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Ebook PDF Ten Cates Oral Histology Development Structure and Function 9Th Edition Ebook PDF Version Full Chapter
Ebook PDF Ten Cates Oral Histology Development Structure and Function 9Th Edition Ebook PDF Version Full Chapter
CHAPTER OUTLINE
The Tooth, 1 Hard Tissue Formation, 6
Enamel, 1 The Organic Matrix in Hard Tissues, 6
Dentin, 1 Mineral, 6
Pulp, 2 Mineralization, 6
Supporting Tissues of the Tooth, 3 Crystal Growth, 8
Periodontal Ligament, 3 Alkaline Phosphatase, 8
Cementum, 3 Transport of Mineral Ions to Mineralization Sites, 9
Oral Mucosa, 3 Hard Tissue Degradation, 10
Salivary Glands, 4 Summary, 10
Bones of the Jaw, 5
Temporomandibular Joint, 5
This chapter presents an overview of the histology of the tooth and its Anatomically the tooth consists of a crown and a root (see Figures
supporting tissues (Figure 1-1), and the salivary glands, the bones of 1-1 and 1-2); the junction between the two is the cervical margin. The
the jaw, and the articulations between the jaws (temporomandibular term clinical crown denotes that part of the tooth that is visible in the
joints) as a basis for subsequent detailed consideration. oral cavity. Although teeth vary considerably in shape and size (e.g., an
incisor compared with a molar), histologically they are similar.
THE TOOTH Enamel
Teeth constitute approximately 20% of the surface area of the mouth, Enamel is an eccentric hard tissue because of its origin, chemically
the upper teeth significantly more than the lower teeth. Mastication is distinct nature of the various noncollagenous matrix proteins expressed
the function most commonly associated with the human dentition, but by ameloblasts, and its large mineral crystals. Enamel has evolved as
teeth also are essential for proper speech. In the animal kingdom, teeth an epithelially derived protective covering for the crown of the teeth
have important roles as weapons of attack and defense. Teeth must be (see Figures 1-1 and 1-2). The enamel is the most highly mineralized
hard and firmly attached to the bones of the jaws to fulfill most of these tissue in the body, consisting of more than 96% inorganic material in
functions. In most submammalian vertebrates the teeth are fused directly the form of apatite crystals and traces of organic material. The cells
to the jawbone. Although this construction provides a firm attachment, responsible for the formation of enamel, the ameloblasts, cover the
such teeth frequently are broken and lost during normal function. In entire surface of the layer as it forms but are lost as the tooth emerges
these cases, many successional teeth form to compensate for tooth loss into the oral cavity. The loss of these cells renders enamel a nonvital
and to ensure continued function of the dentition. and insensitive matrix that, when destroyed by any means (usually wear
The tooth proper consists of a hard, inert, acellular enamel formed or caries), cannot be replaced or regenerated. To compensate for this
by epithelial cells and supported by the less mineralized, more resilient, inherent limitation, enamel has acquired a high degree of mineralization
and vital hard connective tissue dentin, which is formed and supported and a complex organization. These structural and compositional features
by the dental pulp, a soft connective tissue (Figure 1-2; see also Figure allow enamel to withstand large masticatory forces and continual assaults
1-1). In mammals, teeth are attached to the jaw by tooth-supporting by acids from food and bacterial sources. The apatite crystals within
connective tissues, consisting of cementum, periodontal ligament (PDL), enamel pack together differentially to create a structure of enamel rods
and alveolar bone, which provide enough flexibility to withstand the separated by interrod enamel (Figure 1-3). Although enamel is a dead
forces of mastication. In human beings and most mammals, a limited tissue in a strict biologic sense, it is permeable; ionic exchange can
succession of teeth still occurs, not to compensate for continual loss of occur between the enamel and the environment of the oral cavity, in
teeth but to accommodate the growth of the face and jaws. The face particular the saliva.
and jaws of a human child are small and consequently can carry fewer
teeth of smaller size. These smaller teeth constitute the deciduous or Dentin
primary dentition. A large increase in the size of the jaws occurs with Because of its exceptionally high mineral content, enamel is a brittle
growth, necessitating not only more teeth but also larger ones. Because tissue that cannot withstand the forces of mastication without fracture
the size of teeth cannot increase after they are formed, the deciduous unless it has the support of a more resilient tissue, such as dentin.
dentition becomes inadequate and must be replaced by a permanent Dentin forms the bulk of the tooth, supports the enamel, and compensates
or secondary dentition consisting of more and larger teeth. for its brittleness.
1
2 CHAPTER 1 Structure of the Oral Tissues
Dentin is a mineralized, elastic, yellowish-white, avascular tissue and containing the cytoplasmic extensions of the cells that once formed
enclosing the central pulp chamber (Figure 1-4; see also Figures 1-1 it and later maintain it (see Figure 1-4, B). These cells are called
and 1-2). The mineral is also apatite, and the organic component is odontoblasts; their cell bodies are aligned along the inner edge of the
mainly the fibrillar protein collagen. A characteristic feature of dentin dentin, where they form the peripheral boundary of the dental pulp
is its permeation by closely packed tubules traversing its entire thickness (see Figure 1-4, A). The very existence of odontoblasts makes dentin a
vastly different tissue from enamel. Dentin is a sensitive tissue, and
more important, it is capable of repair, because odontoblasts or cells
in the pulp can be stimulated to deposit more dentin as the occasion
demands.
Pulp
The central pulp chamber, enclosed by dentin, is filled with a soft
connective tissue called pulp (see Figure 1-4, A). Dentin is a hard tissue;
Clinical crown the pulp is soft (and is lost in dried teeth, leaving a clearly recognizable
empty chamber). Despite distinctive histologic features, dentin and
pulp are related embryologically and functionally and should be
Enamel
considered together. This unity is exemplified by the classic functions
Dentin of pulp: it is (1) formative, in that it produces the dentin that surrounds
Gingiva it; (2) nutritive, in that it nourishes the avascular dentin; (3) protective,
in that it carries nerves that give dentin its sensitivity; and (4) reparative,
Anatomical in that it is capable of producing new dentin when required.
crown
In summary, the tooth proper consists of two hard tissues: the acellular
enamel and the supporting dentin. The latter is a specialized connective
tissue, the formative cells of which are in the pulp. These tissues bestow
PDL
Pulp
Cementum
Bone
Rod
FIGURE 1-1 The tooth and its supporting structure. PDL, Periodontal
ligament.
Interrod
Rod
FIGURE 1-2 Vertical cone beam CT slice of mandibular molars and FIGURE 1-3 Enamel. Electron micrograph showing that enamel consists
premolars. (Courtesy M. Schmittbuhl.) of crystallites organized into rod and interrod enamel.
CHAPTER 1 Structure of the Oral Tissues 3
Odontoblasts
Predentin Odontoblasts process
Predentin
Dentin
Odontoblasts
A B
Pulp
FIGURE 1-4 Dentin and pulp. A, The odontoblasts (cells that form dentin) line the pulp. B, These cells at
higher magnification show processes extending into dentin.
on teeth the properties of hardness and resilience. Their indestructibility a mineralized connective tissue similar to bone except that it is avascular;
also gives teeth special importance in paleontology and forensic science, the mineral is also apatite, and the organic matrix also contains collagen.
for example, as a means of identification. The cells that form cementum are called cementoblasts.
The two main types of cementum are cellular and acellular. The
cementum attached to the root dentin and covering the upper (cervical)
SUPPORTING TISSUES OF THE TOOTH portion of the root is acellular and thus is called acellular, or primary,
The tooth is attached to the jaw by a specialized supporting apparatus cementum. The lower (apical) portion of the root is covered by cellular, or
that consists of the alveolar bone, the PDL, and the cementum, all of secondary, cementum. In this case, cementoblasts become trapped in lacunae
which are protected by the gingiva (see Figures 1-1 and 1-5). within their own matrix, much like osteocytes occupy lacunae in bone;
these entrapped cells are now called cementocytes. Acellular cementum
Periodontal Ligament anchors PDL fiber bundles to the tooth; cellular cementum has an adaptive
The PDL is a highly specialized connective tissue situated between the role. Bone, the PDL, and cementum together form a functional unit of
tooth and the alveolar bone (Figure 1-5). The principal function of the special importance when orthodontic tooth movement is undertaken.
PDL is to connect the tooth to the jaw, which it must do in such a way
that the tooth will withstand the considerable forces of mastication.
This requirement is met by the collagen fiber bundles that span the
ORAL MUCOSA
distance between the bone and the tooth and by ground substance The oral cavity is lined by a mucous membrane that consists of two
between them. At one extremity the fibers of the PDL are embedded layers: an epithelium and subjacent connective tissue (the lamina propria;
in bone; at the other extremity they are embedded in cementum. Each Figure 1-6). Although its major functions are lining and protecting, the
collagen fiber bundle is much like a spliced rope in which individual mucosa also is modified to serve as an exceptionally mobile tissue that
strands can be remodeled continually without the overall fiber losing permits free movement of the lip and cheek muscles. In other locations
its architecture and function. In this way the collagen fiber bundles can it serves as the organ of taste.
adapt to the stresses placed on them. The PDL has another important Histologically, the oral mucosa can be classified into three types:
function, a sensory one. Tooth enamel is an inert tissue and therefore (1) masticatory, (2) lining, and (3) specialized. The masticatory mucosa
insensitive, yet the moment teeth come into contact with each other, covers the gingiva and hard palate. The masticatory mucosa is
we know it. Part of this sense of discrimination is provided by sensory bound down tightly by the lamina propria to the underlying bone (see
receptors within the PDL. Figure 1-6, B), and the covering epithelium is keratinized to withstand
the constant pounding of food during mastication. The lining mucosa,
Cementum by contrast, must be as flexible as possible to perform its function of
Cementum covers the roots of the teeth and is interlocked firmly with protection. The epithelium is not keratinized; the lamina propria is
the dentin of the root (see Figures 1-1, 1-2, and 1-5, B). Cementum is structured for mobility and is not tightly bound to underlying structures
4 CHAPTER 1 Structure of the Oral Tissues
PDL
Dentin
Dentin
Pulp
A B
Bone
Cementum
PDL
Collagen
SALIVARY GLANDS
Saliva is a complex fluid that in health almost continually bathes the
parts of the tooth exposed within the oral cavity. Consequently, saliva
represents the immediate environment of the tooth. Saliva is produced
by three paired sets of major salivary glands—the parotid, submandibular,
and sublingual glands—and by the many minor salivary glands scattered
throughout the oral cavity. A precise account of the composition of saliva
is difficult, because not only are the secretions of each of the major and
minor salivary glands different, but their volume may vary at any given
time. In recognition of this variability, the term mixed saliva has been
used to describe the fluid of the oral cavity. Regardless of its precise
FIGURE 1-6 Oral mucosa. A, Note the difference between tightly bound composition, saliva has several functions. Saliva moistens the mouth,
mucosa of the gingiva (gum) and mobile mucosa of the labial sulcus facilitates speech, lubricates food, and helps with taste by acting as a
(alveolar mucosa). B, In histologic sections, the gingival epithelium is solvent for food molecules. Saliva also contains a digestive enzyme
seen to be tightly bound to bone by a dense fibrous connective tissue
(amylase). Saliva not only dilutes noxious material mistakenly taken into
(CT), whereas the epithelium of the lip (C) is supported by a much looser
the mouth, it also cleanses the mouth. Furthermore, it contains antibodies
connective tissue.
and antimicrobial substances, and by virtue of its buffering capacity plays
an important role in maintaining the pH of the oral cavity.
(see Figure 1-6, C). The dorsal surface of the tongue is covered by a The basic histologic structure of the major salivary glands is similar.
specialized mucosa consisting of a highly extensible masticatory mucosa A salivary gland may be likened to a bunch of grapes. Each “grape” is
containing papillae and taste buds. the acinus or terminal secretory unit, which is a mass of secretory cells
A unique feature of the oral mucosa is that the teeth perforate it. surrounding a central space. The spaces of the acini open into ducts
This anatomic feature has profound implications in the initiation of running through the gland that are called successively the intercalated,
periodontal disease. The teeth are the only structures that perforate striated, and excretory ducts (Figure 1-7), analogous to the stalks and
epithelium anywhere in the body. Nails and hair are epithelial appendages stems of a bunch of grapes. These ducts are more than passive conduits,
CHAPTER 1 Structure of the Oral Tissues 5
Lobule
Main
excretory duct
Striated duct
Intercalated duct
Canaliculus
between cells
Spherical secretory
end piece
FIGURE 1-7 Diagrammatic illustration of the ductal system of a salivary
gland.
B
of the capsule to form a specialized movable disk. The articular surfaces when stacked together, these cells form the lattice of a crystal.
of the bone are covered not by hyaline cartilage but by a fibrous layer that The number of repetitions of this arrangement produces crystals of
is a continuation of the periosteum covering the individual bones. A simpli- various sizes. Generally the crystals are described as needlelike or platelike
fied way to understand the function of the TMJ is to consider it as a joint and, in the case of enamel, as long, thin ribbons. Some believe that the
with the articular disk being a movable articular surface. formation of crystals is preceded by an unstable amorphous calcium
phosphate phase.
A layer of water, called the hydration shell, exists around each crystal.
HARD TISSUE FORMATION Each apatite crystal has three compartments: the crystal interior, the
The hard tissues of the body—bone, cementum, dentin, and enamel—are crystal surface, and the hydration shell, all of which are available for
associated with the functioning tooth. Because the practice of dentistry the exchange of ions. Thus magnesium and sodium can substitute in
involves manipulation of these tissues, a detailed knowledge of them the calcium position, fluoride and chloride in the hydroxyl position,
is obligatory (and each is discussed separately in later chapters). The and carbonate in the hydroxyl and phosphate positions. Fluoride substitu-
purposes of this section are (1) to explain that a number of common tion decreases the solubility of the crystals, whereas carbonate increases
features are associated with hard tissue formation, even though the it. Magnesium inhibits crystal growth. The apatite crystal can retain its
final products are structurally distinct; (2) to indicate that the functional structural configuration while accommodating these substitutions.
role of a number of these features is still not fully understood; and (3) In summary, biologic apatite is built on a definite ionic lattice pattern
to describe the common mechanism of hard tissue breakdown. that permits considerable variation in its composition through substitu-
Three (i.e., bone, cementum, and dentin) of the four hard tissues tion, exchange, and adsorption of ions. This pattern of ionic variability
in the body have many similarities in their composition and formation. reflects the immediate environment of the crystal and is used clinically
They are specialized connective tissues, and collagen (principally type to modify the structure of crystals by exposing them to a fluoride-rich
I) plays a large role in determining their structure. Although enamel is environment.
not a connective tissue and no collagen is involved in its makeup, its
formation still follows many of the principles involved in the formation
of hard connective tissue. Hard tissue formation may be summarized
MINERALIZATION
as the production by cells of an organic matrix capable of accommodating Over the past few years, there has been a shift in the perception
mineral. This rather simple concept, however, embraces a number of of biologic mineralization, from a physiologic process highly dependent
complex events. on sustained active promotion to one relying more on rate-limiting
activities, including release from inhibition of mineralization. Essentially,
The Organic Matrix in Hard Tissues when calcium phosphate deposition is initiated, the crux is then to
A hallmark of calcified tissues is the various matrix proteins that attract control spontaneous precipitation from tissue fluids supersaturated in
and organize calcium and phosphate ions into a structured mineral calcium and phosphate ions and to limit it to well-defined sites.
phase based on carbonated apatite. The formative blast cells of calcified Formative cells achieve this by creating microenvironments that
tissues produce the organic matrix constituents that interact with the facilitate mineral ion handling and by secreting proteins that stabilize
mineral phase. These cells specialize in protein synthesis and secretion, calcium and phosphate ions in body fluids and/or control their deposi-
and they exhibit a polarized organization for vectorial secretion and tion onto a receptive extracellular matrix. Genome sequencing
appositional deposition of matrix proteins. and gene mapping have shown that several of these proteins are
Of great interest is the fact that the proteins involved in these hard located on the same chromosome and that there is synteny across
tissues, with one exception (enamel), are similar, comprising a pre- several species.
dominant supporting meshwork of type I collagen with various added Collectively, these proteins are referred to as the secretory calcium-
noncollagenous proteins functioning primarily as modulators of binding phosphoprotein gene cluster that comprises (1) salivary proteins,
mineralization. Table 1-1 provides a comparative analysis of the (2) some enamel matrix proteins, and (3) bone/cementum/dentin matrix
characteristics of the various calcified tissues. This basic similarity of proteins. These proteins derive from the duplication and diversification
constituents is consistent with the general role of collagen-based hard of a common ancestral gene during evolution, with an enamel-related
tissues in providing rigid structural support and protection of soft gene as an early intermediate in the process.
tissues in vertebrates. Enamel has evolved to function specifically as an Two mechanisms have been proposed for initiating mineralization
abrasion-resistant, protective coating that relies on its uniquely large of hard connective tissue. The first involves a structure called the matrix
mineral crystals for function. The organic matrix of enamel consists vesicle (Figure 1-10), and the second is heterogeneous nucleation.
essentially of noncollagenous proteins that have no “scaffolding” role. In the first mechanism the vesicle exists in relation to initial min-
However, enamel is not the only calcified tissue without collagen. eralization. The matrix vesicle is a small, membrane-bound structure
Mineralization of cementum situated along the cervical margin of the that buds off from the cell to form an independent unit within the
tooth occurs within a matrix composed largely of noncollagenous matrix first-formed organic matrix of hard tissues. The first morphologic
proteins also found in bone. In invertebrates, the shell of mollusks evidence of a crystallite is seen within this vesicle. The matrix vesicle
consists of laminae of calcium carbonate separated by a thin layer of provides a microenvironment in which proposed mechanisms for initial
organic material—acidic macromolecules, among others. mineralization exist. Thus it contains alkaline phosphatase, calcium-
adenosinetriphosphatase, metalloproteinases, proteoglycans, and anionic
Mineral phospholipids, which can bind calcium and inorganic phosphate and
The inorganic component of mineralized tissues consists of hydroxy- thereby form calcium–inorganic phosphate phospholipid complexes.
apatite, represented as Ca10(PO4)6(OH)2 and which has undergone a Matrix vesicles have had an interesting history since their discovery,
number of substitutions with other ions. This formula indicates only initially questioned as an artifact of tissue preparation.
the atomic content of a conceptual entity known as the unit cell, which In the second mechanism, during the formation of collagen-based
is the least number of calcium, phosphate, and hydroxyl ions able to calcified tissues, deposition of apatite crystals is catalyzed by specific
establish stable relationships. The unit cell of biologic apatite is hexagonal; atomic groups associated with the surface, holes, and pores of collagen
CHAPTER 1 Structure of the Oral Tissues 7
Proteoglycans
Controversial SLRP SLRP SLRP
Matrix Proteinases
1. MMP-20 (enamelysin) Collagen-processing enzymes Collagen-processing Collagen-processing enzymes
and others needed to degrade enzymes and others and others needed to degrade
matrix needed to degrade matrix matrix
2. KLK-4
Mineral
Hydroxyapatite > 90% ribbons Hydroxyapatite 67% Hydroxyapatite 45% to Hydroxyapatite 50% to 60%
(R) expand (mature crystallites 50%
can be millimeters in length)
Uniform small plates Uniform small plates Uniform small plates
Location of Between amelogenin Inside, at periphery, and Inside, at periphery, and Inside, at periphery, and
mineral nanospheres; related to between type I collagen fibril between type I collagen between type I collagen fibril
ribbons? fibril
Nucleated from Controversial—Amelogenins? Matrix vesicles then moving Matrix vesicles then Matrix vesicles then moving
mineralization front, although moving mineralization mineralization front, although
additional mechanisms are front, although additional additional mechanisms are
most likely involved mechanisms are most most likely involved
likely involved
Nonamelogenins?
Dentin?
Prematrix
None present; crystallites abut Always present Always present; usually Present only during formative
plasma membrane of very thin phase
ameloblasts
Continued
8 CHAPTER 1 Structure of the Oral Tissues
Cells
Formative Ameloblasts very tall and thin; Odontoblasts tall with long Cementoblasts short Osteoblasts short
multiple morphologies cytoplasmic processes
Microenvironment Putatively sealed by secretory Incomplete, leaky junctions; Cells widely spaced No junctions at the level of the
and ruffle-ended ameloblasts; cells act as limiting cell body; cells act as limiting
leaky relative to smooth- membrane membrane
ended ameloblasts
Life span of Limited to time until crown For life of tooth with gradual Probably for life of tooth Limited; associated with
formative cells erupts loss as pulp chamber occludes appositional growth phase
Maintenance None Odontoblast process Cementocytes Osteocytes
Life span of NA For life of tooth, with gradual Limited by overall thickness Long until area of bone
maintenance loss as pulp chamber occludes of the layer undergoes turnover
cells
Degradative None per se; cells secrete Odontoclasts Odontoclasts/ Osteoclasts (limited life span)
proteinases cementoclasts
Dentin, fibrillar cementum, and bone are collagen-based tissues. Enamel is outside rather than inside the body. Enamel, dentin, and cementum
are not vascularized, and they do not turn over. Enamel, dentin, and primary cementum are acellular, but dentin contains the large, arborizing
processes of odontoblasts embedded in the matrix.
AEFC, Acellular extrinsic fiber cementum; CIFC, cellular intrinsic fiber cementum; SLRP, small leucine-rich proteoglycans (biglycan, decorin);
MMP, metalloproteinase; KLK-4, kallikrein-4; NA, not applicable.
Updated from Nanci A, Smith CE: Matrix-mediated mineralization in enamel and the collagen-based hard tissues. In Goldberg M, Boskey A,
Robinson C, editors: Chemistry and biology of mineralized tissues, Rosemont, IL, 1999, American Academy of Orthopaedic Surgeons.
fibrils (Figures 1-11 and 1-12). Currently there is uncertainty as to Crystal Growth
whether more mineral resides within collagen or in the spaces between When an apatite crystal has been initiated, its initial growth is rapid
fibrils. Although a direct role by collagen has not been excluded, regula- but then slows down. Several factors influence crystal growth and
tion of this process is believed to be achieved by noncollagenous composition, but especially important is the immediate environment
proteins; however, the precise function of these proteins and the manner of the growing crystal. For example, noncollagenous proteins can bind
in which they achieve their effect are still not fully understood. One selectively to different surfaces of the crystal, preventing further growth
item of particular interest is how these molecules interact with type I and thereby determining the final size of the crystal. The accumulation
collagen. Current views on the mineralization of collagen are discussed of inorganic pyrophosphoric acid (pyrophosphate, PPi) at the crystal
in Box 1-1. surface also blocks further growth.
Neither of these mechanisms is involved in the mineralization of
enamel; matrix vesicles are absent, and enamel contains no collagen. Alkaline Phosphatase
Initiation of enamel mineralization is believed to be achieved by crystal Alkaline phosphatase activity is always associated with the production
growth from the already mineralized dentin, by matrix proteins secreted of a mineralized tissue, and the implicated isozymes are part of the
by the ameloblasts, or by both processes. mammalian alkaline phosphatase gene family. Because the major isozyme
CHAPTER 1 Structure of the Oral Tissues 9
Pore
Surface hole
Hole
Collagen fibril
as calcium enters the cell through specific calcium channels, it is seques- lacuna under osteoclasts. The exact extent of the degradation of its
tered by calcium-binding proteins that in turn are transported through organic matrix constituents and the exact manner by which their frag-
the cell to the site of release. The second suggests that a continuous and ments leave the site of resorption are still not fully defined; in bone,
constant flow of calcium ions occurs across the cell without the concentra- transcytosis is involved (see Chapter 6). Such tissues as cementum and
tion of free calcium ions ever exceeding 10−6 mol/L. Finally, intracellular dentin do not normally undergo turnover, but all hard tissues of the
compartments (e.g., endoplasmic reticulum and mitochondria) also play tooth can be resorbed under certain normal eruptive conditions (e.g.,
a role in calcium handling. Calcium has been localized to these structures deciduous teeth) and under certain pathologic conditions, including
not only in hard tissue–forming cells but also in most other cells, and excessive physical forces and inflammation. The cells involved in their
it is believed that the sequestration of calcium to these organelles is a resorption have similar characteristics to osteoclasts but generally are
safety device to control the calcium concentration of the cytosol. referred to as odontoclasts (see Chapter 10).
Collagen hole-
overlap region Ca2
PO43
fibers. In enamel, mineralization initiates either in relation to preexisting creates a sealed environment that is first acidified to demineralize the
apatite crystals of dentin or enamel matrix proteins. Alkaline phosphatase hard tissue. After exposure to the acidic environment, the organic matrix
is associated with mineralization, but its role is still not fully understood. is broken down by proteolytic enzymes. In enamel, the challenge is to
The breakdown of hard tissue involves the macrophage system, which maintain a relatively neutral pH environment that will prevent mineral
produces a characteristic multinucleated giant cell, the osteoclast. To dissolution and allow optimal activity of the enzymes that break down
break down hard tissue, this cell attaches to mineralized tissue and the organic matrix components.
2
General Embryology
CHAPTER OUTLINE
Germ Cell Formation and Fertilization, 12 Formation of the Neural Tube and Fate of the Germ Layers, 17
Prenatal Development, 12 Folding of the Embryo, 17
Induction, Competence, and Differentiation, 13 The Neural Crest, 18
Formation of the Three-Layered Embryo, 14
This chapter provides basic general embryology information needed chromosomes can result from the failure to separate of a homologous
to explain the development of the head, particularly the structures in chromosome pair during meiosis, so that the daughter cells contain 24
and around the mouth. It supplies a background for understanding (1) or 22 chromosomes. If, on fertilization, a gamete containing 24 chro-
the origins of the tissues associated with facial and dental development mosomes fuses with a normal gamete (containing 23), the resulting
and (2) the cause of many congenital defects manifest in these tissues. zygote will possess 47 chromosomes; one homologous pair has a third
component. Thus the cells are trisomic for a given pair of chromosomes.
If one member of the homologous chromosome pair is missing, a rare
GERM CELL FORMATION AND FERTILIZATION condition known as monosomy prevails. The best-known example of
The human somatic (body) cell contains 46 chromosomes, 46 being trisomy is Down syndrome, or trisomy 21. Among features of Down
the diploid number for the cell. Two of these are sex chromosomes; the syndrome are facial clefts, a shortened palate, a protruding and fissured
remaining are autosomes. Each chromosome is paired so that every tongue, and delayed eruption of teeth.
cell has 22 homologous sets of paired autosomes, with one sex chromo- Approximately 10% of all human malformations are caused by an
some derived from the mother and one from the father. The sex alteration in a single gene. Such alterations are transmitted in several
chromosomes, designated X and Y, are paired as XX in the female and ways, of which two are of special importance. First, if the malformation
XY in the male. results from autosomal dominant inheritance, the affected gene generally
Fertilization is the fusion of male and female germ cells (the sper- is inherited from only one parent. The trait usually appears in every
matozoa and ova, collectively called gametes) to form a zygote, which generation and can be transmitted by the affected parent to statistically
commences the formation of a new individual. Germ cells are required half of the children. Examples of autosomal dominant conditions include
to have half as many chromosomes (the haploid number), so that on achondroplasia, cleidocranial dysostosis, osteogenesis imperfecta, and
fertilization the original complement of 46 chromosomes will be dentinogenesis imperfecta; the latter two conditions result in abnormal
reestablished in the new somatic cell. The process that produces germ formation of the dental hard tissues. Dentinogenesis imperfecta
cells with half the number of chromosomes of the somatic cell is called (Figure 2-1) arises from a mutation in the dentin sialophosphoprotein
meiosis. Mitosis describes the division of somatic cells. gene. Second, when the malformation is a result of autosomal recessive
Before mitotic cell division begins, DNA is first replicated during inheritance, the abnormal gene can express itself only when it is received
the synthetic (S) phase of the cell cycle so that the amount of DNA is from both parents. Examples include chondroectodermal dysplasia,
doubled to a value known as tetraploid (4 times the amount of DNA some cases of microcephaly, and cystic fibrosis.
found in the germ cell). During mitosis the chromosomes containing All of these conditions are examples of abnormalities in the genetic
this tetraploid amount of DNA are split and distributed equally between makeup or genotype of the individual and are classified as genetic
the two resulting cells; thus both daughter cells have a diploid defects. The expression of the genotype is affected by the environment
DNA quantity and chromosome number, which duplicates the parent in which the embryo develops, and the final outcome of development
cell exactly. is termed the phenotype. Adverse factors in the environment can result
Meiosis, by contrast, involves two sets of cell divisions occurring in in excessive deviation from a functional and accepted norm; the outcome
quick succession. Before the first division, DNA is replicated to the is described as a congenital defect. Teratology is the study of such
tetraploid value (as in mitosis). In the first division the number developmental defects.
of chromosomes is halved, and each daughter cell contains a diploid
amount of DNA. The second division involves the splitting and
separation of the chromosomes, resulting in four cells; thus the final
PRENATAL DEVELOPMENT
composition of each cell is haploid with respect to its DNA value and Prenatal development is divided into three successive phases (Figure
its chromosome number. 2-2). The first two, when combined, constitute the embryonic stage,
Meiosis is discussed in this textbook because the process occasionally and the third is the fetal stage. The forming individual is described as
malfunctions by producing zygotes with an abnormal number of an embryo or fetus depending on its developmental stage.
chromosomes and individuals with congenital defects that sometimes The first phase begins at fertilization and spans the first 4 weeks or
affect the mouth and teeth. For example, an abnormal number of so of development. This phase involves largely cellular proliferation
12
CHAPTER 2 General Embryology 13
and migration, with some differentiation of cell populations. Few internal structures (morphogenesis). The second phase is a particularly
congenital defects result from this period of development because, if vulnerable period for the embryo because it involves many intricate
the perturbation is severe, the embryo is lost. embryologic processes; during this period, many recognized congenital
The second phase spans the next 4 weeks of development and is defects develop.
characterized largely by the differentiation of all major external and From the end of the second phase to term, further development is
largely a matter of growth and maturation, and the embryo now is
called a fetus.
Embryonic Fetal
410
400
390
380
370
360
350
50
40
30
20
10
7 14 21 28 35 42 49 56 32 33 34 35 36 37 38 39 40
4 8 32
50
Proliferation Morphogenesis and
and migration differentiation
40
Crown-rump length (mm)
Dental lamina
30
Bilaminar embryonic disc
Arches
Blastocyte
Cleavage
0
Days 0 7 14 21 28 35 42 49 56
Postovulatory age (days)
FIGURE 2-2 Sequences of prenatal development. The upper diagram shows the distinction between embryonic
and fetal stages. The lower part of the embryonic diagram is expanded in the bottom diagram, which distinguishes
the stages of proliferation and migration and morphogenesis and differentiation. The timing of key events
also is indicated. (Modified from Waterman RE, Meller SM.(1978) Congenital craniofacial abnormalities. In:
Shaw JH, Sweeney EA, Cappuccino CC, Miller SM, eds. Textbook of oral biology. Philadelphia: WB Saunders
Co, pp. 863-96.)
14 CHAPTER 2 General Embryology
Cell death
a
b
Survive
a
b Proliferate
c
a
b
Differentiate
c
d
FIGURE 2-4 The effect of expression of cell-surface receptors (colored membrane-bound forms) to capture
different combinations (a-d) of growth factors (colored geometric forms) on cell behavior. If no receptors are
expressed, cell death ensues.
CHAPTER 2 General Embryology 15
Embryoblast
Embryoblast
Primary
yolk sac
Primary
yolk sac
Trophoblast
Morula Blastocyst
Trophoblast
FIGURE 2-5 Differentiation of the morula into a blastocyst. At this time cells differentiate into the embryoblast
(involved in development of the embryo) and the trophoblast (involved in maintenance). (Adapted from Hertig
AT, Rock J, Adams EC, Mulligan WJ (1954) On the preimplantation stages of the human ovum: a description
of four normal and four abnormal specimens ranging from the second to the fifth day of development. Carnegie
Inst Wash Publ 603, Contrib Embryol 35:199–220.)
Developing
placenta
A Amniotic B
Amniotic cavity
Ectoderm
cavity
Endoderm
Ectoderm
Secondary
Endoderm yolk sac
Prochordal
plate
Secondary
yolk sac
Endometrium
Endometrial
epithelium
FIGURE 2-6 A, Schematic representation and B, histologic section of a human blastocyst at 13 days. An
amniotic cavity has formed within the ectodermal layer. Proliferation of endodermal cells forms a secondary
yolk sac. The bilaminar embryo is well established. (B, Adapted from Brewer JI (1938) A human embryo in the
bilaminar blastodisc stage (the Edwards-Jones-Brewer ovum). Contrib Embryol Carnegie Instn 27:85–93.)
The embryoblast cells form the embryo proper, whereas the trophoblast sac), which develops from the migration of peripheral cells of the
cells are associated with implantation of the embryo and formation of extraembryonic endodermal layer. This configuration is completed
the placenta (they are not described further here). after 2 weeks of development (Figure 2-6). During that time the axis
At about day 8 of gestation, the cells of the embryoblast differentiate of the embryo is established and is represented by a slight enlargement
into a two-layered disk called the bilaminar germ disk. The cells situated of the ectodermal and endodermal cells at the head (cephalic or rostral)
dorsally, or the ectodermal layer, are columnar and reorganize to form end of the embryo in a region known as the prochordal (or prechordal)
the amniotic cavity. Those on the ventral aspect, the endodermal layer, plate, where ectoderm and endoderm are in contact (Figure 2-7, A; see
are cuboidal and form the roof of a second cavity (the secondary yolk also Figure 2-6, A).
16 CHAPTER 2 General Embryology
Caudal
Primitive streak
y1 y
Primitive node
A
x1 x
Rostral
Prochordal plate
Amniotic
cavity
Mesoderm Ectoderm
Notochord
Endoderm
Secondary
yolk sac
Mesoderm Ectoderm
Endoderm
Endoderm
Future Mesoderm
buccopharyngeal
membrane
FIGURE 2-7 Gastrulation–conversion of the bilaminar embryo into a trilaminar embryo. The left column
illustrates the plane of section for the middle and right columns. The middle column provides a three-dimensional
view, and the right column provides a two-dimensional representation. A, The floor of the amniotic cavity,
formed by the ectodermal layer of the bilaminar embryo. Ectodermal cells converge toward the midline to
form the primitive streak, a narrow groove terminating in a circular depression called the primitive node.
Ectodermal cells then migrate through the streak and between the ectodermal and endodermal layers in
lateral and cephalic directions (arrows). A notochord process extends forward from the primitive node. B, A
transverse section through x-x1, showing the notochord flanked by mesoderm. C, A section through y-y1.
D, Notochord pushing rostrally as seen in longitudinal section.
CHAPTER 2 General Embryology 17
During the third week of development, the embryo enters the period
of gastrulation during which the germ layers forming the bilaminar
embryonic disk are converted to a trilaminar disk (see Figure 2-7). As
previously described, the floor of the amniotic cavity is formed by
ectoderm, and within it a structure called the primitive streak develops
along the midline by cellular convergence (see Figure 2-7, A). This
structure is a narrow groove with slightly bulging areas on each side.
The rostral end of the streak finishes in a small depression called the
primitive node, or pit. Cells of the ectodermal layer migrate through
the streak and between the ectoderm and endoderm. The cells that pass
through the streak change shape and migrate away from the streak in
lateral and cephalic directions. The cells from the cephalic regions form
the notochord process, which pushes forward in the midline as far as
the prochordal plate. Through canalization of this process, the notochord
is formed to support the primitive embryo.
Elsewhere alongside the primitive streak, cells of the ectodermal
layer divide and migrate toward the streak, where they invaginate and
spread laterally between the ectoderm and endoderm. These cells,
sometimes called the mesoblast, infiltrate and push away the extraem-
bryonic endodermal cells of the hypoblast, except for the prochordal
plate, to form the true embryonic endoderm. They also pack the space
between the newly formed embryonic endoderm and the ectoderm to
form a third layer of cells, called the mesoderm (see Figure 2-7, B-D).
In addition to spreading laterally, cells spread progressively forward,
passing on each side of the notochord and prochordal plate. The cells
that accumulate anterior to the prochordal plate as a result of this
migration give rise to the cardiac plate, the structure in which the heart
forms (see Figure 2-7, A). As a result of these cell migrations, the
notochord and mesoderm now completely separate the ectoderm from
FIGURE 2-8 Scanning electron micrograph views of formation and
the endoderm (see Figure 2-7, C), except in the region of the prochordal closure of the neural fold elevations. (Courtesy G. Schoenwolf).
plate and in a similar area of fusion at the tail (caudal) end of the
embryo, called the cecal plate.
adjacent to the neural tube and notochord. The lateral plate mesoderm
Head fold
cavitates to form a space (coelom), and the mesoderm bounding the
cavity lines the body wall and gut. Intermediate mesoderm is relocated
to a position on the dorsal wall of the coelom. The endoderm
forms the gut. Figure 2-12 indicates the final disposition of the
mesoderm and the derivatives of the ectoderm, endoderm, and cranial
neural crest.
Primitive
Developing brain gut
C D
Cardiac
plate
Buccopharyngeal
membrane
E
CHAPTER 2 General Embryology 19
Ectoderm
Amniotic cavity
A B
Paraxial mesoderm
Mesoderm Endoderm Intermediate mesoderm
Notochord Lateral plate mesoderm
Amniotic cavity
Amniotic cavity
Paraxial
mesoderm
Paraxial
Intermediate
C mesoderm D
mesoderm
Intermediate
mesoderm Lateral plate
Cavitation occurring mesoderm
Endoderm in the lateral plate
migration mesoderm. This cavity
to form gut will form the coelom.
Paraxial
mesoderm
Intermediate
mesoderm
E
Lateral plate
mesoderm
FIGURE 2-11 Cross-sectional profiles. A, The mesoderm, situated between the ectoderm and endoderm
in the trilaminar disk. B, Differentiation of the mesoderm into three masses: the paraxial, intermediate, and
lateral plate mesoderm. C to E, With lateral folding of the embryo, the amniotic cavity encompasses the
embryo, and the ectoderm constituting its floor forms the surface epithelium. Paraxial mesoderm remains
adjacent to the neural tube. Intermediate mesoderm is relocated and forms urogenital tissue. Lateral plate
mesoderm cavitates, the cavity forming the coelom and its lining the serous membranes of the gut and
abdominal cavity.
20 CHAPTER 2 General Embryology
Intermediate plate
Endoderm
Epithelial component of
trachea, bronchi and lungs,
epithelium of gastrointestinal tract,
liver, pancreas, urinary
bladder and urachus,
epithelial component of
pharynx, thyroid, tympanic
cavity, pharyngotympanic
tube, tonsils, and parathyroids
FIGURE 2-12 Derivatives of the germ layers and cranial neural crest.
Signaling molecules belonging to the bone morphogenetic proteins, the head. Embryonic connective tissue elsewhere is derived from
Wnt (wingless homologue in vertebrates), and fibroblast growth factor mesoderm and is known as mesenchyme, whereas in the head it is
signaling pathways, and secreted by the surrounding nonneural ectoderm known as ectomesenchyme, reflecting its origin from neuroectoderm.
and underlying mesoderm play a critical role in inducing the neural In a dental context the proper migration of neural crest cells is essential
crest cell cascade. At the molecular level, neural crest cell competence for the development of the craniofacial skeleton and the teeth. In
is indicated by the expression of members of the Snail (Snail and Slug) Treacher Collins syndrome (Figure 2-15), for example, full facial develop-
zinc-finger transcription factor family that repress the expression of ment does not occur because the neural crest cells fail to migrate
the cell adhesion molecule E-cadherin. properly to the facial region. All the tissues of the tooth (except enamel
Neural crest cells in the head region have an important role. In and perhaps some cementum) and its supporting apparatus are derived
addition to assisting in the formation of the cranial sensory directly from neural crest cells, and their depletion prevents proper
ganglia, they also differentiate to form most of the connective tissue of dental development.
CHAPTER 2 General Embryology 21
A B C
D E
FIGURE 2-14 Migration and differentiation of cranial neural crest cells
(NCCs). A, Migrating NCC. B and C, Neuronal differentiation of NCC.
D, Skeletal differentiation of NCC. E, Neurocranium (bone, red; cartilage,
blue). (From Trainor P, Specification of neural crest cell formation and
migration in mouse embryos. Semin Cell Dev Biol 16[6]:683-693, 2005.)
BOX 2-1 Neural Crest Cells and Their Application in Regenerative Medicine
Neural crest cells comprise a migratory stem and progenitor cell population that pluripotency, their derivation is still ethically controversial, and the potential for
forms within the first 3 to 4 weeks of human embryonic development. Derived host rejection remains high. In contrast, adult stem cells are available from
from the ectoderm during the period of neurulation, neural crest cells are essential numerous tissue sources and can be derived from an affected individual without
for embryo development and throughout adult life. These cells give rise to the ethical concern or fear of transplant rejection. The identification of multipotent
precursors of cranial cartilage and bone and therefore to most of the craniofacial neural crest cell progenitors in adults has facilitated their therapeutic application
skeleton. They generate neurons and glia within the peripheral and enteric nervous in tissue engineering and repair. However, in contrast to stem cells, only 1% to
system and the meninges surrounding the brain. They differentiate into melano- 3% of neural crest cells exhibit true multipotency. Instead, the vast majority of
blasts, the pigment cells of the skin, odontoblasts, smooth muscle cells of the neural crest cells exhibit a limited capacity for producing identical daughter cells.
cardiovascular system, and hormone-secreting cells of the adrenal gland. In fact, Furthermore, despite their persistence in adults, neural crest cells are generated
there is barely a tissue or organ throughout the human body that does not receive only transiently during embryo development. Therefore neural crest cells are
a contribution from neural crest cells. more akin to progenitor cells than stem cells. Nonetheless, studies of neural
Advances in the neural crest cell field continue to uncover the genes, proteins, crest cell contribution to the sciatic nerve in rats revealed that pure populations
and regulatory networks that endow neural crest cells with their stem and progeni- of neural crest cells can be isolated through flow cytometry, and more important,
tor cell–like properties and astonishing array of cell fates. However, much of that these isolated neural crest cells retain the capacity to form neurons and
the focus on neural crest cells currently revolves around their contributions to glia after transplantation into host avian embryos. Similar populations of neural
congenital disorders and diseases, which are collectively termed neurocristopathies. crest cells also persist in the gut, heart, epidermis, bone marrow, cornea, dental
This includes disorders of craniofacial development such as cleft palate and pulp, hard palate, and oral mucosa of adult organisms, providing multiple accessible
craniosynostosis; anomalies of cardiac development including persistent truncus sources of cells for replacement therapy.
arteriosus; malformation of gastrointestinal development as occurs in Hirschsprung The developmental potential of neural crest stem and progenitor cells may,
disease; and cancers such as neuroblastoma and melanoma, which affect the however, decrease with age. Whereas mouse embryo–derived gut neural crest
peripheral nervous system and skin, respectively. Understanding the genetic progenitor cells migrate great distances away from a transplantation site in avian
etiology and cell and tissue pathogenesis of individual neurocristopathies offers embryos and differentiate into neurons, adult gut–derived neural crest progenitor
the potential for developing reparative, regenerative, or preventive therapies for cells only engraft structures in the proximity of their site of transplantation.
treating neurocristopathies. Nonetheless, gut-derived neural crest progenitor cells transplanted into the
Stem cell transplantations have been touted as a therapeutic strategy in the aganglionic gut of a rat model of the Hirschsprung disease engrafted and dif-
treatment of neurocristopathy disorders and diseases. Although embryonic stem ferentiated into neurons. Furthermore, neural crest cells isolated from fetal human
cells were once considered ideal for this purpose because of their extraordinary gut tissue remained viable, engrafted, and established functional connections
Continued
22 CHAPTER 2 General Embryology
BOX 2-1 Neural Crest Cells and Their Application in Regenerative Medicine—cont’d
after transplantation into the bowel of immunodeficient mice. In addition, enteric stem cells (of which epidermal neural crest stem cells are a component) as a
neural crest cell progenitors derived from human-induced pluripotent stem (iPS) potential source of cells to be used in stem cell therapies.
cells, can migrate, engraft, and differentiate into neurons, rescuing disease-related In addition to autologous transplantation without immune rejection, the isolation
mortality in mice with Hirschsprung disease. This raises the possibility of generating of adult neural crest progenitor cells, or their induced pluripotent stem cell (iPS)
neural crest progenitor cells via iPS cells or isolating them directly from the derivation from patients affected with a neurocristopathy, provides a powerful
ganglionic region of the gut of a patient with Hirschsprung disease, and then platform for modeling disease and informing its pathogenesis, as well as drug
transplanting these cells into the aganglionic region of the same individual. This screening for therapeutics. This is particularly evident in ongoing studies of
approach may provide a treatment option for Hirschsprung disease without incurring Hirschsprung disease and familial dysautonomia, a neurodegenerative disorder of
problems with histocompatibility and immunosuppression, which are typical of the peripheral nervous system that is characterized by autonomic dysfunction.
transplantation surgery.
Neural crest cells derived from the epidermis of the skin also appear to hold Conclusions
considerable therapeutic promise. Not only are they readily accessible for isolation, Although the neural crest is a discrete population, generated only transiently in
but the hair follicle contains a mixed population of epidermal, keratinocyte, and the embryo, numerous populations of neural crest stem and progenitor cells have
melanocyte stem cells, each of which exhibits a high degree of plasticity. Within been isolated from embryonic and adult tissues. Neural crest–derived stem cells
the hair follicle is a multilayered region of the outer root sheath called the bulge. are extremely useful for disease modeling, for drug screening, and in stem cell
The bulge is where new hair growth occurs and, interestingly, the inner layers therapy. They are easily accessible, are relatively easy to maintain in culture,
are derived from neural crest cells. Neural crest–derived cells, harvested from and provide an autologous source of tissue for replacement therapies, thereby
the bulge region, can undergo self-renewal, indicating these cells are stem cells. bypassing immunorejection. These approaches, when used in combination with
Furthermore, these cells are multipotent, and under differentiation conditions advances in genome engineering, make it possible to isolate neural crest progenitor
produce colonies of neurons, smooth muscle cells, rare Schwann cells, melanocytes, cells from an affected individual, correct a genetic defect in those cells, and
and even chondrocytes. These cells have therefore been called epidermal neural then transplant those cells back into the same individual, possibly preventing or
crest stem cells, and the bulge in which they are found represents their niche. correcting the disorder. As proof of principle, a similar type of combinatorial
Recently, stem cells isolated from hair follicles were shown to repair sciatic stem cell and gene editing approach has recently been used successfully in the
nerve function in vivo in mice. Isolated stem cells from the hair follicle were used treatment of sickle cell anemia.
in transplants to treat two different injured nerves, the sciatic and tibial nerve. Paul A. Trainor
After transplantation, the follicle stem cells incorporated into the nerve, precipitating Stowers Institute for Medical Research
the recovery of proper nerve function. Functional studies of the gastrocnemius Kansas City, Missouri
revealed consistent contractions upon stimulation. Furthermore, tibial nerve function
was recovered in mice that received a follicle stem cell transplant, as demonstrated Recommended Reading
by normal walking ability. In contrast, control mice with a severed sciatic nerve Le Dourain NM, Kalchein C, editors: The neural crest, Cambridge, 1999, Cambridge University
but without transplantation displayed no muscle contraction upon stimulation. Press.
Saint-Jeannet JP, editor: Advances in experimental medicine and biology, New York, 2006,
Taken together, these results demonstrate that transplantation of follicle stem Landes Bioscience.
cells promotes regenerative axonal growth, resulting in the recovery of peripheral Trainor PA, editor: Neural crest cells: evolution, development and disease, New York, 2014,
nerve function. These experiments elegantly demonstrate the potential of follicle Elsevier.
A B
RECOMMENDED READING Moore KL, et al, editors: The developing human: clinically orientated
embryology, ed 8, Philadelphia, 2008, Saunders.
Cordero DR, et al: Cranial neural crest cells on the move: their roles in Sadler TW, editor: Langman’s essential medical embryology (vol 1), Baltimore,
craniofacial development, Am J Med Genet A 155:270, 2011. 2005, Lippincott Williams & Wilkins.
Minoux M, Rijli FM: Molecular mechanism of cranial neural crest cell
migration and patterning in craniofacial development, Development
137:2605, 2010.
3
Embryology of the Head, Face, and
Oral Cavity
CHAPTER OUTLINE
Neural Crest Cells and Head Formation, 23 Development of the Skull, 36
Branchial (Pharyngeal) Arches and the Primitive Mouth, 26 Development of the Mandible and Maxilla, 36
Fate of Grooves and Pouches, 26 Mandible, 36
Anatomy of an Arch, 27 Maxilla, 38
Fusion of Processes, 28 Common Features of Jaw Development, 39
Formation of the Face, 28 Development of the Temporomandibular Joint, 39
Formation of the Secondary Palate, 29 Congenital Defects, 39
Formation of the Tongue, 34
Knowledge of the evolutionary development of the skull, face, and jaws the neural tube is produced by the formation and fusion of the neural
is helpful in understanding the complex events involved in cephalogenesis folds, which sink beneath surface ectoderm (see Figure 2-3). The anterior
(formation of the head). Early chordates have a fairly simple anatomic portion of this neural tube expands greatly as the forebrain, midbrain,
plan with (1) a notochord for support, (2) a simple nervous system and hindbrain form (Figure 3-3), and the part associated with the
and sense organs, (3) segmented muscle blocks, and, at the beginning hindbrain develops a series of eight bulges, the rhombomeres (Figure
of the pharynx in its lateral wall, (4) a series of branchial arches supported 3-4). Lateral to the neural tube is the paraxial mesoderm, which partially
by cartilage associated with clefts to permit gaseous exchange. The first segments rostrally to form somatomeres and fully segments caudally
vertebrates evolved from this simple plan and were jawless (agnathia). to form somites, the first in the series being the occipital somites (see
Cartilaginous blocks (occipital and parachordal) evolved to support Figure 3-3).
the notochord in the head region, along with cartilaginous capsules NCCs from the midbrain and the first two rhombomeres transform
(nasal, optic, and otic) to protect the sense organs. These cartilages and migrate as two streams to supply additional embryonic connective
collectively form the neurocranium. The branchial arches, as mentioned, tissue needed for craniofacial development (see Figure 3-4). The first
are supported by a series of cartilaginous rods originally numbered 0, stream provides much of the ectomesenchyme associated with the face,
1, 2, and so on that constitute the viscerocranium. The first cartilage whereas the second stream is targeted to the first arch where they
(cartilage 0) of the branchial arches migrated to the neurocranium to contribute to formation of the jaws. NCC subpopulations, depending
provide additional support as the trabecular cartilage. Because of this, on their anteroposterior location along the neural tube, are subject to
the actual second arch cartilage became the first arch cartilage (Figure a very complex temporal and spatial set of signaling events. A plethora
3-1, A and B). The neurocranium and viscerocranium together form of molecules are used as cues to guide them to their ultimate destination
the chondrocranium. within restricted areas of the head. Their eventual differentiation is also
From this simple model, vertebrates came to possess jaws (gnathos- tightly controlled through reciprocal signaling with neighboring
tomata) through modification of the jointed first arch cartilage, with ectodermal cells. The various intracellular signaling events and cross
the upper element, the palatopterygo quadrate bar, becoming the upper talk between cells eventually culminate to elicit various cellular responses
jaw and the lower element, Meckel’s cartilage, becoming the lower jaw including proliferation, migration, differentiation, and survival or
(Figure 3-1, C). The fibrous connection between the two formed the apoptosis.
jaw joint. In addition to jaws, vertebrate evolution also brought about NCCs from rhombomere 3 and beyond migrate into arches that
massive expansion of the head region and associated larger neural and will give rise to pharyngeal structures. Because homeobox transcription
sensory elements. For protection, dermal bones developed as additional factor genes are not expressed anterior to rhombomere 3, a different
bony skeletal elements to form the vault of the skull and the facial set of coded patterning genes has been adapted for development of
skeleton, which included bony jaws and teeth. This cephalic expansion cephalic structures (Figure 3-5). This new set of transcription factor
demanded a source of new connective tissue, and as explained in Chapter genes, reflecting the later development of the head in evolutionary
2, this source is the neuroectoderm, from which neural crest cells (NCCs) terms, includes orthodenticle homeobox 2 (Otx2), muscle segment
migrate and differentiate into ectomesenchyme. Figure 3-2 shows a homeobox (Msx), the distal-less homeobox (Dlx), and the BarH-like
comparison between the cranial components of the primitive vertebrate homeobox (Barx). Homeobox genes also are implicated in dental
skull and the cranial skeleton of a human fetus. development, and their effects are discussed in Chapter 5.
Some NCC populations require instructions from their local
microenvironment. The resulting cross talk involves common signaling
NEURAL CREST CELLS AND HEAD FORMATION pathways, such as sonic hedgehog (Shh), fibroblast growth factor (Fgf),
The folding of the three-layered embryo has been described, and the and bone morphogenetic proteins (Bmp). Enzymes that modify
rostral or head fold is important at this point. As discussed in Chapter 2, chromatin architecture regulating the accessibility of transcription factors
23
24 CHAPTER 3 Embryology of the Head, Face, and Oral Cavity
0
0
0 1 2 1 2 1
3 2 3 4
3
A B C
FIGURE 3-1 A and B, The viscerocranium and the movement of arch 0 to the neurocranium. C, The jaws
developed from the first branchial arch cartilage of the viscerocranium. (Redrawn from Osborn JW, editor: Dental
anatomy and embryology, vol 2, Oxford, UK, 1981, Blackwell Scientific.)
Chondocranium
Otic capsule
Orbital region
Dermocranium
(membrane bones)
Vertebrae
Nasal capsule
Notochord
A
Pharynx
Viscerocranium
Parietal bone
Frontal bone
Maxilla
Squamous part
of temporal bone
Zygomatic arch
Mandible Styloid process
Tympanic ring
Hyoid bone Vertebrae
Thyroid cartilage
FIGURE 3-2 The major components of (A) the primitive vertebrate cranial skeleton and (B) the distribution
of these same components in a human fetal head. B, Bones of the cranial vault and face are formed by
intramembranous ossification (coarse stippling), whereas bones of the cranial base form by endochondral
ossification (fine stippling). (From Carlson BM: Human embryology and developmental biology, Philadelphia,
2004, Mosby.)
CHAPTER 3 Embryology of the Head, Face, and Oral Cavity 25
4 5
3 6
2 7
8
Somites 1
Midbrain
in
ra
db
Somatomeres
Hin
Midbrain
Forebrain
Mesenchyme
FIGURE 3-4 The source and pattern of neural crest migration to the
developing face and branchial arch system. The midbrain and rhombo-
meres 1 and 2 contribute to the face and first branchial arch.
and morphogenesis but also because of their implication in positioning branchial grooves. On the inner aspect of the pharyngeal wall are cor-
cellular structures and coordinating activities, such as cell intercalation. responding small depressions called pharyngeal pouches that separate
One such structure is the cilium, which is found on the surface of most each of the branchial arches internally. Table 3-1 summarizes the
vertebrate cells and acts as a mechanical/chemical sensor. Ciliary dysfunc- derivatives of the branchial (pharyngeal) arch system.
tion is present in some syndromes, such as facial-digital syndrome and
Bardet-Biedl syndrome, which exhibit facial changes, as well as cleft Fate of Grooves and Pouches
palate and micrognathia. Experimentally, it has been shown that a neural The first groove and pouch are involved in the formation of the external
crest–targeted mutation of the kif3 gene, encoding for a kinesin-like auditory meatus, tympanic membrane, tympanic antrum, mastoid
protein implicated in ciliogenesis and intraflagellar transport, affects
polarized growth and cell shape, resulting in shortened mandibles and
defects in development of the cranial base.
Frontal
prominence
Stomatodeum
First arch
Second arch
A B
FIGURE 3-7 A 26-day-old embryo. A, Front view. B, Side view. The structures limiting the stomatodeum
are clearly recognizable. (Courtesy H. Nishimura.)
CHAPTER 3 Embryology of the Head, Face, and Oral Cavity 27
Frontal Frontal
prominence prominence
Stomatodeum Stomatodeum
A B
FIGURE 3-8 A, Development of pharyngeal arches and the grooves between them in a 35-day-old embryo.
B, Midline section showing reflection of the arches on the pharyngeal wall and the pharyngeal pouches
separating them. The dotted line (arrow) represents the site where the buccopharyngeal membrane was.
TABLE 3-1 Derivatives of the Branchial also largely obliterated by the development of the palatine tonsil; a part
persists as the tonsillar fossa. The third pouch expands dorsally and
(Pharyngeal) Arch System
ventrally into two compartments, and its connection with the pharynx
Arch Groove Pouch is obliterated. The dorsal component gives origin to the inferior
First 1. Mandible and maxilla 1. External 2. Tympanic parathyroid gland, whereas the ventral component, with its anatomic
auditory membrane counterpart from the opposite side, forms the thymus gland. The fourth
meatus pouch also expands into dorsal and ventral components. The dorsal
2. Meckel’s cartilage: 3. Tympanic cavity component gives origin to the superior parathyroid gland, and the
a. Incus and malleus 4. Mastoid antrum ventral portion gives rise to the ultimobranchial body, which in turn
of inner ear gives rise to the parafollicular cells of the thyroid gland. The fifth pouch
b. Sphenomalleolar 5. Eustachian tube in human beings is rudimentary and thus disappears or becomes
ligament incorporated into the fourth pouch.
c. Sphenomandibular
ligament
Anatomy of an Arch
Second 1. Reichert’s cartilage: Obliterated 1. Largely obliterated Every branchial arch has the same basic plan. The inner aspect is covered
a. Styloid process of by the 2. Contributes to by endoderm and the outer surface by ectoderm, except for the first
temporal bone down- tonsil arch because it forms in front of the buccopharyngeal membrane and
b. Stylohyoid ligament growth of therefore derives completely from ectodermally covered surfaces. The
c. Lesser horns of the the second central core consists of mesenchyme derived from lateral plate mesoderm
hyoid bone arch invaded by NCCs, referred to as ectomesenchyme. This “neural-derived”
d. Upper part of the mesenchyme condenses to form a bar of cartilage, the arch cartilage
body of the hyoid (Figure 3-9). The cartilage of the first arch is called Meckel’s cartilage,
bone and that of the second Reichert’s, after the anatomists who first described
Third 1. Lower part of the body Inferior parathyroid them. The other arch cartilages are not named. The contribution of
of the hyoid bone gland Meckel’s cartilage is discussed subsequently. Reichert’s cartilage gives
2. Greater horns of the Thymus rise to a bony process, the stylohyoid ligament and the upper part of
hyoid bone the body and lesser horns of the hyoid bone. The cartilage of the third
Fourth 1. Cartilages of the Superior parathyroid arch gives rise to the lower part of the body and greater horns of the
larynx gland hyoid bone and that of the fourth arch to the cartilages of the larynx.
Ultimobranchial body Some of the mesenchyme surrounding this cartilaginous bar develops
Fifth Transient Transient Transient into striated muscle. The first arch musculature gives origin to
Sixth Transient Transient Transient the muscles of mastication, and the second arch musculature to the
muscles of facial expression. Each arch also contains an artery and a
nerve (Table 3-2). The nerve consists of two components, one motor
antrum, and pharyngotympanic or eustachian tube. The second, third, (supplying the muscle of the arch) and one sensory. The sensory nerve
and fourth grooves normally are obliterated by overgrowth of the second divides into two branches: a posttrematic branch, supplying the epi-
arch forming a transitory cervical sinus that sometimes persists and thelium that covers the anterior half of the arch, and a pretrematic
opens onto the side of the neck (branchial fistula) or on the neck and branch, passing forward to supply the epithelium that covers the posterior
inside the pharynx (pharyngocutaneous fistula). The second pouch is half of the preceding arch. The nerve of the first arch is the fifth cranial
28 CHAPTER 3 Embryology of the Head, Face, and Oral Cavity
FIGURE 3-9 Progressive stages in development of pharyngeal arches and their derivatives during the second
month in utero. (Redrawn from Shaw JH et al: Textbook of oral biology, Philadelphia, 1978, Saunders.)
TABLE 3-2 Innervation and Vascularization of the palatal processes, does actual fusion occur (Figure 3-11). To avoid
confusion, the conventional term process (rather than the more accurate
of Pharyngeal Arches
terms swelling or prominence) is used to describe the further development
Arch Blood Vessel Nerve of the face and oral cavity.
First First aortic arch Mandibular (and maxillary) division of the To recapitulate, the primitive stomatodeum is at first bounded above
trigeminal nerve (cranial nerve V) (rostrally) by the frontal prominence, below (caudally) by the developing
Second Second aortic arch Facial (VII) heart, and laterally by the first branchial arch. With spread of the arches
Third Third aortic arch Glossopharyngeal (IX) midventrally, the cardiac plate is distanced from the stomatodeum, and
Fourth Fourth aortic arch Vagus (X) the floor of the mouth is now formed by the epithelium covering the
mesenchyme of the first, second, and third branchial arches.
At about day 24 of gestation, the first branchial arch establishes
(or trigeminal) nerve, that of the second is the seventh cranial (or facial) another process, the maxillary process, so that the stomatodeum is
nerve, and that of the third is the ninth cranial (or glossopharyngeal) limited cranially by the frontal prominence covering the rapidly expand-
nerve. Structures derived from any arch carry with them the nerve ing forebrain, laterally by the newly formed maxillary process,
supply of that arch. Thus the muscles of mastication are innervated by and ventrally by the first arch (now called the mandibular process;
the trigeminal nerve. Figure 3-12).
Fusion of Processes
FORMATION OF THE FACE
The first, second, and third branchial arches play an important role in
the development of the face, mouth, and tongue. Classically, the formation Early development of the face is dominated by the proliferation and
of the face is described in terms of the formation and fusion of several migration of ectomesenchyme involved in the formation of the primitive
processes or prominences (Figure 3-10). In some instances these processes nasal cavities. At about day 28 of gestation, localized thickenings develop
are swellings of mesenchyme that cause furrows between apparent within the ectoderm of the frontal prominence, just above the opening
processes, so that the ostensible fusion of processes actually involves of the stomatodeum. These thickenings are the olfactory placodes. Rapid
the elimination of a furrow. Only in certain instances, such as the union proliferation of the underlying mesenchyme around the placodes bulges
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DANCE ON STILTS AT THE GIRLS’ UNYAGO, NIUCHI
I see increasing reason to believe that the view formed some time
back as to the origin of the Makonde bush is the correct one. I have
no doubt that it is not a natural product, but the result of human
occupation. Those parts of the high country where man—as a very
slight amount of practice enables the eye to perceive at once—has not
yet penetrated with axe and hoe, are still occupied by a splendid
timber forest quite able to sustain a comparison with our mixed
forests in Germany. But wherever man has once built his hut or tilled
his field, this horrible bush springs up. Every phase of this process
may be seen in the course of a couple of hours’ walk along the main
road. From the bush to right or left, one hears the sound of the axe—
not from one spot only, but from several directions at once. A few
steps further on, we can see what is taking place. The brush has been
cut down and piled up in heaps to the height of a yard or more,
between which the trunks of the large trees stand up like the last
pillars of a magnificent ruined building. These, too, present a
melancholy spectacle: the destructive Makonde have ringed them—
cut a broad strip of bark all round to ensure their dying off—and also
piled up pyramids of brush round them. Father and son, mother and
son-in-law, are chopping away perseveringly in the background—too
busy, almost, to look round at the white stranger, who usually excites
so much interest. If you pass by the same place a week later, the piles
of brushwood have disappeared and a thick layer of ashes has taken
the place of the green forest. The large trees stretch their
smouldering trunks and branches in dumb accusation to heaven—if
they have not already fallen and been more or less reduced to ashes,
perhaps only showing as a white stripe on the dark ground.
This work of destruction is carried out by the Makonde alike on the
virgin forest and on the bush which has sprung up on sites already
cultivated and deserted. In the second case they are saved the trouble
of burning the large trees, these being entirely absent in the
secondary bush.
After burning this piece of forest ground and loosening it with the
hoe, the native sows his corn and plants his vegetables. All over the
country, he goes in for bed-culture, which requires, and, in fact,
receives, the most careful attention. Weeds are nowhere tolerated in
the south of German East Africa. The crops may fail on the plains,
where droughts are frequent, but never on the plateau with its
abundant rains and heavy dews. Its fortunate inhabitants even have
the satisfaction of seeing the proud Wayao and Wamakua working
for them as labourers, driven by hunger to serve where they were
accustomed to rule.
But the light, sandy soil is soon exhausted, and would yield no
harvest the second year if cultivated twice running. This fact has
been familiar to the native for ages; consequently he provides in
time, and, while his crop is growing, prepares the next plot with axe
and firebrand. Next year he plants this with his various crops and
lets the first piece lie fallow. For a short time it remains waste and
desolate; then nature steps in to repair the destruction wrought by
man; a thousand new growths spring out of the exhausted soil, and
even the old stumps put forth fresh shoots. Next year the new growth
is up to one’s knees, and in a few years more it is that terrible,
impenetrable bush, which maintains its position till the black
occupier of the land has made the round of all the available sites and
come back to his starting point.
The Makonde are, body and soul, so to speak, one with this bush.
According to my Yao informants, indeed, their name means nothing
else but “bush people.” Their own tradition says that they have been
settled up here for a very long time, but to my surprise they laid great
stress on an original immigration. Their old homes were in the
south-east, near Mikindani and the mouth of the Rovuma, whence
their peaceful forefathers were driven by the continual raids of the
Sakalavas from Madagascar and the warlike Shirazis[47] of the coast,
to take refuge on the almost inaccessible plateau. I have studied
African ethnology for twenty years, but the fact that changes of
population in this apparently quiet and peaceable corner of the earth
could have been occasioned by outside enterprises taking place on
the high seas, was completely new to me. It is, no doubt, however,
correct.
The charming tribal legend of the Makonde—besides informing us
of other interesting matters—explains why they have to live in the
thickest of the bush and a long way from the edge of the plateau,
instead of making their permanent homes beside the purling brooks
and springs of the low country.
“The place where the tribe originated is Mahuta, on the southern
side of the plateau towards the Rovuma, where of old time there was
nothing but thick bush. Out of this bush came a man who never
washed himself or shaved his head, and who ate and drank but little.
He went out and made a human figure from the wood of a tree
growing in the open country, which he took home to his abode in the
bush and there set it upright. In the night this image came to life and
was a woman. The man and woman went down together to the
Rovuma to wash themselves. Here the woman gave birth to a still-
born child. They left that place and passed over the high land into the
valley of the Mbemkuru, where the woman had another child, which
was also born dead. Then they returned to the high bush country of
Mahuta, where the third child was born, which lived and grew up. In
course of time, the couple had many more children, and called
themselves Wamatanda. These were the ancestral stock of the
Makonde, also called Wamakonde,[48] i.e., aborigines. Their
forefather, the man from the bush, gave his children the command to
bury their dead upright, in memory of the mother of their race who
was cut out of wood and awoke to life when standing upright. He also
warned them against settling in the valleys and near large streams,
for sickness and death dwelt there. They were to make it a rule to
have their huts at least an hour’s walk from the nearest watering-
place; then their children would thrive and escape illness.”
The explanation of the name Makonde given by my informants is
somewhat different from that contained in the above legend, which I
extract from a little book (small, but packed with information), by
Pater Adams, entitled Lindi und sein Hinterland. Otherwise, my
results agree exactly with the statements of the legend. Washing?
Hapana—there is no such thing. Why should they do so? As it is, the
supply of water scarcely suffices for cooking and drinking; other
people do not wash, so why should the Makonde distinguish himself
by such needless eccentricity? As for shaving the head, the short,
woolly crop scarcely needs it,[49] so the second ancestral precept is
likewise easy enough to follow. Beyond this, however, there is
nothing ridiculous in the ancestor’s advice. I have obtained from
various local artists a fairly large number of figures carved in wood,
ranging from fifteen to twenty-three inches in height, and
representing women belonging to the great group of the Mavia,
Makonde, and Matambwe tribes. The carving is remarkably well
done and renders the female type with great accuracy, especially the
keloid ornamentation, to be described later on. As to the object and
meaning of their works the sculptors either could or (more probably)
would tell me nothing, and I was forced to content myself with the
scanty information vouchsafed by one man, who said that the figures
were merely intended to represent the nembo—the artificial
deformations of pelele, ear-discs, and keloids. The legend recorded
by Pater Adams places these figures in a new light. They must surely
be more than mere dolls; and we may even venture to assume that
they are—though the majority of present-day Makonde are probably
unaware of the fact—representations of the tribal ancestress.
The references in the legend to the descent from Mahuta to the
Rovuma, and to a journey across the highlands into the Mbekuru
valley, undoubtedly indicate the previous history of the tribe, the
travels of the ancestral pair typifying the migrations of their
descendants. The descent to the neighbouring Rovuma valley, with
its extraordinary fertility and great abundance of game, is intelligible
at a glance—but the crossing of the Lukuledi depression, the ascent
to the Rondo Plateau and the descent to the Mbemkuru, also lie
within the bounds of probability, for all these districts have exactly
the same character as the extreme south. Now, however, comes a
point of especial interest for our bacteriological age. The primitive
Makonde did not enjoy their lives in the marshy river-valleys.
Disease raged among them, and many died. It was only after they
had returned to their original home near Mahuta, that the health
conditions of these people improved. We are very apt to think of the
African as a stupid person whose ignorance of nature is only equalled
by his fear of it, and who looks on all mishaps as caused by evil
spirits and malignant natural powers. It is much more correct to
assume in this case that the people very early learnt to distinguish
districts infested with malaria from those where it is absent.
This knowledge is crystallized in the
ancestral warning against settling in the
valleys and near the great waters, the
dwelling-places of disease and death. At the
same time, for security against the hostile
Mavia south of the Rovuma, it was enacted
that every settlement must be not less than a
certain distance from the southern edge of the
plateau. Such in fact is their mode of life at the
present day. It is not such a bad one, and
certainly they are both safer and more
comfortable than the Makua, the recent
intruders from the south, who have made USUAL METHOD OF
good their footing on the western edge of the CLOSING HUT-DOOR
plateau, extending over a fairly wide belt of
country. Neither Makua nor Makonde show in their dwellings
anything of the size and comeliness of the Yao houses in the plain,
especially at Masasi, Chingulungulu and Zuza’s. Jumbe Chauro, a
Makonde hamlet not far from Newala, on the road to Mahuta, is the
most important settlement of the tribe I have yet seen, and has fairly
spacious huts. But how slovenly is their construction compared with
the palatial residences of the elephant-hunters living in the plain.
The roofs are still more untidy than in the general run of huts during
the dry season, the walls show here and there the scanty beginnings
or the lamentable remains of the mud plastering, and the interior is a
veritable dog-kennel; dirt, dust and disorder everywhere. A few huts
only show any attempt at division into rooms, and this consists
merely of very roughly-made bamboo partitions. In one point alone
have I noticed any indication of progress—in the method of fastening
the door. Houses all over the south are secured in a simple but
ingenious manner. The door consists of a set of stout pieces of wood
or bamboo, tied with bark-string to two cross-pieces, and moving in
two grooves round one of the door-posts, so as to open inwards. If
the owner wishes to leave home, he takes two logs as thick as a man’s
upper arm and about a yard long. One of these is placed obliquely
against the middle of the door from the inside, so as to form an angle
of from 60° to 75° with the ground. He then places the second piece
horizontally across the first, pressing it downward with all his might.
It is kept in place by two strong posts planted in the ground a few
inches inside the door. This fastening is absolutely safe, but of course
cannot be applied to both doors at once, otherwise how could the
owner leave or enter his house? I have not yet succeeded in finding
out how the back door is fastened.