7 Retinoic Acid Signaling and the Zebrafish Dentition …
179
In contrast, enamel makes up the outer covering layer of the tooth, especially
at the points where the tooth is exposed to the environment. Unlike dentin, it is
not possible to remodel tooth enamel once it forms. Typically, ameloblasts, the cell
type that secretes enamel during development, are only present in the tooth germ
before maturation, and most of the cell layer in which they reside is lost as the
tooth matures, is exposed to the environment, and begins to be used. However, in a
continuously growing tooth like a rat incisor, part of the ameloblast cell layer persists
into adulthood. Enamel is comprised of orderly arrangements of hydroxyapatite
crystals that are much more densely mineralized than dentin and that represent one
of the hardest biological structures known (Peyer and Zangerl 1968). In addition to
contributing to their primary function, the strength and hardness of the dentin and
enamel composition of teeth, has facilitated preservation of teeth as fossils. As such,
teeth are probably the most important single anatomical structure in understanding
vertebrate evolution (Qu et al. 2015).
Pioneering Studies of RA in Odontogenesis: Consequences
of VA Deficiency
The first studies that addressed a role of VA in tooth formation were only indirectly interested in the development of the dentition, being more concerned with the
global effects of VA on mammalian physiology and tissue homeostasis. The fact
that VA-dependent effects on tooth formation were found at all probably rests on
the chance that rodents, as a primary experimental model for these studies, exhibit
a unique form of continuous tooth growth and development. Rodent incisors, which
are required for tasks such as gnawing through extremely fibrous foodstuffs, like
nut shells, and breaking down woody material for nest building, continue to form
their mineralized structures even in the adult as they are constantly being worn down
by friction (Fig. 7.2). Defects in rodent incisor growth would be expected in VAdeficient animals if RA is required for any aspect of the biological processes that
replenish mineralized tissue. Furthermore, this connection would suggest other possible roles for RA in earlier stages of tooth development, since early development
and later growth likely involve at least some overlapping cellular mechanisms.
Numerous early twentieth century studies involving VA-deficient diets failed to
report dental or skeletal abnormalities in rats and a few other species, possibly due
to difficulties in completely removing VA from the diet (e.g. Hess et al. 1921).
However, even then, there was some indication that VA might indeed be important to
tooth formation, mainly because tooth development was often observed to be more
robust in animals given a VA-rich diet (e.g. Mellanby 1921). It was not until 1925
that specific effects on continuously growing incisor tooth formation were reported
amongst the pleiotropic defects exhibited by rats fed a particular VA-deficient diet
(Wolbach and Howe 1925). The primary phenotypes observed were in the dentin and
enamel tissues, as well as in the progenitor odontoblast and ameloblast cell layers.
179
In contrast, enamel makes up the outer covering layer of the tooth, especially
at the points where the tooth is exposed to the environment. Unlike dentin, it is
not possible to remodel tooth enamel once it forms. Typically, ameloblasts, the cell
type that secretes enamel during development, are only present in the tooth germ
before maturation, and most of the cell layer in which they reside is lost as the
tooth matures, is exposed to the environment, and begins to be used. However, in a
continuously growing tooth like a rat incisor, part of the ameloblast cell layer persists
into adulthood. Enamel is comprised of orderly arrangements of hydroxyapatite
crystals that are much more densely mineralized than dentin and that represent one
of the hardest biological structures known (Peyer and Zangerl 1968). In addition to
contributing to their primary function, the strength and hardness of the dentin and
enamel composition of teeth, has facilitated preservation of teeth as fossils. As such,
teeth are probably the most important single anatomical structure in understanding
vertebrate evolution (Qu et al. 2015).
Pioneering Studies of RA in Odontogenesis: Consequences
of VA Deficiency
The first studies that addressed a role of VA in tooth formation were only indirectly interested in the development of the dentition, being more concerned with the
global effects of VA on mammalian physiology and tissue homeostasis. The fact
that VA-dependent effects on tooth formation were found at all probably rests on
the chance that rodents, as a primary experimental model for these studies, exhibit
a unique form of continuous tooth growth and development. Rodent incisors, which
are required for tasks such as gnawing through extremely fibrous foodstuffs, like
nut shells, and breaking down woody material for nest building, continue to form
their mineralized structures even in the adult as they are constantly being worn down
by friction (Fig. 7.2). Defects in rodent incisor growth would be expected in VAdeficient animals if RA is required for any aspect of the biological processes that
replenish mineralized tissue. Furthermore, this connection would suggest other possible roles for RA in earlier stages of tooth development, since early development
and later growth likely involve at least some overlapping cellular mechanisms.
Numerous early twentieth century studies involving VA-deficient diets failed to
report dental or skeletal abnormalities in rats and a few other species, possibly due
to difficulties in completely removing VA from the diet (e.g. Hess et al. 1921).
However, even then, there was some indication that VA might indeed be important to
tooth formation, mainly because tooth development was often observed to be more
robust in animals given a VA-rich diet (e.g. Mellanby 1921). It was not until 1925
that specific effects on continuously growing incisor tooth formation were reported
amongst the pleiotropic defects exhibited by rats fed a particular VA-deficient diet
(Wolbach and Howe 1925). The primary phenotypes observed were in the dentin and
enamel tissues, as well as in the progenitor odontoblast and ameloblast cell layers.