporate various ingredients with specific functions, including abrasives, fluorides, anti-sensitivity agents and, depending on the formulation, surfactants.
But a greater amount of foam does not by itself demonstrate a greater removal of plaque.
A randomised clinical trial carried out over eight weeks compared an SLS toothpaste with an SLS-free one in 120 participants. The researchers found no statistically significant differences between the two groups in plaque indices or in gingival bleeding. [1]
They did find, however, a difference in the participants' perception:
the SLS toothpaste was rated better for taste, sensation of freshness and foaming effect.
This raises an interesting distinction.
One thing is how much a product cleans. Another is how much it makes us feel that it is cleaning
So why are surfactants used?
Because they fulfil real functions.
SLS has detergent and surfactant properties, can encourage the dispersion of the toothpaste and has activity against certain microorganisms.
It also provides abundant foam and contributes to a user experience that consumers immediately recognise as characteristic of a toothpaste.
The scientific literature also points to practical reasons for its use: foaming capacity, sensory acceptance and low cost compared with other surfactants. [2]
Therefore, the rigorous question is not: "Is SLS useless?"
It does have functions.
The more interesting question is another one:
what does it really contribute to the result of brushing, and what effects does it simultaneously produce on the tissues with which it comes into contact?
The oral mucosa is not an inert surface
A surfactant does not distinguish between the surface we want to clean and the living tissues of the mouth.
And here a lesser-known part of the scientific literature on SLS appears.
Phenomena of irritation and desquamation of the oral epithelium associated with toothpastes and hygiene products containing SLS have been described.
A systematic review on desquamation of the oral mucosa found cases associated with SLS and observed that the extent of the desquamation was related to its concentration. [3]
This does not mean that using a toothpaste with SLS necessarily causes visible lesions in all people.
It means something much more specific:
SLS is not biologically indifferent to the oral mucosa.
What happens to the mucosal barrier?
The oral mucosa constitutes a biological barrier.
Its function is not only to cover the inside of the mouth: it also regulates the interaction between our tissues and the substances present in the oral environment.
Various experimental works have studied how SLS interacts with that barrier. The scientific literature has linked its exposure, under certain conditions, to inflammation, desquamation and increased permeability of the mucosa to chemical substances. [3]
This requires an important qualification.
It does not mean that any daily use of a toothpaste with SLS automatically produces a clinically relevant alteration of the barrier.
Nor does it demonstrate that other substances present in a toothpaste necessarily cross the mucosa.
But it does demonstrate that considering a surfactant simply as an ingredient that "makes foam" describes only part of its interaction with the mouth.
Saliva is not water: it is an active biological system
When a toothpaste enters the mouth, it does not come into contact only with the teeth.
Saliva contains proteins, glycoproteins, enzymes, immunoglobulins and numerous components that participate in lubrication, protection of the mucosae, microbial balance and the first phases of digestion.
Among them are mucins, which help to form a protective film over the oral tissues, and enzymes such as salivary α-amylase, which begins the digestion of starch already in the mouth.
Therefore, any substance used during brushing temporarily comes into contact with a biochemical system that was already functioning before the toothpaste was introduced.
The relevant question is not only what an ingredient does to the tooth.
We can also ask ourselves:
what does it do to the biological medium surrounding the tooth?
Surfactants, proteins and mucins
This question is especially interesting in the case of surfactants.
SLS has a high affinity for proteins and is known for its capacity to modify their structure. In the oral medium, this property can also affect the glycoproteins that form part of the mucin layer that protects the surface of the mucosa. [4]
The scientific literature has precisely proposed the interaction of SLS with this protective layer as one of the mechanisms related to irritation and to the changes observed in the permeability of the oral mucosa. [4]
This introduces an important difference.
Mucin is not a residue that we need to eliminate.
It forms part of the natural mechanisms by which the mouth protects and lubricates its tissues.
For this reason, when we study a detergent used in oral hygiene, it is not enough to ask whether it eliminates residues or produces foam. We must also study which biological structures it interacts with while performing that function.
Can an ingredient of toothpaste interfere with the enzymes in saliva?
Yes, at least certain interactions are documented.
Interactions between surfactants and other active components of toothpaste have also been studied.
In in vitro experimental studies, the presence of SLS has reduced the uptake of fluoride by enamel in combinations with both sodium fluoride (NaF) and sodium monofluorophosphate (MFP). [5]
This result does not by itself establish the responsible mechanism, nor does it allow it to be automatically extrapolated to all commercial formulations.
This does not mean that SLS "cancels out the fluoride".
It shows something different and possibly more interesting:
the ingredients of a toothpaste do not act in isolation. They can interact with each other and also with the natural biochemical processes of the mouth.
What happens to the salivary protein film?
Teeth and the surfaces of the mouth are continuously coated by components originating from saliva.
The so-called acquired pellicle forms rapidly on enamel and contains numerous salivary proteins and glycoproteins. It does not simply constitute dirt: it participates in the interaction between enamel and the oral environment.
It has been observed experimentally that different toothpaste formulations can modify the properties of films formed by salivary proteins. [6]
After exposure to toothpaste, saliva can deposit proteins again and progressively rebuild that film. However, different combinations of detergents and fluorinated compounds can produce different behaviours.
Once again, this does not by itself demonstrate clinical harm.
But it shows why it is excessively simplistic to imagine brushing as an interaction between a product and an inert mineral surface.
The oral medium responds.
The mouth is also the beginning of the digestive system
Digestion does not begin in the stomach.
Mastication physically fragments food while saliva mixes it and certain enzymes already begin its transformation. Salivary α-amylase, for example, initiates the breakdown of starches.
For this reason it is legitimate to investigate whether the ingredients that we repeatedly introduce into the mouth can temporarily modify the activity of its enzymes.
There are experimental data on the interaction of certain surfactants with natural enzymes. For example, the effect of sodium lauroyl sarcosinate — a surfactant different from SLS — on salivary amylase and various digestive enzymes has been studied experimentally. This is, however, old experimental evidence that does not allow the conclusion that normal use of a toothpaste alters human digestion in a clinically relevant way. [7]
The difference is essential:
a demonstrated molecular interaction does not automatically equate to a relevant physiological consequence.
But nor should it be ignored.
A complete formulation, not a list of independent ingredients
All of this raises a broader problem.
When we read the composition of a toothpaste, we tend to mentally analyse each ingredient separately:
fluoride, surfactant, abrasive, humectant, preservative, flavouring...
But in the mouth they do not arrive separately.
They arrive simultaneously, within a formulation, and they encounter saliva, proteins, enzymes, microorganisms, particles, mucosae and dental surfaces.
For this reason, knowing the safety or the function of each individual ingredient is necessary, but it does not necessarily answer all the questions about the interactions between the formulation and the oral ecosystem.
And it is precisely here that it is always worth distinguishing three levels:
what we know, what we can explain by means of a plausible mechanism, and what has not yet been demonstrated.
SLS and recurrent aphthous ulcers
The relationship between SLS and recurrent aphthous stomatitis has also been studied.
A systematic review of randomised clinical trials found four crossover studies, with a total of 124 participants. Taken together, SLS-free toothpastes were associated with improvements in the studied parameters of the ulcers, although the authors noted that better-designed studies are needed to strengthen the available evidence. [8]
And the individual results help to explain why absolute conclusions should be avoided.
In a trial with 90 participants, eliminating SLS did not significantly reduce the number of ulcers or the number of episodes, but a significant reduction was observed in the duration of the ulcers and in pain during the period of use of the SLS-free toothpaste. [9]
For this reason it would be incorrect to state that:
"SLS causes aphthous ulcers."
The available evidence allows a more limited statement:
in people with recurrent aphthous stomatitis, SLS-free toothpastes may be beneficial for some parameters of the disease, although the evidence is still limited.
And the particles present in a toothpaste?
Toothpastes can contain solid materials, including different forms of silica used for their physical and abrasive properties. [10]
Here it is worth carefully separating what is known from what still constitutes a question.
The fact that a material is described as micronised does not by itself allow its entire particle size distribution to be known. Nor does it automatically allow the conclusion that it is a nanomaterial. [10]
To establish this, it would be necessary to know data such as the granulometric distribution, the size of the primary particles and their state of aggregation or agglomeration.
And then another question arises.
If certain experimental conditions show that a surfactant can modify the barrier properties of the oral mucosa, can it also modify its interaction with other particulate components present simultaneously in the formulation?
It is a scientifically legitimate question.
But it does not equate to an answer.
The evidence we have examined does not allow the assertion that the SLS used in a toothpaste causes the systemic penetration of the particles present in it.
Confusing a plausible hypothesis with a demonstrated effect would be as incorrect as ignoring the question because we do not yet know the answer.
What we know and what we still do not know
We know that surfactants fulfil technological and detergent functions.
We know that foam influences consumer perception, but does not by itself constitute a measure of cleaning efficacy. In a clinical trial, an SLS-free toothpaste obtained results comparable to the one containing SLS for plaque and gingival bleeding. [1]
We also know that SLS can interact with the oral mucosa and that there is evidence of irritation and desquamation under certain conditions. [3]
And there are clinical indications that some people with recurrent aphthous ulcers may benefit from SLS-free toothpastes. [8]
What we cannot conclude from these data is that the surfactants in toothpastes produce systemic diseases, metabolic alterations, or necessarily facilitate the entry of particles into the body.
For those assertions we would need different evidence.
The question, therefore, may not be whether a toothpaste contains "chemical" ingredients — everything around us is chemistry — but how much we really know about the interactions between those ingredients and a biological medium as complex as the mouth.
A simple question
For decades we have learned to associate a mouth full of foam with a clean mouth.
Chemistry explains why that foam appears.
Research allows us to study what the ingredient that produces it actually does.
And when we distinguish one thing from the other, a much simpler question remains:
how much of the foam we expect when brushing responds to a need of our mouth, and how much responds to what we have learned to expect from a toothpaste?
Scientific references
[1] Hamza B. et al. The effectiveness of dentifrices without and with sodium lauryl sulfate on plaque, gingivitis and gingival abrasion—a randomized clinical trial. Clinical Oral Investigations (2016).
[2] American Dental Association. Toothpastes — detergents such as SLS and sodium N-lauryl sarcosinate are used for foaming and may increase solubility of plaque/accretions during brushing.
[3] González-Moles MÁ et al. Oral mucosal peeling related to dentifrices and mouthwashes: A systematic review. Medicina Oral, Patología Oral y Cirugía Bucal (2019).
[4] Lippert F. An introduction to toothpaste — its purpose, history and ingredients. Formulation ingredients for toothpastes and mouthwashes (review).
[5] Barkvoll P. Effect of sodium lauryl sulfate on the uptake of fluoride from NaF and MFP by etched enamel in vitro. J Biol Buccale (1991);19(3):235–239. PMID 1939046.
[6] Veeregowda DH, van der Mei HC, Busscher HJ, Sharma PK. Influence of fluoride-detergent combinations on the visco-elasticity of adsorbed salivary protein films. Eur J Oral Sci (2011);119(1):21–26. DOI 10.1111/j.1600-0722.2010.00798.x.
[7] Bauer CW, La Sala EF. The Effect of Sodium N-Lauroyl Sarcosinate and of Sodium Dehydroacetate on the Enzymes of the Gastrointestinal Tract. J Am Pharm Assoc (1956);45(10):675–678. DOI 10.1002/jps.3030451007.
[8] Alli BY, Erinoso OA, Olawuyi AB. Effect of sodium lauryl sulfate on recurrent aphthous stomatitis: A systematic review. J Oral Pathol Med (2019);48(5):358–364. DOI 10.1111/jop.12845.
[9] Shim YJ, Choi J-H, Ahn H-J, Kwon J-S. Effect of sodium lauryl sulfate on recurrent aphthous stomatitis: a randomized controlled clinical trial. Oral Dis (2012). PMID 22435470.
[10] Hamza B. et al. Toothpaste Abrasion and Abrasive Particle Content: Correlating High-Resolution Profilometric Analysis with Relative Dentin Abrasivity (RDA). Dent J (Basel) (2023);11(3):79. DOI 10.3390/dj11030079.
Review note: the references have been added to the main scientific claims. The SLS–fluoride passage has been restricted to what the in vitro study directly demonstrates; the passage on enzymes now specifies that the study concerns sodium lauroyl sarcosinate, not SLS.
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