Develpoment of palate/ dental crown & bridge courses

INDIAN DENTAL ACADEMY
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Education
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Introduction
 According to Todd – development is progress towards
maturity.
 According to Moyer – development refers to all the naturally
occurring unidirectional changes in the life of an individual
from its existence as a single cell to its elaboration as a
multifunctional unit terminating in death.

Fertilization
 Development begins with fertilization
 Fertilization – is a process by which the male
gamete the sperm, and the female gamete oocyte
unite to form zygote.

 Gametes are located in the sex organs - Gonads
 Male gonad – testis
 Female gonad – ovary
 Spermatogenesis – formation of sperm in the testis
 Oogenesis – formation of oocyte in the ovary
 Gametogenesis – formation of sperm & oocyte

Chromosomes
 Human cell contain – 46 ch
– diploid
 Autosomes – 44
 Sex chromosomes or
allsomes – 2 [x or y ]
 In man - 44 + xy
 In women – 44 + xx
 Gametes contain – 23 ch -
haploid

 Fusion of 2 cells with 46 ch is not possible
 If happens new cell will have 92 ch
 Thus requires a cell with 23 ch [gametes], so that on
fertilization cell with 46 ch will be reestablished
 Process of formation of gametes is called - meiosis

Gametogenesis

Prenatal life
 Can be divided into
 I phase – comprises about 4 weeks, involves cellular
proliferation, migration & some differentiation
 II phase – next 4 weeks, characterized by differentiation
 III phase – end of 2nd phase to the term, maturation &
growth occurs
 I & II phase collectively called embryo
 III phase is called fetus

Folding of embryo

Effect of folds on positions of
other structures

Pharyngeal arches

Structure – Seen in pharengeal
arch

Development of palate :
molecular basis
 Signalling of palatal epithelial mesenchyme interactions is
probably involves both extracellular matrix and soluble
factors.
 E. g: EGF , TGF alpha and beta, etc
 Cyclic AMP just increases prior to shelf fusion.
 Palatal cells contains more glucocorticoids receptors at this
stage of embryogenesis than the liver, brain or limbs.

 Three elements that make up the palate:-
a) the two lateral maxillary shelves
b) the primary palate of the frontonasal prominence
 Initially they are widely separated.
 Due to the vertical orientation of the lateral shelves on either
side of the tongue.

 Palatal development begins in week 5, but weeks 6-9 are
most critical.
 Formation of intermaxillary segment from merged medial
nasal prominences.
 Primary palate forms from median palatine process ossifies
as the premaxillary portion of the maxilla.

 During 8th week I.U.L a remarkable transformation in position
of the lateral shelves takes place.
 They alter from vertical to horizontal as a prelude to their
fusion and partitioning the oronasal chamber.
 The transition is completed within hours.

Mechanisms proposed for this rapid
elevation of the palatal shelves-
1) Variations in vasculature and blood flow these to these
structures.
2) Biochemical transformations in physical consistency of the
connective tissue matrix of the shelves
3) Sudden increase in their tissue turgor
4) Rapid differential mitotic growth
5) An intrinsic shelf force
6) Muscular movements
7) Withdrawal of the embryo’s face against the heart
prominence by uprighting of the head, facilitates jaw opening.
8) Mouth opening reflexes have been implicated in the
withdrawal of the tongue from between the vertical shelves.
9) Pressure differences between the nasal and oral regions due
to tongue muscle contraction.

 During palate closure, the mandible becomes more
prognathic.
 The vertical dimension of the stomodeal chamber increases.
 Maxillary width remain stable, allowing shelf contact to occur.
 Forward growth of Meckel’s cartilage relocates the tongue
more anteriorly, simultaneously with upper facial elevation.
 The epithelium overlying the edge of the palatal shelves is
thickened.
 Their fusion is crucial to intact palatal development.
 Fusion also occurs between the dorsal surfaces of the fusing
palatal shelves and the lower edge of the midline nasal

 The fusion seam initially form anteriorly in the hard palate
region, with subsequent merging of the soft palate region.
 A combination of degenerating epithelial cells and a surface
coat accumulation of glycoprotein facilitates epithelial
adherence between contacting palatal shelves.
 The medial edge epithelium of the palatal shelves undergoes
cytodifferentiation involving a decline of epidermal growth
factor receptor that lead to cell death.
 Programmed cell death of the fusing epithelia is essential to
mesenchymal coalescence of the shelves.

 Fusion of the three palatal components initially produces a
flat, arched roof to the mouth.
 The fusing lateral palatal shelves overlap the anterior primary
palate.
 The sloping pathways of the functional incisive neurovascular
canals that carry the previously formed incisive nerve and
blood vessels.
 The site of junction of the three palatal components is marked
by the incisive papilla overlying the incisive canal.

 The line of fusion of the lateral palatal shelves is traced by the
midpalatine suture.
 And on the surface by the midline raphe of the hard palate.
 This fusion seam is minimized in the soft palate by invasion of
extraterritorial mesenchyme.

OSSIFICATION
 Ossification of the palate proceeds during 8th week I.U.L
 From the spread of bone into the mesenchyme of the fused
lateral palatal shelves and from trabeculae appearing in the
primary palate as ‘premaxillary centers'.
 All derived from the single primary ossification centers of the
maxilla.
 Posteriorly, the hard palate is ossified by trabeculae
spreading from the single primary ossification centers of each
of the palatine bones.

 Midpalatal sutural structure is first evident at 10 and half
weeks, when an upper layer of fiber bundles develops across
the midline.
 In infancy, the midpalatal suture is coronal section has a y
shape and it binds the vomer with palatal shelves.
 In childhood, the junction between the three bones rises into
a t shape, with the interpalatal section taking a serpentine
course.
 In adolescence, the suture becomes so interdigitated thatwww.inidiandentalacademy.com

 The palatine bone elements of the palate remain separated
from maxillary elements by transverse palatomaxillary sutures
into adulthood.
 Ossification does not occur in the most posterior part of
palate , giving rise to the region of the soft palate.

• Development of muscles
 Myogenic mesenchymal tissue of the 1st , 2nd and 4th
branchial arches migrate into this faucial region, supplying the
musculature of the soft palate and fauces.
 The tensor veli palatini is derived from 1st arch, the levator
palatini and uvular from 2nd arch, and faucillar pillar muscles
from the 4th arch.

 The tensor veli palatini is the earliest of the five palatal
muscle to develop, forming myoblast at 40 days.
 It is followed by palatopharyngeus (45days), levator veli
palatini (8th week), palatoglossus (9th week) and the uvular
muscle at the 11th week.
 The hard palate grows in legnth, breadth and height,
becoming an arched roof for the mouth.

 The fetal palate increases in length more rapidly than in width
between 7 and 18 weeks i.u.l
 After which the width inceases faster than the length.
 In early prenatal life the palate is relatively long, but from the
4th month i.u.l. it widens as a result of midpalatal sutural
growth and appositional growth along the lateral alveolar
margins.

 At birth, the length and breadth of palate are almost equal.
 The post natal increase in palate length is due to appositional
growth in maxillary tuberosity region and to some extent, at
the
transverse maxillopalatine suture.

 Growth at midpalatine suture ceases between 1 and 2 years
of age,
but no synostosis occurs to signify its cessation.
 Growth in width of midpalatal suture is larger in its posterior
region than anterior so that the posterior part of nasal cavity
widens more than its anterior part.
 Obliteration of the midpalatal suture may starts in
adolescence ,
but complete fusion is rarely found before 30 years of age.

 Lateral appositional growth continues until 7years of age, by
which time the palate achieves its ultimate anterior width.
 Posterior appositional growth continues after lateral growth
has ceased. So that the palate become longer than wider
during late childhood.
 During infancy and childhood, bone apposition also occurs on
the entire inferior surface of the palate, accompanied by
resorption from its superior surface.
 This remodeling results in descent of the palate and
enlargement of nasal cavity.

 The appositional growth of the alveolar processes contribute
to
deepening as well as widening of the vault of the bony palate,
at the
same time adding height and breadth to maxilla.
 The lateral alveolar processes help to form an anterio-
posterior
palatal furrow , which together with a concave floor produced
by
tongue curls from side to side results in a palatal tunnel
ideally www.inidiandentalacademy.com

 A variable number of transverse palatal rugae develop in the
mucosa covering the hard palate.
 They appear even before palatal fusion, which occurs at 56th
day i.u.
 The rugae are prominent in the infant.
 The anterior palatal furrow is well marked during the 1st year
of life and normally flattens out into the palatal arch after 3-4
years of age.

Clinical considerations
 Clefts are the most common congenital malformations.
 Cleft is a congenital abnormal space or gap.
 Facial cleft is 2nd most common congenital deformity after
club foot.
 Male : female 2:1
 Isolated cleft palate > female
 Cleft lip and palate > males

 X-linked cleft palate has been mapped to the Xq 13 – Xq 21
regions of human x chromosome.

 Delay in the elevation of palatal shelves from the vertical to
horizontal while the head is growing continuously results in a
widening gap between the shelves so that they cannot meet,
and
therefore cannot fuse.
 When eventually they do become horizontal, this leads to
clefting
of the palate.

 The entrapment of epithelial rests or pearls in the line of
fusion particularly the midline raphae of the hard palate,may
give rise to median palatal rest cysts.
 A common superficial expression of these epithelial
entrapment is development of epithelial cysts or nodules
known as Epstein’s pearls.
 Small mucosal gland retention cyst (Bohn’s nodule) may
occur on the buccal and lingual aspects of the alveolar ridges,
and dental lamina cyst composed of epithelial remnants of
this lamina may develop on the crest of alveolar ridges.
 All these superficial cysts of the palate of new born usually
disappears by 3rd postnatal month.

 An anterior midline maxillary cyst developing in the region of
the primary palate cannot be of fissural origin, but a
nasopalatine duct cyst enchroaching anteriorly into the
palate.
 Cysts are rare in the soft palate because of the mesenchymal
merging of the shelves in this region, although submucousal
clefts may occur.

 A common genetically anomaly of the palate is a localised
midpalatal overgrowth of bone, of varying size, known as
torus
palatinus.
 This may enlarge in adulthood

Bohn’s Nodules
Torus palatinus

References :
 Human Embryology, 7th edition, Inderbir Singh
 Langman’s Medical Embryology, 11th editio, T.W.Sadler
 B.D.Chaurasia Human anatomy, head and neck, part III
 Palate development : mechanism and malformation:
M.W.J.Ferguson
 Handbook of Craniofacial development, Sperber

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