Development of Maxilla1 / orthodontic courses by Indian dental academy
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Transcript of Development of Maxilla1 / orthodontic courses by Indian dental academy
Development of Maxilla
Prenatal:
It can be studied under following headings:
- Maxilla proper.
- Premaxilla.
- Palatine bones.
Maxilla proper: It develops from maxillary prominence out ending
cranioventrally from much large mandibular prominence derived
from first arch, maxillary process of mandibular arch. Like the
mandible it first appears as a membranous ossification but unlike
mandible, its further development and growth are little affected by
appearance of secondary cartilage.
First ossification center around of weeks IVL ossification in
maxilla commences little later than in mandible. The center of
ossification first appears in a bond of fibrocellular tissue which lies
on the outer side of cartilage of nasal capsule immediately lateral
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and slightly below infraorbital nerve where it gives of its anterior
superior alveolar nerve. It lies above the part of dental lamina from
which enamel organ of canine tooth gum areas.
Ossification spreads backwards towards the developing zygomatic
bone below the orbit and forward in front of anterior superior
alveolar nerve below the terminal part of infra orbital nerve,
towards developing premaxilla. At this stage bone takes the shape
of curved strip vertically with convex side medially.
From the anterior extraction, frontal process develops which with a
corresponding process of premaxilla forms frontal process of adult
bone. These processes of maxilla and premaxilla unite so rapidly
that no suture appears between them from the beginning.
The developing maxilla forms a bony trough for I.O. nerve. It
forms outer alveolar plate by the downward growth in relation to
canine-deciduous molar tooth germs.
Maxilla continues to grow mainly upward and downward, backward
and with the development palatal process also spreads in midline.
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A secondary cartilage appears in the zygomatic process and its
proliferation considerable adds to back of maxilla. During this
period palatine process with grow backward and a large mass of
bone of maxilla is formed. From this region lingual alveolar palate
develops some what later than buccal plate. The trough of bone
formed will be later divided by septa into alveoli small areas of
secondary cartilage may be formed in midline of developing hard
palate.
Secondary ossification centers are:
1. Zygomatic.
2. Orbitonasal.
3. Nasopalatine.
4. Intermaxillary.
The two intermaxillary ossification centers generate alveolar ridge
and primary palate region which is demarcated by a fissure between
LI and canine teeth.
Comparison between maxillary and mandibular development
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This bone disappear as a separate entity by fusion of the fissures
during first post nasal. Both commence as centers of ossification in
close life relations to a nerve at a place of bifurcation and close
relation to elements of cartilaginous facial skeleton. Both have
neural and alveolar elements. Both develop secondary cartilage in
their backward extraction. However, condylar cartilage remains
active for a long perio and zygomatic is limited to period of faetal
life.
Maxilla has no muscular process and mandible has no palatine
process.
Growth of maxilla is surface deposition and sutural.
Growth of mandible is surface deposition and replacement by
cartilage.
Development of Premaxilla:
By two ossification center (first 7 weeks and above incisive form,
2nd 10 weeks and ventral margin of nasal septum. Premaxilla is
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formed by frontonasal process and limited with the junction of
maxillary process.
At seven weeks of age a separate center of ossification appears for
premaxilla and it retains the identity for a very short period of time
and during 8 th week union takes place with maxillary ossification.
Thus a single mass of bone called maxillary corpus is formed at the
each side of face and later frontal process will arise which units
with frontal process of maxilla. A heavy trabecularized network of
bone appears on labial aspect of canine alveolar which spreads and
fuses with underlying frontal process. The alveolar processes arise
which surround the developing incisor tooth germ.
On the facial aspect, union between maxilla and premaxilla
disappears before birth but seen on palatal aspect after birth.
Development of Palatine bone:
It develops as a fibrocellular condensation on medial side of
cartilaginous nasal capsule. Ossification starts at 7-8 weeks IUL in
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the region of tuberosity in close relation to descending palatine
nerve. Ossification extrudes upwards and horizontally.
At first, the vertical plate of palatine bone is separated from
maxilla by lateral wall of nasal capsule.
Development of Maxilla
Prenatal:
By 8 th week of IUL, ossification centers which become maxillary
and mandibular skeleton become apparent in the lateral face.
Bilateral frontal bones cover the forebrain above the eyes. Small
nasal bones appear anterior to the nasal capsule. The premaxillary
ossification centers may appear as separate or united sites on
anterior surface of nasal capsule. The zygomatic bone and temporal
bone appear posterior to maxillary bone.
By 12 weeks, premaxillary and maxillary bones have increased in
size. During 10 th weeks, a ‘V’ shaped bone arises just below the
nasal septum of ethamoid and is called Vomer and its two diverging
parts grow up on either side of septum. The increase in height of
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the face occurs with addition to the size of ethamoid and the vomer
bone. The sphenoid is located just behind the ethmoid along the
base of skull.
During the faetal period, bone is deposted on the entire external
surface of maxilla and resorption occurs in each alveolus
surrounding the tooth buds and on the lingual surface of alveolar
ridges. Maxillary arch length increases by both anterior and
posterior growth. The orbit floor displaces throughout life
(prenatal) inferiorly bone resorbs on the nasal side of the palate and
forms on oral surface.
In the anterior palate, premaxilla has lingual and plates of bone
around incisor teeth. a suture septum the right and left sides. A
posterior suture septal, the premaxillary form from the maxillary
bones. At this stage the palate is relatively small compared with
cranial skeletal. Later, the palate becomes much larger.
By 8 th month of IUL, the bony configuration of palate is well
established and the sutures are still evident. Additional growth of
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the palate occurs around periphery which assures that growth of the
palate will keep pace with the growth of face.
Post natal
a) Sutures
Growth of the maxilla depends upon the influence of several
functional matrices that act upon different areas of bone. Thus
theoretically can be divided into:
The basal body develops beneath the infraorbital nerve, later
surrounding it to form infraorbital canal. The orbital unit responds
to growth of eye ball. Nasal unit responds to septal cartilage for its
growth and the teeth provide functional matrix for the alveolar unit.
The pneumatic unit reflects maxillary sinus expansion, which is
more a responder than a determiner of the skeletal unit.
The complexity of action of these function at forces on the facial
bones results in different effects on different sutures.
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Superozygomatic suture predominantly A-P direction. In order to
keep pace with growth of brain and spheno-occipital synchondrosal
cartilage.
Nasomaxillary suture A-P direction (predominantly) and creates
elevation of bridge of nose.
Frontomaxillary
Fronto zygomatic
Frontonasal Predominately vertically
Fronto ethmoidal
Ethmoido maxillary
Facial width is relatively less on preparation to neurocranium in
neonate than adult. The face of new born is twice as broad in
comparison with its height than in adult.
Growth at all these sutures is greatest until age of 4 years and
completes by the end of first decade and of more spurt during
puberty. Thereafter these sutures mainly act as sites of fibrous
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union allowing for adjustments brought about by surface deposition
and remodeling.
Surface remodeling
Remodelling takes place over all the surfaces of maxilla. Growth of
alveolar process will add to the vertical height of face and depth of
palate. Bone deposition on the posterior surface of maxillary
tuberosity induces corresponding anterior displacement of entire
maxilla. The growth pattern of dento-alveolar arch differs from
other surfaces. It is related to the sequence of tooth eruption.
Resorption along the anterior surface of body of maxilla creates
supra-alveolar concavity (point A).
The final form of maxillary complex is balanced by bone deposition
and resorption. It differs between individuals and same individual
at different periods.
Deposition is most active at the alveolar process, undersurface of
hard palate. Both resorption occurs in interior of the maxilla
(increasing size of sinuses), upper surface of hard palate. The
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overall effects is to increase the vertical component of facial
growth and reduce the forward component giving a characteristic
fracture of modern human face as compared with that of anthropoid
apes and early human races.
Surface deposition and resorption are more predominate during 2 nd
decade of life, predominately in vertical direction.
Development of Palate:
The palate develops from the elements:
- Primary palate portion of the frontonasal process.
- Two lateral maxillary processes.
and palate is formed from one medial and two lateral palatine
process.
The term palate refers to the tissues that interposes between oral
and nasal cavity. The median palatal process is also called as
primary palate which begins at 6 th week of IUL. It develops as a
wedge shaped mass between the maxillary process of the
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developing upper jaw. From this primary palate the developing four
maxillary teeth are supported.
At the end of 6 th week, the lateral palatine process which form
secondary palate develop from the medial edges of maxillary
processes. The lateral palatine process grow medially first, then
grow downward or vertically on either side of tongue.
Shelf elevation:
At about 8 ½ week of IUL, the lateral palatine shelves roll over the
body of tongue. The process of elevation occurs when the shelves
have developed sufficient strength to slide over tongue. It results
from combined action of shelf and tongue movement. Palates shelf
elevation begins in this posterior region and depresses the tongue
downward and forward, which releases the out part of shelves. Thus
the tongue utilizes lateral space occupied and broadens.
Palatal shelf closure:
After the shelves are in a horizontal position there is a final growth
spurt, and shelf contact occurs in midline.
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Closure fusion of LPP occurs first just posterior to median palatine
process. It is a process of contact with loss of intervening
epithelium and growth of connective tissue across the midline.
After this initial contact, there is fusion of LPP with MPP
anteriorly.
Posteriorly, closure takes place gradually over the next several
weeks and involves merging of the two LPP by cell proliferation at
the depth of midline grade behind the initial fusion. Fusion of LPP
also occurs with nasal septum except post where soft palate and
ovula remain unattached .
At about 12 week of IUL, palate is invaded anterior by bone from
premaxillary, maxillary and palatal centers to form hard palate and
post by muscle to form soft palate.
Premaxillary ossification center ( primary) 8 week of IUL
( Secondary)
Maxillary ossification center (single and appears at 6 week of IUL)
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Palato maxillary suture
Palatine ossification 8 th week ossification starts.
The fusion of three palatal components initially induced a flat,
unarched roof of mouth. The line of fusion of lateral, palatal
shelves is traced in adult the midpalatal suture. The mid palatal
suture strength is first widest at 10 ½ weeks. In adults it becomes
so interdigitated that mechanical interlocking and islets of bone are
formed (after 30 years). In adulthood palatine bone elements of the
palate remain separated from maxillary elements by transverse
palato-maxillary sutures.
The ossification does not occur in most posterior part of palate
giving rise to region of soft palate.
At birth, length and breadth of hard palate are almost equal. The
postural increase in palatal length is due to appositional growth at
tuberosity and to some extent at transverse maxillopalatine suture.
Growth at midpalatine suture ceases between 1 and 2 years of age.
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Lateral appositional growth continues till 7 years by which time
palate achieves its ultimate anterior width. Posterior appositional
growth continues after lateral growth has ceased so that palate
becomes longer than wider during late childhood.
The rougae which are most prominent in infant hold the nipple. The
anterior palatal furrow is more marked during 1 st year and life
(active suckling period). This normally flattens by 3-4 years once
the suckling is stopped. If complicated of thumb sucking, it may
remain in childhood.
Greater palatine foramen is situated between 2 nd and 3rd maxillary
molar about 1cm from the palatal gingival margin towards midline.
In child with only primary dentition erupted, the injection should
be made approximately 10mm posterior to the distal surface of the
second primary molar. It is not necessary to outer greater palatine
foramen. A few drops of solution can be injected slowly at the
point where the nerve is emerging from the foramen. The distal line
from the most posterior erupted teeth.
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- Deficiencies of maxillary prominence and brachial arch
ectomesenchyme may result in facial bones.
- Deficient maxillary development may also be associated with
clefts of upper lip and palate, downs syndrome.
- Entrapment of epithelial rest cells in the live of fusion of the
palatal shelves, may give rise to palatal rest cyst. The
common forms are Eptin pearls along the medial raphe of
hard palate and junction of hard and soft palate. Bohns
modules are mucosal found retention cysts occurring on
buccal and lingual aspect of alveolar ridges.
- Torus palatinus is a common genetic commonly of palate
with localized midpalatal over growth. It may enlarge in
adulthood and interfere with appliances.
- Delay in elevation of palatal shelves leads to clefting of the
palate.
- Inadequate use of the nasal cavity by mouth breathing has
been associated with the narrow pinched fall and high-
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vaulted palatal arch of adenoid facies. The erupt space of
nasal cavity may influence facial growth and form the cause
and effect relationship of this facial form with mouth
breathing has not been substantiated.
- Shapes of palate (u, v, high roofed).
- Cleft palate is a result associated with habits of non-fusion.
- R & L valves of embryonic palate. It may be of different
degrees. In the least severe type, the defect is confined to
soft palate and in severe cases it is continuous with cleft of
lip.
- Epigraphers is a teratome arising specifically from the palate.
- Absence of neural crest ectomesenchyme in frontonasal
prominence may result in cleft lips.
- Hemifacial microsomin produces asymmetric face on affected
side ear, zygomatic bone and mandible will be
underdeveloped.
- Supernumerary the pattern of bone remodeling.
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- It the palate thickness same all over?
- It narrows posteriorly.
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Development of Mandible
Introduction:
Human mandible does not have a single design for life. Rather it
adapts and remodels through different stages of life. It is rather a
exceptional bone in that it is largely derived from membrane bone,
yet main site of growth is at cartilage.
History:
Hunter (1961) proposed that mandible grows by apposition in on its
posterior border with resorption on anterior border. Humphry
(1966) supported the Hunter’s theory. He tied the wire around the
growing mandible of pig and found that wire was embedded in
posterior portion of mandible after portion of mandible after
growth.
Alizarin study by Weinman in 1944 suggested that condyle was
potential of growing in superior and posterior direction. Rickett’s
in 1950 supported this.
Prenatal:
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At about 6 week of IUL, as the nasal capsule becomes the
prominent cartilage in the upper face, Meekel’s cartilage bars
become apparent in mandibular arches (1 st pharyngeal arch).
The posterior part of each of these bars enlarge to become the
(dorsal) malleus, which articulates with a second small cartilage,
the incus. These two cartilages become enclosed in otic capsule.
They form a joint called primary TMJ articulation of these two
cartilages occurs until they undergo endochondral bone formation
during 18 week IUL. At this time secondary TMJ formed anterior to
middle ear and begins functioning. The shift of primary to
secondary occurs as Meekle’s cartilage is fused to mandible.
The mandible is formed in the lower or deeper part of 1 st arch. It is
preceded by Mekels cartilage. Mekels cartilage attains its full form
of 5mm by 6 weeks and then stretches downwards and forwards as
an unbroken rod of cartilage. In midline the ventral line turns
upward in contact with cartilage of opposite side. It is surrounded
in its whole length by a thick investment of fibrocellular tissue.
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Except for the dorsal part, the remaining part is associated with the
development of mandible.
The mandibular nerve: The main nerve issues from the skull medial
and ventral to dorsal end of cartilage and comes into direct relation
with it about the junction of its dorsal and midline 1/3rds. Here it
gives lingual and inferior alveolar nerve. The lingual nerve passes
medial to the cartilage and inferior A-N on lateral aspect. Running
forward terminates by dividing into ----- and incisive branches.
Body of the mandible:
Figure
The body of the mandible continues to develop as a rectangular
membrane bone. The ossification center appears at 7 week of IUL I
the angle by mental and incisive nerve. This is the area of future
mental foramen. From this center, the formation of bone spreads
rapidly backward below the mental nerve, which then lies in on
notch in bone and on the lateral side of inferior alveolar nerve. The
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bone in front of the region of the notch for mental nerve grows
medially below the incisive nerve and spreads upwards between
this nerve and Meckels cartilage, thus the incisive nerve contained
in a trough of bone. The notch containing the mental nerve is
converted into mental foramen. The bony trough grows rapidly
forward towards the midline where it comes in close relationship
with similar bone formation of opposite side but its separated from
connective tissue union takes place before the end of first year
postnatally. A similar spread of ossification (between 4-12months)
takes place in backward direction. Thus by these process, original
primary center of ossification produces the body proper of
mandible form mandibular foramen to symphises.
Fate of Meckels cartilage:
With the exception of at midline, the anterior part of mandible,
from in front of mental foramen included cartilage in its substance.
This part of cartilage first surrounded by on extension of bone from
the medial plate and then gradually resorbed and replaced by an
extension of ossification from membrane bone around it. The rest
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of Meckels cartilage disappears completely except for a part of its
fibrous covering which persists as sphenomandibular and spheno-
alveolar ligament.
The ramus:
The backward extension of mandible to form the ramus is produced
by a spread of ossification from the body, behind and above
mandibular foramen. As in body, here too the ramus and its
processes are first mapped out by extension of this condensation.
The formation of bone occurs rapidly so that the coronoid and
condylar processes are ossified to a greater extent. The further
growth of these processes is modified by secondary cartilages.
Alveolar bone:
As the enamel organ of deciduous tooth germs reach the early bell
stage, the bone of the mandible begins to come into close
relationship to them. This is brought about by the upward growth,
on each side, of the lateral and medial plates of mandibular bone
above the level where the roof of the canal for the incisive and
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inferior alveolar nerve is formed. By this growth, the developing
teeth come to lie in a trough of bone. This trough is later divided
into small alveoli for the teeth by the formation of septa between
two walls.
Secondary cartilage:
These occur at various sites in the region of membrane bone
formation, also called as accessory cartilage. They have no
connection with primary cartilage. The primary cartilage is hyaline.
These cartilages have less intercellular matrix than hyaline. These
cartilages increase in size by proliferation and transformation of the
cells of thick layer of fibrous cellular tissue covering them.
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Condylar cartilage:
There are three sites of secondary cartilage formation appears
between 10-14 th weeks of IUL. The largest and first one is condylar
cartilage. It appears on superior and lateral aspects of condylar
process. The cartilage forms a cone-shaped mass which not only
occupied the whole of condylar process but reaches forward and
downward into ramus upto level of mandibular foramen. Cartilage
in anterior part shows ossification and its continues till 5 month
IUL where only cartilage is left unresorbed beneath the
proliferating tissue of condylar articular surface. this persists until
the end of second decade of life. During this period, thickeness of
zone of cartilage disappears and the replacing bone forms whole of
condyle. This cartilage is responsible for whole of normal growth
period and increases length of mandible.
Coronoid cartilage:
Found along the anterior border and summit of coronoid process.
All the traces of cartilage disappears long before birth.
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Symphyseal cartilage:
This is the 3 rd cartilage occurring at the symphyseal end of each
half of bony mandible. These enable the mandible to grow in with
till they persist. Once the union of mandible occurs at birth, they do
not take any further part in growth.
At birth mandible has wide mandibular angle (135°), ramus is small
compared to body and chin is poorly developed.
Clinical importance:
The shape and size of the fetal mandible undergoes transformation
during its growth and development. The ascending ramus of
neonatal mandible is low and wide and coronoid process is
relatively large and projects well above the condyle. The
mandibular canal runs low in the body.
As the mandibular body is showing the direction of mental foramen
during infancy and childhood changes. The mental neuromuscular
bundle arises at right angles of slightly forward direction at birth.
In adulthood it is characteristically directed backward. This change
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may be due to forward growth in the body of mandible while
neurovascular bundle drags along. This changing direction of
foramen has clinical implication in administration of local
anesthetic i.e. in infancy and childhood syringe needle may be
applied at right angles where as in adult it has to be applied
obliquely from behind. The location of the mental foramen also
alters its vertical relationship within the body of mandible from
infancy to old age. When teeth are present it located midway
between upper and lower border of mandible and in edentulous
mandible appears to be near the upper margin.
The alveolar process develops as a protective trough in response to
tooth buds and becomes superimposed upon basal bone of
mandibular body. This bone fails to develop if teeth are absent and
resorbs in response to tooth extraction. The orthodontic movement
of teeth takes place in alveolar bone (bed) and does not involve
basal bone.
Torus mandibular is exostasis which usually develops bilaterally in
the canine-premolar region.
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During fetal life the relative sizes of the maxilla and mandible vary
wide. Initially at 6 week IUL, mandible is considerably larger than
maxilla. By about 8 week, greater development of maxilla.
Subsequently relatively larger growth of mandible results at 11
week and lower and upper grows are of equal size between 13-20
week, mandibular growth lags behind due to change over from
Meckels cartilage to condylar secondary cartilage. At birth
mandible tends to be retrognathic though two jaws are of equal
size. This is normally corrected by postnatal growth to develop
Angle Class I relationship (maxillo-mandibular). Inadequate growth
results in Class II and overgrowth into Class III relation.
The mandible may be grossly deficient or absent. This condition is
known as agnathia. Aplasia of mandible and hyoid bone is a rare
and lethal condition called as 1 st and 2nd arch syndrome. In this
syndrome ischaemic necrosis of the mandible and hyoid bone
occurs after formation of ear.
Micrognathia is characteristic of several syndromes.
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- Pierre robin syndrome.
- Cat-cry syndrome.
- Treacher Collin’s (mandibulofacial).
- Down’s syndrome (trisomy 21).
- Turners syndrome.
There may be double condyle or bifid condyle that results from
persistence of septa dividing fetal condylar cartilage. Unilateral
condylar hyperplastic is also common.
Prognathism is usually inherited condition hyperpituitarism may
produce mandibular over growth.
Angulation of angle of mandible is 135° at childhood and
senilehood and at adult hood decreases to 160°.
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