Question: How does cheese protect tooth enamel?
About the article "Cheese", section "Dental health".

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Some studies claim that cheddar, mozzarella, Swiss and American cheeses can help to prevent tooth decay.
Several mechanisms for this protection have been proposed:
 The calcium, protein, and phosphorus in cheese may act to protect tooth enamel.
 Cheese increases saliva flow, washing away acids and sugars.
The bell stage is known for the histodifferentiation and morphodifferentiation that takes place.
The dental organ is bell-shaped during this stage, and the majority of its cells are called stellate reticulum because of their star-shaped appearance.
The bell stage is divided into the "early bell stage" and the "late bell stage".
Cells on the periphery of the enamel organ separate into four important layers.
Cuboidal cells on the periphery of the dental organ are known as outer enamel epithelium (OEE).
The columnar cells of the enamel organ adjacent to the enamel papilla are known as inner enamel epithelium (IEE).
The cells between the IEE and the stellate reticulum form a layer known as the stratum intermedium.
The rim of the enamel organ where the outer and inner enamel epithelium join is called the "cervical loop".
In summary, the layers in order of innermost to outermost consist of dentin, enamel (formed by IEE, or 'ameloblasts', as they move outwards/upwards), inner enamel epithelium and stratum intermedium (stratified cells that support the synthetic activity of the inner enamel epithelium) What follows is part of the initial 'enamel organ', the center of which is made up of stellate reticulum cells that serve to protect the enamel organ.
This is all encased by the OEE layer.
Other events occur during the bell stage.
The dental lamina disintegrates, leaving the developing teeth completely separated from the epithelium of the oral cavity; the two will not join again until the final eruption of the tooth into the mouth.
The crown of the tooth, which is influenced by the shape of the inner enamel epithelium, also takes shape during this stage.
Throughout the mouth, all teeth undergo this same process; it is still uncertain why teeth form various crown shapes—for instance, incisors versus canines.
There are two dominant hypotheses.
The "field model" proposes there are components for each type of tooth shape found in the ectomesenchyme during tooth development.
The components for particular types of teeth, such as incisors, are localized in one area and dissipate rapidly in different parts of the mouth.
Thus, for example, the "incisor field" has factors that develop teeth into incisor shape, and this field is concentrated in the central incisor area, but decreases rapidly in the canine area.
The other dominant hypothesis, the "clone model", proposes that the epithelium programs a group of ectomesenchymal cells to generate teeth of particular shapes.
This group of cells, called a clone, coaxes the dental lamina into tooth development, causing a tooth bud to form.
Growth of the dental lamina continues in an area called the "progress zone".
Once the progress zone travels a certain distance from the first tooth bud, a second tooth bud will start to develop.
These two models are not necessarily mutually exclusive, nor does widely accepted dental science consider them to be so: it is postulated that both models influence tooth development at different times.
Other structures that may appear in a developing tooth in this stage are enamel knots, enamel cords, and enamel niche. 
The microstructure of the enamel of VPL/JU/NKIM/25 has been studied.
Unlike other gondwanatheres, it has enamel consisting of three layers—radial enamel, tangential enamel, and PLEX.
The rows of small, round enamel prisms are separated by interprismatic matrix that forms crystalls oriented at right angles relative to the prisms.
Prisms arise at the enamel-dentine junction, run through the enamel, and meet the outer enamel at a high angle.
These features of the enamel are apparently adaptations that protect the tooth from cracks. 
Alteration during tooth development.
Tooth abnormalities caused by environmental factors during tooth development have long-lasting effects.
Enamel and dentin do not regenerate after they mineralize initially.
Enamel hypoplasia is a condition in which the amount of enamel formed is inadequate.
This results either in pits and grooves in areas of the tooth or in widespread absence of enamel.
Diffuse opacities of enamel does not affect the amount of enamel but changes its appearance.
Affected enamel has a different translucency than the rest of the tooth.
Demarcated opacities of enamel have sharp boundaries where the translucency decreases and manifest a white, cream, yellow, or brown color.
All these may be caused by a systemic event, such as an exanthematous fever.
Turner's hypoplasia is a portion of missing or diminished enamel on a permanent tooth usually from a prior infection of a nearby primary tooth.
Hypoplasia may also result from antineoplastic therapy.
Dental fluorosis is condition which results from ingesting excessive amounts of fluoride and leads to teeth which are spotted, yellow, brown, black or sometimes pitted.
Enamel hypoplasia resulting from syphilis is frequently referred to as Hutchinson's teeth, which is considered one part of Hutchinson's triad. 
The high mineral content of enamel, which makes this tissue the hardest in the human body, also makes it susceptible to a demineralization process which often occurs as dental caries, otherwise known as cavities.
Demineralization occurs for several reasons, but the most important cause of tooth decay is the ingestion of fermentable carbohydrates.
Tooth cavities are caused when acids dissolve tooth enamel: :Ca10(PO4)6(OH)2("s") + 8H+("aq") → 10Ca2+("aq") + 6HPO42-("aq") + 2H2O("l") Sugars from candies, soft drinks, and fruit juices play a significant role in tooth decay, and consequently in enamel destruction.
The mouth contains a great number and variety of bacteria, and when sucrose, the most common of sugars, coats the surface of the mouth, some intraoral bacteria interact with it and form lactic acid, which decreases the pH in the mouth.
Then, the hydroxyapatite crystals of enamel demineralize, allowing for greater bacterial invasion deeper into the tooth.
The most important bacterium involved with tooth decay is "Streptococcus mutans", but the number and type of bacteria varies with the progress of tooth destruction.
Furthermore, tooth morphology dictates that the most common site for the initiation of dental caries is in the deep grooves, pits, and fissures of enamel.
This is expected because these locations are impossible to reach with a toothbrush and allow for bacteria to reside there.
When demineralization of enamel occurs, a dentist can use a sharp instrument, such as a dental explorer, and "feel a stick" at the location of the decay.
As enamel continues to become less mineralized and is unable to prevent the encroachment of bacteria, the underlying dentin becomes affected as well.
When dentin, which normally supports enamel, is destroyed by a physiologic condition or by decay, enamel is unable to compensate for its brittleness and breaks away from the tooth easily.
The extent to which tooth decay is likely, known as cariogenicity, depends on factors such as how long the sugar remains in the mouth.
Contrary to common belief, it is not the amount of sugar ingested but the frequency of sugar ingestion that is the most important factor in the causation of tooth decay.
When the pH in the mouth initially decreases from the ingestion of sugars, the enamel is demineralized and left vulnerable for about 30 minutes.
Eating a greater quantity of sugar in one sitting does not increase the time of demineralization.
Similarly, eating a lesser quantity of sugar in one sitting does not decrease the time of demineralization.
Thus, eating a great quantity of sugar at one time in the day is less detrimental than is a very small quantity ingested in many intervals throughout the day.
For example, in terms of oral health, it is better to eat a single dessert at dinner time than to snack on a bag of candy throughout the day.
In addition to bacterial invasion, enamel is also susceptible to other destructive forces.
Bruxism, also known as clenching of or grinding on teeth, destroys enamel very quickly.
The wear rate of enamel, called attrition, is 8 micrometers a year from normal factors.
A common misconception is that enamel wears away mostly from chewing, but actually teeth rarely touch during chewing.
Furthermore, normal tooth contact is compensated physiologically by the periodontal ligaments (pdl) and the arrangement of dental occlusion.
The truly destructive forces are the parafunctional movements, as found in bruxism, which can cause irreversible damage to the enamel.
Other nonbacterial processes of enamel destruction include abrasion (involving foreign elements, such as toothbrushes), erosion (involving chemical processes, such as dissolving by soft drinks or lemon and other juices), and possibly abfraction (involving compressive and tensile forces).
Though enamel is described as tough, it has a similar brittleness to glass making it, unlike other natural crack-resistant laminate structures such as shell and nacre, potentially vulnerable to fracture.
In spite of this it can withstand bite forces as high as 1,000 N many times a day during chewing.
This resistance is due in part to the microstructure of enamel which contains processes, enamel tufts, that stabilize the growth of such fractures at the dentinoenamel junction.
The configuration of the tooth also acts to reduce the tensile stresses that cause fractures during biting.
Gastroesophageal reflux disease can also lead to enamel loss, as acid refluxes up the esophagus and into the mouth, occurring most during overnight sleep.