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PRE-NATAL GROWTH
&DEVELOPMENT
INDIAN DENTAL ACADEMY
Leader in continuing dental education www.indiandentalacademy.com
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What is EMBRYOLOGY? Embryology is the study of prenatal development
of embryo and fetuses.
SIGNIFICANCE OF EMBRYOLOGY -Gives knowledge concerning beginning of human
life and changes occurring during prenatal development. -Understanding normal post-natal growth-and development of various craniofacial abnormalities
INTRODUCTION
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Period of ovum- fertilization to 2 weeks
Period of embryo – 2nd to 8th week
Period of fetus - 9th week to term
Imp-week 4-8,teratogens
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He who sees things grow from the beginning will have the finest view of
them……..
-ARISTOTLE
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Day 0
FERTILIZATION
Human development begins at fertilization, the process during which a male sperm unites with a female oocyte to form a single zygote.
Human development begins at fertilization, which occurs in the ampulla of the uterine tube
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Zygote-contains chromosomes and genes that are derived from both mother and father.
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THE FIRST WEEK CLEAVAGE OF ZYGOTE:
-Cleavage usually occurs as the zygote passes along the uterine tube.
-Cleavage consist of repeated mitotic divisions of zygote.
-The zygote divides into 2 cells, which then divides into 4,8 and so on.
-The cells are called
“BLASTOMERES’’.
- 12 to 16 blastomeres,
it is called as MORULA (fruit of mulberry tree).
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Day 1-3
Cleavage
blastomeres
morula
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2 cell 4 cell 8 cell
REF-THE DEVELOPING HUMAN, MOORE AND PERSAUDwww.indiandentalacademy.com
FORMATION OF BLASTOCYST As morula enters uterus, a fluid-filled space called
blastocyst cavity appears in morula. As fluid increases, it separates blastomeres into two
parts:- Outer cell layer, Trophoblast.
-Inner cell mass, which act as primordium of embryo called Embryoblast
Day 4-7
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Implantation
6 days after fertilization, blastocyst adheres to endometrial surface.
As soon as it attaches, the trophoblast starts proliferating rapidly and differentiates into 2 layers.
-Cytotrophoblast (inner layer). -Syncytiotrophoblast (outer
mass with finger-like processes).
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Implantation
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Implantation of blastocyst commences at the end
of 1st week and completed
by end of 2nd week.
The syncytiotrophoblast release proteolytic enzymes which promotes proteolysis and invasion of maternal endometrium..
The Second week
Completion of implantation:Day 8-14
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DAY 9
Isolated cavities called lacunae appear in syncytiotrophoblast
Adjacent lacunae fuse to form lacunar networks
Capillaries around embryo become dilated to form - sinusoids
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Syncytiotrophoblast erodes sinusoids and maternal blood flows freely In lacunar networks
Communication with eroded endometrial capillaries
Primitive circulation between endometrium and placenta-uteroplacental
circulation
DAY 12
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Site at which blastocyst EMBRYONIC POLE.gets implanted
CLINICAL RELEVANCE
Syncytiotrophoblast releases HUMAN CHORIONIC GONADOTROPHIN ( HCG ) HORMONE… which gives a positive pregnancy test at the end of the second week.
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FORMATION OF AMNIOTIC CAVITY, EMBRYONIC DISC AND YOLK SAC:
As implantation of blastocyst progresses, a small cavity appears in the inner cell mass called “AMNIOTIC CAVITY”.
The blastocyst cavity / Exocoelomic cavity soon modifies to
form “PRIMARY YOLK-SAC”.
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So now there are 2 cavities:1. “AMNIOTIC CAVITY” (above)2. “PRIMARY YOLK-SAC” (below - later forms secondary yolk
sac)
Soon the inner cell mass form 2 types of cells which lie Between these 2 cavities
Epiblast: High columnar cells related to amniotic cavity. Hypoblast – squamous or cuboidal cell mass adjacent to primary
yolk sac
The epiblast and hypoblast together forms the “BILAMINAR EMBRYONIC DISC”.
Second weekBILAMINAR DISC STAGE
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Defect in endometrium persists for 2 days- filled by a closing plug- fibrinous coagulum of blood.
In extra-embryonic mesoderm fluid filled spaces appear which fuse to form Extraembryonic Coelom
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DAY 14
2 processes occur simultaneously:
Formation of extraembryonic somatic and splanchnic mesoderm due to split of extraembryonic mesoderm by extraembryonic coelom.
Extraembryonic coelom is now called chorionic cavity.
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Defect in endometrium disappears
Cells from hypoblast migrate along inside of Primary yolk sac – pinched off and smaller secondary yolk sac forms
Proliferation of cytotrophoblastic cells into syncytiotrophoblast leads to Formation of primary chorionic villi (later forms placenta).
DAY 13
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DAY 14
The amniotic cavity (epiblast at floor)
and secondary yolk sac (hypoblast at roof)
resembles 2 balloons pressed together inside larger balloon (chorionic sac) suspended by connecting stalk - umbilical cord
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DAY 14
Epiblastic cells- formation of primitive streak
Hypoblastic cells in a localized area are now columnar and form a thickened circular area called pre-chordal plate which indicates the future site of the mouth and is an important organizer of the head region
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THE THIRD WEEK
GASTRULATION : is a formative process by which the 3 germ layers & axial orientation are established in the embryo
-Primitive streak.
-Germ layers.
-Formation of notochord
NEURULATION.
NEURAL CREST FORMATION.www.indiandentalacademy.com
GASTRULATION:
the Bilaminar embryonic disc is converted to a Trilaminar embryonic disc.
It is the beginning of morphogenesis (development of body form).
It begins with formation of primitive streak at the surface of the embryonic disk.
Third week
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PRIMITIVE STREAK: It results from
proliferation and migration of the cells of epiblast to the median plane of the embryonic disc.
The primitive streak elongates by addition of cells to its caudal end
its cranial end proliferates to form primitive node.
DAY 15,16
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As soon as the primitive streak appear, it is possible to identify the embryo’sCranio -caudal axis
Primitive groove develops in the primitive streak that is continuous with a small depression in the primitive node, the primitive pit.
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FATE OF PRIMITIVE STREAK
Normally the primitive streak undergoes disappears by the end of fourth week.
Remnants of primitive streak may persist and give rise to a large tumor – SACROCOCCYGEAL TERATOMA.
Need to be surgically excised .
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Fetal Alcohol Syndrome
clinically described 30 years ago (1973),
caused by maternal alcohol consumption during pregnancy.
Alcohol crosses the placenta from maternal circulation into fetal circulation
consists of a variable degree of birth defects and mental retardation, initially identified by a reduced head size and distinctive facial features
This Syndrome is 100% preventable.
FAS
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Fetal Alcohol SyndromeFAS
• Maternal alcoholism causes effects of 2 types
• In moderation i.e. 1-2 ounces/day (30ml) can cause fetal alcohol effects (FAE) -behavioral & learning defects
• Chronic consumption leads to FAS.
• Moderate &chronic consumption in the 1st trimester causes these effects. However development of brain spans the entire period of gestation, hence total abstinence from alcohol is advised
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FAS
CHARACTERISTICS:Microcephaly - leads to small head circumference Palpebral fissure - short opening of eye Epicanthal folds - fold of skin at inside of corner of eye Midface - flat Nasal Bridge - low Philtrum - Indistinct, Upper Lip - thin Micrognathia - small jaw Ears –the curve at top part of outer ear is underdeveloped and folded over parallel to curve beneath. Gives the appearance of a "railroad track"
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MANAGEMENT:
early intervention is critical to determine prognosis for a child with FAS
earlier provision of medical, clinical and educational intervention- better outcome
special needs pre-school programme constant follow up
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FORMATION OF GERM LAYERS:
Soon after primitive streak appears, cells leave its deep surface and migrate to form a loose network of embryonic connective tissue called Mesenchyme
The mesenchyme forms the supporting tissue of the embryo.
Third week
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the mesenchyme forms a layer called Intraembryonic mesoderm.
Some cells of the Epiblast displace the Hypoblast forming intraembryonic or embryonic endoderm in the roof of Yolk sac.
Cells remaining in the epiblast forms the Intraembryonic or Embryonic ectoderm in the floor of the amnion.
Third week
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All the above cells have the potential to proliferate and differentiate into diverse types of cells, such as fibroblast, chondroblast and osteoblast.
In short the cells of the epiblast, through the process of gastrulation, give rise to all 3 germ layers in the embryo.
Third week
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DERIVATIVES OF GERM LAYERS
ECTODERM: Epidermis, hair, nail. Central and peripheral nervous system. Mammary, pituitary and subcutaneous gland. Enamel of teeth. MESODERM :Connective tissue, cartilage, bone. Striated and smooth muscle. Heart, blood and lymphatic vessels. kidneys, ovaries, testes, spleen, cortex of adrenal gland. ENDODERM: Epithelial lining of gastrointestinal and respiratory tracts, urinary bladder and urethra. Epithelial lining of tympanic cavity, tympanic antrum, auditory tube.
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FORMATION OF NOTOCHORD
Some mesenchymal cells migrate cranially from the primitive node and pit, forming a median cellular chord, the notochordal process.
The process soon acquires a lumen, the notochordal canal and grows cranially until it reaches the prechordal plate.
DAY 18
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The notochordal process cannot extent beyond the prechordal plate.
Place of fusion of upper ectoderm and lower endoderm, which will form the OROPHARYNGEAL MEMBRANE.
Various cellular events take place in the notochordal process which give rise to the NOTOCHORD.
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prochordal plate
Notochordal canal
cloacal membrane
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IMPORTANCE OF NOTOCHORD: Defines primordial axis of embryo and gives
rigidity. Serves as basis for development of axial
skeleton (bones of head and vertebral column). Indicates future site of vertebral bodies.
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NEURULATION
Formation of neural plate and neural folds and closure of these folds to form the neural tube constitute Neurulation.
Neural plate and Neural tube: As the notochord develops, the embryonic ectoderm
over it thickens to form an elongated, slipper-like plate of thickened epithelial cells, the “neural plate” .
DAY 19,20
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Neural plate formation is induced by developing notochord.
The ectoderm of neural plate called Neuroectoderm gives rise to the “CENTRAL NERVOUS SYSTEM” i.e. the Brain and spinal chord
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NEURULATION
At about 18th day, the neural plate invaginates along its central axis to form median “Neural groove”, which has neural folds on each side.
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The neural fold are the first signs of brain development.
By the end of 3rd week the neural folds begin to move together and fuse, converting neural plate into a “neural tube”
NEURULATION
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NEURAL CREST FORMATION
As the neural folds fuse to form the neural tube, some neuroectodermal cells lying along the crest of each neural fold lose their epithelial affinities and attachments to neighboring cells.
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Soon it forms a flattened irregular mass, the neural crest, between the neural tube and the overlying surface ectoderm.
Neural crest soon separates into right and left parts that migrates to the dorsolateral aspects of the neural tube and give rise to the sensory ganglia of the spinal and cranial nerves.
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CREST CELLS DERIVATIVES.
Neurolemmal sheath of peripherl nerves. Meningeal coverings of the brain and the
spinal cord. Formation of pigment cells. Several skeletal and muscular components in
the head
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NEURAL TUBE DEFECTS- primarily results from failure of neural folds to fuse and form the neural tube in the brain region.
e.g.- ANENCEPHALY- anterior brain structures are lost and replaced by soft spongy mass.
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Development of somites
As the notochord and neural tube form,intraembryonic mesoderm on each side proliferates to form a column of PARAXIAL MESODERM.
INTERMEDIATE MESODERM
LATERAL MESODERM
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Development of somites DAYS 20-30
• Paraxial mesoderm differentiates into paired cuboidal bodies- somites
• First appear in occipital region
• 42-44 pairs of Surface elevations by 5th week
• Develop craniocaudally
• Form axial skeleton www.indiandentalacademy.com
4th week onwards...
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Paraxial mesoderm.
Lateral plate mesoderm.
Neural crest cells .
Ectodermal placodes
Mesenchyme for formation of head region is derived from:
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PHARYNGEAL APARATUS “Branchial”- branchia, gill
resemblance to fish embryo - Pharyngeal arches (mesoderm) - Pharyngeal clefts (ectoderm) - Pharyngeal pouches (endoderm) - Pharyngeal membranes
clefts separate arches externally. Pouches separate arches internally.
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PHARYNGEAL ARCHES Pharyngeal arches consist of core of mesenchymal tissue
covered on the outside by surface ectoderm and on inside by endoderm.
Apart from this, the arches also have migrated neural crest cells, which contribute to skeletal components of the face.
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By the end of the 4th week , 4 pairs of pharyngeal arches are visible externally as rounded ridges on each side of the future head and neck regions.
5tharch-often absent. If present the 5th and 6th arches are rudimentary & not visible on the surface.
Neural crest cells, in addition to forming nerve tissue, produce the bones of the cranium.
Within the pharyngeal arches, neural crest cells and lateral plate mesoderm give rise to bones of the jaw and lower face, the viscerocranium
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Each arch is characterized by its own Cartilaginous rod that forms the skeleton of the arch muscular component nerve component and arterial component.
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DERIVATIVES OF PHARYNGEAL Apparatus
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SKELETAL DERIVATIVES
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MUSCLE DERIVATIVES
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NERVE SUPPLY
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ARTERIAL SUPPLY
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The first pharyngeal arch is often called the mandibular arch. First arch splits giving rise to 2 regions:
- cranial part called Maxillary Process- Caudal part called Mandibular Process
MAXILLARY PROCESS gives rise to Maxilla MANDIBULAR PROCESS gives rise to Mandible
FIRST PHARYNGEAL ARCH
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MAXILLARY PROCESS: mesenchyme of the maxillary
process gives rise to premaxilla, maxilla, zygomatic bone and part of temporal bone
through membranous
ossification.
FIRST PHARYNGEAL ARCH
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MANDIBULAR PROCESS:
Cartilage of the 1st arch
is meckel’s cartilage.Dorsal end-ossifies to
form malleus and incusMiddle part regresses,
but perichondrium forms sphenomandibular ligament
FIRST PHARYNGEAL ARCH
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Meckle’s cartilage
Ventral part-forms horse shoe shaped structure in the shape of future mandible and has close positional relationship to developing mandible but makes no contribution to it.
Mesenchymal tissue lateral to cartilage undergoes intramembranous ossification to form mandible and meckel’s cartilage disappears
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MUSCULATURE:
Temporalis Masseter Pterygoids Anterior belly of digastric Mylohyoid Tensor tympani Tensor palatini.
FIRST PHARYNGEAL ARCH
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NERVE SUPPLY: Nerve supply to muscles
of the 1st arch is by mandibular branch of trigeminal nerve.
Sensory supply to the skin of face by ophthalmic, maxillary, and mandibular branches of trigeminal nerve.
FIRST PHARYNGEAL ARCH
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Called the hyoid arch as part of the hyoid bone develops here
The cartilage of 2nd arch is called as Reichert’s cartilage.
SECOND PHARYNGEAL ARCH
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It gives rise to, Stapes Styloid process of
temporal bone Stylohyoid ligament Lesser horn and
upper part of body of hyoid bone.
SECOND PHARYNGEAL ARCH
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MUSCLES: Stepedius. Posterior belly of
digastric. Auricular. Muscles of facial
expression
SECOND PHARYNGEAL ARCH
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NERVE: Facial nerve supplies
all these muscles.
SECOND PHARYNGEAL ARCH
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CARTILAGE of 3rd pharyngeal arch produces,
Lower part of body of hyoid bone.
Greater horn of hyoid bone.
THIRD PHARYNGEAL ARCH
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MUSCLE: Stylopharyngeus
muscle.
NERVE: Glossopharyngeal
nerve.
THIRD PHARYNGEAL ARCH
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CARTILAGINOUS component of 4th and 6th pharyngeal arches fuse to form,
Thyroid cartilage. Cricoid cartilage. Arytenoid cartilage. Corniculate cartilage. Cuneiform cartilage.
FOURTH AND SIXTH PHARYNGEAL ARCHES
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MUSCLES:4th arch: cricothyroid, levator palatini, constrictors of pharynx ,
6th arch: intrinsic muscles of
larynx.
FOURTH AND SIXTH PHARYNGEAL ARCHES
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NERVE: 4TH arch: Superior laryngeal branch of vagus nerve. 6th arch: Recurrent laryngeal branch of vagus nerve.
FOURTH AND SIXTH PHARYNGEAL ARCHES
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ARTERIAL SUPPLY Pharyngeal arch arteries are called aortic arches
from arch 1 & 2-arteries significantly smaller Arch 1- part of maxillary artery Arch 2- hyoid & stapedial arteries Arch 3- part of carotid system Arch 4- left side-arch of aorta Right side-subclavian artery Arch 6- pulmonary arteries
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Human embryo has 5 pairs of pharyngeal pouches, the last one is atypical and often considered as part of the 4th pouch.
Composed of Endoderm
PHARYNGEAL POUCHES
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It comes in contact with the epithelial lining of the 1st pharyngeal cleft, which is a future external auditory meatus.
The distal portion widens into sac-like structure forming primitive tympanic cavity, the proximal part remains narrow, forming Auditory (Eustachian) tube.
lining of the tympanic cavity- forms tympanic membrane or eardrum.
FIRST PHARYNGEAL POUCH1st pouch forms stalk-like diverticulum- Tubotympanic recess.
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Buds are secondarily invaded by mesodermal tissue thus forming primordium of palatine tonsil
3rd and 5th month- tonsil is infiltrated by lymphatic tissue.
Part of pouch remains and forms tonsillar fossa in adult.
second PHARYNGEAL POUCH
The epithelial lining of 2nd pouch proliferates and form Buds that penetrate into surrounding mesenchyme.
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3rd and 4th pouches are characterized by , DORSAL WING and VENTRAL WING
In 5th week, from 3rd pouch Dorsal wing- Inferior parathyroid gland. Ventral wing- Thymus gland.
THIRD PHARYNGEAL POUCH
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Both gland primordia lose their connection with pharyngeal wall, the thymus then migrates in a caudal and medial direction, pulling the Inferior parathyroid gland with it.
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The primordia finally rest on the dorsal surface of the thyroid gland and forms inferior parathyroid gland.
The thymus gland moves rapidly to its final position in the thorax, fuses with counterpart from opposite side.
THIRD PHARYNGEAL POUCH
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Of the 4th pouch Dorsal wing- superior
parathyroid gland.
It also loses contact with wall of pharynx and migrate caudally and medially and finally is located on the dorsal surface of thyroid.
FOURTH PHARYNGEAL POUCH
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Last pharyngeal pouch to develop Usually considered to be a part of 4th pouch. Gives rise to – Ultimobranchial body, which gets incorporated
into thyroid gland giving rise to parafollicular or ‘c’ cells of thyroid gland which secrete calcitonin, hormone involved in regulation of calcium level in blood.
FIFTH PHARYNGEAL POUCH
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Derivatives PHARYNGEAL POUCHES
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located between arches externally
these are spaces, thus contain no germ layer components
Four pharyngeal clefts, of which only 1st contributes to the definitive structure - external auditory meatus.
DERIVATIVES OF PHARYNGEAL CLEFTS/grooves
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Active proliferation of mesenchymal tissue of 2nd arch, results in overlapping of it over 3rd and 4th arch causing the 2nd , 3rd and 4th clefts lose contact with the outside and forms a cervical sinus which eventually obliterates as neck develops.
DERIVATIVES OF PHARYNGEAL CLEFTS
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Pharyngeal Membranes:
Appear in the floors of the pharyngeal grooves and form where the epithelia of the groove & pouches approach each other
as most clefts are filled in, only first membrane develops. this lies close to external auditory meatus and develops into the
Tympanic membrane
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Primordial mouth or stomodeum appears as slight depression of surface ectoderm
It is separated from cavity of primordial pharynx by oropharyngeal membrane
Bilaminar-ectoderm and endoderm
STOMODEUM
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• Ruptures at 26 days
• Communication of primordial cavity and foregut with amniotic cavity
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CLINICAL COMMENT Most congenital anomalies in head-neck region originate during transformation of the pharyngeal apparatus into its adult derivatives. Thus the term “branchial anomalies” results from persistence of parts that normally disappear as adult structures develop.
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BRANCHIAL FISTULAS: -an abnormal canal that opens internally into tonsillar sinus and
externally in the side of the neck. persistence of parts of the 2nd pharyngeal groove and pouch. Fistula ascends from its opening in the neck through the
subcutaneous tissue and platysma muscle to reach the carotid sheath – passes between the internal & external carotid arteries and opens into the tonsillar sinus
CLINICAL CORRELATION
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BRANCHIAL CYST: Remnants of parts of cervical sinus and/or the
2nd pharyngeal groove may persist and form a spherical or elongated cyst.
They may be associated with
branchial sinuses and drain
through them,
these cysts often
lie free in the neck just inferior
to the angle of the mandible
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May develop anywhere along the anterior border of SCM muscle
Slowly enlarging painless swelling in the neck.
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NEURAL CREST CELLS: Essential for formation of craniofacial region but
disruption results in severe craniofacial malformation : 1ST ARCH SYNDROME-
Treacher collins syndrome (mandibulofacial dysostosis)
Pierre-Robin sequence Digeorge sequence (3rd and 4th pharyngeal pouch
syndrome). Goldenhar syndrome (Hemifacial microsomia ).
CLINICAL CORRELATION
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TCS
First described by Thomson and Toynbee in 1846-47 Later, essential components described by Treacher Collins
in 1960
Autosomal dominant inheritance
Associated with increased paternal age
Prevalence of 1 in 50,000
Treacher collins syndrome (mandibulofacial dysostosis)
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Characteristics: Fishlike” facial appearance Usually bilateral and symmetric expression Degree of malformation at birth is stable and non-progressive Dolichofacial pattern Hypoplastic supraorbital rims and underdeveloped zygomatic bones resulting in malar hypoplasia.
TCS
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TCS
“Cleft palate in 35% Downward slanting palpebral fissures Retrusive mandible and maxilla High mandibular plane angle– Anterior open bite Antegonial notching Malformed external ear Normal intelligence
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Treacher Collins syndrome1. Preoperative frontal view of 16-year-old patient with Treacher
Collins Syndrome. No previous correction had been performed.2. Postoperative frontal view 1 year after orthognathic surgery. 3. Pre and postoperative lateral views of same patient.
1. 2. 3.
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PRS
Triad of micrognathia, glossoptosis and cleft palate First described by St. Hilaire in 1822 Pierre Robin first recognized the association of
micrognathia and glossoptosis in 1923 Prevalence: 1 of every 8,500 newborns
PIERRE ROBIN SEQUENCE
Alters 1st arch structures, with mandible most severely affected. www.indiandentalacademy.com
The initiating defect is micrognathia which results in posterior displacement of the tongue i.e. glossoptosis and obstruction to full closure of palatine processes resulting in bilateral cleft palate
PRS
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Occurs because the 3rd and 4th pharyngeal pouches fail to differentiate into thymus and parathyroid glands.
Congenital thymic aplasia and absence of parathyroid glands with or without cardiovascular defects.
DIGEORGE SEQUENCE:
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characteristics Congenital hypo-parathyroidism Increased susceptibility to infections Shortened philtrum of lip Low set notched ears Nasal clefts micrognathia, And cardiac abnormalities – defects of aortic
arch & heart
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Characteristics Maxilla, temporal,& zygomatic bones are reduced in size and
flattened. Facial asymmetry Ear, eye, and vertebral defects are common. i.e. Occuloauriculovertebral disease Epibulbar Dermoids which are benign tumors located just inside the opening of the eye or the eyeballs, cause problems with vision.
HEMIFACIAL MICROSOMIA/GOLDENHAR SYNDROME:
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Preoperative frontal view of 17-year-old patient after inadequate orthognathic surgical correction.
Postoperative frontal view after distraction osteogenesis and dermal fat graft to left cheek.
Preoperative left oblique view shows deformity and after reconstruction
GS
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Development of
face
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2 organizing centers- Forebrain (prosencephalic) centre
Hindbrain (rhombencephalic) centre
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5 facial primordia Neural crest: source for almost all connective tissues in the face
DEVELOPMENT OF FACE
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Boundaries of stomodeum.
Paired maxillary prominences- lateral boundary
Paired mandibular prominences- caudal boundary
Nasal part of FNP- rostral boundary
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Facial prominences-active centers of growth – 4th to 8th week Connective tissue continuous from one prominence to another.
DEVELOPMENT OF FACE
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Lower jaw and lower lip are the first parts of the face to form.
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Nasal placodes & nasal pits- by the end of fourth week Primodia of the nose and and nasal cavities.
DEVELOPMENT OF FACE
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Nasal prominences , nasal pits
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Maxillary prominences grow- pushing nasal prominences medially
Nasolacrimal groove
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MNP
MP
LNP
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• Auricular hillocks- seen by the end of fifth week.
• Neck region
• Primordia for external acoustic meatus and auricle.
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• By the end of sixth week
• Maxillary prominence merges with lateral nasal prominence
• Continuity between side of nose and cheek region
• Nasolacrimal ductNLG
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NASOLACRIMAL DUCT
Rod like ectodermal thickening in the floor of Nasolacrimal groove.
Later as a result of cell degeneration cord canalizes into Nasolacrimal duct.
Part of duct which fails to canalize – ATRESIA OF NASOLACRIMAL DUCT.
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Medial nasal prominences merge with each other and with fused lateral nasal & maxillary prominences
Intermaxillary segment
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Intermaxillary segment gives rise to
Philtrum of the upper lip. Premaxillary part of the maxilla and its
associated gingiva. The primary palate.
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MNPLNP
MP
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1. Frontonasal prominence: forehead, dorsum & apex of nose2. Lateral nasal prominence: alae of nose3. Medial nasal prominence: nasal septum, philtrum, premaxilla, primary palate4. Maxillary prominence: upper cheek, most of maxilla and lip5. Mandibular prominence: mandible, chin, lower lip, lower cheek
Disruptions in theformation of theseprominences leadsto facial clefting andother defects.
Summary of Facial Development
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DEVELOPMENT OF PRIMARY PALATE
Palatal development spans week 5-12 , but weeks 6-9 are most critical
Formation of intermaxillary segment from merged medial nasal prominences
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Primary palate begins to develop from deep part of the intermaxillary segment of maxilla.
Initially this segment is a wedge shaped mass of mesenchyme between internal surface of maxillary prominence.
Primary palate forms the premaxillary part of the maxilla.
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DEVELOPMENT OF SECONDARY PALATE
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Sixth week
Secondary palate develops from two mesenchymal projections that extend from internal aspects of the maxillary prominences. ( lateral palatine processes )
project inferomedially.
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As jaw develops tongue moves inferiorly palatal shelves ascend to a horizontal position and fuse in the median plane.
Palatal shelves also fuse with the nasal septum and posterior part of primary palate.
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NASAL SEPTUM develops as a downgrowth from internal aspects of merged medial nasal prominences.
Fusion between nasal septum and palatine processes ninth to twelfth week.
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Bone develops in the primary palate, forming Premaxillary part of the maxilla.
Gradually bone extends into the lateral palatine processes to form HARD PALATE.
Posterior part do not ossify SOFT PALATE.
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Nasal septum
Bone development
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Theories for palatal shelf elevation Causes extrinsic to palatal shelves
1. Descent of the tongue due to pronounced sagittal growth spurt of the Meckle's cartilage and the mandible (Coleman 1965; Burdi & Silvey 1969)
2. Myoneural activity within the tongue causing descent (Wragg et al 1969)
3. shelves being pushed up by the tongue (Walker 1971)
4.mouth opening reflexes (Humphrey 1969)
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Intrinsic causes –
1. Hydration and polymerization of intercellular substances producing an elastic elevating force (Walker 1961)
2. differential growth of one side of the palatal shelf (Wood & Kraus, 1962)
3. turgor produced by a build up of mucopolysaccharides , predominantly hyaluronic acid (Andersen et al 1967)
4. serotonin release from neural tissue (Zimmerman et al 1981)
5. degree of mesenchymal cell activity at different sites and stages of palatal development (Singh and Moxham 1993)
Ref- fundamentals of craniofacial growth - Sperberwww.indiandentalacademy.com
Most accepted theory-
elevation of the palatal shelves to horizontal position is believed to be caused by an intrinsic shelf elevating force that is generated by the hydration of hyaluronic acid in the mesenchymal cells within the palatal process
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CLEFT LIP & PALATE Cleft lip and cleft palate are related embryologically but
are distinct entities Cleft lip: 1 in 750; Cleft palate: 1 in 2500 Effects on appearance, speech, feeding
Associated Dental Abnormalities Supernumerary Teeth- 20% Dystrophic Teeth- 30% Missing Teeth- 50% Malocclusion- 100%
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Genetics
Non-syndromic inheritance is multifactorial Cleft Lip, With or Without Cleft Palate:
• One Parent-2%• One Sibling- 4% Two Siblings- 9%• One Parent + One Sibling- 15%
Cleft Palate:• One Parent- 7%• One Sibling- 2% Two Siblings- 1%• One Parent + One Sibling- 17%
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Genetics
Increased clefts with chromosome aberrations
Clefts a part of a Syndrome 15-60% of time
More than 200 syndromes include clefts
Cleft Palate- Apert’s, Stickler’s, Treacher Cleft Lip +/- Palate- Van der Woude’s, Waardenberg’s
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Epidemiology
Cleft Lip +/- Palate- 2 Male: 1 Female Cleft Palate - 2 Female: 1 Male
(palatine processes fuse one week later in females) Cleft Lip +/- Palate- Native Americans > Oriental and
Caucasians > Blacks Cleft Palate- Same among ethnic groups Environmental: Ethanol, Rubella virus, thalidomide,
aminopterin, smoking Increased Clefts with maternal diabetes mellitus and
amniotic band syndrome Increased Clefts with increased paternal age
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Unilateral Cleft Lip• Forms as a persistent labial groove• Labial groove should disappear as the maxillary prom. fuse with merged medial nasal prominences• Stretching of epithelium causes tissue breakdown and cleft formation www.indiandentalacademy.com
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Nasal floor communicates with oral cavity Maxilla on cleft side is hypoplastic Columella is displaced to normal side Nasal ala on cleft side is laterally, posteriorly, and inferiorly
displacedwww.indiandentalacademy.com
Bilateral Cleft Lip• Similar to unilateral cleft lip• Central soft-tissue mass that moves freely
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Clefting of alveolar process of maxilla as well as lip Complete cleft extends to incisive foramen Complete bilateral anterior cleft isolates the anterior and
posterior parts of the palate Result from failure of lateral palatine processes to fuse to
primary palate
Anterior Cleft Anomalies
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Posterior Cleft Anomalies
Clefts extending through both soft and hard palate to the incisive fossa
Isolates anterior and posterior parts of palate Result from failure of lateral palatine processes to grow
medially and fuse to each other
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Complete Cleft Palate
Complete bilateral cleft of the lip and alveolar process of the maxillae with complete bilateral cleft of the anterior and posterior palate
Complete bilateral cleft of the lip and alveolar process of the maxillae with bilateral cleft of the anterior palate and unilateral cleft of the posterior palate
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Development of tongue
Development begins around the end of fourth week in relation to pharyngeal arches in the floor of mouth.
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Swellings from the first pharyngeal arch
Median tongue bud 2 distal buds (tuberculum impar)
anterior two thirds of epithelium proliferates tongue
Downwards (thyroglossal duct)
To form the thyroid gland.
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Two swellings caudal to foramen cecum
COPULA HYPOBRACHIAL
EMINENCE
Ventromedial parts ventromedial parts
of 2nd arch of 3rd and 4th arch
Overgrown by hypo forms the posterior
Brachialeminence two thirds of the
tongue.
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1st Brachial Arch
2nd Brachial Arch
3rd Brachial Arch
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Copula overgrown by hypopharyngeal eminence
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1st Brachial Arch
2nd Brachial Arch
3rd Brachial Arch
4th Brachial Arch
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Terminal sulcus-line of fusion of the anterior and posterior parts of the tongue.
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Nerve supply of tongue
Anterior two-thirds
lingual branch of chorda tympani
mandibular div of tri- branch of facial.n ( taste
geminal.n (sensory) buds except for vallate
papillae )
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Posterior third
glossopharyngeal.n superior laryngeal
branch of vagus.n
MUSCLES – all muscles of tounge are supplied by hypoglossal nerve except for palatoglossus which is supplied by pharyngeal plexus fibres from the vagus nerve.
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• Aglossia.
In this condition, a portion or all of the tongue
is absent. Rarely is all the tongue absent.
Microglossia
Migrognathia and limb defects (Hanhart’s syndrome)
APPLIED ASPECTS
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Macroglossia
A congenital macroglossia is generally caused by an overdevelopment of the muscular portion of the tongue.
Lymphangiomas may occur alone or (more frequently) in association with hemangiomas The tongue is the most common oral location for this lesion. Together with hemangioma, lymphangioma is an important cause of congenital macroglossia.
Macroglossia may develop after removal of teeth. This develops as a hypertrophy (increase in cell size) when the teeth no longer contain the tongue within the previously established boundaries.
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Ankyloglossia : In this condition, the tongue is restricted in its movements by a
strand of mucosa - lingual frenum that attaches the anterior third of the tongue to the floor of the mouth and the lingual gingival mucosa.
Extends to the tip of tongue interfering with free protrusion
Persons with this condition are commonly called "tongue-tied." Treatment is surgical. www.indiandentalacademy.com
Congenital Lingual Cysts and Fistulas
Remnants of thyroglossal duct
Dysphagia
Fistulas open through foramen caecum
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SKULL
NEUROCRANIUM VISCEROCRANIUM( clavaria & base of skull ) ( skeleton of face and associat
ed structures )
• Membranous
• cartilaginous
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Cartilagenous neurocranium
Development of neurocranium
Neural crest cells
Paraxial mesoderm
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Ossification pattern-• Occipital bone• Body of sphenoid• Ethmoid bone
Other structures-• Vomer bone of nasal septum• Petrous and mastoid part of temporal bone
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Membranous neurocranium
Origin of mesenchyme
Neural crest cells Paraxial
mesoderm
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Membranous neurocranium
Calvaria
• Frontal bone • Parietal bone• Squamous part of temporal bone• Occipital bone
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Role of fontanelle
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VISCEROCRANIUM
CARTILAGINOUS VISCEROCRANIUM
• Middle ear ossicles
• Styloid process
• Hyoid bone
• Laryngeal cartilages
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MEMBRANOUS VISCEROCRANIUM
• Maxilla
• Zygomatic bone
• Squamous temporal
• mandible
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Apert and Crouzon Syndrome’s
1906, Apert described a child with acrocephalosyndactyly
1912, Crouzon described mother & daughter with craniofacial dysostosis
Both are autosomal dominantIncidence is ~ 15 to 16 per 1,000,000 births
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Typical characteristics Craniosynostosis
• Coronal sutures fused at birth• Larger than average head circumference at birth
Midfacial malformation and hypoplasia Shallow orbits with exophthalmos Apert Syndrome: symmetric syndactyly (=fusion of digits)
of hands and feet
Apert and Crouzon
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Apert and Crouzon
syndactyly
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Facial features Shallow orbits with exophthalmos Retruded midface with relative prognathism Beaked nose Hypertelorism Downward slanting palpebral fissures
Apert and Crouzon
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Development of mandible
Intramembranous Meckle’s cartilage – role
• Primitive structural support• Morphogenic template
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MECKLE’S CARTILAGE
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DEVELOPING MANDIBLE MECKEL’S CARTILAGE
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Mandibular nerve – lingual branch• inferior alveolar branch – mental
- incisive
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Primary ossification center
Anterior and posterior extension of growth
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Height of bone is increasing at the same time as antero – posterior growth.
Mental nerve comes to lie in a shallow groove & then a definite notch
Formation of trough composed of lateral and medial plates. Notch containing nerve converted into foramen.
Closure & formation of incisive canal – part of mandibular canal
Neural element
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Developing tooth germs
Formation of alveolar process – upward extension of neural element
Medial and lateral alveolar plates - formation of secondary trough
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Development of ramus Backward extension of neural element behind and above mandibular
foramen
Pre-osteoblast condensation
Coronoid and angular processes added for muscular attachment
Point of divergence is marked by – Lingula www.indiandentalacademy.com
By 10TH week the rudimentary mandible is formed almost entirely by membranous ossification, with little direct involvement of MECKEL’S CARTILAGE
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Secondary cartilages
Condylar cartilage
Coronoid cartilage
Symphyseal cartilage
Distinguish from the primary Meckel's cartilage:- histologic structure
(large haphazardly arranged chondrocytes
& sparse intercellular matrix)
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CONDYLAR CARTILAGE
10 week of IUL –first appears as a fringe Cone shaped structure
14TH week of IUL – By endochondral ossification this mass of cartilage converted quickly to bone.
This cartilage persists until the end of the second decade of life, providing a mechanism for growth of the mandible.
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CORONOID CARTILAGE
About 16th week of IUL
Strip along anterior border and tip of coronoid process
Grows as response to the developing temporalis muscle
Fuses with ramus & disappears before birth
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SYMPHYSEAL CARTILAGE
Two in number 7 month of IUL in the mental region Fuses with mandible during the first year of post-natal life
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Development of nasomaxillary complex
Maxilla – intramembranous
Maxilla develops from the centre of ossification in the mesenchyme of the maxillary process of the first arch
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No arch cartilage or PRIMARY CARTILAGE , but centre of ossification is associated closely with the cartilage of the nasal capsule.
Centre of ossification-at division of infraorbital into anterosuperior dental nerve.
spread of ossification – Upwards – frontalDownwards – lateral alveolar plateInward – palatal processBackward – zygomatic processForwards – pre-maxillary region
Medial alveolar plate along with Lateral alveolar plate trough around maxillary tooth germ
MAXILLA
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SECONDARY CARTILAGE
Zygomatic or malar cartilage appears in the developing zygomatic process and for a short time adds considerably to development of maxilla.
Body of maxilla is relatively small because the maxillary sinus is not developed.
Formation of sinus takes place in 16th week as a shallow groove on the nasal aspect of the developing maxilla.
At birth sinus is still the rudimentary structure about the size of a small pea.
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COMMON FEATURE OF DEVELOPMENT OF JAWS
Both maxilla and mandible start developing from centres of ossification in close relation to bifurcation of corresponding nerves
They form from 2 facial swellings which have the same origin
Each has a relation to a primary cartilaginous skeleton
Both form a neural element & alveolar element.
Finally, both develop SECONDARY CARTILAGE to assist in their growth.
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CLINICAL
CONSIDERATIONS
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Down Syndrome (Trisomy 21)
1866, described by John Landon Down
Most common
Prevalence 1 in 700 births Maternal age >35 carries
increased risk
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Etiology: non-disjunction mutation resulting in Trisomy 21
Non-disjunction-error in cell division; Failure of chromatids of a chromosome to disjoin during
meiosis
Down Syndrome
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Trisomy=3 chromosomes present instead of the usual pair; associated with 3 main syndromes
Trisomy 21 – Down syndrome Trisomy 18 – Edwards syndrome Trisomy 13 – Patau syndrome
Infants with trisomy 18 &13 are severely malformed and mentally retarded and usually die early in infancy
Down Syndrome
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• Growth retardation
• Mental retardation
• Clinodactyly of 5th digit (=incurving)
• Simian crease(=single transverse palmar crease)
• Congenital heart defects
Characteristic features:
Down Syndrome
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Facial Characteristics Broad face Midface hypoplasia Flat occiput Flat nasal bridge Epicanthal folds Up-slanting palpebral fissures Progressive enlargement of lips Small ears
Down Syndrome
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