DENT3002-Oral Histology and Embryology F

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DENT3002 – Oral Embryology and Histology (2 credits)
Dr. O. Ogle , DDS, OMFS
18 Lectures
Compiled by: Lorenzini H. Grant

from DDS Class of 2016
DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

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DENT3002 –Oral Histology and Embryology (2 credits)
Lecture Topic
1 Embryology of Head, Face and Oral Cavity
2 Developmental Anomalies and Syndromes
3 Cleft disorders
4 Inheritances of Dental and Facial Traits
5 Craniofacial Growth and Development
6 Development and Growth of the Maxilla and the Mandible
7 Development of Teeth
8 Dentin Structure
9 Dental Pulp
10 Dentinal Structure
11 Cementum,Cementoenamel Junction (CEJ)
12 Dentinal Sulcus, Dentogingival Junction
13 Supporting Structure
14 TMJ Histology and Embryology
15 Oral Flora [PP]
16 Salivary gland diseases [PP]
17 Salivary glands [PP]
18 Anthroprometrics of the Face [PP]
Lecture 01 – Embryology of Head and Neck

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Main divisions of Prental Development
• Weeks 1 – 3 (0-21days) -Fertilization, Implantation and Gastrulation

Weeks 3 – 8 (22 – 56 days) -Embryo
• Weeks 9 – birth (2.5 mths to birth)- Fetus
• Structural development of the head and neck occurs between the third and eighth
weeks of gestation.
• 5 pairs of branchial arches form on either side of the pharyngeal foregut on day 22.
These are the embryologic basis of all the differentiated structures of the head and neck.
• Each arch consists of 3 layers: an outer covering of ectoderm, an inner covering of

endoderm, and a middle core of mesenchyme.
• The arches are separated into external, ectoderm-lined pharyngeal clefts and internal,
endoderm-lined pharyngeal pouches. \
• The face is formed between week 3 – 8.
Weekly development- Week 1
• Sperm enters the oval cytoplasm in the uterine tube.
• The maternal and paternal chromosomes combine to form a zygote, completing

fertilization.
• The zygote is transported to the uterus, where it undergoes a series of mitotic divisions
and transforms into the ball of small cells termed blastomeres.
WEEK 1 contd.
• The blastomere becomes the morula, a ball of 16 cells (after 4 mitotic divisions), and
begin to form an internal cavity – the blastocyst.
• The blastocyst consists of two layers of cells:
1) an inner layer termed the embryoblast that becomes

the embryo.
2) an outer layer termed the trophoblasts that forms

the embryonic part of the placenta.
At the end of the first week, the superficial implantation of the blastocyst into the uterine wall is
complete.

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WEEK 3
Formation of primitive streak & the germ layers
Trilaminar Embryo. The formation of three layers (ectoderm, mesoderm & endoderm) is called
Gastrulation
Weekly Development
• WEEK 3
• Week # 3 is marked by the formation of the trilaminar embryonic disc by the process of
gastrulation: the inner layer is termed endoderm, the middle layer- mesoderm, and the
outer layer- ectoderm.
• A midsagittal groove appears as a result of invagination of the ectoderm centrally and

simultaneous elevation of ectodermal tissue alongside the groove to form the neural
folds.
• Primitive streak - midline thickening of epiblast at caudal (hind) end gives rise to
mesenchymal cells that migrate between epiblast and hypoblast.

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• The neural fold fuse with each other in the mid line beginning at the junction of the future
brain and spinal cord to form the neural tube.
• A population of ectodermal cells adjacent to the neural fold gives rise to the formation of
the neural crest.
• These neuroectodermal crest cells (stem cells) migrate widely throughout the developing
embryo in a relatively cell-free extracellular matrix and differentiate into a wide array of
cell and tissue types, influenced by the local environment.
Most connective and skeletal tissues of the cranium and face comes from the derivatives of
neural crest cells.
The optic primordia is formed as a thickened area with a shallow sulcus on the lateral
forebrain of the neural tube in the region of the future diencephalon.
Neural crest cells intervene between the optic vesicle and the overlying ectoderm and give rise
to specialized neuroectodermal elements of the eye and adnexum
• By the end of the third week, growth of the cephalic portion of the neural tube gives rise
to the frontal nasal process and the branchial arches, the first stages of a recognizable
face.
• THE THREE GERM LAYERS GIVE RISE TO ALL THE TISSUES AND ORGANS OF
THE EMBRYO
• Ectoderm: CNS & spinal cord, neural crest, adrenal medulla, peripheral nervous
system, epidermis, pituitary.
• Mesoderm: Bone & connective tissue, smooth & striated muscle, heart, blood & lymph
cells, kidneys, gonads
• Endoderm: Many epithelial linings e.g. gut, buccal mucosa, respiratory tract, thyroid,
liver, pancreas
• At ~18days neural groove forms producing neural folds.

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Neural crest formation: cells on the crest of the neural folds migrate
ventrolaterally to either side of the neural tube
Somite formation: mesoderm on either side of the notochord thickens to

form longitudinal columns of paraxial mesoderm
These paraxial columns start dividing into pairs of somites by end of third
week.
Somites are compact aggregates of mesenchymal cells from which cells

migrate to give rise to vertebrae, ribs, axial musculature etc
Neural Tube defects
• The neural tube is the embryonic structure which develops into the
brain and spinal cord. Very early in a baby's development,
a layer of cells folds over and "zips up" to form the neural
tube .
• If the neural tube fails to "zip up" completely at some

point, the baby will be affected with an abnormality called
a neural tube defect. Spina bifida and anencephaly are
the most common neural tube defects.
• Malformations of CNS are relatively common (3 in

1000 births).
• Most due to defects in closure of neural tube
• Failure of closure results in serious developmental
abnormalities
Failure of caudal neuropore closure leads to various forms of spina bifida:
• A congenital defect in which the neural arches fail to close,

so exposing the contents of the spinal canal posteriorly.
Usually occurring in the lumbosacral region (lower back) of
the spine.

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Failure of rostral neuropore to close leads to acrania & anencephaly
Anencephaly
• When the neural tube fails to close at the head, the brain and the
skull bones do not develop normally. This condition is called
anencephaly.
• Infants born with this problem die at, or soon after, birth.
Closure of rostral neuropore produces three primary brain vesicles

(forebrain, midbrain & hindbrain)
Forebrain and hindbrain each subsequently develop into two secondary

vesicles
Lumen of neural tube froms ventricles of the brain
Problems related to the vesicles in the Brain
e.g. hydrocephalus results from blockage of flow of cerebrospinal

fluid in the ventricles
• The CSF normally flows through one ventricle to the next, and
down the spinal cord.
• Hydrocephaly occurs when there is an abnormal

accumulation of cerebrospinal fluid (CSF) inside each of the four ventricles of the brain.
• When the circulation of CSF is blocked it accumulates in the brain.
Because the skull of babies does not fuse quickly, the accumulation of this fluid causes the
head to enlarge due to the swelling of the ventricles.

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Week 4
Branchial arches develop at beginning of the 4th week from some neural crest cells.
Neural crest cells migrate to future head and neck region and 4 pairs of arches appear at end of
4th week separated by branchial grooves
NEURAL TUBE:/BRANCHIAL ARCH FORMATION – 25 DAYS
Stomodeum
Typical Branchial Arch consists of:
Artery
* Cartilage
* Muscle
* Nerve
BRANCHIAL APPARTUS – contributes to development of the face, neck, nasal cavities,

mouth, larynx & pharynx
Malformations of head and neck are produced mainly during development of the branchial
apparatus.

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The adult derivative of each arch is supplied by the cranial nerve that is specific for that
particular arch.
• 1st ARCH – maxillary & mandibular branches of trigeminal (V) nerve

• 2nd ARCH – facial (VII) nerve
• 3rd ARCH – glossopharyngeal (IX) nerve
• 4th ARCH – superior laryngeal branch of vagus (X) nerve
• 5th ARCH – only rudimentary if present
• 6th ARCH – recurrent laryngeal branch of vagus (X) nerve
First Arch Syndrome

Development of the tongue, face, lips, jaws, palate, pharynx and neck
involves modifications of the branchial apparatus into adult structures
MAJOR: Treacher Collins, Pierre Robbins

MINOR: mandibulofacial dysostosis
micrognathia with peromelia
otomandibular dysostosis
acrofacial dysostosis.
First and Second Arch Syndromes
• Hemifacial mirosomia
• Goldenhar-Gorlin Syndrome (Goldenhar Syndrome is now considered a variant of
craniofacial microsomia)
• Craniofacial microsomia: generic name for HMS and Goldenhar syndromes .Also called:
Facio-Auriculo-Vertebral Spectrum

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• Treacher-Collins Syndrome also called mandibulofacial dysostosis

• highly variant degrees of involvement (complete,
incomplete, and abortive forms) are seen
• the syndrome is characterized by hypoplasia of the facial
bones - especially the zygoma and the mandible
• the clinical appearance is a result of the zygoma failing to
fuse with the maxilla, frontal, and temporal bones.
facial features include :

Hypoplastic cheeks, zygomatic arches, and mandible.
High arched or cleft palate
Macrostomia (abnormally large mouth)
Anti-mongoloid slant to the eyes
Anterior open bite
Increased anterior facial height
Hemifacial Microsomia
Classifications of HFM
[Puzansky -1969]
• Type I. Mild hypoplasia of the ramus, and the body of the mandible is minimally or
slightly affected..
• Type II. The condyle and ramus are small; the head of the condyle is flattened; the
glenoid fossa is absent; the condyle is hinged on a flat, often convex, infratemporal
surface; the coronoid process may be absent.
• Type III. The ramus is reduced to a thin lamina of bone or is completely absent. There
is no evidence of a temporomandibular joint.

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Munroe’s Classification for Hemifacial Microsomia

Type IA: The craniofacial skeleton is only mildly hypoplastic and the occlusal plane is
horizontal.
• Type IB: the skeleton is as in IA, but the occlusal plane is canted.
• Type II: the condyle and part of the affected ramus are absent.
• Type III: in addition to the findings in Type II, the zygomatic arch and glenoid fossa are
absent;
• Type IV: This is an uncommon type with hypoplasia of the zygoma and medial and
posterior displacement of the lateral orbital wall;
• Type V: the most extreme type has inferior displacement of the orbit with a decrease in
orbital volume.
Vargervik Classification
• "I (A). The classic type characterized by unilateral facial underdevelopment without
microphthalmos or ocular dermoids but with or without abnormalities of the vertebrae,
heart or kidneys.
• "I (B). Similar to type I (A) except for the presence of microphthalmos.
• I (C). Bilateral asymmetric type in which one side is more severely involved.
• I (D). Complex type that does not fit the above but does not display limb deficiency,
frontonasal phenotype or ocular dermoids.
• II. Frontonasal type. Relative unilateral underdevelopment of the face in the
presence of hypertelorism with or without ocular dermoids and vertebral, cardiac, or
renal abnormalities.
• IV. (A) Unilateral or (B) Bilateral. Goldenhar type with facial underdevelopment in
association with ocular dermoids, with or without upper lid coloboma.
OMENS Classification on Reporting on CFMS

• O = orbital
• M = mandibular
• E = ear
• N = facial nerve
• S = soft tissue.
Theories of Aetiology of CFMS
• VASCULAR: - Stapedius Artery (Poswolo)

Focal hemorrhage or devascularization
• Retinoic Acid Syndrome
Crest cells have large amt of RA binding sites
Acutane type chemicals bind to RA sites & kills stem cells
Early distruction  craniofacial microsomia
Late disruption destroys placode cells and causes Treacher Collins syndrome

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Week 4 Continued
• The recognizable face begins its development in the 4th week from 5 primordia that
surround a central area of depression - the stomadeum or the oral pit.
• These 5 primordia are:
1) the single cranially located frontal nasal process
2) the two maxillary processes – bilaterally located
3) the two mandibular processes.
• The maxillary and mandibular processes are derived from the first branchial arch.
• The first branchial arch (also termed the mandibular arch) forms the lateral wall and
base of the stomodeum ( the primitive mouth).
• The remaining branchial arches constitute the lateral and anterior walls of the primitive
oropharynx and with the corresponding pharyngeal pouches between them eventually
give rise to the features of the face.
The mandibular processes are the first to merge with each other at the mid line and
eventually give rise to the mandible and the lower part of the face and tongue. This is
completed by the end of this week (4th).
The dorsal end of the first arch cartilage, also termed Meckel cartilage, ossifies to form
the malleus and incus of the middle ear. The dorsal end of the second arch cartilage, also
termed Reichert cartilage, ossifies to form the stapes of the middle ear and the styloid
process of the temporal bone.
Clinical Relations
• The most common congenital anomaly of the branchial clefts is remnants of the
second branchial cleft which may degenerate into cystic cavities termed branchial
cleft cysts.
• The external component of this cleft is

found at the anterior junction of the
middle and lower thirds of the
sternocleidomastoid muscle and its
track usually passes over the
glossopharyngeal nerve and between
the internal and external carotid
arteries to the tonsillar fossa.

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Bilateral Branchial Cleft Cysts
Craniofacial Microsomia
• The disorder is characterized by a wide spectrum of symptoms and physical

features that may vary greatly in range and severity from case to case.
• It involve the cheekbones, jaws, mouth, ears, eyes, and/or bones of the spinal column
(vertebrae)
• most cases affect only one side of the body (unilateral)
• 10 to 33 percent of affected individuals have such malformations on both sides of the
body (bilateral), with one side typically more affected than the other (asymmetry).
• In the majority of cases, the right side is more severely affected than the left.
• an affected individual's face may appear smaller on one side than the other (hemifacial
microsomia)
• may include underdevelopment of the cheekbones (malar hypoplasia), bones of the
upper and lower jaws (maxillary and mandibular hypoplasia), and the bones forming
a portion of the lower skull (temporal hypoplasia)
• incomplete development of certain muscles of the face

• an abnormally wide mouth (macrostomia)
• cleft palate
• cleft lip
• abnormalities of the teeth
• malformation (microtia) of the outer ears (auricles or pinnae)
• absent external ear canals (atresia)
• abnormal outgrowths of skin and cartilage on or in front of the ears (preauricular
tags)

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Week 5
• The maxillary processes continue to enlarge, encroaching on the stomadeum, to form a

primitive oral cavity.
• The first branchial arch gives rise to muscles of mastication (temporalis, masseter,
lateral pterygoid, medial pterygoid).
• The mylohyoid, anterior belly of digastric, tensor tympani, and tensor veli palatini
muscles also are derived from the first branchial arch.
• The second branchial arch develops into the muscles of facial expression.
• At the end of the fourth week, a median swelling, also termed median tongue bud,
appears in the floor of the primitive pharynx just rostral to the foramen cecum.
• The tongue is derived from the first through fourth branchial arches.
• The posterior one third develops from the copula formed by the ventromedial part
of the second branchial arches and the hypopharyngeal eminence from the
ventromedial part of the third and fourth branchial arches.
Development of Tongue
The median tongue bud appears on the floor of the primitive pharynx at the end of
the 4th week
Two distal tongue buds appear on each side of

median bud and ultimately grow over the median
bud.
The fused distal buds form the anterior two-
thirds of the tongue
The posterior third derived from the
hypobranchial eminence which grows over the
copula
(Median bud does not form a recognizable part
of the adult tongue).
• The general mucosal sensory innervation of the anterior two thirds of the tongue
(derived from the first arch) is from the lingual branch of the trigeminal nerve - the
nerve of the first branchial arch.
• The chorda tympani branch of the facial nerve - the nerve of the second branchial
arch - supplies the taste buds of the anterior two thirds of the tongue, except the
vallate papillae.
• The glossopharyngeal nerve - the nerve of the third branchial arch - supplies the taste
buds in the vallate papillae and most of the posterior one third of the tongue.
• The superior laryngeal branch of the vagus nerve - the nerve of the fourth
branchial arch -innervates a small patch of the tongue anterior to the epiglottis.

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Hypoglossal nerve innervates the tongue muscles when they

develop
Sensory innervation explained by developemnt from branchial

arches
Good things to know!
Tongue malformations uncommon except for:
• Fissuring
• Hypertrophy of taste bud papillae (found in Down
syndrome)
• Cleft of tongue which can arise when there is incomplete fusion
of the distal tongue buds
Development of Palate
• Adult palate develops from primary and secondary palates between 5th and 12th week.
• Critical time with regard to malformations is from 6th to 9th week
12 pairs of cranial nerves develop during 5th and 6th weeks
Classified into three groups according to their embryological origin
• Somatic efferent nerves: innervate muscles of the head (III, IV, VI & XII)
• Nerves of branchial arches: supply structures derived from branchial arches (V, VII,
IX, & X)
• Special sensory nerves: (I, II & VIII)
• Cells of the cranial, spinal and autonomic ganglia (and most of the autonomic
nervous sytem) are derived from the neural crest cells
Week 6
• The medial nasal processes approach each other to form a single globular process
that in time gives rise to the nasal tip, columella, prolabium, frenulum, and the
primary palate.
• The frontonasal process collapses inward to form the nasal septum
• Toward the end of the sixth week, the maxillary process fuses with the medial nasal
fold of the globular process, forming a true nostril as it gives rise to the lateral lip
element.
• Posterior to this anterior fusion of the maxillary process to the nasal processes, the
developing nasal floor is open to the oral cavity. Within the primitive stomadeum, lateral

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palatine processes develop from the medial edges of the maxillary process to give rise
to the secondary palate. .
• At this stage, the developing tongue nearly fills the oronasal cavity completely and
reaches the nasal septum.
Week 6 continued
• During this sixth week, the external ear develops from 6 mesenchymal swellings
(hillocks) that surround the first branchial cleft.
• The first 3 hillocks arise from the mandibular arch (first branchial arch); the second
3, from the hyoid arch (second branchial arch).
• From ventral to dorsum, the hillocks of the first arch become the tragus, helix,
and the cymba concha.
• The hillocks on the second arch become the antitragus, antihelix, and concha.
• The branchial cleft lengthens to form the primordium of the external auditory
canal.
Week 8
• Complete closure of the lower facial fissures or grooves.

• The upper and lower jaws are formed with the complete fusion of the maxillary and
mandibular processes.
• The eyes begin to take a more medial position. The anterior rotation of the eyes
continues throughout the remainder of the gestational period and well into childhood.
• Ossification centers arise within the mesenchyme (membranous ossification).
• The primordial elements of the chondrocranium begin to undergo endochondral
ossification to form the bones of the basicranium (sphenoid, petrous part of
temporal and occipital bones) and the nasal ethmoid significantly later in fetal life.
• Maxillary bone ossification centers arise within the zygomatic and squamoid portion of
the temporal region.
• The mesenchyme encompassing Meckel cartilage undergoes membranous
ossification to form the body of the mandible.

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Lecture 2 : Developmental Abnormalities and Syndrome
Branchial Grooves and Pharyngeal Pouch Derivatives
POSSIBLE SITES OF FACIAL CLEFTS

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Craniofacial Dysmorphological Syndromes

a) Syndromes associated with brain development
* Holoprosencephaly
b) Syndromes of mandibulofacial and acrofacial dysostosis
* Mandibulofacial dysostosis (Treacher Collins syndrome)
• * Preaxial acrofacial dysostosis (Nager syndrome)
c) Oculo-auriculo-vertebral spectrum
* Hemifacial microsomia
DISORDER WITH CLEFT PALATE AS AN OBLIGATORY OR LIKELY ASSOCIATED

FINDING
• Pierre Robin syndrome/sequence

• Velo-cardio-facial syndrome (DiGeorge syndrome; Shprintzen syn.)
• Ectrodactyly-ectodermal dysplasia-clefting syndrome (EEC)
Holoprosencephaly (Alobar, semilobar,lobar)
6-12 per 100,000 births. Three variations
A cephalic disorder in which the prosencephalon (the forebrain of the embryo) fails
to develop into two hemispheres.
• An anterior midline defect that results in a series of induction malformations
characterized by midline facial and CNS defects.
• The condition can be mild or severe but in most cases the malformations are so severe
that babies die before birth.
Associated with:
• chromosomal abnormalities (such as trisomy 13, 15, 18 or
genes in chromosomes 2, 7, 18, 21)
• maternal diabetes mellitus
• fetal infections of CMV, toxoplasmosis, syphilis
• exposures to phenytoin, retinoic acid, and alcohol.
VELO-CARDIO FACIAL SYNDROME

(DiGeorge Syndrome or Shprintzen Syndrome)
• 1 per 3,000-5,000 births
• DiGeorge Syndrome: the second most common cause of Mild case of
congenital heart defects after Down Syndrome. holoprosencephaly
• Abnormal development of the face, thymus and parathyroid
glands and heart.
• Micro-deletion of a small segment of the long arm (q11.2) of chromosome 22

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Di George Syndrome Include:
• Congenital heart disease (74%) – tetralogy of

Fallot, interrupted aortic
• Palatal abnormalities (69%) – CP, VPI and
submucosal cleft palate
• Characteristic facial features(95%) -hypertelorism
• Learning difficulties (70 - 90%).
• Hypocalcemia and immune deficiency (50%)
Clinical Features
Short stature, microcephaly, learning challenges
• Eye problems, hearing problems, emotional and behavioral

problems
• Low muscle tone, cleft palate, gastro-intestinal problems
• Scoliosis, immune system problems, heart defects
Ectodermal Dysplasia
A group of conditions in which there is abnormalities in the
development of ectodermal structures: skin, hair, nails, teeth, or sweat
glands.
• There are many different types of ectodermal dysplasia.

• The most common form of ectodermal dysplasia usually affects
men.
Features of Ectodermal Dysplasia
Features of Ectodermal dysplasia
Abnormal nails Heat intolerance
Abnormal or missing teeth Inability to sweat
Absent or decreased tears Poor temperature
Poor vision regulation
Decreased skin color Large forehead
(pigment) Low nasal bridge
Lower than normal Poor hearing
number of teeth per arch Thin, sparse hair
Thin skin

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Mandibulofacial Dysostosis (Treacher Collins Syndrome)
• 1 in 50,000 births
• Autosomal dominant.
• The cause of Treacher Collins Syndrome is a genetic mutation. “Treacle” gene on
chromosome 5
• TCOF1 is the only gene currently known to be associated with TCS, a mutation in this
gene is found in 90-95% of the individuals with TCS
Clinical Features of Mandibulofacial Dysostosis

• EAR • FACIAL BONES
• abnormal • malar hypoplasia
external ears • high or cleft
• hearing loss palate
• anomalies of • mandibular
middle and inner hypoplasia
ears.
• EYE
• ptosis of upper
eyelid
• cleft of the lower
eyelid (coloboma)
• down slanting
palpebral fissures
Patient with Treacher Collins Syndrome
Hemifacial Microsomia
Also known as Oculo-Auriculo-Vertebral Dysplasia

Goldenhar Syndrome
• First and Second Branchial Arch Syndrome

• A congenital disorder that affects the development of the lower
half of the face, most commonly the ears, the mouth and
the mandible.

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• It is the second most common facial birth defect after clefts, with an incidence in the
range of 1 in 3500 to 4500
• CAUSE: during the fetal stage of pregnancy, at approximately 4 weeks of gestation,

some form of vascular problem leads to clotting and a decrease blood supply to the
developing face. This can be caused by a physical trauma.
• The loss of the blood supply restricts the developmental ability of the affected area of the
face
HFM Clinical Features
• Clinical presentation is variable.

• May involve just the ear - small,
underdeveloped ear with tags or pits
• Facial asymmetry
• Missing or malformed portions of the
mandible.
• Maxillary and mandibular hypotrophy.
Classification of HFM
OMENS:
o Orbital
o Mandible
o Ear
Nerves
 Soft tissue
Kabans Classification
• TYPE 1: Mild hypoplastic state involving muscles of mastication, glenoid fossa, smaller
mandibular ramus and condyles. Normal TMJ
function. May or may not involve ear.
• TYPE 2: A and B
A: small coned shaped condylar head,
hypoplastic glenoid fossa. Normal TMJ
function
B: severe hypoplasia of condyle and ramus. No

real TMJ

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Treatment for Hemifacial Microsomia

Treatment for Hemifacial MICROSOMIA
Ear Reconstruction:age 6 to 7 Closure of open bite:
Presurgical jaw orthopedic Extrusion of maxillary teeth
Mandibular Surgery: Maxillary jaw surgery
Costochondral rib grafts Final orthodontics
Distraction osteogenesis Cosmetic procedures:
Interarch splints Assymetric genioplasty
Treatment of occlusion with Alloplastic grafts
guiding elastics Rhinoplasty
Soft tissue augmentation
Orthodontic Appliances
Low-intensity pulsed ultrasound (LIPUS)
Premature Closure of Cranial Sutures

Scaphocephaly: premature closure of sagittal suture (long and narrow head)
• Trigonocephaly: premature closure of the metopic suture (wedge-like triangular

appearing forehead)
• Brachycephaly : premature closure of both coronal sutures (braod and short skull
shape)

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• Oxycephaly (Turricephaly): premature closure of sagittal suture, later followed by

premature closure of the coronal sutures
• (point-up and long head)
• Plagiocephaly - anterior type:
• premature closure of one of the coronal sutures
• (Uneven height of the orbits. A flat and recessed forehead on the involved side.)
Scaphocephaly – long narrow head
Trigonocephaly
WEDGE SHAPED – Triangle shaped head
Brachycephaly
Broad and short skull shape

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Oxycephaly –Pointed Up and Long Head
Plagiocephaly-UNEVEN ORBITS AND FLAT FOREHEAD
Craniofacial Dysostosis (Crouzon Syndrome)
• A genetic disorder known as a branchial arch syndrome.

• Affects the first branchial (or pharyngeal) arch, which is the precursor of
the maxilla and mandible.
• During development, the skull and facial bones of the infant fuses early or are unable to
expand preventing normal bone growth.
• For dentists, this disorder is important to understand since many of the physical
abnormalities are present in the head, and particularly the oral cavity.
• 1 in 25,000 births
• Associations with mutations in the genes of FGFR2 and FGFR3
• FGFR2 (fibroblast growth factor receptor2 ) mutations (95%); chromosome 1, 10 (10q26)
• Crouzon syndrome is autosomal dominant

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Crouzon Syndrome:Clinical Features
• Premature closure of coronal sutures

• Cranial deformity
• Abnormal bony orbit
• Exophthalmos; strabismus; hypertelorism/
• Small beak-shaped nose
• Severe maxillary hypoplasia
• Relative mandibular prognathism
Crouzon Syndrome :Dental Features
• Narrow/high-arched palate.
• Posterior bilateral crossbite – due to hypoplastic maxilla.
• Congenitally missing teeth
• Crowding of teeth in maxilla
• Due to maxillary hypoplasia, Crouzon patients generally have an “ underbite” and
subsequently cannot chew using their incisors.
• Will eat fried chicken with a fork or breaking off pieces of a sandwich rather than biting
into it.
Clinical features of Crouzon Syndrome

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Acrocephalosyndactyly (Apert Syndrome)
• A branchial arch syndrome similar to Crouzon Syndrome.

• An autosomal dominant disorder due to a C to G mutation at the position 755 in the
FGFR2 gene, which causes a Ser to Trp change in the protein.
• This is a male-specific mutation: with the mutation always occurring on the paternally
derived allele.
• The incidence rises incrementally with the age of the father. Old fathers
Amino Acid Coding

One letter Three letter
Amino acid Possible codons
code code
A Ala Alanine GCA, GCC, GCG, GCT
B Asx Asparagine or Aspartic acid AAC, AAT, GAC, GAT
C Cys Cysteine TGC, TGT
D Asp Aspartic acid GAC, GAT
E Glu Glutamic acid GAA, GAG
F Phe Phenylalanine TTC, TTT
G Gly Glycine GGA, GGC, GGG, GGT
Apert Syndrome
1 in 100,000 births
• FGFR2 (fibroblast growth factor receptor 2) mutations (100%) Chromosome 1, 10
(10q26)
• Syndrome expresses signs and syptoms related to craniosynostosis and limb
anomalies (Syndactyly)
Clinical Features
Craniosynostosis Syndactyly
• Synostosis of the • Symmetrical syndactyly
coronal sutures of the hands and feet.
• Brachycepahalic • A short thumb with radial
• Exophthalmos deviation
• Hypertelorism • Complex syndactyly (two or
• Midface hypoplasia more digits fused together)
• Retrusive Maxilla. of the index, long and ring
• Anterior open bite and finger
posterior crossbite • Symbrachyphalangism
(congenital ankylosis of the
proximal joints of the fingers
and toes)
• Simple syndactyly of the
fourth webspace

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Images of patients with Aperts Syndrome (Craniofacial Dysostosis)
Malocclusion in Apert Syndrome
Hands and Feet
Note the fusion of the digits of the hands and feet.
Dental Features of Apert Syndrome

Class 3 occlusion ( lower jaw forward in relationship to upper jaw)

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Dental features of Apert Syndrome

A high-arched palate • Congenitally missing
• Narrow palate teeth
• Anterior open bite • Crowding of the
** (important teeth.
feature)
Cleidocranial Dysplasia
A hereditary congenital disorder due to HAPLOINSUFFICIENCY by mutations in
the CBFA1 gene also called Runx2, located on the short arm of chromosome 6.
• HAPLOINSUFFICIENCY: When a diploid organism has only a single functional copy of

a gene (with the other copy inactivated by mutation) and the single functional copy of
the gene does not produce enough of a gene product, leading to an abnormal or
diseased state. It is responsible for some autosomal dominant disorders.
• Autosomal dominant
• Rearrangement of long arm of chromosome 8 (8q22) and the long arm of
Chromosome 6 (6q)
Clinical features
• hypoplasia or aplasia of clavicle
• hypermobility of shoulders
• short stature (affected entire skeleton)
• short middle phalanges of the 5th fingers
• large head and brachycephalic
• hypertelorism
• pronounced frontal, parietal, occipital bossing (Arnold head)
Cleidocranial dysplasia: Dental Features

• Maxillary hypoplasia
• Highly arched palate
• Delayed, unerupted, impacted, and supernumerary teeth of the permanent dentition

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Cleidocranial Dysplasia :Images
CD-Dental Features
Lecture 03- Clefting Disorders
Epidemiology of Cleft Disorders

• WHITE : 1: 1,000 LIVE BIRTHS
• ASIAN : 1: 500 LIVE BIRTHS
• BLACK: 1: 2,500 LIVE BIRTHS
U.S.A 1:750
Frequency of Clefts
Frequency of Clefts
• Combined CL/CP: 46 %
• Isolated CP: 28 %
• Isolated CL(+/- ALVEOLUS): 18 %
• Bilateral Clefts: 8%

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Facts about Clefting
• Male are affected more often than female.

• Isolated unilateral clefts (CL +/- CP) occur twice as frequently on the left side as on the
right and are 9 times more common than bilateral clefts.
• For parents with cleft lip and palate or for a child with cleft lip and palate, the risk of
having a subsequent affected child is 5%
• The risk increases to 9% with 2 previously affected children.
• The risk to subsequent siblings increases with the severity of the cleft
• Isolated Clefts of the secondary palate are far more likely to be associated with
syndromes than are clefts involving the lip alone or the lip and palate.
• Lip clefts are usually nonsyndromic and believed to be either multifactorial in origin or
the result of changes at a major single-gene locus.
• 86% of patients with bilateral clefts of the lip present with palatal clefts.
• 68 % of unilateral clefts of the lip are associated with palatal clefts.
Syndromic Clefts
• The most commonly recognized syndrome associated with clefts of the lip and palate is
Van der Woude syndrome.
• This syndrome is an autosomal dominant disorder.
• It is characterized by clefts of the lip and/or palate and blind sinuses, or pits, of the
lower lip.
Etiology
• Isolated clefts are not linked to exposure to any single teratogenic agent except the
anticonvulsant drug phenytoin. (Use of phenytoin during pregnancy is associated
with a 10-fold increase in the incidence of cleft lip)
• The incidence of cleft lip in infants born to mothers who smoke during pregnancy is twice
that of those born to nonsmoking mothers.
• 12-14% of clefts are associated with syndromes.
• MULTIFCTORIAL
• MULTIGENETIC
• HEREDITARY IN 20 – 30% OF CASES

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i.e.: clefts run in families in 25% of cases. The parents of a cleft patient have a 5% chance of
having another child with CL/P.
Other Etiological Factors
• NUTRITION
• AGE OF THE PARENT
• VITAMIN DEFICIENCIES
• RADIATION
• DRUGS
• HYPOXIA
• VIRUSES
Development of the Palate
• Adult palate develops from primary and secondary palates between 5th and 12th week.
• Critical time with regard to malformations is from 6th to 9th week
Primary palate (median palatine process) forms

from the medial nasal prominences.
Secondary palate forms from lateral palatine

processes
After the 7th week, these fuse along the midline and with the
primary palate and nasal septum

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Problems of the Cleft Palate Patient
• EAR PROBLEMS
• NASAL PROBLEMS
• DENTAL PROBLEMS
• SPEECH DIFFICULTIES
• DENTOFACIAL DEFORMITIES
Surgical Treatment of the Cleft Palate patient
• Pre-surgical orthopedics: birth – 3 months

• Lip repair: 3 months. (Rule of tens)
• Closure of palate: 12 – 18 months
• Pharyngeal flap: 5 years (if necessary)
• Alveolar bone graft: 9 years
• Orthognathic Surgery: M= 18 yrs .F= 15 yrs
• Rhinoplasty: Late teens
Rule of tens
Baby should be at least:
10 weeks old
10 gms of Hemoglobin
10 lbs of weight.
Note the dentoalveolar defects in patients with unilateral cleft

lip.
Unilateral cleft lip Bilateral Cleft Lip
Lip Adhesion
• Surgical lip adhesion may be used for bilateral clefts as an

alternative to presurgical orthopedics.
• In lip adhesion, the soft tissues of the lip are united,
essentially converting a wide complete cleft to an incomplete
cleft.

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• Function of the obiculoris muscle along with the surgically

created Simmonart’s band will reposition the protruding
premaxilla.
Lateral Clefts
Problems of Cleft Palate
• FEEDING
• EAR INFECTIONS
• POSSIBLE LOSS OF HEARING
• URI’s
• HYGIENE PROBLEMS
• DENTAL MALOCCLUSIONS
• SPEECH DIFFICULTIES
Anatomy of the Palate
Submucus Cleft
• A submucous cleft palate is defined by the presence of a bifid or

double uvula, muscular diastasis of the soft palate (zona
pellucida), and notching of the posterior border of the hard palate.
• An occult submucosal cleft palate is an absence or deficiency of
the musculus uvulae with a diastasis of the levator veli palatini but
without the presence of a bifid uvula or grooving of the oral
surface of the soft palate.
• An occult submucous cleft is best visualized endoscopically as
the absence of the bulge on the nasal surface of the soft palate
during speech.

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Lecture 04- Inheritance of Dental and Facial Traits
Basic Review of Definitions

• Chromosome: gene containing body found in nucleus
• DNA (deoxyribonucleic acid): codes of genetic information; nuclear DNA and mitochondria
DNA
• Nucleotide (base): A (adenine), G (guanine), T (thymine), C (cytocine), U (uracil); purine (A
& G), pyrimidine (T & C)
Codon: 64 codens; 60 in 20 amino acid; 1 starting (AUG) and 3 termination (UAA, UAG, UGA)
codens
Gene: unit of genetic information
Locus: position of gene in a chromosome
Allele: alternative form of gene in the same locus
Karyotype: chromosomal institution of each species
Genome: full DNA content of the chromosome set
Autosomes: the chromosomes which determines the body development
Sex Chromosomes: the chromosomes which determines the sex development
Classification of Genetic Disorders
a) Chromosomal Disorders
b) Single-Gene Disorders
c) Multifactorial Disorders
Chromosomal Abberations
Accounts for 50% of first trimester spontaneous abortion. Common: 7 in 1000 live births.
An excess or deficiency of whole chromosome or chromosomal segments upsets the

normal balance of the genome
• A) Excess or loss of one or more Chromosomal Abberation Examples

chromosome: monosomy, trisomy, AUTOSOMES: Monosomy 21 (Antimongolism)
Aneuploidy, triploidy, tetraploidy: Trisomy 21 (Down syndrome),
13, and 18
• B)Deletion: breakage and loss of a piece of a
chromosome SEX CHROMOSOMES: Monosomy X
(Turner’s syndrome) Trisomy XXX XXY
(Klinefelter syndrome); XYY
• C)Translocation: breakage of two
chromosomes with transfer of the broken
fragments MOSAICISM: Two cell lines of an individual
Happens in the cleavage of zygote (non-
• D)Isochrome formation: abnormal splitting of disjunctionin mitosis)
the centromere during mitosis, resulting in the 46/47: (+21), (XY/XXY) 45/46: (X/XX), (X/XY)
loss of one arm and the duplication of the other
• E) Chromosomal mosaicism

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Down’s Syndrome (Mongolism)
• Epicanthal folds, superolateral slanted

palpebral fissures
widespread eyes
• broad nasal bridge
• small ears,
• macroglossia with protrusive tongue
Children with Down’s Syndrome
Trisomy 18-Edwards Syndrome
• closely set eyes

(hypotelorism)
• low-set ears
• small mouth
(microstomia).
• Severe cardiac anomalies.
XO- Turners Syndrome
• Female characteristics
• Short stature
• Broad chest with widely spaced nipples.
• Low hairline at back of neck
• Low-set ears
• Drooping eye lids
• Increased weight, obesity
• Nonverbal Learning Disability (problems with
math, social skills and spatial relations)

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Turner’s Syndrome –Dental Features
• Short body of mandible

• Short hard palate with narrow width
• Lateral palatine ridges
• Class 2 malocclusion
Klinefelter Syndrome
XXY Males
Tall stature
Large breast
Small testicles and penis
Lack of facial, pubic and underarm hair.
High incidence of tooth decay.
Patterns of Gene Inheritance
1) Caused by mutant gene

2) Characteristic pedigree patterns
3) Rare: 1 in 2000 or less
4) Over 6000 known genetic disorder, 2000 are known to be simple
Mendelian genetic disorders. And among them, 75% affects craniofacial expression
Pattern of Single Gene Inheritance
• Autosomal vs. X-linked
• Dominant vs. Recessive
• Dominant: a trait determined by a dominant allele: a trait that is visible or measurable

and that prevents the appearance of the recessive; an allele is expressed whether
homozygous or heterozygous.
• Recessive: a trait determined by a recessive allele; a trait that is not visible or
measurable when paired with the dominant allele; an allele is expressed only when
homozugous.
• Codominance, Incomplete dominance
• Codominance: both allele of a pair are fully expressed in heterozygotes (ex. ABO blood
typing)
• Incomplete dominance:A heterozygous condition in which both alleles at a gene locus
are partially expressed, often producing an "intermediate phenotype". Example: Red and
white flower parents give pink flower offspring, a third phenotype. This is the "blending"
of parent phenotypic characteristics.

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Genotype vs. Phenotype
• Genotype: actual genetic makeup of an individual; genetic constitution referred to a

single locus
• Phenotype: the observable or measurable characteristics of an individual as determined

by the genotype and the influence of environment; expression of the genotype as a
morphological, biological, or physical trait.
• Autosomal dominant inheritance

• Autosomal recessive inheritance
• X-linked dominant inheritance
• X-linked recessive inheritance
Autosomal Dominant Inheritance
• affects every generation (no skipping)

• - affected person – affects 1/2 of offspring
• - unaffected person – does not transmit
• - males and females are equally affected
• - pedigree: male-to-male transmission pattern
Dentinogenesis Imperfecta (Hereditary

Opalescent Dentine)
• Autosomal dominant inheritance (A/D)

• Type I (associated with osteogenesis
imperfecta - OI): A/D
• Type II (not associated with OI): A/D 1 in
8,000
• Type III (Brandywine type): A/D
•
Pedigree Chart of Dentinogenesis Imperfecta
• DGI and Dental Dysplasia (DD): autosomal dominant genetic conditions.

• Abnormal dentine structure affecting either the primary or both the primary and
secondary dentitions.
• Teeth appear amber, brown/blue or opalescent brown.
• Radiographically - the crowns may appear bulbous, pulp chambers are often small or
obliterated and the roots are often narrow with small or obliterated root canal

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Dentinogenesis Imperfecta
Amelogenesis Imperfecta (Hereditary enamel dysplasia) (Hereditary brown enamel)
• abnormal formation of the enamel (external layer of teeth).
• can have different inheritance patterns depending on the gene that is altered.
• mutations in the AMELX, ENAM, MMP20, and KLK-4 genes have been found to cause
amelogenesis imperfecta (non-syndromic form)
• Most cases are caused by mutations in the ENAM gene and are inherited in an
autosomal dominant pattern.
Autosomal Recessive Inheritance
• characteristically appears only in siblings

• - skip generations – parents, offspring not affected
• - 1/4 of siblings of proband (propositus) affected
• - males and females are equally likely to be affected
• - pedigree: parents may be consanguineous

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Amelogenesis Imperfecta (Hereditary enamel dysplasia) (Hereditary brown enamel)
TYPES:
Hypoplastic (defective formation of matrix) - enamel does not grow to its full thickness.
Hypocalcified (defective mineralization of the formed matrix) soft enamel which can be
removed with an instrument
Hypomaturation (enamel crystallites remain immature) enamel chips away easily
1. Hypoplastic (defective formation of matrix)
(enamel does not grow to its full thickness)
Autosomal Recessive Inheritance
appears only in siblings

skip generations – parents, offspring not affected
1/4 of siblings of proband (propositus) affected
males and females are equally likely to be affected
pedigree: parents may be consanguineous
X linked Dominant Inheritance
Affected male – affects all daughters; affects no sons

Affected female – affects 1/2 of her children
(as in autosomal dominant inheritance)
the trait in affected females is twice as common as in affected males (males and females are
not equally affected)
Pedigree: never father-to-son transmission
Amelogenesis Imperfecta - Hypoplastic Type: X-linked Dominant Trait

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• Intermediate inheritance (Incomplete dominance)
Heterozygous are different from both homozygotes (sickle cell anemia; sickle cell traits: a
portion of cells show sickling phenomenon or mild anemia)
• Sex-limited traits: precocious puberty in male;

hydrometrocolpos in female
• Sex-influenced traits: baldness in male; congenital adrenal hyperplasia in female
• Penetrance: all or none phenomenon
• Expressivity: severity
• Pleiotropy: one gene, more then one effect e.g. syndromes, phenylketonuria,
galactosemia
• Genetic heterogeneity: several genes, one effect
• e.g: profound childhood deafness, osteogenesis imperfecta
• Imprinting: expression of the trait based on the presence of either the material or
paternal allele (and that allele only) [To date, about 40 imprinted genes have been
identified in humans of chromosome 1, 6, 7, 11, 12, 13, 14, 15, 18, 19, and 20]
Inheritance of Craniofacial Traits
• Pierre Robin syndrome: sporadic, non-genetic condition, low recurrence risk
• Ectodermal dysplasia-Ectrodactyly-Cleft syndrome: A/D; penetrance (+) ; variable

expressivity
• Mandibulofacial dysostosis (Treacher Collins syndrome) : A/D; 1/2 spontaneous

mutation; penetrance (+)
• Hemifacial microsomia: sporadic; possible A/D or R; variable expressivity
• Craniofacial dysostosis (Crouzon & Apert syndromes): A/D; sporadic occurrence;

penetrance (+)
• Cleidocranial dysplasia: A/D or R; sporadic

occurrence; penetrance (+)
• Osteogenesis imperfecta: 4 types, 2 are A/D; 1 is A/R; 1 is both A/D and R
• Achondroplasia: A/D, penetrance (+)
Indication of a Genetic Condition rather than Environmental Etiology
a) The occurrence of the disease in definite proportions among persons related by descent,
when environmental causes can be ruled out.
b) The failure of the disease to appear in unrelated lines (ex. in spouses or in-laws)
c) A characteristic onset age and course, in the absence of known precipitating factors.

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d) Greater concordance in monozygotic than in dizygotic twins.
e) The presence in the patient of a characteristic phenotype, often including mental retardation,
and a demonstrable chromosomal
abnormality, with or without a family history of the same or related disorders.
Lecture 05- Growth and Development
Definition of Growth and Development
Growth: Growth is The quantitative increase in protoplasmic mass (physical size). It includes
the cellular and extracellular components.
• Occurs in a carefully regulated fashion.
Growth occurs in three ways:

• a) cell hyperplasia: a steadily decreasing process from conception through adulthood
• b) cell hypertrophy: this occurs at any age.
• c) the growth of extracellular matrix
Development : refers to the increase in skill, capacity, and complexity of function, or change in
relative position of a part of the body as a result of differential growth, or change in the
hierarchy.
• Related to growth, but is not synonymous. In the normal individual, they are parallel
processes that are defined differently.
• Development is a progression of changes, either quantitative or qualitative, that lead
from an undifferentiated or immature state to a highly organized, specialized, and mature
state.
• Example: the development of motor skills in a child. The development in neuromuscular
control lead to greater dexterity
Measures of Growth and Development
• I. Chronological (time)
• II. Biological/Physical
– 1. Sex development (secondary sex characteristics)

– 2. Physiological (metabolic rates; blood chemistry)
– 3. Skeletal (timing of the appearance of ossifying center; timing of the suture
closure; ossification and hand-wrist X-ray; pubic symphysis staging)
– 4. Dental (presence of dental development stages; crown and root
formation,eruption and emergence pattern; attrition pattern)
– 5. Morphological (size and shape changes; height, weight, head circumference
measurement)

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• III. Cognitive assessment

• IV. Psychosocial
Chronological in Growth and Development
Growth period Approximate age
1. Pre-natal 0-280 days

Ovum 0-14 days ( first 2 weeks)
Embryo 14 days to 8 weeks
Fetus 9 weeks to birth
2. Premature infant: 27 weeks to 37 weeks (3rd trimester)
3. Birth Average: 280 days
4. Neonate (new born) First 4 weeks after birth
5. Infancy (infant) First year
6. Early childhood(pre-school): 1 year to 6 years
7. Late childhood (juvenile): 6 years to 10 years
8 Adolescence (teens)
Females: 8 or 10 to 18 years Males: 10 or 12 to 20 years
Puberty (average): Females: 13 years Males: 15 years
9. Adult 18 or 20 years and above

– middle aged 40 – 60 years
– elderly: 60 and above
Maternal Factors affecting Fetal Development

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Effects of Aging
Effects of Aging
Skeletal System: Urinary System:
Degenerative changes; Osteoarthritis -Nephron units decrease;
Reduction in urine
Integumentary System: - Decrease bladder
Dry, thin, and inelastic skin. - Prostate issues in men
Sagging; Wrinkling and folding Respiratory System:
-the expanding and contracting ability of
Cardiovascular System: rib cage decreases;
cage Atherosclerosis;
Hypertension
Decrease of respiratory efficiency
Special Senses: Tooth loss is not part of the normal
Presbyopia; Cataract; Glaucoma; aging process.
Decline of hearing Teeth becomes more yellow/brown
Reduction of taste with age. The underlying dentinbuds
darkens and becomes yellow
because it is thickening.
Teeth may become more brittle with
age and crack.
Salivary flow decreases - contributes
to dental problems
Effects of Aging
• With time, the enamel on the teeth is subjected to wear due to chewing, grinding, and
acidic foods. Dentine may appear through the enamel. Sensitivity may become a
problem.
• Tooth loss in the elderly is mainly due to the decline in the fiber content and blood
vessels of the gum tissues. Increase periodontal disease.
• Gum disease in older people is a result of cumulative diseases – diabetes, poor

circulation, inadequate diet, medications that cause xerostomia (dry mouth)
Controlling Factors in Craniofacial Growth
• Genetics: facial dimension is polygenic and less than 25 % of the variability of any
dimension in children can be explained by consideration of that dimension in parents.
• Function: function is one of the primary factor in controlling
craniofacial growth. “Functional Matrix Hypothesis”.
• General body growth: Craniofacial growth is related to the general body growth and
exhibit similar patterns as the general body growth.

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• Neurotrophism: Neurotrophism ( the quality of having a special affinity for nervous

tissue) could act indirectly by the nerves inducing and affecting soft-tissue growth and
function, which in turn would control or modify skeletal growth and morphology.
• Orthodontic forces: utilized to affect jaw growth and alter tooth positions.
• Malnutrition: it is assumed that gross malnutrition affects craniofacial growth in humans

but there is little specific information available.
• Malfunction: malfunctions in the craniofacial regions plays an important role in altering

the morphology of the normal growth patterns, especially in nasorespiratory malfunction.
• Gross craniofacial anomalies: original dysplasia will affect later adaptive growth. .
Adenoid Faces
• Large adenoids obstruct nasopharynx forcing individual to breath through their

mouth.
• Mandible grows in a compensatory downward arch so as to open the airway

and improve breathing
Clinical Features of Adenoid Faces
• OBTUSE GONIAL ANGLE: growth of mandible in downward direction
• Long corpus of mandible
• Long lower third of face – due to mandibular growth and open bite.
• Anterior open bite – opens the air way and improves breathing

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Functional Matrix Hypothesis
• The functional matrix is primary and, size, shape, spatial position, and growth of any
skeletal unit is secondary, compensatory, and mechanically obligatory to changes in its
related functional matrix” (Moss, 1968)
• RULE: Form follows function
Types of Functional Matrix
Types of Functional Matrix

Periosteal matrix 2. Capsular matrix
(e.g., muscles) (e.g., brain, oral cavity)
active growth, deposition and resorption affect passive growth, no deposition
size and/or shape no resorption affect location
Growth Craniofacial Growth
Active growth (Periosteal)+ Passive growth Active growth process

(Capsular) =Total growth 1) Sutural growth
2) Bone remodeling
3) Cephalic cartilage growth +
Passive growth process =
1) The growth of neural,
orbital, CSF, and other
masses and real substances
2) The expansion of oro-
nasopharyngeal and other functioning
spaces
Craniofacial Bone Development
1. Orthotypic bone development
a) Endochondral ossification: e.g.,ethmoid

bone, hyoid bone
b) Intramembranous ossification: e.g.,
parietal, frontal, maxillary, zygomatic bones
2. Heterotypic bone development
a) Fibroblasts into osteocytes: e.g., tendon

b) Chondrocytes into osteocytes: e.g
chondroid bone)

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Intramembranous Bone Formation
• Intramembranous ossification is the embryonic development of flat

bones from a connective tissue matrix.
• Centrally located stem cells within the connective tissue differentiate
(specialize) into osteoblasts, forming the ossification center.
• Ossification takes place at numerous sites
Chondrocranium
Chondrocranium contributes to:
• the occipital bone

• ethmoid bone
• sphenoid bone
• temporal bone
Mechanism of Bone Growth
1. Growth processes
a) deposition and resorption
b) coupling effect
2. Growth fields
a) connective tissues surrounding the bone (osteogenic membranes)
b) cartilage
3. Growth sites
– special growth fields of the bone and cartilage
4. Growth remodeling
a) the maintenance of bone
b) the size and shape change of the bone nes
5. Growth movements
• a) drift (active growth)
• b) displacement or translation (passive growth)
Growth Sites of Craniofacial Complex

1) Sutures
2) Maxillary tuberosity
3) Mandibular condyle
4) Posterior border of mandibular ramus
5) Dentoalveolar process
6) Synchondroses of basicranium
7) Nasal cartilages

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Some principles of Craniofacial Growth
1. The growth of cranial vault, cranial base, and orbits is almost complete at 7 years old.
2. As a general rule, the growth of the cranial vault, base, and orbit can be considered
completed at 10 years old
the nasal region, 10 year old

the maxillary region, 15 years old
mandible, 20 years old.
1) Sutures
2) Maxillary tuberosity
3. Infant/adult face comparisons:
a) Increase in size is continuous but not uniform. This is due to the growth velocity
change and differential growth.
b) The face reaches the adult size in the order of:
• facial width
• facial depth
• facial height.
c) Since there is variation in velocity, the proportions of the face, change with ages.
4. Facial growth curve lies between neural and somatic curves.
Growth
a. From 6 years old to adulthood, facial volume increased by 40 %
b. The facial volume of males is larger than that of females in all ages, except in the 11-12
years old group.
c. At the age of 14 to 15 years old, female facial growth is almost completed. The males will
continue facial growth for few more years – 18 to 20 years old

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Growth of Cranial Vault
• Growth of the cranial vault is made possible by differential growth at the sutures in
response to the growth of brain.
1. The internal part of the cranial vault is mostly resorptive with depository areas. The
external part of the cranial vault is mostly depository
2. Result: the cranial vault will increase in size as well as in thickness with age.
Growth of Cranial Floor
• 1. Resorptive regions are shown in black and depository

areas in gray.
• 2. With the exception of the petrous part of the temporal bone,

the rest of the cranial floor/fossa is resorptive.
• 3. Results: increase of cranial height due to the resorption of

the cranial floor, except
the petrous portion.
Growth of the Nasomaxiillary Complex
The growth of the nasomaxillary complex occurs in two ways:
• 1) by apposition of bone at the sutures that connect the maxilla

to the cranium and cranial base
• 2) by surface remodeling
• As growth of the surrounding soft tissues moves the maxilla

downward and forward, it opens up space at its superior and
posterior sutural attachment. New bone is added on both sides of the sutures.
The growth sites of the nasomaxillary complex are:
* the sutures
* the maxillary tuberosity
* dentoalveolar processes.
The dentoalveolar process contributes to the 40% increase of height.

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Growth pattern in the Anterior Surface of the Maxilla
As the maxilla is displaced downward and forward, the anterior surface

of the maxilla is resorptive (resorption surface shown in red) except a
small area around the anterior nasal spine, which is depository
Growth of the Mandible
• During mandibular growth, the mandible is displaced (or translated) downward and
forward, while growth is actually upward and backward.
• The growth sites of the mandible are:
– The condylar process

– posterior border of ramus
– dentoalveolar process
• As the mandible grows in length, the ramus is extensively
remodeled. There is resorption (-) of the anterior border of
the ramus and deposition (+) at the posterior border of the
ramus.
• Removal of the anterior border of the ramus makes
room for the eruption of permanent molars
Growth of Mandibular Condyle

• A major site of growth, having considerable clinical significance.
• An endochondral growth mechanism.
• The condylar cartilage is unique and differs in histologic organization from most other
growth cartilages involved in endochondral bone formation. It is not structurally
comparable to a long bone's cartilaginous epiphyseal plate
The condyle performs a functional role. It:

(1) provides a pressure-tolerant articular contact
(2) it makes possible a multidimensional growth capacity in response to ever-
changing, developmental conditions and variations.
• The proliferative process produces the "upward and backward" growth movement of the
condyle.
• The cap of condylar cartilage has multidirectional proliferative capacity.
• The condyle grows from a stable cranial base. Growth at the condylar head lengthens
the vertical rami of the mandible and moves the chin downward and forward.
• Disruptions in condylar growth produces facial asymmetries.

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Condylar Hyperplasia
Growth at Mandibular Condyle
• The rate and directions of condylar growth are subject to the influence of
extracondylar agents, including intrinsic and extrinsic biomechanical forces and
physiologic inductors. Condylar growth is not preprogrammed.
• Condylar prechondroblasts are randomly arranged providing an opportunity for

selected, multidirectional growth potential.
Functional Matrix Modification
Forces placed on the facial skeleton can change its shape and growth
pattern:
orthodopedic functional appliances – e.g headgear , chip cup

appliance, osteogenesis distraction, palatal expanders orthodontic
treatment teeth.

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Lecture 06- Development and Growth of the Maxilla and Mandible
Maxillary Growth
• As the maxilla increases in size, there is a companion process of remodeling which

functions to maintain the constant proportions of its shape and the relative positions of
its component parts.
• The remodeling proceeds by a process of outer surface deposition in conjunction with
inner surface resorption.
• Different parts of the maxilla grow in a wide variety of individual directions.
Several factors contribute to maxillary growth.

• the growing tongue, eye and brain produces a continual separation of adjacent sutures
which stimulates bone growth at the suture sites.
• the cartilaginous nasal septum is a primary force in pacing morphogenesis of the
maxilla and other adjacent bones.
• the forward and downward growth of the nasal septum serves to “carry” the maxilla with
it, thus separating its various sutures and stimulating new bone deposition within the
sutural surfaces.
Maxillary Growth
Separation of Sutures by Soft Tissue Growth
Suture Growth of the Maxilla
• Growth by suture activity combined with cartilage expansion ceases after about the
seventh postnatal year and over-all surface apposition then comes to represent the
dominant mechanism of growth.

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• During periods of sutural growth, the particular sutures that are believed to contribute
predominantly to maxillary growth are those articulating with the frontal, zygomatic,
ethmoid, and palatine bones.
• The continued downward and forward growth is due to growth at the posterior margins
and in the alveolar areas
Sutures do not have intrinsic growth potential. They produce new bone at the sutural
edges of the bone fronts in response to external stimuli.
Bone growth at the cranial sutures relies on proliferation of osteogenic progenitor cells and/or
differentiation of osteoblasts.
This process relies on the production of sufficient new

bone cells to be recruited into the bone fronts, while
ensuring that the cells within the suture remain
undifferentiated.
• The number of suture layers varies according to

different authors.
• Using the human zygomaticomaxillary suture as a

template, Kokich (1986) identified three layers and
found the same in most of other sutures.
• Cranial suture can arbitrarily be divided into three

layers: a central zone sandwiched in between two
osteogenic zones. However there were no sharp
boundaries between zones
• More proliferative cells are present in the

osteogenic zone than in the central zone
MidPalatal Suture -5 layers

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Sutural Growth of the Maxilla
• Proliferation in the osteogenic zone serves to replenish progenitor osteoblasts for the
bone fronts.
• Central zone proliferation contribute progenitor fibroblasts, endothelial cells, and a self-
renewing mesenchymal cell population for the maintenance of the matrix.
Mid Palatal Suture
The Maxillary Tuberosity
• During growth, the entire maxilla is moved in a progressively

anterior direction. As it does so, new bone deposits are
simultaneously added onto the periosteal surfaces of the
maxillary tuberosity.
• These additions increase the longitudinal dimensions of the

growing maxilla and, at the same time, functioning to lengthen
the dental arch as the teeth increase in number.
• During the active period of maxillary growth, deposits of bone

on the posterior-facing surfaces are in the form of fine
cancellous, nonlamellar bone tissue which later receives
lamellar compaction.
• Since the tuberosity faces posteriorly and somewhat laterally,

apposition of new bone on its periosteal surface brings about
growth in corresponding posterior and lateral directions. This
produces a lengthening and a slight widening of the maxillary
arch at the posterior end
Maxillary
Development
• As new bone deposits are added onto posterior

surfaces of the maxillary body, the anterior-
posterior dimensions of the maxilla increase.
However, constant relative positions of the various
parts of the face must be maintained during these

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increases. The relative position of the orbits remain constant.
• This is accomplished by a combination of bone deposition on the posterior surfaces of

the zygomatic processes with resorption from its anterior face. Thus, as the maxilla
lengthens by new growth on its posterior margin, the zygomatic process moves
continuously backwards by a process of relocation
Bone Growth by remodelling

Bone Cells
• OSTEOBLAST: mononucleate cells that are responsible for

bone formation.
• H&E staining: basophilic cytoplasm of due to the presence of

a large amount of rough endoplasmic reticulum.
• The nucleus is spherical and large.
• An active osteoblast is characterized morphologically by a

prominent Golgi apparatus that appears histologically as a clear
zone adjacent to the nucleus
Osteoblast
Osteocyte
• most numerous cell found in mature bone.

• stellate shape of various sizes.
• a mature osteocyte contains a single nucleus that is located toward the vascular side
and has one or two nucleoli and a membrane.
• reduced size endoplasmic reticulum, Golgi apparatus and mitochondria.
cell processes that radiate towards the mineralizing mat

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Osteoclasts
• a type of bone cell that

removes bone tissue by
removing its mineralized
matrix and breaking up
the organic bone.
• a large cell that contains
15-20 closely packed

oval-shaped nuclei.
• cytoplasm has a
homogeneous, "foamy"
appearance.
Osteopontin
• Osteopontin (OPN) is a highly phosphorylated sialoprotein that is

a prominent component of the mineralized extracellular matrices of bones and teeth.
• OPN is a highly negatively charged, extracellular matrix protein.
• Osteopontin is an important factor in bone remodeling.
• It plays a role in anchoring osteoclasts to the mineral matrix of bones.
Maxillary Development
• The orbital side of the frontal process and the anterior face of the separate zygomatic
bone are resorptive in nature and grow and move in a general posterior course.
• The lateral rim of the orbit is also resorptive and grows posteriorly
• The zygomatic bone is shifted in a backward direction corresponding to the posterior

growth at the maxillary tuberosity and is relocated in position to maintain its relative
location in the entire facial complex.
The Maxillary Dental Arch
• The dominant area of growth occurs at the posterior margin of the arch on the maxillary
tuberosity.
• Accompanying this, bone deposition takes place along the

entire inner side of the maxillary arch together with
resorption from the labial and buccal sides

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• This combination of resorption from the labial side and deposition on the lingual surface
of the arch serves to shift the premaxillary area toward the midline.
• Since the premaxillary area is growing in a posterior direction, it comes to lie in

successive new locations which were formerly wider in their lateral dimensions. This
allows for teeth to change from primary dentition to the larger adult size teeth.
• The width of the anterior maxilla reaches its adult size by age 7 – 8 and does not
grow any more after that. .
The Pre-Maxilla
Dental Arch
• The width of the dental arch increase progressively and proportionally in size by
continued bone deposition along the lateral (buccal) surface of the maxillary tuberosity in
the molar area posterior to the zygomatic process (premolar areas)
• This surface contour at the tuberosity is so oriented that it faces in two general
directions: posterior and lateral - and surface bone additions serve to bring about
increased growth in corresponding posterior and lateral directions.
• Growth of the palatal shelf occurs by addition on the oral surface with corresponding
proportionate removal from the opposite nasal surface. This serves to move the dental
arch downwards as well as increasing the nasal passage way.
• The palatal shelf of the maxilla varies regionally from a relatively thin sheet of simple
lamellar bone to a thick plate composed of two cortical tables enclosing a middle
cancellous diploe.
• Both types of palatal bones grow differently
• In the lamellar type of structure, the thin sheet of palatal bone receives uniform lamellar
deposition on its oral side in combination with resorptive removal from the nasal side .
• Palatal areas involving a much thicker shelf than the single cortical plate grow and move
in an oral direction by a combined process of periosteal apposition and endosteal
resorption on the oral lamina together with endosteal apposition and periosteal
resorption on the nasal lamina. The cancellous bone tends to maintain its volume

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Dentate Areas of the Maxilla
• As the maxilla moves anteriorly, teeth and teeth buds are carried in a like course and
bony adjustments made during relocation.
• Teeth are subjected to movements during growth in order to accommodate the general
process of growth itself.
• Tooth migrations through bone represents a physiologic adaptation to maintain the
constant relationships in position between tooth and specific areas of growing, moving
bone.
Developing Tooth Bud in Maxilla
• Movement of the unerupted tooth germ within growing

bone also serves a secondary function in the maintenance of
contact between adjacent teeth.
• Alveolar crest height increases with tooth eruption

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Growth of the Mandible
Mandibular Growth Patterns
• The mandible is unique as it is the only movable component of the facial skeletal and
suspended in space by various muscles and ligaments.
• As it grows, it is required to perform sophisticated movements associated with
mastication as well as speech.
• The bulk of its growth takes place during adolescence
• The mandibular ramus height and length in both sexes show progressive increase in
dimensions during all stages of mandibular growth.
• Males show a greater mandibular height and length compared to females at all stages
except during the first year and in some cases to 36 mths.
• The increase in the height and length shows a growth spurt at puberty and continuous
growth through the adolescence years.
• The ramus plays a key role in placing the corpus and dental arch into an ever-changing
match with the growing maxilla and can adapt the growth to limitless structural
variations. Form follows function.
• Vertical growth of the mandible exceeds horizontal growth

• Although the mandible of both males and females grows in the same direction, Ramus
inclination was observed to decrease with skeletal maturity in females, whereas an
overall increase was seen in males. This suggests that there is more bone deposition on
the posterior border than on the lower border of the
gonion (angle) in males.
• Females tend to show a better correlation
between skeletal maturity and growth changes in
the mandible.
Mandible
• Formed from 1st arch

• Within the first arch a cartilaginous bar known
as Meckel’s cartilage is formed.
Meckel’s Cartilage
• Two cartilages – L and R
• The dorsal end of each cartilage is connected with

malleus; the ventral ends meet each other in the region of
the symphysis menti which will contain the incisor teeth.

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• Connective tissue below the malleus becomes ossified to become the mandible.
Facts about Meckel’s Cartilage
• Meckel’s cartilage is the cartilage of 1st arch and has a role in developing mandible but
no contribution.
• Two cartilages don’t meet in the midline but separated by thin band of
mesenchyme.
• On the lateral aspect of meckel’s cartilage during 6th week condensation of mesenchyme
occurs.
• At 7 weeks intramembranous ossification starts in this condensation forming the 1st
bone of mandible
• Bone formation starts along the lateral aspect of Meckel’s cartilage
• The ramus of mandible forms by rapid spread of ossification posteriorly into

mesenchyme of 1st arch, turning away from Meckel’s cartilage, this point is marked by
the lingula
Fate of Meckel’s Cartilage
• In the posterior extremity it forms the malleus of inner ear & sphenomalleolar ligament.
• From sphenoid to the div of mandibular nerve into inf alv n and lingual n the cartilage is
totally lost but persist as sphenomandibular ligament.
• From linula to point canine area, cartilage is totally resorbed.
• From this point forward there is evidence that cartilage makes contribution by means of
endochondral ossification
Early Mandibular Growth
• The growth of the mandible is strongly influenced by appearance of three secondary

cartilages:
• Condylar cartilage
• Coronoid cartilage
• Symphysial cartilage
• Symphysial cartilage: Two in number and appears in CT between the two ends of
Meckel’s cartilage. Obliterated within the 1st year of birth.

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Condylar Cartilage
• Appears at 12th week of development

• Forms a carrot shaped mass and occupies developing
ramus
• This mass is converted to bone by endochondral
ossification
• By 20 weeks only thin layer of cartilage remains in the
condylar head and persists till the end of 2nd decade of
life and provides mechanism of growth of mandible
•
Steps in Endochondral Bone Growth Cranial Bones
1 Development of the cartilage model
2 Growth of the cartilage model
3 Development of the primary ossification center: nutrient artery

penetration the cartilage and induces perichondrium cells to differentiate into
osteoblasts; later becomes periosteum. Osteoblasts deposit spongy bone;
primary ossification spreads from out to inward and towards both ends of cartilage model.
4 Development of the secondary ossification center - occurs after birth
Endochondral Bone Formation
TMJ of an Infant

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Mandibular Condyle in a Young Child
• Some chondrocytes
hypertrophy and burst; causing a
pH change which initiates
calcification of the cartilage
model.
• The enlarged chondrocytes

die, leaving cavities in the
cartilage.
• Blood vessels enter the

cartilage, bringing fibroblasts that
become osteoblasts. Spongy
bone develops at the primary
ossification center.
Intramembranous Bone Formation
• 1. Mesenchymal cells aggregate, differentiate into

osteoblasts, and begin ossification. The location
where ossification begins is the ossification center,
from which developing bone grows out in
projections called spicules.
• 2. Blood vessels grow into the area to supply the

osteoblasts. Spicules connect, trapping blood
vessels inside bone.
• 3. Spongy bone develops, which can be remodeled

into osteons of compact bone, periosteum or
marrow cavities.

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Mandible
• the mandible only articulates with one other bone of the craniofacial complex and tends
to be influenced by the growth of the maxilla.
• it is largely affected by the position of the tongue.
• It is more susceptible to environmental factors than intrinsic malformations
• increased tongue size, nasal patency and breathing efficiency, can cause “mandibular
compensation” which may affecting its growth pattern.
• Mandibular growth also follows the pattern of resorption at one surface along with
deposition on the contralateral surface.
• After birth the mandible initially grows to accommodate the developing tongue (up
to 11 months)
• As the mandible grows the general shape changes from a round, smooth contour
anteriorly to adopt a more sharp and narrow adult shape.
• progressive dental eruption and mastication further contribute to the growth.
• Dental eruptions will lead to vertical growth.
• Mastication is associated with muscle mass development. This causes an increase in
the dimensions of the mandibular notch (antigonial notch) and associated muscle
attachment sites.
• Like the maxilla, the mandible also grows downward and forward.

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Lecture 07 – Development of Teeth –Amelogenesis and Dentinogenesis
Tooth Development
• Teeth form from embryonic cells

• Primary teeth start to form between the sixth and eighth weeks.
• Permanent teeth begin to form in the twentieth week. We are born with some permanent
tooth bud
• If teeth do not start to develop at or near these times, they will not develop at a later date
and will be congenitally missing.
There is a factor within the tissues of the first branchial arch that initiates the development of
teeth.
The tooth bud (tooth germ) is an aggregation of cells that eventually forms a tooth.
These cells are derived from the ectoderm of the first branchial arch and the
ectomesenchyme of the neural crest.
The tooth bud is organized into three parts: the enamel organ, the dental papilla and
the dental follicle.
The enamel organ is composed of the outer enamel epithelium, inner enamel epithelium,
stellate reticulum and stratum intermedium.
These cells give rise to ameloblasts, which produce enamel and the reduced enamel
epithelium.
The location where the outer enamel epithelium and inner enamel epithelium join is called
the cervical loop.
The growth of cervical loop cells into the deeper tissues forms Hertwig's Epithelial Root
Sheath, which determines the root shape of the tooth.
Dental Papilla
• The dental papilla contains cells that develop into odontoblasts – dentin forming cells.
• The junction between the dental papilla and inner enamel epithelium determines the
crown shape of a tooth.
• Mesenchymal cells within the dental papilla are responsible for formation of
tooth pulp.
The dental follicle gives rise to three important entities:
• cementoblasts - forms the cementum of the tooth.

• osteoblasts - give rise to the alveolar bone around the roots of teeth.
• fibroblasts. develops into the periodontal ligaments which connect teeth to the alveolar
bone through cementum.
•

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Tooth Bud Stage of Tooth Development
A: enamel organ
B: dental papilla
C: dental follicle
Bud Stage
• Begins when epithelial cells proliferate into the ectomesenchyme of the jaw - usually
when the fetus is around 6 weeks old. The tooth bud is the group of cells at the end of
the dental lamina. The tooth bud does not have a clear arrangement of cells.
• Along with the formation of the dental lamina, 10 round epithelial structures, each
referred to as a bud, develop at the distal aspect of the dental lamina of each arch.
These correspond to the 10 deciduous teeth of each dental
arch.
Each bud is separated from the ectomesenchyme by a basement

membrane.
Ectomesenchymal cells congregate deep to the bud, forming a

cluster of cells, which is the initiation of the condensation of the
ectomesenchyme. The remaining ectomesenchymal cells are
arranged in a more or less haphazardly uniform fashion.

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Dental Lamina
• The dental lamina is attached to the surface layer of

the gum (stained red
Tooth bud at the stage when both enamel and dentin

formation begins
Cap Stage
• The first signs of an arrangement of cells in the tooth

bud.
• A small group of ectomesenchymal cells stop

producing extracellular substances, and aggregate to
form a clump of cells called the dental papilla.
• The tooth bud then grows around the

ectomesenchymal aggregation, taking on the
appearance of a cap, and becomes the enamel
organ.
• A secondary condensation of ectomesenchymal

cells called the dental follicle surrounds the enamel
organ and limits the dental papilla.
• The enamel organ will produce enamel, the dental papilla will produce dentin and
pulp, and the dental follicle will produce all the supporting structures of a tooth
Cap Stage formation of Tooth in Maxilla and Mandible
Maxilla Mandible

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Bell Stage
• In the bell stage histodifferentiation and

morphodifferentiation takes place.
• The dental organ is bell-shaped during this

stage, and the majority of its cells are called
stellate reticulum because of their star-
shaped appearance.
• Cells on the periphery of the enamel organ separate into three important layers:
• Cuboidal cells on the periphery of the dental organ are known as outer enamel
epithelium.
• Columnar cells of the enamel organ adjacent to the dental papilla are known as inner
enamel epithelium.
• The cells between the inner enamel epithelium and the stellate reticulum form a layer
known as the stratum intermedium.
Bell Stage of Tooth Development

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Bell Stage- The cervical loop
• The rim of the dental organ where the outer and inner enamel epithelium join is called
the cervical loop.
• It is a specific epithelial structure at the apical side of the tooth germ.
• During root formation the inner layers of epithelium disappear and only the basal layers
are left creating Hertwig's Epithelial Root Sheath (HERS).
• At this point it is referred to as HERS instead of the cervical loop to indicate the
structural difference.
The inner enamel epithelium and stratum intermedium (specialised stratified cells that
support the synthetic activity of the Inner Enamel Epithelium) forms the enamel of the tooth
The enamel forming structures is all encased by the outer enamel epithelium layer.
The dental lamina disintegrates, leaving the developing teeth completely separated from
the epithelium of the oral cavity.
Bell Stage
• The crown of the tooth takes shape during this stage and is influenced by the shape of
the internal enamel epithelium.
• One hypothesis of tooth shape (the "clone model“), proposes that the epithelium
programs a group of ectomesenchymal cells to generate teeth of particular shapes.
• This group of cells, called a clone, coaxes the dental lamina into tooth development,
causing a tooth bud to form.
• Growth of the dental lamina continues in an area called the "progress zone". Once the
progress zone travels a certain distance from the first tooth bud, a second tooth bud will
start to develop
Crown Stage of Tooth Development
• Hard tissues - enamel and dentin - develop during this stage.
• In prior stages, all of the inner enamel epithelium cells were dividing to increase the
overall size of the tooth bud, but the mitosis stops during the crown stage at the location
where the cusps of the teeth form.
• The first mineralized hard tissues form at the cusp tips and at the incisal edge.
Mineralization

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Incisal Tip
Crown Stage of Tooth Development
• At the start of mineralization the inner enamel epithelial cells change in shape from
cuboidal to columnar and the nuclei of these cells move closer to the stratum
intermedium and away from the dental papilla.
• The adjacent layer of cells in the dental papilla increases in size and differentiates into
odontoblasts.
• Odontoblasts would not form if it were not for the changes occurring in the inner enamel
epithelium - -Reciprocal induction
The odontoblasts secrete an organic matrix into their immediate surrounding.

The organic matrix contains the material needed for dentin formation.
As odontoblasts deposit organic matrix, they migrate toward the center of the dental papilla.
Unlike enamel, dentin starts forming in the surface closest to the outside of the tooth and
proceeds inward.
Dentin
• As the odontoblasts migrate toward the center of the dental papilla, cytoplasmic
extensions are left behind.
• The tubular appearance of dentin is a result of the formation of dentin around these
extensions.
Hard Tissue Formation

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• After dentin formation begins, the cells of the inner enamel epithelium secrete an organic
matrix against the dentin.
• This matrix mineralizes and becomes the tooth's enamel.
• Outside the dentin are ameloblasts which continue the process of enamel formation.
• Enamel formation moves outwards, adding new material to the outer surface of the
developing tooth.
Amelogenesis
Amelogenesis is the formation of enamel on teeth and occurs during the crown stage of tooth
development after dentinogenesis.
Although dentine must be present for enamel to be formed, it is also true that ameloblasts must
be present in order for dentinogenesis to continue.
A message is sent from the newly differentiated odontoblasts to the inner enamel
epithelium (IEE), causing the epithelial cells to further
differentiate into active secretory ameloblast.
• Dentinogenesis is in turn dependent on signals

from the differentiating IEE in order for the
process to continue.
• This prerequisite is an example of the biological

concept known as reciprocal induction, in this
instance between mesenchymal cells and
epithelial cells
Secretory Stage of Amelogenesis
• The line at the base of the ameloblasts represents the

proximal cell web (pcw), and that at the apex, the distal
cell web (dcw).

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Secretory Stage of Amelogenesis
• In the secretory stage, ameloblasts release enamel proteins that contribute to the
enamel matrix.
• The enamel protein is then partially mineralized by the enzyme alkaline phosphatase.
• The appearance of this mineralized tissue occurs around the third or fourth month of
pregnancy and marks the first appearance of enamel in the body.
• Ameloblasts deposit enamel at the location of what become cusps of teeth alongside
dentin.
• Enamel formation then continues outward, away from the center of the tooth.
Definitions
• TOMES PROCESSES: histologic landmark identified on an ameloblast.
• During the synthesis of enamel, the ameloblast is moving away from the enamel,
forming a projection surrounded by developing enamel.
• Tomes' processes are these projections and give the ameloblast a "picket-fence"
appearance under a microscope.
• They are located on the secretory, basal end of

the ameloblast.
Maturation Stage of Amelogenesis
• In this stage, the ameloblasts transport some of

the substances used in enamel formation out of
the enamel.

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• The function of ameloblasts changes from enamel production to transportation of

substances.
• Most of the materials transported are proteins used to complete mineralization.
• The important proteins involved are amelogenins, ameloblastins, enamelins
and tuftelins.
At the end of this stage the enamel has completed its mineralization.
Maturation Process
• Tooth along the slope of a cusp showing an incisal

to cervical gradient in enamel maturation.
• As maturation progresses, enamel matrix is lost
and mineral content increases.
• Almost mature enamel (top right) appears whitish
because mineralization
• Note the striae of Retzius and morphology of
maturation stage ameloblasts. (noTomes’
process).
• Striae of Retzius: incremental growth lines or

bands seen in tooth enamel.
• They represent the incremental developental pattern of enamel, the successive

apposition of different layers of enamel during crown formation.
End of Amelogenesis
• During the transport phase of the ameloblasts, they remove water as well as proteins
from the maturing enamel, allowing the latter to achieve complete mineralization.

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• Once the enamel is completely mineralized, the ameloblasts shrink from columnar to
cuboidal or flattened cells, but remain a part of the reduced enamel epithelium that
forms a more or less continuous lining over the completed enamel.
Disturbances in Amelogenesis
• Disturbance to the process will leads to enamel hypoplasia. Chemicals may become
incorporated into the enamel crystals leading to discolored teeth
Enamel Defects in Children
Amelogenesis imperfecta (enamel Amelogenesis can be affected by:

hypoplasia) can be caused by:
 Mother's health during pregnancy
(illnesses, diet deficiency)
• Tetracycline in early years.
 Premature birth. • Early childhood diseases (high fever)
 Medications given to mother prior to • Excess flouride
birth or to child during early childhood • Poor childhood nutrition (deficient
 Early childhood diseases (high fever) diet, lack of calcium, phosphate,
 Chronic / frequent childhood illness vitamins A, C, D)
during first four years of life
 Poor childhood nutrition (deficient diet,
lack of calcium, phosphate, vitamins
A, C, D)
Enamel Hypoplasia
Tetracycline Teeth

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Mild Case of Fluorosis
Reduced Enamel Epithelium
• The reduced enamel epithelium overlies a developing tooth and is formed by two
layers: a layer of ameloblast cells and the adjacent layer of cuboidal cells (outer enamel
epithelium) from the dental lamina.
• As the cells of the reduced enamel epithelium degenerate, the tooth is revealed
progressively with its eruption into the mouth.
• The degeneration of reduced enamel epithelium also mediates the
initial epithelial attachment to the tooth at the CEJ.
(REE) : the epithelium is produced by the combination of the external and internal enamel
epithelium.
• The REE remains covering the enamel crown until the tooth erupts when it fuses with
the oral epithelium.
• The REE remaining on the enamel surface becomes the junctional epithelium.
Junctional Epithelium

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• A circular arrangement of epithelial cells occurring at the base of

the gingival sulcus and attached to both the tooth and the subepithelial connective
tissue
• The reduced enamel epithelium consists of two major cellular layers:
• 1) the reduced ameloblasts that are in contact with the enamel, but are no longer able
to undergo cell division and are no longer functional.
• (2) the external cells of the reduced enamel epithelium consist mostly of stratum
intermedium cells, and cellular remnants of the stellate reticulum and outer
enamel epithelium
• It is the external cells of the reduced enamel epithelium that will eventually give rise to
the junctional epithelium.
• Once enamel is completely mature,

the enamel organ forms the reduced enamel
epithelium.
• At this stage ameloblasts are no

longer distinguishable

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• Note that the enamel organ on the cuspal aspect

of the tooth has reorganized into a reduced
enamel epithelium in which individual cell layers
cannot be distinguished.
• (Decalcified preparation - the fully calcified

enamel has been completely removed, leaving
behind the space it occupied)
Definitions
• Enamel tufts: hypomineralized ribbon-like

structures that run longitudinally to the
tooth axis and extend from the dentinoenamel
junction (DEJ) one fifth to a third into
the enamel.
• They are called ‘‘tufts’’ due to their wavy look

within the enamel microstructure
• Biomechanically, enamel tufts are ‘‘closed

cracks’’ or defects which, in their manner of
propagating, act to prevent enamel fractures.
Enamel Tufts

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• Hunter-Schreger bands. In HSB enamel

prisms are arranged in layers of varying thickness
at about right angles to each other.
• HSB strengthen the enamel and prevent cracks

from propagating through the tooth.
Hunter Schreger Bands
Note :Wave like Grooves Alternating orientation of a group of

enamel rods
Dentinogenesis
• Begins at the late bell stage of tooth development.

• Odontoblasts differentiate from cells of the dental papilla.
• The different stages of dentin formation result in different types of dentin:
mantle dentin
primary dentin
secondary dentin
tertiary dentin.

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Mantle Dentine
Mantle dentin forms from the preexisting ground substance of

the dental papilla.
• The newly differentiated dentin begin secreting an organic
matrix directly adjacent to the inner enamel epithelium closest
to the area of the future cusp of a tooth.
• The organic matrix contains collagen fibers with large
diameters (0.1-0.2 μm in diameter).
• The odontoblasts begin to move toward the center of the
tooth, forming the odontoblast process.
• The odontoblast process causes the secretion of
hydroxyapatite crystals and mineralization of the matrix.
• This area of mineralization is known as mantle dentin and is a
layer usually about 5-30 μm thick.
• Mantle dentin is formed by newly differentiated odontoblasts and
is approximately 150 micrometers wide.
• It lacks phosphoryn, has loosely packed collagen fibrils and is
less mineralized.
Odontoblast
• large columnar cells arranged in an epithelioid sheet.
• Its nucleus is located at the pole aligned away from the

dentine, with its golgi and ER above it
Primary Dentin
• the most prominent dentin in the tooth.
• The odontoblasts increase in size, and decrease the

size the extracellular organic matrix.
• The larger odontoblasts secrets collagen in smaller

amounts, which results in more tightly arranged,
heterogeneous nucleation that is then used primarily
for mineralization.
• Other materials (such as lipids, phosphoproteins ,

and phospholipids) are also secreted.

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Secondary Dentine
• Secondary dentin is formed after root formation

is finished.
• Ocurs at a much slower rate.
• It is not formed at a uniform rate along the entire
tooth, but instead forms faster in the crown area of
the tooth.
• This development continues throughout life and
accounts for the smaller areas of pulp found in older
individuals
Pulp Stone: a calcified mass of secondary dentin within the

dental pulp
Root Dentine
• The dentin in the root of a tooth forms only after the

presence of Hertwig's epithelial root sheath (HERS), near
the cervical loop of the enamel organ.
• Root dentin is considered different from dentin found

in the crown of the tooth (known as coronal dentin)
because of the different orientation of collagen fibers, the
decrease of phosphophoryn levels, and less mineralization.
Phosphoryn
• Phosphophoryn, or dentin phoprotein, is one of three proteins formed from dentin

sialophosphoprotein and is important in the regulation of mineralization of dentin.
• Phosphophoryn is the most acidic protein ever discovered.
• This extreme acidity is achieved by its amino acid sequence. Many portions of its chain
are repeating -D-S-S- (aspartic acid-serine-serine) sequences.
• In protein chemistry, net acidity equates to negative charge.

• Being highly negative, dentin phosphoprotein is able to attract large amounts of calcium.
• Studies also indicate phosphophoryn can initiate HA formation.
CEMENTUM
Cementogenesis
• Occurs late in the development of teeth

• Cementoblasts are the cells responsible for cementogenesis.
• The cementoblasts differentiate from follicular cells, which can only reach the surface of
the tooth's root once Hertwig's Epithelial Root Sheath (HERS) has begun to deteriorate.

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• Two types of cementum form: cellular and acellular.

• Acellular cementum forms first.
Acellular Cementum
• Acellular cementum contains a secreted matrix of

proteins and fibers
• The cementoblasts secrete fine collagen fibrils along
the root surface at right angles before migrating away
from the tooth.
• As the cementoblasts move, more collagen is deposited
to lengthen and thicken the bundles of fibers.
Noncollagenous proteins, such as bone sialoprotein and osteocalcin , are also secreted.
As mineralization takes place, the cementoblasts move away from the cementum, and the fibers
left along the surface eventually join the forming periodontal ligaments.
Cellular Cementum
• Cellular cementum develops after most of the tooth

formation is complete and after the tooth occludes
with a tooth in the opposite arch.
• This type of cementum forms around the fiber bundles
of the periodontal ligaments.
• The cementoblasts forming cellular cementum
become trapped in the cementum they produce.
• The origin of the formative cementoblasts is believed
to be different for cellular cementum and acellular
cementum.
• One of the major current hypotheses is that cells

producing cellular cementum migrate from the
adjacent area of bone, while cells producing acellular cementum arise from the dental
follicle.
• It is known that cellular cementum is not found in teeth with one

root. In premolars and molars, cellular cementum is found only in the part of the
root closest to the apex and in interradicular areas between multiple roots.

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Composition of Cementum
45%-50% Inorganic material and 50-55% Organic portion.
• Consists of: Matrix and collagen fibers.
• Collagen Fibers derived from Fibroblasts (Sharpey’s fibers/Extrinsic fibers) and

Cementoblasts (Fibers in Cementum matrix/Intrinsic fibers)
• Ground substance and organic matrix (Cementoid) formed by Cementoblasts.
• Ground substance includes proteoglycans, glycoproteins and phosphoproteins.
Lecture 09 - The Dental Pulp
• Dental pulp is an unmineralized oral tissue

composed of soft connective tissue, vascular,
lymphatic and nervous elements that occupies
the central pulp cavity of each tooth.
• The pulp has a soft, gelatinous consistency.
• By either weight or volume, the majority of pulp
(75-80%) is water
Development of Dental Pulp
• The dental pulp originates from a solidified

mesenchyma of neuroectodermal tissue
known as the dental papilla that penetrate the
enamel organ during the cap stage of tooth
development.
• Dental Papilla: Ball of condensed ectomesenchymal cells that form dentin and pulp.
• During the transition from bud to cap stages, the ectomesenchyme provides several cell
lineages, to dental papilla mesenchyme and to other tissues that become progenitor
cells for the subsequent development of the periodontium.
Pulp Development
• During the bell stage a discrete structure within the enamel organ, termed the “enamel
knot,” synthesizes and secretes a number of signals that participate in the determination
for the patterns of morphogenesis within the maxillary and mandibular dentitions:
incisiform, caninform, and molariform
• The pulp creates and shapes its own locale in the center of the tooth taking the shape of
the tooth.

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• At the time of eruption, the pulp chamber of a tooth reflects the external form of the
enamel
• During the cap stage there is a proliferation of fibroblasts and mitosis of

undifferentiated mescenchymal cells.
• The start of the maturation of the pulp coincides with the first signs of dentine formation.
• Once the odontoblasts appear and produce the first layer of predentine, the adjacent
dental papilla becomes dental pulp.
Nerves
• Nerve fibers grow towards the dental follicle during the cap stage of tooth development.
• Once there, the nerves develop around the tooth bud and enter the dental papilla when
dentin formation has begun.
Pulp Development
• The maturation of the pulp will progress with directional adjustment of cells and collagen
matrix.
• Blood vessels and nerves with non-mylinated axon also appear at this time.
• Myelinated nerve fibers appear later, after pulp maturation and root formation. There is,
therefore, a lack of sensitivity of the pulp in young patients.
• Immature teeth have fewer myelinated axons than older teeth.
• These fibers do not reach their maximal number until the root completes its apical
development.
Vasculature
• At the start of the bell stage a vascular plexus arises from the main alveolar vessels to
encircle the dental sac and provide necessary nutrients to the enamel organ.
• Capillaries are given off at the outer enamel epithelium but does not enter the enamel
organ.
• At the base, small capillary vessels from the plexus enter the dental papilla
• They divide and become distributed in the core of the connective tissue matrix.
• The peripheral limits of the capillary network is at the pulpal – odontoblastic border.
• Capillaries crowd around the odontoblast during active dentinogenesis
• The coronal vascular complex later anastomose with the radicular vascular.
• During the cap and bell stages the dental papilla is highly vascularized.
• Animal studies and human embryos have demonstrated that the dental papilla begins in
and exists in a rich vascular network.

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• The number of blood vessels reaches a maximum at the beginning of the crown
stage, and a part of the dental papilla eventually forms in the pulp of a tooth.
The Pulp
Grossly, the pulp maybe divided into two compartments:
• The odontogenic compartment
• The pulpal compartment.
• ODONTOGENIC COMPARTMENT: odontoblast, the cell free zone and the parietal
plexus of nerves.
• THE PULP PROPER: the remainder of the pulp chamber. Consists of fibroblast, extra
cellular matrix, blood vessels, nerve and cells required for the maintenance and defense
of the tissue(macrophages, lymphocytes, etc.)
• soft connective tissue that supports the dentin
• four distinct zones
• 1. odontoblastic zone at the periphery
• 2. cell-free zone of Weil – below the ODs
• 3. cell-rich zone
• 4. pulp core – major vessels and nerves

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Secondary Architectual Classification-does not include Odontoblast
Structural Features
The pulp is circumscribed by the specialized
odontogenic region composed of :-
 The odontoblasts (the dentin forming cells)
 The cell-free zone (Weil’s zone), and
 The cell-rich zone
Pulp Zones
• The cell-free and cell-rich zones are usually

indistinct or absent in the embryonic pulp and usually
appear only when dentin formation begins.
• The zones become increasingly prominent as

the pulp ages.
• Both of these zones are less constant and less

prominent near the root apex.

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Central Pulp Zone
• The main body of the pulp that occupies the area circumscribed by cell-rich zones.
• It contains the principal support system for the
peripheral pulp, which includes the large vessels and
nerves from which branches extend to supply the
outer pulp layers.
• The principal cells are fibroblasts.
• The principal extracellular components are ground

substance and collagen.
• The environment of the pulp is unique in that it is

surrounded by an unyielding tissue and fed and
drained by vessels that pass in and out at a distant
site (the tooth apex)
Odontogenic Zone
 The peripheral aspect of dental pulp.

 Differentiates into a layer of dentin-forming odontoblasts.
 Small unmyelinated nerve fibers exist in the region of the
odontoblasts and within
 dentinal tubules.
 These intradentinal nerve fibers contained
 neurotubules, mitochondria, and small vesi-
 cles.
 These axons go as far as a few mm into the dentinal
tubules, but never get to the dentino-enamel junction
Cell Free Zone of Weil
40 microns wide &relatively free of cells

• Traversed by
•blood vessels
•unmyelinated nerves
•cytoplasmic process of fibroblasts
•Represents the space into which odontoblasts move during
tooth development
• Prominent in the coronal pulp and is located immediately subjacent to the odontoblast
layer.
• This region contains numerous bundles of reticular fibers which pass from the central
pulp region, across the cell-free zone and between the odontoblasts.
• Their distal ends incorporated into the matrix of the dentin layer.
• Numerous capillaries and nerves are also found in this zone

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• During the development of a tooth, odontoblast may move toward the pulp in this zone.
• In functional mature teeth there is limited or no movement of odontoblast in this zone.
• Contains Subodontogenic Plexus: the Nerve Plexus of Raschkow and the vascular
plexus
Nerve Plexus of Raschkow
• -Represents the peripheral branches of the nerve that enters through the apical foramen
• -Only present in the crown
• -Nerve bundles are both myelinated and unmyelinated
• -Comprised of Sensory afferents of theTrigeminal
Nerve and sympathetic branches of Superior Cervical
Ganglion
• A plexus of myelinated nerve fibers located between the

core of the pulp of the tooth and the cell-rich zone.
• Axons of Raschkow plexus lose their myeline sheath (but
not their Schwann cells) as they penetrate the cell-rich
and cell-free zones to make synaptic contact with the
odontoblast cell body in the pulp or odontoblastic process
within the dentinal tubule.
• Raschkow plexus is responsible for transmitting pain sensation from the pulp of
the tooth.
Nerve Plexus of Raschkow :Plexus and Nerve Endings
Cell Rich Zone
• Just under the cell-free zone.

• Contain numerous
fibroblasts - the
predominant cell type of
pulp.
• Undifferentiated
mesenchymal cells - can
give rise to odontoblasts, fibroblasts or macrophages.
• The function of undifferentiated cells is that they become either fibroblasts or
odontoblasts or macrophage according to need.
• Zone formed due to migration of cells from pulp proper

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• Odontoblasts themselves are incapable of cell division
• Any dental procedure that relies on the formation of new dentin after destruction of
odontoblasts, depends on the differentiation of new odontoblasts from the multipotential
cells of the cell rich zone.
• Lymphocytes, plasma cells and eosinophils are other cell types found in this area.
Cell Rich Zone
• Cells in this layer produce little collagen, because they are not mature fibroblasts.
• There are cytoplasmic connections between the odontoblasts and the subjacent
mesenchymal cells.
• Through these connections signals of odontoblast injury or death may be provided to

these less differentiated cells that may cause them to divide and differentiate into
odontoblasts or odontoblast-like cells, as required
• Mitosis seen when dead odontoblasts are replaced.
• Undifferentiated mescenchymal cells are found along pulp vessels, in the cell-rich zone
as well scattered throughout the central pulp.
 They appear larger than fibroblasts and polyhedral in shape with peripheral
processes & large oval nuclei.
The Pulp Core
Pulp core or pulp proper
This layer acts as a support system for the peripheral pulp because it contains blood vessels
and nerves.
• These vital structures branch out to supply the other layers of pulp.
• The blood vessels arise from superior and inferior alveolar arteries.
• The nerves follow the course of blood vessels and supply the smooth muscles of these
blood vessels..
Pulp core or pulp proper
• When stimulated by cold, heat, pressure, operative procedure and chemicals, the nerves
cause vasoconstriction of blood vessels.
• These are sympathetic nerves

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Neurovascular Structures of the Pulp Longitiudinal View of Peripheral Nerve
Cells of the Pulp
Fibroblast
• The fibroblasts are stellate shaped cells having extensive process.

• Cells that occur in greatest number in the pulp
• Function is to form, maintain the matrix that consists of collagens, fiber and ground
substance throughout the pulp
Pulp Fibroblast
• Exhibit wide variation in their degree of differentiation.

• They have the ability to directly form calcified tissues, something regular connective
tissue fibroblasts apparently cannot accomplish.
FIBROBLAST CELLS: long and flat with with elongated

processes protruding from the body of each cell, creating the
spindle-like appearance of the cell. the nucleus in the body of the
cell, is oval
• Young teeth- Fibroblasts have abudant cytoplasm having

numerous cell organelles.
• Older pulp - Fibroblasts appear spindle shaped posses

short processes having few cytoplasmic organelles such cells
are called fibrocytes

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Fibrous Pulp
Immunocompetent Cells
They play a major role in local inflammation and

immunity.
They are recruited from the blood stream and remain

as transient inhabitants in the pulp.
These cells are:
1. Macrophages
2. Mast cells
3. Plasma cells
4. Lympocytes,Neutrophils,Eosinophils basophils and
manocytes.
Macrophages and Histiocytes
• Described as histiocytes (or) as resting wandering cells.

• Located close to blood vessels
• Have several phenotype
• Undifferentiated mesenchymal cells around blood vessels (pericytes) can differentiate
into fixed or wandering histiocytes under appropriate stimulation
• Wandering histiocytes (macrophages) may also arise from monocytes that have
migrated from vessels
• Pulpal macrophages and dendritic cells thought to function like Langerhans’ cells (as
antigen presenting cells) have been identified in normal rat pulp.
• These cells seem to be associated with pulpal immunosurveillance.
• Pulp Dendritic Cells are more common than macrophages and proliferate in carious
teeth .
• Macrophages are phagocytes, function of which are engulfment and digestion of
foreign material
• During inflammation they appear in large numbers to aid in defense the organism
• They constitute 8-9% of the pulpal cell population
• Macrophages are cells produced by the differentiation of monocytes in tissues.

• Macrophages often have an elongated irregular shape that reflects their ameboid,
wandering nature.
• When there are many of them in one region, they are not contiguous.

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• A macrophage displays its inclusions only as a result of substantial phagocytic activity,

and so may not be easily recognized in the absence of such activity
Macrophage
Dendritic Cell
• A special type of immune cell that is found in tissues,

such as the skin, dental pulp, that boosts immune
responses by showing antigens on its surface to other
cells of the immune system.
• A dendritic cell is a type of phagocyte and a type of

antigen-presenting cell (APC).
• At certain development stages they grow branched

projections, the dendrites
Plasma cells
• Plasma cells are seen during inflammation of the pulp

• •The plasma cells function in the production of antibodies.
• •Plasma cells may be present in coronal pulp
• •They have small nuclei with radiating chromatin that appears like
a cast wheel.
• These cells are not normally present in healthy pulp tissue but are
associated
• with injury and resultant immune response.

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Mast Cells
• Occur in small groups around blood vessels

• Present only during pulpal inflammation
• Have round nucleus and contain many dark staining granules in the cytoplasm.
• Their number increase during inflammation.
• Mast cells are seldom in large numbers in normal, healthy pulps but are commonly found
in inflamed pulps.
• The granules of these cells contain histamine, a potent inflammatory mediator, and
heparin.
• These cells release these granules or degranulate into the surrounding tissue fluid
during inflammation.
Mast cells are generally located near blood vessels of the pulp.
When degranulation of mast cells releases histamine close to vascular smooth muscle, it
causes vasodilation.
This increases vessel permeability, allowing fluids and leukocytes

to escape. (increase pulpal pressure)
• Mast cells in oral tissues contain the pro-inflammatory cytokine
tumour necrosis factor-α in their granules.
• Release of pro-inflammatory cytokine tumour necrosis factor-α

promotes leukocyte infiltration during inflammation associated
with conditions such as oral lichen planus, gingivitis, pulpitis, and
periapical inflammation through induction of endothelial-leukocyte
adhesion molecules.
Lymphocytes,Eosinophils and Leucocytes
• Usually not found extra-vascularly in the normal pulp.

• During inflammation they increase in number within the pulp.
• Lymphocyte present along the walls of the blood vessels
• Involved in initial immunodefense.
• Usually they are not found in uninflamed pulp
• In non-pathologic state, T lymphocytes found throughout pulp but B lymphocytes

are rare.
• Eosinophils are present in some allergic types of inflammation
• In pulp they are found in an inflammatory exudate

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Extracellular Matrix
• Connective tissue fibers
• Collagen
• Elastin
• Fibronectin
• Ground substance
• Proteoglycans
• Glycosaminoglycans
• Basement membrane
Fibers (Collagen Fibres)
• Extra cellular structural protein is a major constituent of connective tissue.

• Collagen fibers appear throughout the pulp as young fine fibers ranging in diameter from
10-12mm.
• Pulp collagen fibers do not contribute to dentin matrix production
• The fibers form a loose, reticular network to support other structural elements of the
pulp.
• After root completion the pulp matures and bundles of collagen fibers increase in
number.
• They scatter throughout the coronal or radicular pulp, or they appear in bundles.
• These are termed diffuse or bundle collagen.
Most prevalent in root canals, especially near apical region.

Type I: Present as thick striated fibrils
Responsible for pulp architecture.
Type III: Thinner fibrils,mainly distributed in cell free and cell rich zones.
Contributes to the elasticity of pulp
Type IV: Present along the basement membrane of blood vessels.
Type V and VI: form dense meshwork of thin microfibrils through out the stroma
Types of Collagen
Type 1 collagen : a triple helix composed of three chains or strands, each of them with 1050
amino acids and approximately 300 nanometers long. Type I collagen is extremely strong and
forms the primary component of tendons, connective tissue structures that link muscles and
bones. Reinforces bones.
• Type 2 collagen : the major protein in cartilage. Collagen type II fibrils are smaller than
collagen type I fibrils and assume random orientations in a gelatinous matrix of protein-
carbohydrate complexes, where they cross-link with collagen type IX.

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• Type 3 collagen not as strong as collagen type I. Also forms triple helices. Collagen III
is common in arterial walls, in the skin and in the intestines. It is also produced by
fibroblasts to seal up damaged skin in response to injury since it can be produced more
rapidly than collagen type I
Type 4 collagen : Collagen IV: forms bases of cell basement membrane and may be
produced by the cells themselves, rather than by fibroblast
• Type 5 collagen Rcell surfaces, hair and placenta
• Type 6 collagen: forms a filamentous network and has been identified in muscle and
skin. The molecule consists of a short triple helix about 105 nm in length with a large
globular domain at each end.
•
Type Location
Collagen
skin, tendon, bone, dentin, and pulp

I
II cartilage.
III unmineralized connective tissues
IV component of basement membranes
V a constituent of interstitial tissues
VI widely distributed in low concentrations in

soft tissues at interfibrillar filaments.
VII component of basement membranes
Collagen Turnover
• Collagen turnover is maintained by fibroblasts

• •During bacterial infection & inflammation, collagenolytic activity is accelerated
following collagenase produced by bacteria, PMN & fibroblasts
• • Collagen synthesis is accelerated during reparative dentin formation

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Elastic Fibers
• This has the ability to expand and contract like a rubber band
• •Elastic fibers are first formed in bundles of thin micro filaments
called Oxytalan fibers
• •Elastin is then deposited in between oxytalan fibers.
• •Always associated with larger blood vessels
• - bundles of proteins (elastin) found in extracellular
matrix of connective tissue and produced by fibroblast.
Fibronectin
• It plays a role in cell-cell & cell-matrix adhesion

• Has a major effect on the proliferation, differentiation & organization of cells.
• Seen around the blood vessels
• Also found in odontoblast layer with fibers passing into predentin
• Due to its close interaction with odontoblasts and extracellular fibers, fibrinoectin helps to
maintain cell morphology and provide a tight seal at this site.
• Fibronectin may be involved in cell migration and anchorage in the wound healing
process of the connective tissue of pulp.
• It regulates the migration and differentiation of secondary odontoblasts
• Adherent property of fibronectin is due to cell surface glycoprotein receptors called

Integrins
Ground Substance
• It is a structureless mass that makes up the bulk of the pulp

• Consists of complexes of proteins,carbohydrate and water.
• Broadly classified as:
– Glycoaminoglycans
– Proteoglycans
• More specifically, these complexes are composed of combinations of
glycosaminoglycans - hyaluronic acid,
chondroitin sulfate
other glycoproteins
Glycosaminoglycans
• GAG found in pulp is mainly chondroitin sulphate, dermatan sulphate & hyaluronic acid.
• Proteoglycans occupy larger area and they provide protection against compression.
• During dentinogenesis,the ground substance show affinity for collagen and influence
fibrinogenesis.
• They have capacity to bind with calcium and help in mineralisation

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Basement Membrane
• A basement membrane separates the internal enamel epithelium from the dental pulp.
• In mature pulp, basement membrane forms interface along endothelial cells & schwann
cells
• In the central part of the pulp arterioles have thicker layer of muscle cells and dense
basement membrane interspersed between endothelium and muscle cells
Basement membrane is a product of connective tissue and epithelium. It is composed of:
• Collagen type IV
• Laminin -adhesive glycoprotein
• Fibronectin
• Heparin sulfate
• Collagen IV provides binding sites for the rest of basement membrane components
• Laminin binds to both cells of connective tissue and

epithelium
• Composed of 2 layers:
– lamina densa-electron dense
– lamina lucida-electrolucent
• Act as sieve between epithelium and connective

tissue.
• Helps in organization and differentiation by enabling interactions between extra

cellular molecules and cell surface receptors
• Eg: Odontoblasts during tooth development
Radicular Pulp
• Radicular pulp is that pulp extending from the cervical region of the crown to the root
apex.
• They are not always straight but vary in shape, size and number.
• Root shape determines pulp shape
• The radicular portion is continuous with the periapical tissues through the apical
foramen or foramina.
Carries blood to and from the coronal pulp through the apical canal.
Regulate blood flow to coronal pulp
Allows transmission of immune cells from peripheral vascular or PDL vascularture to coronal
pulp.

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The Apical Foramen
• The pulp organs are continuous with the periapical tissue through
the apical foramen.
• The average size of the apical foramen is:
• maxillary teeth: 0.4 mm
• mandibular teeth: 0.3 mm
Apical Foramen
Innervation of the Pulp
• In the root, plexus of Raschkow or other
• Plexus of nerves does not exists..
Nerve in Root to crown
 The nerve bundles pass upward → fanout and branch beneath the
cell-rich zone, and ramify into a plexus of single nerve axons .
 A fibers emerge from their myelin sheath to form subodontoblastic

plexus
 As the root begins to develop, the apical foramen is actually larger

than the pulp chamber, but it becomes more constricted at the
completion of root formation.
 Accessory Canals
The pulp cavity is sometimes connected with the periodontal tissue with
an opening rather than the apical foramen, the lateral, accessory or
supplementary canal.
They are numerous in the apical third of the root and in the bifurcation of
multirooted teeth.
If the root canal breaks up into

multiple tiny canals, it is
referred to as a delta system
because of its complexity.

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Aetiology of Accessory Canals
1. Degeneration of the epithelial root sheath of Hertwig before odontoblasts differentiation.

2. Large blood vessel disturbs the course of the root sheath.
3. Lack of union of the tongue like projection (in multi-rooted teeth).
Odontoblasts
The odontoblasts are arranged in a single layer where:

 In the pulp chamber the cells are crowded and appear pseudostratefied
columnar.
 Near the beginning of the root canal they become columnar in shape.
 In the mid portion of the root canal they become cuboidal in shape.
 In the apical area of the root canal they become flat cells.
Odontoblast Coronal pulp Radicular pulp.
Cells1 More less
layer2 Columnar A squamous

to cuboidal in layer of flattened
med. cells.
Vascular Supply
 Vessel course up the RC and branches laterally toward the odontoblast layer.
 Ramify in coronal pulp to form a capillary plexus
 To provides odont. source of metabolites.
Capillary blood flow :
 In the coronal portion of the pulp is nearly twice that in the

root portion.
Arteriovenous anastomoses (AVAs)
 Direct communication between Artery and Vein. No capillary

bed.
 Radicular pulp >Coronal pulp
 Regulate the pulp circulation
to avoid thrombosis and hemorrhage.
 It shunt blood away from areas of pulpal injury

(redirect incoming blood)

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Lecture 10 – Dentinal Structure
• Dentinal hypersensitivity, or cervical dentinal sensitivity, is defined as pain arising

from exposed dentine typically in response to thermal, chemical, tactile or osmotic
stimuli.
• Dentine may become exposed because the enamel or cementum which normally
covers the dentine surface is removed or denuded as a result of attrition, abrasion or
erosion.
Dentin Sensitivity
• Dentin sensitivity is due to open dentinal tubules which provide a direct link between the
external environment and the internal pulp of the tooth.
• Even after long periods of exposure to the oral environment, dentinal sensitivity may still
be a significant problem despite the exposed tubules becoming occluded by the smear
layer or pellicle
• Dentin sensitivity affects about 20 – 25 of the population
Dental Pellicle
• Dental pellicle is a protein film that forms on the surface enamel by selective binding
of glycoproteins from saliva that prevents continuous deposition of salivary calcium
phosphate.
• It forms in seconds after a tooth is cleaned.
• It is also protective to the tooth from the acids produced by

oral microorganisms after consuming the available carbohydrates
• The teeth most commonly affected by dentinal hypersensitivity are the upper premolars
followed by the upper first molars with the incisors being the least sensitive teeth.
• Most sufferers of dentine hypersensitivity range in age from 20 to 40 years with the peak
incidence occurring at the end of the third decade and decreases during the fourth and
fifth decades of life.
Odontoblastic transduction theory
• According to this theory, odontoblastic processes are exposed on the dentine surface
and can be excited by a variety of chemical and mechanical stimuli.
• As a result of such stimulation neurotransmitters are released and impulses are

transmitted towards the nerve endings.
• To date no neurotransmitters have been found to be produced or released by

odontoblastic processes.

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Neural theory
• An extension of the odontoblastic theory.
• This theory postulates that thermal, or mechanical stimuli, directly affect nerve endings
within the dentinal tubules through direct communication with pulpal nerve fibres.
• While this theory has been supported by the observation of the presence of
unmyelinated nerve fibres in the outer layer of root dentin and the presence of putative
neurogenic polypeptides, this theory is still considered theoretical with little solid
evidence to support it
Hydrodynamic theory
• The most widely accepted theory for dentinal hypersensitivity.
• This theory postulates that fluids within the dentinal tubules are disturbed either by
temperature, physical or osmotic changes and that these fluid changes or movements
stimulate a baroreceptor which leads to neural discharge.
• The most widely accepted theory for dentinal hypersensitivity.
• Dentin contains many thousands of microscopic tubular structures that radiate outwards
from the pulp.
• These dentinal tubules are 0.5-2 micrometres in diameter.
• Changes in the flow of the plasma-like biological fluid present in the dentinal tubules can
trigger mechanoreceptors present on nerves located at the pulpal aspect thereby
eliciting a pain response.
• This hydrodynamic flow can be increased by cold, air pressure, drying, sugar, sour
(dehydrating chemicals), or forces acting onto the tooth.
• Hot or cold food or drinks, and physical pressure are typical triggers in those individuals
with teeth sensitivity.
Clinical Management
• For deep tooth brush abrasions – restore the area with composit restorations.
• Chemical agents can consist of
– amorphous calcium and phosphate

– potassium nitrate
– strontium chloride
– fluoride therapy
– calcium sodium phosphosilicate.

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Commercial Products
• Sensodyne (GlaxoSmithKline) and Crest Sensitive
• (, Proctor and Gamble) contains Potassium nitrate.
• Sensodyne Original and Sensodyne Mint toothpastes: Strontium chloride and

strontium acetate respectively.
• The mode of action is linked to their ability to form mineralized deposits within the tubule
lumen and on the surface of the exposed dentine that help prevent transmission of the
applied stimulus.
Flouride
• Flouride decrease permeability of dentin.

• Topical fluoride applications create a barrier by precipitating calcium fluoride (CaF2) on
the tooth surface, blocking patent dentinal tubules and, hence, reducing permeability and
hypersensitivity.
• The resins contained in fluoride varnishes might provide an additional barrier effect
• Clinical studies indicate that a single application of topical fluoride varnish reduced
cervical dentin hypersensitivity for 24 weeks
Dentoenamel Junction (DEJ)
• Dentin - derived from the mesoderm - is a flexible, mineralized tissue composed of 70%
(weight %) inorganic material, 20% organic material and 10% fluid.
• Enamel - derived from ectoderm - is a very brittle tissue composed of mostly

hydroxyapatite mineral (∼96%), water (∼3%), and trace organic matrix (∼1%)
• (DEJ) is an interface between two mineralized tissues with different compositions and
biomechanical properties
• Formation of the DEJ begins at the early stages of tooth morphogenesis and is thought
to be linked to a mixture of dentin proteins secreted by odontoblasts and enamel
proteins from ameloblasts.
• The proteins associated with DEJ formation are collagen fibril bundles that cross the
transition zone and insert into enamel are generally responsible for the variations and
distribution deviations in composition and structure of the organic matrix within the DEJ.
• The mineral crystallinity within the DEJ is not much different from the mineral in dentin.
• There is a narrow area of higher mineralization of enamel in the region adjacent to the
DEJ.
• Enamel close to the tooth surface is less mineralized than the enamel at the DEJ.

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• This difference in mineral content is important, because the higher the mineralization
the more susceptible to mineral dissolution.
• The decrease of mineral content at the outer enamel surface will provide superior
resistance to attack from the acidic by-products associated with dental plaque.
• However, the increased minerals within enamel near the DEJ may help explain why
dental decay tends to penetrate more rapidly once it nears the DEJ
• The DEJ structure is a series of 25-200 μm diameter scallops that contain 80-120 nm
parallel Type-I collagen fibrils extending from the dentin into enamel, which might play a
role in crack prevention.
• The modulus gradient has been associated with variations of mineralization and the
associated collagen to mineral ratio within the DEJ as compared to dentin and enamel.
• For a given material the Modulus (E) is the ratio of stress* to strain or the “stretchability”
of the material.
• A brittle material would have a much smaller strain value before breaking.
• MODULUS OF ELASTICITY: eelastic material always spring back into shape when the
force is removed.
• THEY OBEY HOOKS LAW = deformity is directly proportional to the force.

• The modulus gradient is the difference in ability to stretch between two materials in
contact.
• When a force is applied to an elastic body, the body will deform.
• Strain is the deformation per unit of the original length.
• The stiffness between dentin and enamel are different.
DEJ
L - limit of
proportionality
E - elastic limit
Y - yield point
X - stress removed here,
body has
'
permanent strain 0X
B - breaking stress

-102-
Forces
Enamel is a brittle substance which is strong in compression.

Dentin is more elastic and will deform.
Compressive strength is the capacity of a material to withstand axially directed pushing
forces – biting and chewing.
When the limit of compressive strength is reached, brittle materials are
crushed. Proprioceptive sensation of teeth and TMJ prevents this from occuring.
• When a specimen of material is loaded in such a way that it extends it is said to be

in tension.
• When the material compresses and shortens it is said to be in compression.
• The major difference between the two types of loading is the strain which would have
opposite signs for tension (positive—it gets longer) and compression (negative—it gets
shorter).
• Both are governed by Hooks law. The breaking point is = the crushing point.
Red dot represents the crushing point
In a compression test, there is a linear region where

the material follows Hooke's Law.
Dento-enamel Junction (DEJ)
• Finite-element models of forces applied to teeth shows that in the scallop model, the
net-compression towards the DEJ was higher than net-tension away from it.
• As a consequence, the dentin and enamel is pushed towards each other during loading.
• The width of the transition zone, microhardness and elastic modulus of the DEJ is critical
in preventing fractures of the enamel.
• The width of the transition zone at the occlusal position is wider than that at the cervical
position.
• The matrix/mineral ratios of the DEJ are higher than those of enamel (more organic)
and lower than those of dentin (more mineral)
• MATRIX MINERAL ROTION: CH (matrix) to phosphate (mineral)
• The molecular structure of organic matrix in the DEJ is different from that in dentin.

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Buccal cusp Buccal cervical

Tooth
occlusal site site
1 10.8±3.5 6.3±1.4
2 12.2±2.6 6.0±0.9
3 12.7±2.8 5.8±1.0
4 14.2±2.5 6.2±1.5
5 14.8±3.3 7.3±1.8
*
Overall Mean ±SD 12.9±3.2 6.3±1.3
• Enamel initially forms at the occlusal/cuspal

locations followed by enamel formation across the crown
to the cervical area.
• The difference in development times of enamel at

occlusal and cervical positions might account for the
difference in structural width of the DEJ between
positions.
• The difference might also be related to

differences in function with the occlusal surfaces exposed
to greater loads during mastication than the cervical area.
(Form follows function)
Dentin Structures

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Mantle Dentine
• The peripheral portion of dentin, adjacent to the enamel or cementum, consisting of

coarser fibers than the circumpulpar dentin.
• It is unique to the rest of primary dentin.
• Mantle dentin is formed by newly differentiated odontoblasts and forms a layer
approximately 150 micrometers wide.
• Unlike primary dentin, mantle dentin lacks phosphoryn, has loosely packed collagen
fibrils and is less mineralized.
• Below it lies the circumpulpal dentin.
The outer layer of primary dentin, which is synthesised at

the onset of dentinogenesis, is called mantle dentin.
Mantle dentin is slightly less mineralized than other layers

of the primary dentin i.e. circumpulpal dentin.
Dentin
Primary Curvature is: S-shaped - lazy “s” of the primary

curvature. In the coronal portion of the tooth, dentin has a
“S”shaped curvature
Secondary Curvature: jagged or wrinkled texture.

• Curvatures result from movement of
• odontoblasts during development.
• In the root portion of the tooth, dentin has a more straight path.
•

-105-
Dentin Tubular Branching

• There are different types of branches of dentinal tubules which are differentiated on the
basis of size, location and direction of the branches in relation to the main tubule.
• Major branches of the tubules are found peripherally up to approximately 250 mm from
the outer surface in both coronal and root dentin.
• These branches form a delta and the
diameter of the tubules ranges from 0.5 to
1.0 mm
• Fine branches are typical of root dentin and
in any location where the number of tubules
is low. They vary in diameter from 0.3 to 0.7
mm and they branch off from the main
tubule at about a 45o angle.
• Microbranches can be found anywhere in
dentin.
• They are up to about 0.1 mm in diameter
and branch off from the tubule at a 90o

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Owen Contour Lines
Accentuated incremental lines in dentin caused by sublethal systemic insults such as infectious
disease which injure odontoblasts.
**Incremental lines or bands within mature dentin
Interglobular Dentin
• Areas of unmineralized or
hypomineralized dentin where globular areas of
mineralization have failed to coalesce

-107-
Granular Layer-Tomes Processes
• The superficial layer of dentin

adjacent to cementum. This is only found
in root dentin
Regular Secondary Dentine
Age Changes
The predominant age related changes in dentin are represented by a gradual
enlargement of the peritubular dentin and formation of secondary dentin.
• The widening of peritubular dentin leads to narrowed or occluded tubules.
Age Changes:
 Increase of volume at the expense of pulp
 Increase of secondary and tertiary dentin, more dead tracts and sclerotic dentin
found
 Increase in secondary dentin makes the teeth appear darker
DENTIN:
Dentin is softer than enamel, but still harder than bone. It consists mainly of apatite crystals of
calcium and phosphate, which is only about 70% mineralization and contains proportionally
more collagen fibers and cells. Dentin is produced by the odontoblasts, cells that line the pulp

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cavity of the tooth. Dentin is a living tissue which has the ability for constant growth, repair and
reacts to physiologic or functional and pathologic or disease stimuli. Primary dentin is formed
during tooth formation. Once a tooth becomes functional, subsequent formation of dentin results
in secondary dentin, somewhat less mineralized and with more irregular tubules than the
primary dentin.
Tertiary or reparative dentin forms in response to injury: dental abrasion, attrition, cavity
preparation, erosion or dental caries. Tertiary dentin appears to have less structural
organization and strength than the original dentin which it replaces. Although the exact form
and the regularity of tertiary dentin appears to be dependent on the intensity of the external
stimulus. Hypercalcification of dentin tubules can also occur in response to injury and is
referred to as sclerotic dentin. The amount of sclerotic dentin increases with age, proceeding
from the root apex towards the crown. There are also obvious optical changes in the tissue,
which becomes translucent, while normal dentin is normally opaque.
Undergoes numerous other alterations associated with caries, aging or induced through
treatment or medications.
• Demineralization
• Deproteinization
• Hypermineralization
Age changes in dentin include:
increase of thickness and volume at the expense of pulp,
decline in number and density of odontoblasts and other cell types with decreases in
the root being greater than those in the crown region,
an increase of secondary and tertiary dentine, more dead tracts and sclerotic dentin
found.
Aging teeth develop secondary dentin over time that also makes the teeth appear darker.13-14
• Changes in dentine due to aging results from transformation of morphological features

causing changes to their hardness and modulus of elasticity.
• The thickness of mantle dentine and globular dentine decreases with aging.
The hardness and modulus of elasticity of dentine increases with age.

-109-
Lecture 11- Cementum, Cementoenamel Junction, PDL
Cementum
• Cementum formation begins when both epithelial cells of Hertwig’s root sheath
(HERS) and mesenchymal cells of the dental follicle are in proximity to the developing
root surface.
• The Hertwig's epithelial root sheath (frequently abbreviated as "HERS") is a

proliferation of epithelial cells located at the cervical loop of the enamel organ in
a developing tooth.
• Hertwig's epithelial root sheath initiates the formation of dentin in the root of a tooth by
causing the differentiation of odontoblasts from the dental papilla.
• The root sheath eventually disintegrates, but residual pieces that do not completely
disappear are seen as epithelial cell rests of Malassez

-110-
Cementogenesis
(1) HERS becomes disintegrated prior to any

cementum deposition.
(2) mesenchymal cells from the dental follicle

penetrate the HERS bilayer and deposit initial
cementum matrix.
Immediately adjacent epithelial cells are separated from

the root surface by a basal lamina and do not secrete
any cementum matrix
(3) HERS is removed from the root surface prior to cementum deposition.
• (4) both amelogenin mRNAs and proteins are absent from the root surface and from the
cervical-most ameloblasts.
• (5) cementum protein extracts do not cross-react with amelogenin antibodies on
Western blots.
Cells in immediate proximity to HERS extend processes between HERS cells and gain access
to the developing root surface prior to any cementum deposition.
• The outer HERS basal lamina is removed prior to cementogenesis and inner HERS
basal lamina is penetrated by invading cells from the dental follicle proper.
•
It has been suggested that the process-
forming epithelial cells function to disrupt
Hertwig’s root sheath to provide space for
mesenchymal cells to penetrate the epithelial
barrier.
• Initial cementum matrix deposition

exclusively occurs in areas in which
mesenchymal cells have access to the root
surface.
• Adjacent epithelial cells separated from
the root surface by a basal lamina do not
deposit any cementum
•
The first cementoblasts that appear during root development are mesenchymal cells of
the dental follicle.
• The cervical disintegration of HERS is a key event during cementogenesis allowing for
the perforation and gradual penetration of HERS by mesenchymal cells.

-111-
Periodontal Ligament (PDL)

•
The dental follicle around the developing root is reduced to a thin capsule of
connective tissue that will be remodeled into the (PDL).
• Some of the pluripotential cells of the dental follicle that are capable of producing bone,
cementum and the ligament will be preserved as undifferentiated cells in the mature
periodontal ligament, usually in a perivascular location.
• Remodeling of the ligament begins at the cemento-enamel junction and proceeds
apically
•
Remodeling of the dental follicle into a periodontal ligament (PDL) begins near the
cemento-enamel junction following the formation of the dentogingival fibers (DGF).
• Remodeling begins with the fibers that are closest to the root surface and the bone (B).
• The process then proceeds in an apical direction until the entire follicle is remodeled into
a periodontal ligament, with fibers more or less perpendicular to the root surface.
•

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• The gingival fibers are the connective tissue fibers that are in the gingival
tissue adjacent to teeth and help hold the gums firmly against the teeth.
• They are primarily composed of type I collagen, although type III fibers are also
involved.
• These fibers, unlike the fibers of the periodontal ligament, attach the tooth to the gingival
tissue, rather than the tooth to the alveolar bone.
Dentogingival fibers (DGF)

D: dentin
DF: dental follicle (immature

periodontal ligament)
EF: extrinsic collagen

fibers
F: fibroblasts

-113-
Lecture 12 – Dentinal Sulcus –Dentogingival Junction
• The gingival sulcus is the natural space found between the tooth and the gum tissue that
surrounds the tooth, known as the free gingival margin
• Healthy gums generally have a sulcus depth between 1 to 3mm.
• Sulcus depths greater than 3mm occur in patients that have varying degrees of
periodontal disease.
• This is referred to as a periodontal pocket.
• The gingival sulcus is formed by the space

between:
the sulcular epithelium
the junctional epithelium
the wall of the tooth (enamel or cementum)
Gingival Sulcus :Overview
The cellular turnover of the junctional epithelium is very high.

The intercellular spaces are wider in the junctional epithelium, when compared to those of the
sulcular or oral epithelia.
Numerous substances have been shown to permeate the junctional epithelium, both toward the
sulcus and from the sulcus within the connective tissue
Free Gingiva
The free or marginal gingiva consists of four boundaries:
1 Coronally by the gingival margin
2 Apically by the free gingival groove. (In the absence of
this groove, the apical boundary would correspond to a line
oppoite to the bottom of the sulcus – usually 1.0 – 1.5 mm
apical to the free gingival margin.
3 Medially is the gingival sulcus.
4 Laterally is the oral and vestibular mucosa.

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The attachment of the free gingiva to the tooth surface is mediated by a thin nonkeratinized
epithelium termed the junctional epithelium (JE).
Ultrastructural studies have shown that the attachment of the JE to the tooth surface occurs
through hemidesmosomes (HD) and a basal lamina-like extracellular matrix termed the internal
basal lamina (IBL).
The junctional epithelium is a strategically important interface between the gingival sulcus,
populated with bacteria, and the periodontal soft and mineralized connective tissues that need
protection from becoming exposed to bacteria and their products.
The JE forms the attachment of the oral epithelium to the teeth.
It attaches to enamel, cementum or dentin in that order.
About 1 – 2 mm in corono-apical dimension
• At the end of ameliogenesis ameloblast and stratum intermedium layers of the enamel
organ along with remnants from the stellate reticulum and outer enamel epithelium forms
a thin multilayered epithelium structure that covers the enamel following its formation.
• This is referred to as the reduced enamel epithelium.
• Once the enamel is completely mineralized, the ameloblasts shrink from columnar to
cuboidal or flattened cells, but remain a part of the reduced enamel epithelium that
forms a more or less continuous lining over the completed enamel.
The reduced enamel epithelium consists of two major cellular layers:

(1) the reduced ameloblasts that are in contact with the enamel but no longer functional.
(2) the external cells of the reduced enamel epithelium that consist mostly of stratum
intermedium cells.
The external cells of the reduced enamel epithelium consist of undifferentiated epithelial cells
able to divide and multiply.
It is these external cells of the reduced enamel epithelium that give rise to the junctional
epithelium.

-115-
• With tooth eruption the reduced enamel epithelium slowly dissolves around the tooth as
it enters the mouth
• It eventually settles close to the cervical area of the crown.
• Its length, therefore, varies with the amount of tooth surface that has erupted.
Length of Junctional Epithelium

 Length varies according to stage of eruption
 Tooth first erupts – most of enamel covered by JE
 Tooth reaches occlusal plane – ¼ enamel surface covered
 Eventually JE lies close to CE junction
 Older patients with root exposure (passive eruption or disease) JE proliferates apically -
firm attachment with cementum

The junctional epithelium is a circular arrangement of epithelial cells occurring at the
base of the gingival sulcus and attached to both the tooth and the subepithelial connective
tissue.
When the JE forms from the ameleoblastic tissue it is called primary epithelial attachment.
Summary
 Initially derived from Reduced Enamel Epithelium
 REE replaced once tooth erupts – REE covering
crown lost rapidly and is replaced by squamous
epithelial cells
 Transformed REE & oral epithelium form
dentogingival junction and junctional epithelium
 Final conversion of REE to JE may not occur until
3-4 years post eruption

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• Stratified non-keratinizing squamous epithelium that surrounds the tooth like a collar with
a cross-section resembling a thin wedge.
• One side of the “wedge” is attached by a broad surface to the tooth and the other to the
gingival connective tissue.
• Legend:
• CT, gingival connective tissue
• ES, enamel space
• JE, junctional epithelium
• OE, oral epithelium
• SE, sulcular epithelium
The junctional epithelium has 2 basal

laminas:
one that faces the tooth (internal basal lamina)
one that faces the connective tissue
(external basal lamina).
The internal and external basal lamina are
structural analogs of each other.
Junctional epithelium is unique as it possess 2 basement membranes – the internal and

external basal lamina

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The JE has a high rate of cell turnover

It takes 6 days for cells to go from the stratum
basale to the surface and are sloughed.
During outward migration, the cells maintain
their attachment to the tooth surface.
As the cells migrate, they maintain their
attachment to the underlying basal lamina
• The proliferative cell layer responsible for most cell divisions is located in contact with
the connective tissue, i.e. next to the external basal lamina.
• The desquamative (shedding) surface of the junctional epithelium is located at its
coronal end, which also forms the bottom of the gingival sulcus.
• All cells within the JE are in a coronal migration, including those cells that are in contact
with the tooth surface.
• The basal lamina is a layer of extracellular matrix secreted by the epithelial cells, on
which the epithelium sits
• The basal lamina cannot be distinguished under the light microscope, but only under the
higher magnification of an electron microscope.
• Under the electron micoscope the basal lamina and lamina reticularis are visibly distinct
structures.

-118-
Desmosomes
• Desmosomes are molecular complexes of cell
adhesion proteins and linking proteins that attach the
cell surface adhesion proteins to intracellular
keratin cytoskeletal filaments.
• A type of junctional complex, they are localized spot-
like adhesions randomly arranged on the lateral
sides of membranes.
• Desmosomes help to resist shearing forces and are
found in simple and stratified squamous
epithelium
External Basal Lamina
Internal Basal Lamina

The internal basal lamina consist of a lamina densa and a lamina lucida.
LAMINA DENSA: adjacent to the enamel. An electron-dense zone
LAMINA LUCIDA: area where hemidesmosomes are attached. It is a roughly 40 nanometre
wide electron-lucent zone between the basal cells of the epithelium and the lamina densa.
The attachment of the JE to the tooth surface is also reinforced by gingival fibers.

-119-
• Gingival Fibers: located at the depth of the gingival sulcus and add reinforcement to
the JE.
• The gingival fibers are located in the attached gingiva and help hold the tissue firmly
against the teeth.
• They are primarily composed of type I collagen, although type III fibers are also involved.
• These fibers attach the tooth to the gingival tissue.
• Circular fibers: these fibers are unique in that they exist entirely within the gingiva and
do not contact the tooth
Gingival Fibers
GINGIVAL LIGAMENT = GINGIVAL FIBERS
Layers of Oral Mucosa

-120-
DO NOT HAVE GRANULAR OR CORNIFIED LAYERS
• The JE is divided into three zones:
– Coronal…permeable zone
– Middle…adhesion zone
– Apical …germination zone.
The apical area is only a few cell layers thick.
The attachment to enamel, cementum or to dentin occurs

in the same manner
The apical area is only a few cell layers thick and is the germination layer
The attachment to enamel, cementum or to dentin in the middle area utilizes the same
mechanism.
The cells at the coronal portion is exfoliated (sloughed) in rapid succession.
• The basal cells are cuboidal or flattened.

• They contain more rough endoplasmic reticulum and lysosomes.
• Mitochondria within the cells decreases as the cells migrate towards the surface.
• Cells of the suprabasal layer adjacent to the tooth surface have complex
microvilli that interdigitate.
• The cells at the base have phagocytic properties.
• The basal cells are cuboidal or flattened.

• They contain more rough endoplasmic reticulum and lysosomes.
• Mitochondria within the cells decreases as the cells migrate towards the surface.
• Cells of the suprabasal layer adjacent to the tooth surface have complex
microvilli that interdigitate.
• The cells at the base have phagocytic properties.
Basal Cell Layer
1 cuboidal cells
2 rough endoplasmic reticulum and lysosomes

-121-
• The density of desmosomes that interconnect the cells are far less than that of
oral epithelium and represents wider intercellular junctions.
• Wide intercellular spaces increases the permeability
Soluble substances can diffuse from the oral cavity into the underlying gingival connective
tissue, while both fluids and cells can travel through the junctional epithelium from the
connective tissue into the gingival sulcus and subsequently to the oral cavity.
Apical migration of junctional epithelium along a root surface is an important factor in

periodontal pocket formation and deepening.
Disturbance of the attachment will result in deepening of the periodontal pocket.
Sulcular Epithelium
• The sulcular epithelium (SE) is the stratified, squamous epithelium, non-keratinized or

parakeratinized, that lines the lateral surface of the gingival sulcus.
• It is continuous with the oral epithelium.
• Apically, it overlaps the coronal border of the junctional epithelium.
• It has good resistance to mechanical forces
The SE is the coronal lining of the gingival sulcus extending from the marginal gingiva to the JE.
Made up of basal and prickle cell layers.
The sulcular epithelium resembles the oral/gingival epithelium except that it does not become
fully keratinized (Parakeratinization).
Normally there are no rete pegs in sulcular epithelium but they will form during inflammation.
Normal Gingiva

-122-
Sulcular Epithelium
Sulcular Epithelium
In contrast to the junctional epithelium, the sulcular epithelium is

less permeable
It has mostly protective functions.

-123-
Gingival Epithelium Sulcular Epithelium
Hyperkeratosis Parakeratin
Orthokeratin

-124-
Lecture 13- Supporting Structures
Alveolar Bone
• Alveolar bone or alveolar process is that portion of maxilla or mandible

that supports the roots.
• Anatomically it is the thickened ridge of bone that contains the tooth
sockets on bones that bear teeth.
• The alveolus is the socket in the jaw in which the roots of teeth are
held in the alveolar process.
• The basal bone is the remainder of the maxilla or mandible.
Fig.12.1 Basal Bone
Formation Of Alveolar Bone
• Alveolar bone arise from the outer-most

cells of the dental papilla
• As root and cementum formation begin,
bone is created in the adjacent area.
• The osteoblast cells that deposits alveolar
bone are form from the dental follicle
• It is 65% inorganic and 35% organic
• The organic portion is 30% Type 1 collagen
5% non-collagenous proteins.

-125-
Formation of Alveolar Bone (continued)

• The alveolar bone forms when the tooth
erupts and disappear gradually after the
tooth is lost.
• Intially, bone forms a thin eggshell of
support – the bony – crypt around each
tooth germ.
• As the root grows and lengthens, the
alveolar bone grows with the elongating
erupting tooth and maintains relationship with each tooth root.
• The alveolus is composed of two parts:

– The alveolar bone proper (= alveolus)
– Supporting bone
The alveolar process contains a region of compact bone adjacent to
the periodontal ligament called lamina dura.
The lamina dura attaches to the periodontal ligament
• Alveolar bone proper is that part of the alveolar bone that forms
the sockets.
• Alveolar bone proper is also called cribiform plate because it is perforated by several
openings.
• It is a thin lamella of compact bone in which periodontal fibers are embedded
• It is a special type of compact bone composed of bundle bone and Haversian bone
• It is referred to as bundle bone because it is regularly penetrated by Sharpey’s fibers
from the PDL.

-126-
Alveolar Bone
• Bundle bone is a histologic term for the portion of the bone of the alveolar process that
surrounds teeth and into which the collagen fibers of the periodontal ligament are
embedded.
• Haversian bone: A structural unit of bone consisting of a Haversian canal and
corresponding lamellae of compact bone
Tooth Root and Bone

-127-
Haversian System canals are a series of tubes

around narrow channels formed by lamellae.
• This is seen in compact bone.
• The Haversian canals surround blood
vessels and nerve cells throughout the bone and
communicate
with osteocytes in lacunae through canaliculi.
• This unique arrangement is conducive to
mineral salt deposits and storage.
• Adjacent haversian canals are
interconnected by Volkmann canals.
Haversian Bone
• Alveolar bone is subjected to continuous and rapid remodeling associated with tooth
eruption, then mastication and after tooth extraction if it occurs.
• In physiologic movement of teeth the lamella bone of the alveolus is readily resorbed in
zones of compression and deposited in zones of tension.

-128-
• Radiographically alveolar bone proper is referred to as LAMINA DURA

• It appears radio-opaque on dental radiographs.
• The widening or disaperance of the lamina dura is an expression of pathology.
Alveolar Bone of Maxilla

• Cortical bone thinner than mandible in all areas
• Defects of the buccal side of the premolar – molar area are fairly common because it is
perforated by many small openings through which blood vessels and lymph vessels
pass.
• Cortical bone thinner than mandible in all areas
• Thick cortical bone in premolar – molar area.
• Thicker on the buccal side.
• Thin cortical plate on lingual side of molar teeth.
• Thinner cortical plate than maxilla in buccal of lower anterior.
The remainder of the alveolar process below the

alveolar bone proper is called the SUPPORTING
BONE
• It is attached to the alveolar bone proper.
• Supporting bone is comprised of the
cortical bones at the laterl and medial sides and
spongy bone between the two cortical plates.
Supporting Bone
• The compact supporting bone of the alveolar process extends from the alveolar crest to
the lower border of the socket on the outside surface of the maxilla and mandible.
• This cortical bone has Haversian systems radiating lamellae with lacunae and canaliculi.
Alveolar Bone
• Cancellous bone is located apically between the
alveolar bone and the cortical plates.
• It supports and strengthens the alveolar bone.
Interdental Bone
• INTERDENTAL BONE: the bone between the
roots of single rooted or multi-rooted teeth.
• INTERRADICULAR BONE: the bone between
the roots of multi-rooted teeth

-129-
Trabecular Pattern and Lamina Dura
• There are variations in the thickness of the trabecular

and the size of the marrow spaces.
• From the apex of the mandibular molars the
trabeculae often radiate in a distal direction.
• Radiating trabeculae is not seen in the maxilla as the
maxillary sinus are close to the roots of the molars
Hirschfeld’s Canal
• Canals that extend vertically through alveolar bone between the roots of mandibular and
maxillary anterior teeth premolars
Dimensional Changes of Post-extraction Sockets
The average reduction in width of the alveolar ridges is approximately 4 mm.

The decrease in height is approximately 2 mm.
The alveolar bone continues to slowly resorbed until it reaches the basal bone.
Alveolar Bone Abnormalities
• FENESTRATION: an area where the root penetrates

the cortical bone in the apical region. Usually secondary
to infection
• DEHISCENCE: an area where the root penetrates the
cortical bone in the coronal area.
Fenestration and Dehiscence

-130-
Root Resorption
• Root resorption is the destruction, and subsequent loss, of the root structure of a tooth.
• Root resorption occurs as a result of differentiation of macrophages into osteoclasts in
surrounding tissue which, if in close proximity to the root surface will resorb the root
surface cementum and underlying root dentine
• Root resorption may be internal or external.
• Root resorption can be a transient or a progressive event.
• Unlike deciduous teeth, permanent teeth rarely undergo root resorption

• Root resorption of secondary teeth can occur as a result of pressure on the root surface.
• This can be from trauma, ectopic teeth erupting in the path of the root, inflammation,
excessive occlusal loading, aggressive tumors and growths.
• The most common cause in USA is orthodontic forces.
Deciduous root resorption is a natural process which allows exfoliation of the primary teeth to
make way for the secondary teeth.
Deciduous root resorption is caused by osteoclast differentiation due to pressure
exerted by the erupting permanent tooth.
• Permanent teeth rarely undergo root resorption

• Cementum and predentin covering on dentin are essential elements in the resistance of
the dental root to resorption.
• The most external aspect of cementum is covered by a layer of cementoblasts.
• THIS surface does not provides satisfactory conditions for osteoclast binding.
. Internally, the dentin is covered by predentin matrix, which possesses a similar organic
surface.
• Internally, the dentin is covered by predentin matrix, which possesses a similar organic
surface.
• Osteoclasts do not adhere to nonmineralized collagen matrices.
• The presence of a noncollagenous, organic component within dentin (odontoblast layer
and
• predentin) prevents resorption of the root canal wall
Root Resorption Aetiologies
• Intrapulpal infection : the stimulation factor in internal root resorption and in

periradicular inflammatory root resorption.
• • Periodontal infection: causes external root resorption due to an injury to the

pericementum.
• • Pressure from orthodontic type forces: impacted tooth, or tumor can cause external
root resoption adjacent to the area near the stimulation source.

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Resorption can occur on a luxated tooth that has been replaced in the socket. It is thought the
stimulus for the resorption and ankylosis of the tooth is related to damage to the PDL due to too
long a time out of the mouth, or lack of adequate storage before replacement.
• Trauma causing injury to the dentin, cementum, or PDL can bring about a clastic
response of cells as a normal part of the scavenging function of cells.
• This is normally a transient process, but with added stimulation may continue into a
chronic inflammatory process, creating external resorption of the root surface.
External Root Resorption

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Internal Root Resorption
• In order for root resorption to occur, two things must happen:

• 1. The loss or alteration of the protective layer(pre-cementum or pre-
dentin)
2. Inflammation must occur to the unprotectedroot surface.
Destructive phase:IRR
• Active resorption of injured/necrotic cells by multinucleated giant cells.
• This destruction will continue as long as there is stimulus present to
allow the inflammation to continue.
• The conditions most likely to continue the stimulus would be due to
either mechanical damage to the root surface, or foreign materials or bacteria picked up
at the accident site on the root surface
• If the stimulus only exist for a short period of time, healing will take place without
intervention by the dentist.
Healing phase :IRR

• The critical factor in determining the outcome after a dental traumatic injury has occurred
is the type of cells that repopulate the root surface during the healing phase.
• If cementoblasts are able to cover the damaged root surface, a type of healing termed
cemental healing or surface resorption will occur and the outcome will be favorable.
If osteoblast are able to cover the root surface, the conditions for healing will be unfavorable.
Direct contact with bone will cause bone to heal directly to the root over some areas leading to
ankylosis.
Bone is constantly remodeling.
Bone that’s in contact with root will resorb the root by the osteoclasts but, in the reforming
stage, bone is laid down instead of dentin.
The root is, therefore, slowly replaced with bone.
Ankylosed Teeth
Pathogenesis:IRR
• For internal root resorption to occur, the outermost protective odontoblast layer and
the predentin of the canal wall must be damaged, resulting in exposure of the underlying
mineralized dentin to odontoclasts

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• Odontoclasts bind to extracellular proteins containing the RGD (arginine-glycine-

aspartic acid) sequence of amino acids via integrins.
• Integris are specific surface adhesion glycoprotein membrane receptors containing
different a and b subunits.
• Avb3 integrin plays a key role in the adhesion of clastic cells
Etiologic factors that may cause loss of predentin:

Trauma (the most common predisposing factor - responsible for 45% of cases)
caries and periodontal infections
excessive heat generated during restorative procedures on vital teeth
Calcium hydroxide procedures
vital root resections
anachoresis
orthodontic treatment
cracked teeth
idiopathic dystrophic changes within normal pulps
Etiologic factors that may cause loss of predentin:
• Trauma (the most common predisposing factor - responsible for
45% of cases)
• caries and periodontal infections
• excessive heat generated during restorative procedures on vital
teeth
• Calcium hydroxide procedures
• vital root resections
• anachoresis
• orthodontic treatment
• cracked teeth
• idiopathic dystrophic changes within normal pulps
• Osteoclasts are motile, multinucleated giant cells formed by the fusion of mononuclear
precursor cells of the monocyte-macrophage lineage derived from the spleen or bone
marrow.
• They are recruited to the site of injury or irritation by the release of many
proinflammatory cytokines
• Osteoblasts and osteocytes are derived from skeletal precursor cells.
To perform their function, these motile phagocytic cells must attach themselves to the cemental
surface to become cementoclasts.

-134-
Damaged cemental surfaces exposes the mineralized cemental tissue with RGD peptides.
The polarity of osteoclasts is regulated by their actin cytoskeleton
The resorptive area within the clear zone is isolated from the extracellular environment, creating
an acidic microenvironment for the resorption of hard tissues
• The areas in which cementum is destroyed is filled in with bone.

• Once dentin is exoposed the process continues by odontoclastic function.
• Continuation of the process will lead to complete replacement of the root by bone
Lecture 14 – Temporomandibular Joint Histology and Embryology
TMJ Embryology
• TMJ development takes place between the 7th and 20th week of intrauterine life.
• A particularly sensitive period of morphogenesis is between the 7th and 11th week
There are three stages in TMJ development:
1 blastemic stage (7th-8th week) {temporal and condylar blastemas}.. development of the
condyles, articular fossa, articular disk and capsule.
2 cavitation (9th-11th week): beginning of lower joint space development and condylar
chondrogenesis
3 maturation stage (after the 12th week)
• After the 16th week the joint is completed and assumes its primary joint function.
Condylar Blastemas
• The structures of the TMJ originate from two different blastemas situated at some
distance from each other and operating at different rates and opposing directions.
• A condylar blastema evolving dorsally contributes to the formation of the condylar
cartilage, the disc, the aponeurosis of the external pterygoid muscle, and the capsular
elements of the lower joint level.
• A temporal blastema develops the articular structures of the upper level in a forward
direction
• The condylar blastema grows toward the temporal blastema
Blastemas
• A blastema is a mass of undifferentiated cells that has the capability to develop into an
organ, a body part or an appendage.
• Blastemas are found in the early stages of an organism's development.
• In the 9th week, chondrogenesis begins from the mesenchyme cells, laterally from
meckel’s cartilage, in the middle of the condylar blastema.

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• In the 10th week, the condylar head and the entire conical condyle are apically
surrounded by the lower jaw body, which is ossified intramembraneously.
• Endochondral ossification of the condylar cartilage in the anterior part begins in the
17th week and after the 20th week the cartilaginous form of the condyle is present only
on the surface.
• The mandibular primary growth center starts developing from the 12th week in the
mandibular process of meckel’s cartilage.
• The volume of meckel’s cartilage decreases after the 18th week and later it disappears
during mandibular ossification.
• Meckel’s cartilage is replaced by the body of the mandible and secondary

condylar cartilage.
• A characteristic of mandibular development is bone derivation from the mesenchyme by

intramembranous ossification laterally from meckel’s cartilage, while the development of
carrot-shaped condylar cartilage is placed posteriorly.
Articular Disk
• After the 7th week, a thickening of mesenchymal tissue positioned craniolaterally from
the future condyle occurs.
• This thickened mesenchymal tissue goes on to form the articular disk.
• Due to the forming of the articular space between head of condyle and the fossa, the
articular disk is thinner in the middle section, which later creates the characteristic
biconcave shape.
• From the 12th week, it is in its permanent position between the temporal bone and the
condyle.
• Its cartilaginous structure develops between the 15th and 20th week.
The Joint Capsule

• The mesenchymal development of the articular capsule starts in the 8th week and
stretches from the squamous part of the temporal bone towards the articular disk and
the condyle.
• In the 11th week, the capsule is positioned between the zygomatic arch of the temporal
bone and the condyle and it is attached to the outer portion of the articular disk.
• The upper and lower articular spaces develop from cracks in the thickened
mesenchyme, from which the condyle, the articular disk and the capsule
develops.
• Lower articular space starts developing in the 9th week, and follows the condylar
shape. Its development begins earlier than the superior joint space but progreses
at a slower rate.

-136-
• The upper articular space starts forming in the 11th week between the zygomatic
process of the temporal bone and the articular disk.
• It grows laterally and anteriorly between the 12th and 16th week of development.
• The articular spaces are disproportionate until the 26th week
Glenoid Fossa
• The mandibular (glenoid) fossa is lined by is dense, avascular, fibrous connective

tissue that belnds with the periosteum.
• Otorhinolaryngology and dental medicine are related fields and therefore have a
complex relationship in TMD diagnosis.
• One of the reasons for that is the closeness of embryonic ear development and TMJ
development.
• Another reason is their morphological proximity and the intertwining of the innervation
field of the shared nerves
• Otorhinolaryngology and dental medicine are related fields and therefore have a
complex relationship in TMD diagnosis.
• One of the reasons for that is the closeness of embryonic ear development and TMJ
development.
• Another reason is their morphological proximity and the intertwining of the innervation
field of the shared nerves
Possible causes of TMJ Disease
• Possible causes include:

• Grinding or clenching the teeth, which puts a lot of pressure on the TMJ
• Dislocation of the soft cushion or disc between the ball and socket – anterior
displacement.
• Presence of osteoarthritis or rheumatoid arthritis in the TMJ
• Stress, which can cause a person to tighten facial and jaw muscles or clench the teeth
• People with TMD can have severe pain and discomfort that can be temporary or last for
many years.
• More women than men experience TMD
• TMD is seen most commonly in people between the ages of 20 and 40.
Common symptoms of TMD include:
• Pain or tenderness in the face, jaw joint area, neck and shoulders, and in or around the
ear when chewing, speaking, or open the mouth wide
• Limited ability to open the mouth very wide
• Jaws that get "stuck" or "lock" in the open- or closed-mouth position
• Clicking, popping, or grating sounds in the jaw joint when opening or closing the mouth
(which may or may not be accompanied by pain)

-137-
• A tired feeling in the face

• Difficulty chewing or a sudden uncomfortable bite --
• Swelling on the side of the face
Other common symptoms of TMD include :
• Toothaches
• headaches
• neckaches
• dizziness
• earaches and hearing problems.
Section 2: TMJ Histology
Sagittal section of TMJ :

A: Condylar head
B: Articular disk
C: Lateral pterygoid muscle
Adult TMJ :
•
A: Condylar head
B: Tubercle of temporal bone.
C: Articular fossa
D: Articular disk
E: Upper synovial cavity
F: Lower synovial cavity
G: ateral pterygoid muscle.
H: Upper portion of posterior
disk and capsule
I: Lower portion of posterior disk
and capsule

-138-
Mandibular condyle in a child: growth of condylar head :
• A: Fibrous layer
• B: Reserve zone
• C: Proliferative zone
• D: Hypertrophic zone
• E: Calcifying zone
• F: Bone
Histological Layers that make up the TMJ Articular Surfaces
A . Articular zone - Fibrous Zone
• This most superficial, outermost layer, located next to the joint cavity.
• ii. Made up of dense fibrous connective tissue rather than hyaline cartilage, which gives
it several advantages such as: Improved ability to repair, wear-resistance, and a
decreased susceptibility to the effects of aging.
• iii. The fibers are tightly packed and can withstand the forces of movement.
B. Proliferative zone
• Second zone, composed of undifferentiated mesenchymal tissue.
• ii. This tissue is responsible for the growth of articular cartilage in response to
forces and stress placed on the surface during its loading

-139-
C. Fibrocartilaginous zone - Hypertrophic zone
• Third zone, consisting of collagen fibrils, randomly arranged in a radial pattern, or

a crossing pattern.
• ii. Aids in withstanding compressive and lateral forces.
D. Calcified cartilage zone - Calcifying zone
• Fourth and deepest zone
• ii. Made up of chondrocytes and chondroblasts . (persists until end of teens)
• iii. Within this layer, the chondrocytes become hypertrophic, die, and have their
cytoplasm emptied, to form bone cells.
Adult TMJ
The zones of the mandibular condyle in an adult are:
• articular zone (dense fibrous connective tissue)

• - reduced proliferative zone.
• - fibrocartilaginous zone
• - zone of calcified cartilage
• - bone
• Articular Zone: or superficial zone- composed of fibrous tissue. Fibroblasts scattered in

avascular layer of type 1 collagen fibres arranged in bundles oriented parallel to articular
surface. Connective tissue contains cartilagenous cells.
• Fibrocartilagenous zone: Bundles of collagen fibres arranged in crossing pattern and

some in radiating pattern. Function- resist against compressive or lateral forces
• Fibrocartilage is a tough, dense, fibrous material

• Fibrocartilage consists of a mixture of fibrous tissue and cartilaginous tissue in various
proportions.
• It owes its flexibility and toughness to the fibrous tissue, and its elasticity to the
cartilaginous portion.
• It is the only type of cartilage that contains type I collagen in addition to the type II
Differences between Mandibular Condyle of an Adult vs Child
• In a child there are large areas of hypertrophic cartilage that is contributing to the
growth of the condyle.
• In the adult the cartilage has disappeared. There is fibrocartilagenous and calcified
cartilage.

-140-
• There's still a proliferative layer that can generate more chondrocytes if necessary.
TMJ of a newborn
Newborn TMJ with temporal bone at bottom right and the

disc between it and the condyle.
• Notice lots of cartilage in the condyle and

evidence of endochondral ossification
• Note the highly cellular nature of the disc

compared with the adult. Notice also the hyaline
cartilage and the fibrous / cellular nature of the
condylar surface
the disc is at the bottom and the condyle above it.
• The hyaline cartilage is darkly stained and

separated from the lower joint compartment by cellular
fibrous tissue forming the articular surface.
• Endochondral ossification is taking place

between the upper end of the darkly stained cartilage
and the top of the field

-141-
Articular surface of condylar head :
• A: Fibrous connective tissue layer

• B: Lower synovial cavity
Bony structure with thick covering.
Articular Eminence
D = articular disk
F = fibrous articular tissue
P = proliferative layer FC =
chonrocytes in fibrous matrix
B = bone of articular eminence
Covering has 3 zone

- Articular zone: avascascular fibrous CT
- Proliferative zone
- Fibrocartilaginous zone (from secondary cartilage)
• Develops after birth from transient cartilage

• Provides a cushion
The temporal component of the temporomandibular joint, as with the condyle, may undergo
morphological change in response to occlusal disharmonies and altered jaw function.
In adult humans, changes in the contours of the articular eminence have been correlated with
increasing dental attrition or loss of posterior teeth.

-142-
Articular Disk
Articular disk :
• A: Articular disk.
• B: Upper synovial cavity
•
In newborns, the articular disc is almost completely fibrous and
very cellular, while in adults, it is more cartilaginous with
significantly reduced cellularity.
• This fibrocartilaginous disk greatly reduces friction

between both articular surfaces and protects the hard working
joint from wear and tear.
The disk is made up of bundle of :
• type I collagen bundles

• Collagen is loosely arranged. The disk has its collagen fibers arranged in all directions
• appears "crimped" or wavy

-143-
Fibrocartilage of Disk
• The posterior retrodiscal region is vascular

and made up of loose CT
• It is a band of elastic fibers, that attach the disk

to the anterior lip of the squamostympanic fissure of
the temporal bone and function as brake for the disk.
Posterior Ligament Retrodiscal Tissue
A = retrodiscal tissue
B = articular disk
Retrodiscal Tissue is highly vascularised
Note the blood vessels in the retrodiscal tissue

-144-
The space of the lower joint compartment separates

the fibrous disc (left) from the fibrous articular surface
(right).
The more darkly stained zone beneath the fibrous

articular surface is fibrocartilage and bone is on the
right.
Higher power of the disc on the left and the articular

surface of the condyle on the right.
The surfaces of both are fibrous and cell-free
The fibrous articular surface is supported by

fibrocartilage at bottom right

-145-
The interface between fibrocartilage on the left and

bone on the right.
Development of the muscles of Mastication
The muscular system develops from intraembryonic mesoderm from embryonic cells called the
myoblast.
Muscles of Mastication are derived from the 1st (mandibular arch)
Primary Muscles of Mastication

Masseter
Lateral Pterygoid
Medial Pterygoid
Temporalis
Secondary Muscles of Mastication

Digastric
Mylohyoid
Geniohyoid
Muscles of the pharyngeal arches are:

the muscles of mastication
• (mandibular arch, arch I)

• facial expression (hyoid arch, or arch II)
• palate and pharynx (arches III and IV)
• intrinsic laryngeal muscles, esophagus (arch VI)
• possibly the trapezius and sternomastoid (post arch VI?).

-146-
Muscles of Mastication
• Movements of the TMJ is initiated & effected by muscle coordination.

• Achieved in part through sensory innervations.
• Hilton’s Law:
• The muscles acting on a joint have the same nerve supply as the joint.
• Therefore: Branches of the mandibular division of the fifth cranial nerve supply the TMJ
(auriculotemporal, deep temporal, and masseteric)
• All muscles of the body are derived from mesoderm.

• The muscles of mastication arises from loosely organized mesenchyme in the branchial
arches.
• Myoblasts from the arches migrate to form the muscles of mastication, of facial
expression, and muscles of the pharynx and larynx.
• They are innervated by branchial arch nerves V, VII, IX, and X, respectively
• The process of muscle fiber development occurs within loosely organized masses of
mesoderm in in the branchial arches.
• Skeletal muscle tissue formation begins as specialized mesodermal cells, called
myoblasts which are derive from Cephalic Myogenic Mesodermal Cells
• THE MYOBLASTS elongate, combine to form parallel bundles, and fuse to form
multinucleated cells.
• The central nuclei move to the periphery, and during fetal life myofibrils are seen in the
cytoplasm
• Each muscle fiber develops from several embryonic myoblast cells.

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-1-

DENT3002 – Oral Embryology and Histology (2 credits)

Dr. O. Ogle , DDS, OMFS

Compiled by: Lorenzini H. Grant

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

DENT3002 –Oral Histology and Embryology (2 credits)

Lecture 01 – Embryology of Head and Neck

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

Main divisions of Prental Development

• Weeks 1 – 3 (0-21days) -Fertilization, Implantation and Gastrulation

• Each arch consists of 3 layers: an outer covering of ectoderm, an inner covering of

• The face is formed between week 3 – 8.

Weekly development- Week 1

• Sperm enters the oval cytoplasm in the uterine tube.

• The maternal and paternal chromosomes combine to form a zygote, completing

• The blastocyst consists of two layers of cells:

1) an inner layer termed the embryoblast that becomes

2) an outer layer termed the trophoblasts that forms

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

Formation of primitive streak & the germ layers

• A midsagittal groove appears as a result of invagination of the ectoderm centrally and

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

• At ~18days neural groove forms producing neural folds.

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

Somite formation: mesoderm on either side of the notochord thickens to

Somites are compact aggregates of mesenchymal cells from which cells

Neural Tube defects

• If the neural tube fails to "zip up" completely at some

• Malformations of CNS are relatively common (3 in

Failure of caudal neuropore closure leads to various forms of spina bifida:

• A congenital defect in which the neural arches fail to close,

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

Failure of rostral neuropore to close leads to acrania & anencephaly

Closure of rostral neuropore produces three primary brain vesicles

Forebrain and hindbrain each subsequently develop into two secondary

Lumen of neural tube froms ventricles of the brain

Problems related to the vesicles in the Brain

e.g. hydrocephalus results from blockage of flow of cerebrospinal

• Hydrocephaly occurs when there is an abnormal

• When the circulation of CSF is blocked it accumulates in the brain.

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

NEURAL TUBE:/BRANCHIAL ARCH FORMATION – 25 DAYS

Typical Branchial Arch consists of:

BRANCHIAL APPARTUS – contributes to development of the face, neck, nasal cavities,

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

• 1st ARCH – maxillary & mandibular branches of trigeminal (V) nerve

First Arch Syndrome

MAJOR: Treacher Collins, Pierre Robbins

First and Second Arch Syndromes

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

• Treacher-Collins Syndrome also called mandibulofacial dysostosis

facial features include :

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

Munroe’s Classification for Hemifacial Microsomia

OMENS Classification on Reporting on CFMS

Theories of Aetiology of CFMS

• VASCULAR: - Stapedius Artery (Poswolo)

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

• The external component of this cleft is

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06

Bilateral Branchial Cleft Cysts

• The disorder is characterized by a wide spectrum of symptoms and physical

• incomplete development of certain muscles of the face

DENT3002- Oral and Dental Histology and Embryology DDS Semester 06