Growth and DevelopmentLecture 1

8-24-10

Somatic growth: pattern, variability, timing, and methods of study

Growth

Growth: Increase in size or number

o Anatomic phenomenon
Hyperplasia: Increase in number of cells
Hypertrophy: Increase in size of individual cells
Ex: Secretion of extracellular material: increase in size independent of the number size of cells
o Odontoblast secretion & Ameloblast secretion

Development

Development: Increase in organization, complexity, specialization (loss of potential)

o Physiologic and behavioral phenomenon
o Immaturemature
Pattern: a changing and complex set of spatial proportionalities over time
o Ex: the proportion of head and limbs to body
Head and face = decrease
Newborn = 25%
Adult = 12%
Limbs = increase
o Reflect Proportionality
Cephalocaudal gradient of growth
An axis of increased growth extending from the head toward the feet
The further from the head (ie the lower limb) will have more growth
Size of components of craniofacial complex
o Post natally more facial growth than
cranial growth
Overall body proportions change during the normal
growth and development
o Not all the tissue systems grow at the same rate
Scammons curve
Neural: cranium, brain
o Nearly complete by 6 or 7
Lymphoid: tonsil, adenoid
o Grow far beyond the adult size and then
regress
o Around age 10 = larger than at any
other time
Sometimes the lymphoid tissue
is so large that is interferes with
the air passage
General: bone, muscle, viscera
o S shaped curve
o Childhood growth rate = slow
o Acceleration of growth rate at puberty
Genital

o Grow rapidly at puberty

Craniofacial
o Depends on the distance from the brain
o Maxillacloser to neural
o Mandiblecloser to general
Man and max between the neural and general tissue

Growth Plots
Distance curve (cumulative curve)
Accumulation of data over time
(longitudinal)
Velocity curve (incremental curve)
Amount of growth within an interval
Velocity curve allows seeing
acceleration or deceleration of
over time.
Peak velocity = 14 yrs
Growth Studies
Longitudinal studies: measures individuals
many years
Time consuming
Highlight individual variations
Smaller sample size
Cross-sectional studies: a large group of
individuals representing all ages are measured at
one time
Easier and quicker
Variations conceal details
Larger sample size
Growth variability
Variability within species
Timing
Size
Each individual tends to follow their own
pattern, patterns are similar
Assumption
o Human traits such as height and weight adhere to normal curves
o These curves occur at all ages
o There is normal variability within individuals
o Children outside of 97% of pop should be
referred for
medical
evaluation
o Change of
growth
pattern
(height or
weight) is
reason for
concern
Growth Spurt
All children undergo growth spurts, but timing and amount can vary
Depends on
o Sex: girls, boys

of time
growth

over

o Genetics: early, average, late

Sexual maturation accompanies growth spurt
Events that occur during growth spurt/maturation
o Girls
Increase in weight
Development of 2nd sex characteristics
Breast buds
Genital hair
Increase in height
Menses
Bony change
Hand-wrist
Cervical
o Boys
Increase in weight
Muscle mass
Development of 2nd sex characteristics
Genital hair
Size of genitals
Facial hair: lip and chin
Increase in height
Bony change
o Hand-wrist
o Cervical
Adolescent growth stages vs. 2nd sexual characteristics
o Girls: adolescent growth 3 yrs
Stage 1 (beginning of adolescent growth)
Appearance of breast buds
Initial pubic hair
Stage 2 (peak velocity in height, about 12 months later)
Noticeable breast development
Axillary hair
Darker/more abundant pubic hair
Stage 3 (growth spurt ending, 12-18 months later
Menses
Broadening of hips with adult fat distribution
Breasts completed
o Boys: adolescent growth 5 yrs.
Stage 1 (beginning of adolescent growth)
fat spurt weight gain
Feminine fat distribution
Stage 2 (height spurt beginning, about 12 months later)
Redistribution/reduction of fat
Pubic hair
Growth of penis
Stage 3 (peak velocity in height, 8-12 months later)
Facial hair appears on upper lip only
Axillary hair
Muscular growth with harder/more angular body form

Stage 4 (growth spurt ending,

15-24 months later)
Facial hair on chain and
lip
Adult distribution/color
of pubic and axillary
hair
Adult body form
Growth Spurt variability
o Girls mature about 2 yrs earlier than
boys
o Orthodontic implications: growth
modification
Relation of Growth Spurt and Maturation
o If ages are removed and peak growth
superimposedpeaks are similar
Menses occur on downward slope
Implication: only 2 years of
rapidly decreasing growth
remains
Stages of adolescent Growth Summary
o Girls mature earlier than boys by
about 2 yrs
o Total time of duration
Girls3 years
Boys5 yrs
o Boys are larger because they grow
longer
o Orthodontic implications
Growth modification for girls
starts earlier
Boys can outgrow orthodontic treatment more than girls
Problems with determining growth
spurt/maturation
o Difficult to check secondary sex
characteristics
o Menses means limited growth potential
o Growth spurt/maturation does not
correlate well with age
o Chronologic age vs. development
(biologic) age
Chronologic age is not an
accurate indicator because 2
girls at the same age may be at
different stages of
development/growth spurt
Skeletal, dental, 2nd sex characteristics
o Skeletal age
Hand wrist radiograph
Bottom: See epiphyses
Top: Epiphyses ossified (older)
Cervical vertebrae radiograph
Look at inferior border of
vertebrae

As grow olderget concavity in inferior border of vertebrae

When youngerslope from posterioranterior.as get older,
this superior surface of vert. becomes more straight

Methods of Studying Physical Growth

Measurement approaches
Measure living samples or skeletal remains
Non-destructive
Craniometry
o Measurements of skulls found
among human remains
Precise measurements
Cross-sectional data, only can be measured one time
Anthropometry
o Measurements on living individuals
Longitudinal data, can be measured repeatedly
Soft tissue interference
Cephalometric radiology
o Introduced in 1934 by Hafrath in
Germany and Broadbent in US
Study growth pattern
Evaluate malocclusion
Evaluate outcome of
treatment (superimposition)
2-D image represents 3-D
structure
Three-dimensional imaging:
o Computed tomography (CT)
Conventional CT and cone
beam CT (CBCT)
Rapid scan (less than 1 minute)
Less radiation exposure (3-20% of conventional CT)
No distortion of image
o Magnetic resonance imaging (MRI)
Using electromagnetic spectrum (not Xray)
No radiation exposure
High contrast sensitivity
Experimental approaches
Destructive manipulation of samples
Restrict to non-human species
Ex:
o Vital staining
Alizarin red: timing of dental mineralization
Tetracycline: cause dental staining
o Radioactive tracers
o Implant

Growth and DevelopmentLecture 2

8-26-08

Craniofacial Growth
Review of Last Week
Growth = increase in size or number, anatomic phenomenon
o Hyperplasia = increase in number of cells
o Hypertrophy = increase in size of individual cells
Secretion of extracellular material: increase in size independent of the number or size of cells
o Intersistial growth = growth occurs within the tissue
Characteristics of soft tissues and uncalcified cartilage
o Appositional growth = growth occurs on the surface of the tissue
Characteristics of mineralized tissue
Development = increase in organization, complexity, specialization (loss of potential), physiologic and behavioral
phenomenon
Types of bone formation
Endochondral bone formationinitial formation of cartilage
o Extremities of all long bonesepiphyseal (growth) plate
o Vertebrae
o Ribs
o Condyle
o Cranial base
Intramembranous bone formationno intermediate formation of cartilageNO CARTILAGE!!
o Alveolar bone
o Calvaria
o Long bone
Cranial Structure and Characteristics

Craniofacial cartilage
o Cranial base bones that formformed with cartilage 1st
Ethmoid
Sphenoid
Occipital
o Nasal cartilage
o Condyle
o Small area at junction of right and left mandible
These are Endochondral bones
Nearly avascular
Diffusion of oxygen and nutrients
Multiple centers of ossification
Only small areas of cartiage growth remain between bones after birth
Eventual fusion of those bones

Synchondrosis

Looks like a 2 sided epiphyseal growth plate

Bidirectional growth (cranial bone) vs. unidirectional growth (long bone)
Types of Synchondrosis
o Spheno-ethmoidal synchondrosis
Between the sphenoid and the ethmoid bones

 Active growth prenatally

Allow anterioposterior growth of cranium
Fuses around 6-7 yrs of age in human
o Inter-sphenoid synchondrosis
Between the pre-sphenoid and
basissphenoid
Fuses around the time of birth in human
Does not contribute to postnatal growth
o Spheno-occipital synchondrosis
Between the body of the sphenoid and
occipital bones
Active postnatal growth
Fuses around 13-15 yrs of age
Allows more vertical growth of cranium
Clinical significance of synchondrosis
o Growth of cranial synchondrosis has direct effect on the growth of nasomaxillary complex and mandible
Displaces facial bones (max and mand) inferiorly and increases facial height
o Disease (Achondroplasia) affects the growth of cranial base and midface.
Affects fibroblast growth factor and production
Growth of face is severely retarded
Growth of mandible is pretty normal.
Development of Meckels Cartilage
Bilateral about 7-8 wk in utero
From 1st pharyngeal arch
Bone forming next to it becomes mandible and cartilage
is removed.
Distal extension forms incus and malleus.
Condylar cartilage develops in separate area of
mandible.
Growth Center vs. Growth Site
Growth Center
o Synchondrosis
o Epiphyeal plate a location at which independent, genetically controlled growth can occur
o Innate growth potential and cannot be influenced by environmental circumstances
Growth Site
o Condyle
o All growth centers can be sites, but not all sites can be centers
Intramembranous Bone
Suture growth
o When bone grows inside there is bone formation on the 2 sides of the suture.
o
Surface remodeling
o Sutures connect bones to form cranium
o Maxilla is connect to cranial base with suture
Ossification occurs without cartilage formation
Brain (neural growth causes tension and deposition of bone
When neural growth slows or stops, suture fuse
Periosteal growth can occur at surfaces
o Outer or inner surface
Cranial Intramembranous Bones
o Newborn skull shows sutural areas with minimal bone (fontanellessoft spots)
Connected by dense CT = fontanelles
Close by 8 wks after birth

 Anterior closes after 18 months

o Most of the growth is at the suture
o Premature closure of cranial sutures leads to craniosynostosis (Crouzon, Apert syndromes)
Craniofacial sutures
o FM = Frontmaxillary suture
o ZM = Zygomaticaomaxillary suture
o ZT = Zygomaticotemporal suture
o ZF = Zygomaticofrontal suture
o FN = Frontonasal suture
o Median palatine suture
Increase the facial
height/depth/width
o Transverse palatine suture
Sutures become more
interdigitated with
increasing age.
Bone Growth/Movement
Shaping of surfaces with
different fields of
apposition and
resporption.
o Not every bone
always has one
surface doing
just one thing.
o Some parts will undergo apposition and some will undergo resorption.
Drift: growth movement of bone by the combination of resportion and deposition (apposition)
Displacement: movement of the whole bone as a unit
o Picture: The point has grown outward as a result of increase in the
size of the object itself
Secondary Displacment: The point has grown outward as a result of increase
in the size of another object.
o Pictures #2!
o Primary + Secondary Displacement
The point has grown outward as a result of both primary and
secondary displacement.
Maxillary Growth
o Intramembranous bone formation forms the maxilla
o Growth occurs by
Apposition at the suture that connect the maxilla to the cranium
and cranial base
Displacement from the growth of cranial base (Secondary)
Surface remodeling
o Disease affecting growth of suture will lead to underdevelopment of the maxilla.
o Surface remodeling
Resorption of anterior surfacebone becomes less prominent in adult
Deposition of alveolus with eruption of teeth
Deposition of the maxillary tuberosity
Primary and secondary displacement
o Surface remodeling moves maxilla backward
o Whole maxilla is moving forward.
Palatal Vault Growth
o Resorption from the floor of nose and anterior surface

o
o

Deposition to the roof of the mouth

Drift: downward and backward
Palate moves downward
o Displacement: downward and forward
***Size of the oral cavity does not decrease. With eruption of teeth the sides of the oral
cavity increase dramatically.
Maxillary + Palatal Vault Growth
o Bone remodeling (drift) results in
Upward and backward
Tension at suture causes bone to be added at sutures
Resorption of anterior surface
Deposition at the maxillary tuberosity
Downward
Eruption of teeth bring alveolus down
Vertical drift of palate
Nasal Septum
o Cartilagenous remnant of the chondrocranium that ossifies posteriorly as the vomer bone.
o The anterior part remains as cartilage and continues growing later than most of the rest of the face.
Mandibular Growth
o Endochondral Growth
Conversion of condylar cartilage to bone
Only occurs at the condyle!
o Intramembranous Growth
Remodeling at multiple adjacent site:
Deposition/resorption
o Main direction of growthUpward or backward
Anterior portion stays the same width
Major area of mandibular growth is in posterior
areasroom for posterior teeth to erupt
Growth of mandible will not releive anterior
crowding
Measured by:
Position of chin or basal bone in space
Absolute increase in size
Drift is the result of periosteal remodeling
Deposition and resorption also occur in anterior mandible
Result = definition of chin
Allows: growth of ramus and room for posterior teeth to erupt
Mechanism of growth:
Condyle cartilage is not the major mechanism for growth of mandible
Absolute growth result of:
o Apposition of posterior ramus
o Resorption on anterior ramus
o Condylar growth
o Coronoid process
Dental arch perimeter growth
o Resorption at anterior portion of ramus
o Allows molars to erupt
Displacement
Primary
o Growth of mandible in posterior direction displaces mandible forward and
downward
Secondary

o
o

Soft Tissues
o Lips

Nose

Grwoth of cranium pushing mandible forward and downward

Growth of maxilla pushing mandible downward

Mixed dentition yearsshort lip height, lip incompetence and gummy smile
Adolescenceelongation of lips, lip thickness reaches max then decreases
Growth of nasal bone is complete @ 10 yrs
Nasal cartilage and soft tissue undergo adolescent spurt, which results in more prominent
nose at adolescence (esp boys)
Nose and chin become prominent at adolescence and post
adolescence
Relative decreased prominence of lips

V principle
o An important facial skeleton grwoth mechanismsince many facity
and cranial bone have a V configuration or V shaped region
o Outer surfaceResorption
o Inner surfaceDeposition
o V moves away from its narrow end and enlarges in overall size.
o Applies to the mandible and Palate
Summary of Craniofacial Growth
Actual growth of maxillabackward, upward
o When teeth are eruptingalveolar bone grows downward
Actual growth of mandibleupward, backward
o When teeth are eruptingalveolar bone grows upward
Growth of face
o Result of primary and secondary displacement
o Comparison can be made by superimposition on various cranial base structures
Those structures are also
remodeling (not constant)

Growth and DevelopmentLecture 3

9-02-08

Theories of Craniofacial Development

Three Theories of Craniofacial Skeletal Growth

Genetic Factors
o Exert their influence within the cells in which they are contained
o Determine the characteristics of cells and tissues
o Chondrogenesis is affected by genetic factors
Epigenetic Factors
o Determined genetically
o Are effective outside of the cells and tissues in which they are produced
o Only occur indirectly
o Ex: Sex hormones, growth hormones which are produced a long distance away
Environmental Factors
o Regulate or modify the morphogenesis controlled by the genome
o Ex: muscular forces, food, oxygen
Three major theories as to the location of genetic control:
o Bonethe primary determinant of growth
o Cartilagethe primary determinant of skeletal growth, while bone responds secondarily
o Soft tissue matrixthe primary determinant of growth
Soft tissue surrounds skeletal tissue
Growth Center vs. Growth Site
o Growth Center
A location at which independent, genetically controlled growth can occur
Innate growth potential
Cannot be influence by environmental circumstances
o Growth Site
Location at which growth occurs
All growth centers can be sites, but not all sites can be growth centers
Bone as a growth determinant
o Growth Centersuture, periosteum
o Basis of theoryobservation that overall craniofacial growth pattern is constant
o Examplemaxillary growth result of sutural growth
o Problems with theory:
Lack innate growth potentialfail to grow if transplanted to another location
Influenced easily by environmental circumstancesgrowth at sutures respond to mechanic
forces
o Viability of theory
Dominant theory until 1960s
Currently rejected
Cartilage as a growth determinant
o Growth Centercartilage
o Basis of theorycondylar cartilage and nasal cartilage are growth centers for mandible and maxilla
o Example:
Nasal cartilage growth causes vertical maxillary growth
Surgical procedures removing the nasal cartilage results in midface deficiency
o Problem with theory:
A surgical procedure itself or the interference with blood supply can have caused the midface
deficiency (not necessarily the absence of the cartilage).
Not all skeletal cartilages have innate growth potential

 Epiphyseal plate>cranial synchondrosis>nasal cartilage>condylar cartilage

Condyles
regenerate after
fracture in 75% of
children
o Viability of theory
Some cartilages can
act
as growth centers
(ie
epiphyseal cartilage,
cranial synchondrosis, nasal septum)
Condyle is not a growth center.
Important for growth modification in ortho treatment.
Soft tissue as a growth determinant
o Growth centersoft tissue
o Bases of theory:
Proposed by Moss in the 1960s
functional matrix theory
Growth of face occurs in response to functional needs and neurotrophic influence.
o Example:
Size of cranium based on growth of the brain
Increase pressure of brain on cranium = bigger cranium
Can cause cranium to be 2-3xs normal size
Growth of mandible and maxilla is in response
to
nasal and oral cavities
Growth of eye socket is in
response to eye
development
o Picture:
Bones, cartilage, ligaments protect the functional
matrix.
Orofacial matrix = oral, nasal cavities and pharyngeal spaces.
This one is the most important one for growth of the face.
Growth of skeletal units is secondary to the growth of functiona matrix (soft tissue or
functioning space).
o Problem
Not clear how theory works
o Viability of theory
Suggests that loss of function has considerable effect on growth of structures
Modified by Moss in 1997 to incorporate more genetic background.
Current consensus
o These are only theories
o Bone theory is no longer valid
o Probably a combo of cartilage and functional matrix theories
o Understanding of the influence of genetics on craniofacial structures is increasing, but have much more
to learn

Summary of craniofacial growthMechanisms of growth for cranium, cranial base, maxilla and mandible

Growth of cranium occurs in response of growth of brain

o Growth of cranial base is the result of endochondral bone formation at synchondroses, which have
independent growth potential, at the same time influenced by the growth of brain.
Growth of maxilla and its associated structures occurs from a combo of growth at sutures and surface
remodeling.
o The surrounding soft tissues and nasal septum cartilage may contribute to the forward repositioning of
maxilla.

Growth of mandible occurs by endochondral bone formation at condyle and surface remodeling.
o The growth of muscles and other adjacent soft tissues may contribute to the repositioning of the
mandible.

Distraction Osteogenesis

A biologic process of new bone formation between the surfaces of bone segments that are gradually separated
by incremental traction (0.51.5 mm/day).
o Can be divided by external or internal device.
o External deviceattached to bone
o Internal deviceattached to teeth or bone
o Can be bi/uni-directional.
Advantages of the devices
o Larger distances of movement are possible than with conventional orthognathic surgery
o Deficient jaws can be increased in size at an earlier age.
o Adaptation of soft tissues, histogenesis
Alveolar Distraction
o Augmentation of the maxillary and mandibular alveolar ridges
o Alveolar deformities and defects may result from:
Developmental anomaliescleft palate, congenital tooth absence
Maxillofacial trauma
Periodontal disease leading to bone and tooth loss
o Ex: Bone graft. CT graft
These grafts cannot provide an increase in bone volume.
Alveolar distraction can provide construction of bone.
This is a graft that is used to fix the bone. Can increase bone remodeling.
Periodontal Ligament Distraction (AKA Rapid
Canine Retraction)
o Used to reduce resistance when move
the canine distally.
o Periodontal ligament is stretched.
o New bone is created mesially to the
canine.
o After extraction there is surgical prep
of socket. Socket is extended to same depth as canine.
o Widen socket and increase septum.
o Last step is to undermine the septum.
o More detail:
Remove premolarattach distraction device to move the canine distally to relieve anterior
crowding.
Takes 3 weeks compared to 6 months with traditional methods.

Prenatal Craniofacial Development

Stages of Development

Cleavage Stages
o Fertilization of the egg by the sperm
Distal 1/3 of fallopian/uterine tube
o Development of nonpermeable membrane around egg
o Division of cells into multicelled morula
o Movement through the uterine tube to reach uterine cavity4th day
Implantation6th day

o
o
o

Attachment of blastocyst to uterine wall

Separation into inner embryonic cell mass (embyroblast) and outer covering (trophoblast)
Trophoblast layer produces enzymes to break down uterine wall.
Cells attach to the posterior wall.
Release enzymes to allow deeper attachment.
Blastocyst Stage
o Layers of ectoderm and endoderm form
Ectodermal = columnar
Endodermal = cuboidal
o Yolk sac forms and provides food source until blood vessels
form.
Yolk sac between endodermal and trophoblastic cells.
Mesoderm migration
o Mesoderm migrates anteriorly and laterally between ectoderm and endoderm except at:
Future area of the mouth (prochordal plate)
Anus (cloacal membrane)
Derivatives of Germ Layers
o Ectoderm
Nervous system
Sensory epithelium of eye, ear, nose
Epidermis, hair, nails
Mammary and cutaneous glands
Epithelium of sinuses, oral and nasal cavities,
intraoral glands
Tooth enamel
o Mesoderm
Muscles
CT derivatives:
bone cartilage
blood
dentin
pulp
cementum
periodontal ligament
o Endoderm
GI tract epithelium and associated glands
Neural tube formation
o Ectodermal cells multiply and folding occurs
o Neural tube forms about 4 wks anteriorly and
continues posteriorly
Neural plates curve to form a tube.
Neural Crest cells Separate
o Crest cells break off from neural fold area
o Neural crest cells migrate ventraly along the lateral
wall of the neural tube.
o Become:
Sensory ganglia
Sympathetic neurons
Pigment cells
Cartilage of pharyngeal arches
o Contribute to embryonic connective tissue of the face (pulp,
dentin, cementum)
Neural Crest cell migration

o Migrate ventraly and laterally.

The main point:
Neural crest cells from different sources have to migrate into specific places to form the head and neck area.
If adequate neural crest cells do not migrate or live, certain tissues do not develop.
Teratogen Suspecptibility
Congenital deformities can be hereditary.
Not much can be done to reduce hereditary hazards in humans.
Before 2 weeks, developing human is not susceptible to teratogens.
After 2 weeks, it is most critical time periodthis stage is period of differentiation of tissues/organs.
o Teratogens may be highly defectivedeformities.
After 8th week, the susceptibility will decrease and will only cause minor effects.

Growth and Development Lecture 4

Postnatal Craniofacial Development

Important Points
Dental Development
o Including all primary teeth and 1st permanent molar.
o Begins in the 3rd month uterus.
Calcification occurs around the crown
o A line can form in the crown if any disturbance or
insult occurs.
Birth--a dramatic processLeads to growth
cease and weight decrease during the first 7
10 days after birth
Almost every child has a neonatal line in the
primary teeth
These insult lines are more obvious in permanent teeth
o Picture:
Cross section of enamel.
See striae of retzius.
Reflects apposition of growth in
enamel layer.
Neonatal line shows dramatic
physiological change during the
birth.
o Location of the neonatal line
After birth, any disturbance in
formation of teeth can be tracked
by the neonatal line.
Factors affecting Postnatal Development
Premature birth (low
birth weight)
Chronic illness
Nutritional status
Picture:
o Growth of limbs
of body length
and weight.
o See extremely
rapid growth in
early infancy.
o Growth slows
down after the
1st 6 months.

Premature Birth (low birth weight)

Low birth weight (LBW): fetus < 2500 g
Extreme LBW: fetus < 1000g
o Incidence in developed country = 8%.
o Can be expected to be smaller the first 2 years.
If survives the neonatal periodgrowth of the LBW will follow the normal pattern and gradually overcome the
initial handicap.
Chronic Illness
Disease or illness has negative impact on growth
The severer the disease, the longer the time, the greater the cumulative
impact.
Chart
o Boy with Growth hormone deficiency.
o Red dot is actually growth height.
o Circles is height vs. skeletal development.
o Around 6 yrs there is a delay in growth height compared to
skeleton.
o After treatment was started there was a dramatic increase in
growth.
Nutritional Status
Chronically inadequate nutrition has similar negative impact on growth.
Adequate nutrition is a necessary condition for normal growth but is not a
stimulus.
o Adequate nutritionoverweightproblem in developing
countries.
During the last centurymore rapid growth and earlier maturation.
o Better nutrition
o Chemicals (ie pesticidescan affect hormones and growth)
Children are larger and mature more quickly these days.
Mandible Defiency at birth
Relatively lack of prenatal growth of mandible makes the birth process easier.
Mandible grows more than other facial structures postnatally.
Eyes too far apart/small chin
Prenatal growth of the mandible begins later and continues longer than the midfacial structure and orbital
structure.
The mouth of the neonate
At birth, the alveolar process is covered by gum pads.
Although the upper and lower gum pads touch
o There is no precise jaw relationship.
Tongue of the infant always contacts with the lower lip.
Mouth of Neonate (infantile swallow, adult swallow)
Infantile swallow
o The jaws are apart during swallowing.
o The tongue is pushed forward and placed between the gum pads.
o The tip of the tongue protrudes.
o The mandible is stabilized by the contraction of the tongue and the orofacial musculature and when the
tongue contacts with the lips.
Position of tongue is lower in swallows than the adult/mature swallow.

Adult swallow
o Teeth occlude momentarily during swallowing act
o The tip of the tongue is enclosed in the oral cavity.
o Mandible is stabilized by contraction of the mandibular elevator muscles (not facial muscles).
o Teeth occlude and the tongue is enclosed in the oral cavity.
Vs. infantile where tongue protrudes onto lips.
o After 6 months = infants swallow is more precise in opening and closing.
Transition of swallow
o Infantile swallow disappears during the 1st year of life.
o With eruption of the primary teethtransition from infantile swallow to adult
swallow occurs.
o If sucking habits persist, there will not be a total transition to the adult swallow.
o 60% achieve adult swallow by age 8.
Remaining 40% are still in transition.

Postnatal Facial Development

Striking difference between the newborn and adult skull.
o Baby face is not miniature of adult face.
o Baby: larger eyes, tiny nose, puffy cheeks, high forehead, small mouth, wider
and shorter proportions.
Proportionally, more facial growth than calvarial growth after birth.
o Note on slide: more facial growth than temporal growth after birth.
Newborn face has attained:
o 64% of adult width
o 54% of adult depth
o 41% of adult height.
Maturation of an infants faceadult form occurs with the changes in:
o Size
o Shape
o Position
o Composition of all cranial tissues (bones, muscles, nerves, and sense organs)
o **Differential development process with progressing facial development.
Size
o The oral cavity and nasal spaces, eyes, and brain increase in size, but at
different rates.
o The adult face differs markedly from the infant face in size, proportions,
structure and functions.
Aging
o Further alters appearance as minor skeletal modification continue
Skin loses elasticity
Wrinkle
Fat deposits under mandible and bags around the eyes.
Mandible growth
o In postnatal period, mandible grows proportionally
more than the early developing cranial base and brain.
o Changes in shape
Infancy:
Wide gonial angle
No chin
Small ramus
Immature condyle
Relatively retruded position
Childhood:

Teeth erupt
Gonial angle (mandibular angle) decreases
Chin develops
Adulthood:
Prominent chin
Fully developed alveolus and condyle
Decreased gonial angle
Old age:
Lose teeth and bone mass
Increased gonial angle
o Peak growth for maxilla and mandible occur simultaneously
growth slows and stops at different times.
Mandible continues to increase in length when the maxilla finishes growing.
Grwoth of maxilla is much less than mandible and body height.
Grow in this order: maxillaheightmandible
The anterior part of the nasal septum remains as cartilage and continues growing later than most of the rest of
the face.
The forward growth of the forehead is due to the development of brow ridges and frontal sinus (not aerated at
birth).
Gender differences for skeletal age may be greater than for
dental age.
o Girls attain skeletal maturity earlier than boys
o Some girls may have more mature facial bones but
still have primary teeth.
Maxilla
o Result of
Growth of cranial base
Apposition of bone
Eruption of teeth
o Major growth sites
Sutures
Alveolus (with eruption of teeth)
o Major growth direction
Sutures: upward and backward
At alveolus: downward with eruption of teeth.
o Resulting growth directiondownward and forward.
Mandible
o Result of
Conversion of cartilage to bone
Apposition
Growth of maxilla
o Major growth sites
Ramus
Alveolus
Condyle
o Major growth direction
Condyle and ramus: upward and backward
At alveolus: upward with eruption of teeth
o Resulting growth direction
Downward and forward
Completion of facial growth
o Transverse
About 4 yrs

 First to be completed
Anterioposterior
About 7 yrs in cranial base
Mandible and maxilla continue into late adolescence
Growth of sigmoidal and ethmoidal at cranial base
o Vertical
Late adolescence and early adulthood
Last to be completed
Postnatal facial development
o Remove inhibitions of normal growth
o Promote normal function
o Reduce iatrogenic damage to tissues (surgical scars)
o Consider the effect of growth on the final result when intervention during the growth period is
necessary
o

Variations in Facial Features

Different facial type, relate to shape and form of head
o Changed the shape of nose to balance the
shape of the midface
o Dolichocephalic: long, narrow head form
o Meoscephalic: medium, head form
o Brachycephalic: wide, short head form

Dolichocephalic
o Face:
Narrow, long, and protrusive
o Nose:
Long and protrusive with convex contour

(aquiline)
Slope of the nose tends to follow the same slope of the forehead.
Brachycephalic
o Face:
Wide, short
o Nose:
Shorter with rounded tip
Straight or concave contour
Male and female facial differences
o Male
Proportionaly larger nose
Protrusive, longer, wider, straight or convex (aquiline)
profiled
Profile dropping straight downward from a
protruding forehead
o Female
Thinner and less protrusive nose
Straight or concave profile
More rounded noseoften tips upwarddropping
downward from bulbous forhead
Because of the less protrusive forehead and nose
The upper jaw and cheekbone looks more
prominent

Growth and DevelopmentLecture 5 (continued)

9-09-08

Prenatal Craniofacial Development (continued)

Teratogen Susceptibility

Congenital deformities can be hereditary and/or environmental.

Beyond prenatal exam and parental counseling, not much can be done to reduce hereditary hazards in humans.
On the other hand, to understand the noxious environmental agents, teratogen, and the time of their maximum
effects on fetal development is important to prevent those deformities.
From the picture, we can see before 2 weeks, developing human is not susceptible to teratogens, because at this
early proliferative stage, any damage may be compensated by the remaining cells that have not become
committed or differentiated.
From the 3rd week to the 8th week, it is the most critical time period, because this stage is the period of
differentiation of tissues and organs. Teratogens may be highly effective and result in numerous deformities.
After 8th week, susceptibility to teratogens rapidly decreases and may cause only minor defects. From the
picture, we can see around 7-8th week, palate and teeth are more susceptible to teratogens.
Teratogens
o Infectious agents
o Radiation
Deformities like cleft palate
o Drugs
Ex: Tetracycline during 2nd/3rd trimester = hydroplasia of enamel and discoloration of dentin
Should be avoided unless necessary
o Hormones
o Nutritional Disorders
Ex: Folic Acid deficiency = neural tube defects
o Teratogenic habits: Smoking, Alcohol
Ex: smoking = higher cleft palate incidence
Ex: alcohol = MR = growth defiency

Stages of Embryonic Craniofacial Development (5)

Stage

Time (postfertilization)

Related syndromes

Germ layer formation and initial

organization of structures

Day 17

Fetal alcohol syndrome

Neural tube formation

Day 18-23

Anencephaly

Origin, migration, and interaction of

cell populations

Day 19-28

Hemifacial microsomia
Treacher Collins syndrome
Limb abnormalities

Formation of organ systems

Primary palate
Secondary palate

Day 28-38
Day 42-55

Cleft lip and/or palate, other facial clefts

Cleft palate

Final differentiation of tissues

Day 50-birth

Achondroplasia
Synostosis syndromes (Crouzons, Aperts)

Craniofacial Syndromes

Fetal Alcohol Syndrome

o Characteristics: smooth
philtrum, short nose, thin
upper lip
o Growth deficiency, brain
damage
Treacher-Collins Syndrome
(mandibular dysostosis)
o Failure of neural crest cells
to migrate
o Possible caused secondarily by excessive cell death in the trigeminal ganglion
o Characteristics: Underdevelopment of jaw and zygomatic arch, downward slanting eyes, notch on
eyelids, hearing loss
Hemifacial microsomia
o Usually unilateral/assymetrical
o Characterisized by tissue on one side of the
face is affetcted
o Characteristics: deformed/missing ear,
ramus of
mandible affected
o Currently thought to be caused by early loss
of neural cells
o The farther the cells have to migrate, the
more damage
o Midline structures (palate) no affected as
much.
Those cells migrating to middle of the
face are ok.

Back to development!

Initiation of oral cavity

o Start in the 3rd week as a pit or invagination
underlying the
forebrain.
o Lower part of face/neck are formed by
pharyngeal
arches on both side s of the neck
Derivatives of Pharyngeal/branchial arches
o Formation of the arches occurs at 5-6 weeks
o Only 1st and 2nd extend to the midline.
o Each arch is separated to adj arch by shallow grooves called pharyngeal pouches internally.
o Outer surface of pharyngeal arches are covered by the ectoderm and inside is lined by endoderm
1st arch is lined by the ectoderm of the oral mucosa.
o In each arch there is differentiation of neural crest cells
o Arch 1 (mandibular arch)
Muscles of mastication
Anterior belly of digastrics
Meckels cartilage
Cranial nerve V: Trigeminal
o Arch 2 (hyoid arch
Muscles of facial expression
Posterior belly of digastrics
Cranial nerve VII: facial
o Arch 3
Cranial nerve IX: glossopharyngeal

Arch 4
Cranial nerve X: vagus
Face at 4 weeks
o Oral pit is surrounded by frontal process, two maxillary processes, and mandibular
arch.
Frontal processupper face
First pharyngeal archmaxillary process arises from mandibular arch (later
form cheek, most of upper lip)
Mandibular arch grows toward midline and fusesmandible, lower part of
face, and body of tongue)
Face at 5 weeks
o Formation of nasal pits (as they deepen they form the nostrils)
Face at 6 weeks
o As tissue around nasal pit enlarges2 medial nasal processes form intermaxillary
portion of upper lip (philtrum)
o Maxillary and medial nasal processes fuse (externally) to form upper lip
Connective tissue moves between areas of fusion and bind fused area
o Floor of nostril fuses front to back
o Failure to fusecleft lip
o Upper lip has 3 parts
2 max process grow inward
Medial nasal process grows downward
Face at 7 weeks
o Medial nasal processes merge at deeper levels also and form the intermaxillary
segmentprimary plate
o Yellow colormaxillary process
o Blue colormandibular process
o

Development of Palate

Primary Palatepremaxilla
o Medial palatine process from
medial nasal process
Secondary Palate
o Develop from medial edges of the
maxillary processes
o Fusion of medial palatine process with lateral palatine processes (lateral processes grow medially)
o Contain hard palate and posterior
soft palate
Cross-section of palatal fusion
o 6 week
o 7 weektongue is narrow, fills
oralnasal cavity
o 8 weeklateral palatine processes
slide and roll over body of tongue.
Tongue lowers down and helps
fusion of midline tissue
o 9 weekfusion of lateral palatine
process and with nasal septum.
Later, around 12th week, bone
appears in the palate.
Palatal Fusion

o
o

Anterior portion of palate develops from fusion of maxillary processes and medial nasal processes
Fusion occurs from frontback

Common Facial Congenital Deformities

Cleft lip and palate
o Most common craniofacial defect
o CL/P occur in about 1 in 500-700 births
Male > female
Unilateral >bilateral
Left > right
o CP occurs in 1 in 2000 births
Female > male
o Cleft lip-unilateral
Failure of medial and nasal process and
maxillary process to fuse unilaterallyleads to
nasal distortiontissues pulled toward
attached side
o Cleft lip-bilateral
Failure of medial nasal process and maxillary
process to fuse bilaterally
o Cleft of face
Width of mouth is determined by fusion of the
maxillary process and mandibular process
Failure of maxillary and mandibular processes to fuse produces the cleft of face.
o Other less common cleft
Cleft of nose and upper lip
Failure of fusion of medial
nasal process (around 6th
week)
Cleft of mandible
Failure of mesenchymal cells
mandibular process to merge together (around 6th week)
Synostosis syndrome
o Crouzons
Premature fusion of superior and posterior sutures of maxilla along walls of orbit
Causes midface deficiency
Protrusion of the eyes and wide separation of eyes.

of

Aperts

Severe mental/neurological feedbacksrelease of fused suture is a critical step in treating this.

Usually requires surgical procedures along with orthodontics to correct malocclusion
Premature fusion of superior and posterior sutures of maxilla along walls of orbit
Causes midface deficiency
Maxilla sometimes fused to sphenoid
Hands and feet involved

Tooth Formation Prenatally

During 6th weekperipheries form dental laminant

Divided into 4 stages
o Bud
o Cap
o Bell
o And something another
Considerable calcification is necessary to detect tooth
radiographically.
Most of our info is based on radiographs.
Primary teeth
o 20 primary teeth
Centrals
Laterals
Canines
1st primary molars
2nd primary molars
o Primary tooth development timing
Calcification
Calcification
Begins
Begins
Tooth
Max
Mand

Crown Completed

Crown Completed

Max

Mand

Central

14 wk iu

14 wk iu

1.5 mon

2.5 mon

Lateral

16 wk iu

16 wk iu

2.5 mon

3 mon

Canine

17 wk iu

17 wk iu

9 mon

9 mon

1st molar

15 wk iu

15 wk iu

6 mon

5.5 mon

2nd molar

19 wk iu

18 wk iu

11 mon

10 mon

Primary Tooth Eruption Order

Centralslateral1st molarcanine2nd molars
In permanent dentitionOccurs earlier in boys than girls
In primary dentitiongirls are earlier than boys
Shaded teeth erupt earlier than opposing countpart
Upper lateral = earlier than lower lateral
Upper 1st = earlier than lower 1st
Upper canine = earlier than lower canine
Lower 2nd = earlier than upper 2nd

Important Points
All primary teeth start formation prenatally.
Clinically, teeth are forming before a radiograph detects them.
Teratogens can affect formation of teeth.

Because certain teeth start forming at different times, insults can affect teeth at different places
on their crowns.

Lecture Six: Development and Eruption of the Dentition

Note: my notes that I took during class are in italicsmind you, I dont really understand the guy so a lot of them dont
make sense.

Outline:

Tooth development
Sequence and timing of eruption of the primary and permanent teeth
Pre-emergent eruption and its control
Post-emergent eruption and the circadian
rhythm

TOOTH DEVELOPMENT:
My notes: initiated with dental lamina; oral
epithelium proliferates and goes from bud stage to
cap stage. At the bell stage, the tooth has its final
shape. Followed by odontogenesis mineralization
of dentin and enamel. Tooth starts to erupt and
reaches functional position.

Initiation
Primary teeth
During the 6th week, oral epithelium proliferates and forms the
dental laminae
Dental laminae undergo further proliferation at sites corresponding
to the positions of primary teeth
During 6th and 8th week in uterus, 20 primary tooth buds form
Permanent tooth buds develop lingually at later prenatal period
Permanent molars develop posteriorly to the primary molars
Permanent teeth
5 months IU central incisors
10 months (IU?) premolars
4 months IU first permanent
4 years of age second molars
Most of the other organ systems (i.e. digestive, CV) are all
functioning completely before birth, but development of teeth
continues long after birth
Bud stage (pic)
Bud stage is the initial stage of definitive tooth development
If initiation is stopped, dental agenesis occurs

Cap stage
Early cap stage
Late cap stage
Cells adjacent to the dental
papillae are those outside the
enamel organ divide and grow
around the enamel organ to form
the enamel organ? Enamel organ,
dental papillae, and dental follicle
are developed.
Enamel organ forms enamel
Dental follicle forms cementum,
PDL, and something else?
Differentiation/bell stage
13-14 weeks
The cap continues to grow into a bell shape
Appearance of specialized cells in the tooth germ
The enamel organ is divided into inner and outer enamel epithelium
The dental lamina of the permanent tooth appears as an extension
of the primary
Tooth germ of permanent molars develops the posteriorly extended
dental lamina
Dentinogenesis, Amelogenesis
Cells of the dental papilla adjacent to inner enamel epithelium
differentiate into odontoblasts
o Odontoblasts will produce predentin
o Predentin calcifies to form dentin
Cells of the inner enamel epithelium differentiate into
ameloblasts, which produce enamel
Enamel and dentin formation begins at the tip of the
tooth and progress towards the future root
The inner and outer enamel epithelium come together
in the neck region and form epithelial root sheath, which
initiates root formation
The inner cells of the dental follicle differentiate into
cementoblasts which produce cementum
Tooth assumes its final shape
Ameloblasts and odontoblasts appear
Cells from dental papilla differentiate into odontoblasts
where they will form the dentin
Cells of the inner enamel epithelium differentiate into ameloblasts to form enamel
Two characteristics:
o Shape is defined
o Junction of inner and outer EE and dental papilla
14 weeks IU, primary teeth are in the bell stage
Around 18 weeks IU, odontoblasts of primary teeth start to form dentin and then ameloblasts start to form
enamel

Root Formation
After clinical crown formation, the inner and outer enamel epithelial fold
over at the CEJ
The epithelia without the stellate reticulum is called Hertwigs epithelial
root sheath
Hertwigs epithelial root sheath grows away from the crown, increasing
size, moving the teeth, and allowing room for additional root growth
Root sheath determines number of roots and shape
Primary teeth development timing:

1)
2)
3)
4)
5)

Central incisors
Lateral incisors
First molars
Canines
Second molars

Teeth tend to be delayed more than they are early; same teeth in
the same arch tend to erupt at the same time.

Primary Tooth Spacing

Generalized
Primate
70% of children have space while 30% show no space
Children with space will have decreased chance of crowding in
permanent teeth
Chronology of Permanent Tooth Development:

The first permanent molar is the only permanent tooth starting calcification before birth
Crowns of most permanent teeth show radiographic evidence of calcification after birth
Approximately of an incisor crown calcifies a year; longer for other teeth
By 8-9 years of age, all permanent teeth except third molars should show on radiographs
Only the first molar develops before birth
All crowns are developed before age 8, except 3rd molar
By 8, any disturbance may affect crown formation (i.e. tetracycline)

Chronology of tooth development summary

Usual eruption order of permanent teeth
o Maxillary
M1, I1, P1, P2, C, M2, M3

Mandible
M1, I1, C, P1, P2, M2, M3
Root completion occurs about 2-3 years after eruption
o Implications:
Roots of unerupted teeth should not appear closed
Trauma requiring root canal therapy can be problematic

Rule of four for permanent teeth

At birth, 4 first molars have initiated calcification
At 4 years of age, all crowns have initiated calcification
At 8 years of age, all crowns are complete
At 12 years of age, all crowns emerge
At 16 years, all roots are complete
Dental Ages
Dental age 6
o Eruption of 4 first molars and mandibular central incisors
Dental age 7
o Eruption of maxillary central incisors and mandibular later incisors
Dental age 8
o Eruption of maxillary lateral incisors
o A delay of 2-3 years before any further permanent teeth appear
o From 6-8, the first molar and incisors erupt like a group and then there is a delay of 2-3 years before any
further permanent teeth appear
Dental age 9
o 1/3 of the root of the mandibular canine, first premolar, and maxillary first premolar is complete
o Root development just starts on the mandibular second premolar and maxillary canine and second
premolar
Dental age 10
o of the root of the mandibular canine, first premolar, and maxillary first premolar is completed
o Significant root development of mandibular second premolar and maxillary canine and second premolar
o Completion of roots of mandibular incisors and near completion of the roots of maxillary laterals
Dental age 11
o Eruption of first premolars and mandibular canine
o Completion of the roots of all incisors and first molars
o Eruption of permanent teethnone before this!
Dental age 12
o Eruption of remaining succedaneous teeth and all the 2nd molars
Dental age 13-15
o Completion of the roots of permanent teeth (except 3rd molar)
o By dental age 15, the 3rd molar should be seen on the radiographs

Effects of radiation on tooth development:

Radiation in high doses inhibits further crown and root development

Calcification of crown matrix was not inhibited
o If only cusp tips were calcified at the beginning of radiation, they can continue after radiation
This picture shows effects of radiation, mainly on the mandible (max seems normal)
o For the upper teeth, the second molars have erupted and only 2 permanent canines
o Upper left side, first premolar didnt erupt
o Pt should be around dental age of 12
Mandible: four lower incisors, first molar, this means pt is at least the dental age of 7 at the time of radiation
o Normally at dental age 9, there should be 1/3 of root development for lower canines and lower first
premolars
o However, they dont have root formation in this case
o Crown development of 2nd molar is completed and around 7.5 dental age
o Pt probably had radiation around dental age 8

Stages of tooth eruption

Emergence is the first sign of eruptionbefore emergence, there
is pre-emergent eruption which begins soon after root formation
and long before the teeth are seen in the oral cavity. After
emergence, they continue to erupt at a slower rate to
compensate for occlusal wear and mandibular dropping
Pre-emergent tooth movement
o Bodily movement of tooth germ
Movement within the bone before root formation.
During this phase, the growing tooth germ moves
various directions to maintain position in expanding
jaw.
The primary teeth in the alveolar bone move in the
facial, occlusal direction.
Permanent teeth also move within the jaw (adjust
positions).
o Change of position of permanent teeth
Permanent teeth develop lingually to the primary
predecessor.
Gradually, the developing permanent teeth are
positioned lingual near the apical 1/3 of the
primary teeth.
The premolars are located under the roots of the
primary molar.
This change of position is the result of the eruption of the primary teeth and coincident
increase in the height of the supporting tissue.
Not apical movement of permanent tooth germs.
Pre-emergent eruption
o Begins after root formation
o Resorption of bone/primary tooth roots
o Eruption mechanism moves the tooth occlusally
Post-emergent eruption
o Post-emergent spurt
o Juvenile occlusal equilibrium
o Adult occlusal equilibrium
Pre-Emergent Eruption:
Resorption of bone/primary tooth roots

o Defective bone resorption leads to eruption failure (M-CSF, Rankl, IL-1)

o Heavy fibrous gingiva or multiple supernumerary teeth may mechanically block the eruption
Eruption mechanism moves the tooth occlusally
o Resorption of bone/primary tooth roots and tooth eruption are not controlled by the same mechanism
Osteoclasts are required. If mutation of genes for osteoclasts leads to
defective osteoclasts no more resorption. Experiments have shown
that in absorption and tooth eruption may not be controlled by the same
mechanism.

Defective Osteoclast (pic)

Defective gene for osteoclast maturation defective osteoclast teeth
cannot erupt

Cleidocranial dysplasia (radiograph)

Mutation of an important gene

Bone resorption without eruption (2 radiographs)

Mandible fracture
First pic canines are the same height
Second pic right canine didnt erupt + bone
resorption
Mechanisms for tooth eruption
Root formation/elongation
o Root formation is the consequence, not the cause of eruption
o Root formation is not required for tooth eruption although it may accelerate tooth eruption
o Eruption of rootless teeth (pic)
Radiation experiment on a
monkey
Left: root of teeth are missing ,
but can still erupt though
suggesting root formation is not
required for eruption
Right: control without radiation
Periodontal ligament
o Animal studies showed that substances affecting the
development of cross-links in maturing collagen
interfere with eruption
o Transaction of fibers in the dental follicle prior to the
onset of eruption does not affect eruption rates or
movement
o Different mechanisms for pre-emergent and postemergent eruptions

PDL should not be the primary mechanism of pre-emergent eruption (but may be responsible for
post-emergent eruption
o PDL is considered a factor in tooth eruption because of traction power of the fibers
o More PDL fibers in post-eruption phase compared with pre-eruption phase
o Before emergence of the tooth, the fibers are not as well organized
o Suggests that there may be different mechanisms
Vascular pressure
o Regional changes in vascular pressure have long been proposed as a force of eruption, but the evidence
for this is both inconclusive and contradictory
o Injection of vasodilators above the root apex can cause transient increase in eruption
o Injection of vasoconstrictor can decrease
Dental follicle
o Dental follicle is required for eruption
o Removal of the follicle from the unerupted tooth prevented
the tooth from erupting
o Leaving the follicle intact and substituting and inert object for
the tooth resulted in eruption of the inert object
Clinical Application
o In infant, tooth eruption may be accompanied by a slight
temperature increase, mild irritation of the gums, and general
malaise
o Although some systemic disturbances at the time of the tooth may be expected, severe general
symptoms should not be associated with teething

Post-Emergent Eruption
Post-emergent spurt
o The stage of relatively rapid eruption from the time a tooth first penetrates the gingiva until it reaches
the occlusal level
o Eruption occurs between 8pm and midnight or 1am
o Tooth stops erupting and often intrudes slightly during the early morning and the day
o The circadian rhythm is possibly related to the similar cycle of growth hormone release
Juvenile occlusal equilibrium
o Teeth that are in function erupt at a rate that parallels the rate of vertical growth of the jaws
o As the mandible continues to grow and moves away from the maxilla, tooth eruption matches the jaw
growth
o A pubertal spurt in eruption of teeth accompanies the pubertal spurt in jaw growth
o After a tooth is in occlusion, the rate of eruption is controlled by the forces
opposing eruption from mastication or soft tissues
Adult occlusal equilibrium
o When the pubertal growth spurt ends, teeth continue to erupt at an
extremely slow rate during adult life
o Teeth continue to erupt at an extremely slow rate during adult life
o Occlusal wear of teeth is compensated by additional eruption and facial height
remains constant
o If extremely severe wear occurs, eruption may not compensate and lead to
decrease of facial height
o To compensate for occlusal wear increase in thickness of cementum
Eruption
Teeth tend to erupt in groups
o First permanent molars and incisors
o Canines, premolars, second molars
o Third molars

Root formation at time of eruption

o Incisors about formed
o Premolars and canines about 2/3 formed
Eruption of teeth is more genetically determined than environmentally susceptible
o Only cases of severe malnutrition may cause delayed eruption

Development and eruption of the dentition (lecture 7)

9-30-08

Outline

Clinical problems related to tooth development

Most commonly encountered clinical problems

Problem with tooth development

Enamel hypoplasia
o Infection or trauma of primary tooth may interfere with matrix formation or calcification of permanent
tooth
o Nutritional deficiencies
Vit A
Vit C
Vit D
Calcium
Phosphorus
Excessive fluoride intake

Fusion
o Results from the union of two adjacent tooth germs
involving the dentin
There are really 2 separated roots and pulp
chambers
Look at the lower right anteriors

Gemination
o Results from the splitting of a single tooth germ
Clinically appers as a double tooth or fused tooth.
Single root and single pulp canals.
In less than 1% of population.
Happens in the anterior region.

Peg lateral
o 1-2% of population.
o Smaller conical and tapered to a point in the incisal.

Accessory cusp/tubercle
o Enamel pearl
o Will not allow the normal CT attachment.

o
o

Accessory cups in the cingular area.

Remove the cups from max incisor for O purpose may require endo treatment.

Dilacerations/flexion
o Dilacerations (left)
A severe bend or distortion of a tooth root
o Flexion (right)
A sharp curvature or twist to a root

Congenitally missing teeth

o Heredity
o Localized inflammation or infections
o Systemic conditions
o Can be autosomal dominant, recessive or X linked
o Severe interuterine disturbance can lead to tooth development problems

Failure of initiation
o primary (general) lamina all primary teeth and permanent molar
o successional lamina
o fusion of mandibular processes or premaxilla and maxillary processes

Congenitally missing teeth

o Occurs most commonly at areas of
Fusion of dental lamina, 77% here
The weakest site, increased site of missing teeth
Maxillary laterals
Mandibular centrals
Ends of dental lamina, 24% here
Second premolars
Third molars
o More frequently affected permanent teeth
3rd molar > 2nd molar > premolar > lateral incisor
Congenital missing later incisor can be linked to opposite lateral incisor missing too
o Andontia
congenital absence of all teeth, deficiency or absence of epidermal
glands
o Oligodontia:
absence of six or more permanent teeth
o Hypodontia:
absence of less than six permanent teeth
o MSX1, PAX9, BLX are the mutations of these genes that can lead to missing teeth, but have nothing to
do with the syndromes.

Supernumerary teeth (Cleidocranial dysplasia)

o Problem with excessive initiation, genetically determined
o May link to some skeletal dysplasias
o Most located in the anterior maxillary region, but can be anywhere

o
o
o
o

Can prevent or deflect tooth eruption

Location determines the extent
Impacted supernumerary tooth is found on a radiograph
This can cause crowding and interfere with O

Problems with teeth during eruption

o Number of teeth
The inheritance of the number of teeth is autosomal dominant with variable penetrance
Supernumerary teeth
Congenitally missing teeth
Lost teeth (primary and permanent)
Early loss of primary teeth may result in movement of the remaining teeth, blocking out
unerupted permanent teeth, tipping of
neighboring teeth, extrusion of the opposing
teeth
This change can cause functional interference.
The earlier loss of the lower right canine
(primary) leads to less space for permanent of
canine and shift of midline.
If extraction after the permanent tooth is being to erupt, the perm tooth will reupt
quicker.
If extraction before eruption, the permanent tooth eruption will be delayed.
o Size of teeth
Mismatch of size of teeth and size of basal bone leads to crowding or
spacing, which can lead to malocclusion
Tooth size discrepancy between maxillary and mandibular teeth
Teeth are smaller there will be spacing, teeth are larger there will be
o

crowding
Eruption of teeth: location/direction/amount
Usual eruption order of permanent teeth
Maxillary
o M1, I1, I2, P1, P2, C, M2, M3
Mandible
o M1, I1, I2, C, P1, P2, M2, M3
Development/eruption in the wrong place or
direction
This can lead to esthetic problem or
functional problem.
The teeth can become impacted.
Maxillary canine is the most common
impacted one.
Strong genetically components.
Eruption in undesirable place can cause
o Premature contact and functional shift resulting in cross bite

Double row of teeth

Roots of primary teeth have not resorbed
Check root length with radiograph to make decision about extraction
Check the x-ray to make the decision about extraction
Pressure of tongue will push the permanent teeth forward

Extreme type of ectopic eruption: Transposition

Most common on the maxillary
In 1/300 ortho pts
Generally seen in b/w Incisors and Canines
or b/w Canine and Premolar

With amount of eruption: deficient or eruption failure

Can be localized
Can erupt to the surface, but then fail to erupt further

Types of eruption failure

o Physical obstruction
Scar tissue
Cyst
Other teeth
Lack of ramal remodeling
Trauma
o

Ankylosis
Usually primary molars
5-10% US children have one ankylosed primary molars
Ankylosed tooth may finally resorb and exfoliate
Primary molars that become ankylosed at early age
can become totally submerged, and unlikely exfoliate.
May delay a little bit of the eruption of the successive
tooth.
The primary molar is unlikely to exfoliate and the
permanent is severly delayed and this can cause sever
problems.
Ankylosis of lower primary 2nd M.
Can lead to malocclusion.
Fusion of alveolar bone and cementum or dentin
Fusion usually occurs in root bifurcation
20% of ankylosed teeth are associated with congenitally missing teeth
Failure of Hertwigs epithelilal root sheath could cause ankylosis of teeth

Primary failure of eruption

Infection of condyle can lead to severe growth deficiency
There are lack of bone remodeling and lead to eruption failure
An eruption defect, manifesting as a complete failure of eruption or cessation of initial eruption
with no obvious local or systemic causative factor
Evidence suggests that this disorder has a substantial geographic component??
Tooth forms but does not erupt
Teeth may erupt into initial occlusion and then cease to erupt, or may fail to erupt entirely
Predominantly affects the posterior dentition
Both primary and permanent molars may be affected
Involvement may be unilateral or bilateral
The first and second permanent molars are the most frequently affected teeth
Application of orthodontic force in an attempt to bring the affected teeth into the arch leads to
ankylosis rather than normal tooth movement
Strong family history of eruption failure or eruption problems in the primary dentition
Accompanied with higher level of hypodontia

Diagnosis relies principally upon exclusion, all possible causative factors have been considered
and eliminated

In the permanent teeth

Lower right 1st molar
Other molars didnt erupt at all