The book may actually be correct and Mayo (surprisingly) rather wrong here. According to a 2020 review:
Several published reviews have concluded that milk is of
very low cariogenicity and may have some caries protective
potential. For example, WHO reviewed the strength
of the evidence in 2003 and concluded that a “decreased
risk” of dental caries from milk was “possible.” The evidence
comes from several types of study: epidemiological
studies (interventional and observational), animal experiments,
plaque pH studies, and in vivo and in vitro
enamel and dentine slab experiments. More recent observational
epidemiological studies have adjusted for potential
confounders and have reported that milk consumption
is associated with lower caries experience or
incidence. Other types of study generally support this
conclusion. Reasons for these favourable caries-related
properties include the lower acidogenicity of lactose
compared with other dietary sugars and the protective
effects of calcium, phosphate, proteins, and fats.
The most detailed controlled studies were alas done in (deslivated) rodents or in vitro on enamel slabs...
A severe
test of the cariogenic or cariostatic properties of
milk was developed by Bowen et al. [68, 69], using
desalivated rats which are therefore much more
caries-susceptible. In these experiments, the rats
given milk or lactose-reduced milk remained essentially
caries-free, while those given sucrose or
lactose in water developed caries. The authors
concluded “that (cow’s) milk does not promote
caries, even in the highly caries-conducive environment
engendered,” and “that milk or lactosereduced
milk can be used safely by hyposalivatory
patients as a saliva substitute.” Peres et al. [70]
and Bowen and Lawrence [71], also using desalivated
rats, concluded that “cow’s milk was not
cariogenic” and “cow’s milk is essentially noncariogenic”,
respectively.
Caution is always needed when extrapolating
the findings of animal experiments to the human
situation, and this is important when dietary
phosphate is thought to play a caries-preventive
role [3, 72] as is the case with milk. Although
some caution is advisable, the results of the above
numerous animal experiments give considerable
weight to the evidence that bovine milk is noncariogenic
and may be anti-cariogenic.
Several studies, in human volunteers, have
shown that the fall in plaque pH after drinking
milk is negligible compared with the fall in pH
after drinking solutions of sucrose or lactose, and
that the falls for lactose were smaller than for sucrose
[73–80]. While plaque pH studies are a useful
guide to the fermentability of sugars in foods,
such experiments do not consider the presence
and effect of substances in foods which may protect
against dental caries, such as, for example,
calcium, phosphate and casein in milk.
Artificial caries-like lesions can be induced in
small slabs of enamel by exposing their surface to
acid buffers or by covering the slab with a biofilm
which is then challenged with a variety of substrates.
This method has been used both in the
laboratory (in vitro) and in the mouth (in vivo),
where they are held by a purpose-built intra-oral
appliance, to examine the ability of foods to demineralize
or remineralize tooth enamel. The early
experiments of Weiss and Bibby [81] and Bibby
et al. [82] examined the in vitro effect of bovine
milk (raw, pasteurized, whole or skimmed) and
found that all the milks “reduced the solubility of
enamel,” while similar results were obtained by
Thomson et al. [83–85] using an enamel slab intra-
oral device. Jensen et al. [86], using a similar
system, showed that milk (with 3 levels of fat content)
was not cariogenic for enamel or dentine.
Gedalia et al. [87] and Walker et al. [88, 89] reported
that milk remineralized previously demineralized
enamel slabs in vivo.
In addition to the plaque pH studies mentioned
above, Jenkins and Ferguson [73] conducted
in vitro comparisons of 4% lactose solutions
and cow’s milk. They concluded that, within
the limits of their experiments, their results “gave
no grounds for suggesting that milk has a local effect
on the teeth which would favour caries,” and
suggested that the negligible fall in plaque pH was
partly due to milk’s high buffering power and that
the low level of dissolution of test enamel was due
to the protective action of milk’s high levels of calcium
and phosphate. Rugg-Gunn et al. [77] also
reported that both cow’s milk and human milk
protected enamel from dissolution in in vitro experiments,
compared with sucrose or lactose, but
that human milk was less protective than cow’s
milk, as would be expected from their different
calcium and phosphorus contents.
Eight further in vitro studies have investigated
the caries inducing or caries preventive effect of milk and showed that (a) demineralization of
enamel was reduced by intermittent exposure to
milk [90, 91, 92], and (b) that milk aided the remineralization
of demineralized enamel [90, 93].
Ivancakova et al. [94] and Arnold et al. [95] reported
that milk reduced the rate of root caries
progression.
Not all in vitro studies have suggested that
milk resists demineralization or encourages remineralization.
Prabhakar et al. [96] incubated
enamel slabs with human or bovine milk in vitro
and concluded that plain bovine milk was relatively
cariogenic in the absence of saliva. Likewise,
Muñoz-Sandoval et al. [97] and Giacaman
and Muñoz-Sandoval [98] report that bovine
milk caused demineralization of enamel and dentine
slabs and concluded that “Whole milk… may
be less cariogenic than sucrose but not anticariogenic.”
These differences may be explained by differences
in experimental methods. While the
studies discussed in the previous paragraph used
cell-free demineralization, the 3 studies discussed
in this paragraph used active biofilms, for example,
of Streptococcus mutans, which might result
in a greater challenge.
Although there is no total agreement in the
conclusion drawn, both in vitro and in vivo
enamel slab experiments suggest that bovine milk
has little ability to cause demineralization and, indeed,
is capable of remineralizing previously demineralized
enamel. The calcium, phosphate and
casein components would appear to be crucial determinants
of these favourable properties of bovine
milk.
And an older (2002) review that was mainly focused on mechanisms, but which is open access says in its abstract:
The mechanisms involve several milk components and effects. Caseins and peptides thereof, i.e. casein glycomacropeptide (CGMP) and casein phosphopeptide (CPP), reduce the adhesion of cariogenic mutans streptococci in situ and seem to reduce colonization in the rat. They block adhesion in solution
(clearance), as well as when bound to tooth surfaces. CGMP binds to the tooth as micelle-like structures, which do not bind bacteria. CPP binds as minor complexes with calcium and phosphate, buffering calcium
and phosphate when hydroxyapatite solubility increases by decreasing pH, and possibly explaining the acid-buffering effect from milk and cheese. Further, peptides in the whey fraction, i.e. proteose-peptones, provide protection against tooth tissue demineralization, and other milk peptides, such as kappacin (a k-casein-derived peptide), lactoferrin, lactoperoxidase and lysozyme, possess innate immunity-like functions. Using milk components as a caries-prophylactic measure has not been studied in humans, but
epidemiological studies conrm associations between milk:cheese intake and protection against caries. However, the impact of possible confounders cannot yet be fully evaluated.
Similar 2004 article.
