Prenatal growth & development /diploma orthodontic course by indian dental academy /certified...

PRE-NATAL GROWTH

&DEVELOPMENT

INDIAN DENTAL ACADEMY

Leader in continuing dental education www.indiandentalacademy.com

www.indiandentalacademy.com

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

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

He who sees things grow from the beginning will have the finest view of

them……..

-ARISTOTLE

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

Zygote-contains chromosomes and genes that are derived from both mother and father.

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).

Day 1-3

Cleavage

blastomeres

morula

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

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).

Implantation

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

Isolated cavities called lacunae appear in syncytiotrophoblast

Adjacent lacunae fuse to form lacunar networks

Capillaries around embryo become dilated to form - sinusoids

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

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.

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”.

So now there are 2 cavities:1. “AMNIOTIC CAVITY” (above)2. “PRIMARY YOLK-SAC” (below - later forms secondary yolk

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

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

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.

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

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

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

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

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

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.

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 .

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.

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

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"

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

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

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

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

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.

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

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.

prochordal plate

Notochordal canal

cloacal membrane

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.

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

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

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.

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

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.

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.

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

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.

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

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...

Paraxial mesoderm.

Lateral plate mesoderm.

Neural crest cells .

Ectodermal placodes

Mesenchyme for formation of head region is derived from:

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.

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.

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

Each arch is characterized by its own Cartilaginous rod that forms the skeleton of the arch muscular component nerve component and arterial component.

DERIVATIVES OF PHARYNGEAL Apparatus

SKELETAL DERIVATIVES

MUSCLE DERIVATIVES

NERVE SUPPLY

ARTERIAL SUPPLY

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

MAXILLARY PROCESS: mesenchyme of the maxillary

process gives rise to premaxilla, maxilla, zygomatic bone and part of temporal bone

through membranous

ossification.

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

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

MUSCULATURE:

Temporalis Masseter Pterygoids Anterior belly of digastric Mylohyoid Tensor tympani Tensor palatini.

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.

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

It gives rise to, Stapes Styloid process of

temporal bone Stylohyoid ligament Lesser horn and

upper part of body of hyoid bone.

MUSCLES: Stepedius. Posterior belly of

digastric. Auricular. Muscles of facial

expression

NERVE: Facial nerve supplies

all these muscles.

CARTILAGE of 3rd pharyngeal arch produces,

Lower part of body of hyoid bone.

Greater horn of hyoid bone.

THIRD PHARYNGEAL ARCH

MUSCLE: Stylopharyngeus

muscle.

NERVE: Glossopharyngeal

nerve.

THIRD PHARYNGEAL ARCH

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

MUSCLES:4th arch: cricothyroid, levator palatini, constrictors of pharynx ,

6th arch: intrinsic muscles of

larynx.

NERVE: 4TH arch: Superior laryngeal branch of vagus nerve. 6th arch: Recurrent laryngeal branch of vagus nerve.

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

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

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.

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.

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

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.

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

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

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

Derivatives PHARYNGEAL POUCHES

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

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

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

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

• Ruptures at 26 days

• Communication of primordial cavity and foregut with amniotic cavity

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.

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

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

May develop anywhere along the anterior border of SCM muscle

Slowly enlarging painless swelling in the neck.

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

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)

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.

“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

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.

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

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:

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

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:

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

Development of

2 organizing centers- Forebrain (prosencephalic) centre

Hindbrain (rhombencephalic) centre

5 facial primordia Neural crest: source for almost all connective tissues in the face

DEVELOPMENT OF FACE

Boundaries of stomodeum.

Paired maxillary prominences- lateral boundary

Paired mandibular prominences- caudal boundary

Nasal part of FNP- rostral boundary

Facial prominences-active centers of growth – 4th to 8th week Connective tissue continuous from one prominence to another.

DEVELOPMENT OF FACE

Lower jaw and lower lip are the first parts of the face to form.

Nasal placodes & nasal pits- by the end of fourth week Primodia of the nose and and nasal cavities.

DEVELOPMENT OF FACE

Nasal prominences , nasal pits

Maxillary prominences grow- pushing nasal prominences medially

Nasolacrimal groove

• Auricular hillocks- seen by the end of fifth week.

• Neck region

• Primordia for external acoustic meatus and auricle.

• By the end of sixth week

• Maxillary prominence merges with lateral nasal prominence

• Continuity between side of nose and cheek region

• Nasolacrimal ductNLG

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.

Medial nasal prominences merge with each other and with fused lateral nasal & maxillary prominences

Intermaxillary segment

Intermaxillary segment gives rise to

Philtrum of the upper lip. Premaxillary part of the maxilla and its

associated gingiva. The primary palate.

MNPLNP

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

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

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.

DEVELOPMENT OF SECONDARY PALATE

Sixth week

Secondary palate develops from two mesenchymal projections that extend from internal aspects of the maxillary prominences. ( lateral palatine processes )

project inferomedially.

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.

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.

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.

Nasal septum

Bone development

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)

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

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%

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%

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

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

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

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

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

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

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

Development of tongue

Development begins around the end of fourth week in relation to pharyngeal arches in the floor of mouth.

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.

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.

1st Brachial Arch

2nd Brachial Arch

3rd Brachial Arch

Copula overgrown by hypopharyngeal eminence

1st Brachial Arch

2nd Brachial Arch

3rd Brachial Arch

4th Brachial Arch

Terminal sulcus-line of fusion of the anterior and posterior parts of the tongue.

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 )

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.

• 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

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.

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

NEUROCRANIUM VISCEROCRANIUM( clavaria & base of skull ) ( skeleton of face and associat

ed structures )

• Membranous

• cartilaginous

Cartilagenous neurocranium

Development of neurocranium

Neural crest cells

Paraxial mesoderm

Ossification pattern-• Occipital bone• Body of sphenoid• Ethmoid bone

Other structures-• Vomer bone of nasal septum• Petrous and mastoid part of temporal bone

Membranous neurocranium

Origin of mesenchyme

Neural crest cells Paraxial

mesoderm

Membranous neurocranium

Calvaria

• Frontal bone • Parietal bone• Squamous part of temporal bone• Occipital bone

Role of fontanelle

VISCEROCRANIUM

CARTILAGINOUS VISCEROCRANIUM

• Middle ear ossicles

• Styloid process

• Hyoid bone

• Laryngeal cartilages

MEMBRANOUS VISCEROCRANIUM

• Maxilla

• Zygomatic bone

• Squamous temporal

• mandible

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

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

syndactyly

Facial features Shallow orbits with exophthalmos Retruded midface with relative prognathism Beaked nose Hypertelorism Downward slanting palpebral fissures

Apert and Crouzon

Development of mandible

Intramembranous Meckle’s cartilage – role

• Primitive structural support• Morphogenic template

MECKLE’S CARTILAGE

DEVELOPING MANDIBLE MECKEL’S CARTILAGE

Mandibular nerve – lingual branch• inferior alveolar branch – mental

- incisive

Primary ossification center

Anterior and posterior extension of growth

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

Developing tooth germs

Formation of alveolar process – upward extension of neural element

Medial and lateral alveolar plates - formation of secondary trough

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

Secondary cartilages

Condylar cartilage

Coronoid cartilage

Symphyseal cartilage

Distinguish from the primary Meckel's cartilage:- histologic structure

(large haphazardly arranged chondrocytes

& sparse intercellular matrix)

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.

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

SYMPHYSEAL CARTILAGE

Two in number 7 month of IUL in the mental region Fuses with mandible during the first year of post-natal life

Development of nasomaxillary complex

Maxilla – intramembranous

Maxilla develops from the centre of ossification in the mesenchyme of the maxillary process of the first arch

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

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.

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.

CLINICAL

CONSIDERATIONS

Down Syndrome (Trisomy 21)

1866, described by John Landon Down

Most common

Prevalence 1 in 700 births Maternal age >35 carries

increased risk

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

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

• Growth retardation

• Mental retardation

• Clinodactyly of 5th digit (=incurving)

• Simian crease(=single transverse palmar crease)

• Congenital heart defects

Characteristic features:

Down Syndrome

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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