Craniofacial growth and development

1. Facial growth and
development
Aslam Alkadhimi
Orthodontic Registrar StR 2
Eastman Dental Institute and Buckinghamshire Healthcare NHS Trust

2. Contents
• Philosophy behind growth and development!
• Terminology
• Why do we need to know about G&D
• Prenatal growth
• Postnatal growth
• Relevance of G&D to clinical practice
• Importance of G&D in orthodontics

3. • There must be a beginning of any great matter, but the
continuing unto the end until it be thoroughly finished yields
the true glory. Sir Francis Drake 1578
• The only true wisdom is in knowing you know nothing.
Socrates
• According to Socrates, we are full of wisdom when it comes
to facial growth!!

4. Terminology
• Growth refers to changes in magnitude and size.
• This is why economists refer to growth of economy when they mean
expansion of economy in amount and magnitude.
• Growth is divided into pre and postnatal growth; the prenatal growth
starts from the second trimester until birth while the postnatal one
starts from birth until death.
• On the other hand, development accounts for how growth happens.
• The term development is used almost always to refer to an increase
in complexity.

5. Terminology

6. Critical period
• Genes orchestrate the phenomena of growth and development
• The stage at which individual has reached a particular age is referred
to as maturational/biological age
• Critical period
• Most brain cells form by 6 months of age
• Bone and cartilage continue to divide until 15-20 years …NB
• During fetal and early infancy, brain is susceptible to damage

7. What tissues does our head develop from?

8. Pre somite Somite Post somite
8-21 days 21-31 days 32-56 days

9. Prenatal growth

10. Neural crest
Endoderm
Ectoderm

11. What gives rise to the face?
Frontonasal prominence
1st pharyngeal arch
2nd pharyngeal arch

12. 4 weeks 6 weeks 7 weeks
Midface development

13. Development of midface
The frontonasal prominence (red) contributes to the
forehead (A), the middle of the nose (B),
the philtrum of the upper lip (C) and the
primary palate (D), while the lateral nasal
prominence (blue) forms the sides of the
nose (B,D).
The maxillo-mandibular prominences
(green) give rise to the lower jaw
(specifically from the mandibular
prominences), to the sides of the middle
and lower face, to the lateral borders of
the lips, and to the secondary palate (from
the maxillary prominences).

14. Derivatives of pharyngeal arches

15. Palate development

16. CL/P common birth defect
Sporadic cases with no family history may be more related to
environmental risks, Presence of one or more affected
relative in the same family strongly suggests that genetic
Factors are the main contributor.

17. Post somite period
• 2nd month of development
• Facial features become more recognizable as human
• The external appearance of embryo is changed by an increase in head size and
formation of limbs, face, ears and eyes.
Fetal period
• 9th week to birth
• At the beginning of 3rd month, the head constitutes half of overall length
• Beginning of 5th month, head is 1/3rd of the total length
• At birth, it is 1/4th of total length

18. Developmental anomalies
There are four clinically significant types of congenital anomaly
• Malformation : A morphological defect of an organ, part of an organ, or
larger region of the body that results from an intrinsically abnormal
developmental process.
• Disruption :A morphological defect of an organ, part of an organ, or a
larger region of the body that results from the extrinsic breakdown of, or
an interference with, an originally normal developmental process
• Deformation : An abnormal form, shape, or position of a part of the body
that results from mechanical forces
• Dysplasia : An abnormal organization of cells into tissue (s) and its
morphological result (s).

19. Chromosome abnormalities
• TURNER’S SYNDROME:- Turner syndrome is
caused by the absence of two complete
copies of the X chromosome in some or all
the cells.
• Multiple eye findings including cataract,
blue sclera.
• Colour Blindness
• Depressed Corners of mouth
• High arched palate
• Dental malocclusion
• Micrognathia

20. Chromosome abnormalities
TRISOMY 21/DOWNS SYNDROME:-
• Hypoplastic maxilla and nasal bones
• Flattening of nasal bridge, orbital ridges, and
maxilla
• Short hard palate
• Cleft lip/palate about 3 times frequency in
normal population
• Protruding fissured tongue with
hypertrophy of papillae
• Dentition delayed, increased periodontal
disease, and reduced dental caries

21. Chromosome abnormalities
CROUZONS SYNDROME/CRANIOFACIAL DYSOSTOSIS:-
• Premature closure, especially of coronal suture, occasionally lambdoidal..
• Variable cranial form depending on order and rate of progression of suture
closure
• Optic nerve damage
• High arched palate
• V-shaped maxillary dental arch.
• Crowding of the upper teeth.
• Class III Malocclusion
• Mental retardation occasionally seen
• anomalies of the hands and feet may or may not occur.

22. Neural crest cells and craniofacial defects
• Treachers colins syndrome
• Pierre Robin syndrome
• De george anomaly
• Occuloauriculo vertbral spectrum(golden har syndrome)

23. Treachers Collins Syndrome
• under development of the zygomatic bones,
mandibular hypoplasia, down slanting palpebral
fissures, malformed external ears
• Autosomal dominant trait with 60% cases
• Macrostomia
• Hypoplastic mandible with concave undersurface
• Hypoplastic zygomatic arches
• cleft palate
• Dental malocclusion common
• Pinna frequently deformed, crumpled forward, or
• misplaced
• Absence of external auditory canal

24. Pierre Robin Syndrome
• Altered first arch structure
• Occur independently or in association with other malformations
• Development of mandible most severely affected
• micrognathia, cleft palate and glossoptosis (posteriorly placed
tongue)
• Robin’s syndrome may be due to genetic or environmental factors
• May also occur as a deformation
• The primary defect includes poor growth of the mandible and as a
result a posteriorly placed tongue that fails to drop from between the
palatal shelves preventing their fusion

25. Marfan’s Syndrome
• Autosomal dominant trait
• prominent supraorbital ridges
• Long narrow face
• High arched palate
• Mandibular prognathism
• Myopia
• Blue sclerae
• Chest deformities
• Hyperextensibility of joints
• Hernias
• Muscular underdevelopment

26. De George anomaly
Characterized by :
• have immunological deficiencies, hypocalcaemia and poor prognosis
• Origin of the defect is caused by abnormal development of neural
crest cells that contribute to formation of all affected structures
• In addition to genetic causes , alcohol and maternal diabetes can
produce such defect
• defects in the palate
• mild differences in facial features,

27. Oculoauriculovertebral spectrum
• craniofacial abnormalities involving the maxillary, temporal and
zygomatic bones which are small and flat
• Ear (anotia-no ear), eye(tumors and dermoid in eye balls)
• Asymmetry -65% cases
• Other malformation-tetralogy of fallot (con.heart disease),
malformations of kidney and intestine

28. Hemifacial Microsomia
• Hemifacial microsomia (HFM) is a congenital disorder that affects the
development of the lower half of the face
• Most commonly the ears, the mouth and the mandible.
• It usually occurs on one side of the face, but both sides are
sometimes affected.
• If severe, it may result in difficulties in breathing due to obstruction of
the trachea—sometimes even requiring a tracheotomy.
• With an incidence in the range of 1:3500 to 1:4500, it is the second
most common birth defect of the face, after CLP.

29. Hemifacial Microsomia
• The condition develops in the fetus at approximately 4 weeks
gestational age, when some form of vascular problem such as blood
clotting leads to insufficient blood supply to the face.
• This can be caused by physical trauma, though there is some evidence
of it being hereditary.
• This restricts the developmental ability of that area of the face.
• Currently there are no definitive reasons for the development of the
condition.

30. Hemifacial Microsomia
• Type I : Mild hypoplasia of the ramus , and the body of the mandible
is slightly affected.
• Type II : The condyle and ramus are small, the head of the condyle is
flattened , the glenoid fossa is absent , the condyle is hinged on a flat,
often convex, infratemporal surface , the coronoid may be absent.
• Type III: The ramus is reduced to a thin lamina of bone or is
completely absent. There is no evidence of a TMJ.

31. Hemifacial Microsomia

32. OMENS classification
Each of the involved structures is graded from 0 to 3 according
to the severity of clinical manifestations (Horgan et al. 1995).
E, ear malformations;
M, mandibular hypoplasia;
N, facial nerve paralysis;
O, orbital anomalies;
S, soft tissue deficiency.

33. Mandibular asymmetry

34. Mandibular asymmetry

35. Mandibular asymmetry
What is going
on here?

36. Mandibular asymmetry
An example of a Technetium
isotope scan used to assess the
growth activity of skeletal sites.
In the example shown there is
no increased uptake in the
condylar regions.

37. Post natal growth
Theories of growth control
• 1-Genetic
• 2-sichers sutural
• 3-scott’s cartilaginous
• 4-Moss’ functional matrix
• 5-Petrovic’s servosystem

38. 1-Genetic theory
• Assumption that genes determine all aspects of facial growth and
facial form.
• Little correlation between facial features of parent and child.
• Some genetic control.
• Evidence supports polygenic inheritance.
Mossey 1999

39. 2-The sutural theory/Sicher’s hypothesis
• This theory was developed by Joseph Weinmann and Harry Sicher
who suggested that primary growth of the craniofacial skeleton was
genetically regulated, being controlled within the sutures and
cartilages.
• For the cranial vault and maxillary complex, sutural growth was
regarded as being the prime mediator of bony expansion and, in
the case of the maxilla, downward and forward displacement
relative to the anterior cranial base (Sicher and Weinmann, 1 944).

40. 3- The cartilaginous theory/ Scott’s hypothesis
• Within this theory, great emphasis was placed upon the role of
cartilage in producing the driving force of craniofacial growth: in
particular, the nasal septal cartilage generating a downward and
forward displacement of the maxillary complex, synchondroses
elongating the cranial base and the condylar cartilage directing
downward and forward growth of the mandible (Scott, 1 954). The
mandible was perceived as essentially a bent long bone, with the
mandibular condylar cartilage being equivalent to the epiphyseal
plates of long bones whose growth forces the mandible
downward and forward away from the cranial base.

41. 4-The functional matrix theory/Moss’
hypothesis
• Melvin Moss, who suggested that the genetic control of growth is
lying in the soft tissue only while hard tissues respond to
functional adaptation of soft tissues, adopted it (Moss, 1 968, Moss
and Rankow, 1 968, Moss, 1 997a, Moss and Salentijn,1 969, Moss,
1 997b).
• Craniofacial skeleton composed of many functional cranial
components each functional cranial component is comprised of the
following two elements: skull=skeletal unit+ functional matrices

42. 5-The servosystem theory/Petrovic’s
hypothesis
• Alexandre Petrovic proposed that two principle factors which determine
growth of the craniofacial region (Petrov ic et al., 1 975):
• Genetically regulated growth of the primary cartilages within the cranial
base and nasal septum determine growth of the midface and provide a
constantly changing reference input, which is mediated via the dental
occlusion
• The mandible is ab le to respond to this occlusal changing by muscular
adaptation and locally induced condylar growth. Strength of this theory is
that it incorporates both genetic and environmental influences and
assumes a role for both cartilaginous and periosteal tissues during growth
of the head.

43. Growth of cranium
1. Fronto-ethmoidal synchondrosis Fuses at 2 y
ears.
2. Spheno-ethmoidal synchondrosis - Fuses at 7 y
ears.
3. Intersphenoidal synchondrosis - Fuses at very
early IU life
4. Spheno-occipital synchondrosis - Fuses at 12-1
4 years

44. Achondroplasia
• One of the most common developmental abnormalities that affect the
skull base.
• Achondroplasia (genetic form of dwarfism) has either a hereditary or
sporadic aetiology, but mainly associated with developmental retardation
of the cartilaginous growth, resulting in very short limbs and small midface
(Shiang et al., 1 994). Facial features include:
• Frontal bossing
• Depressed nasal bridge
• Midface hy poplasia and subsequently Class III malocclusion

45. Growth of the maxilla

47. Growth of the mandible

48. Growth of the mandible

49. Growth rotations
• Bjork study
• Started his study in 1951
• Had a sample size of 100 children between the age group of 4 – 24
yrs.
• Used metal implants to find the sites of growth and resorption in
individual jaws.
• Also examined individual variation in direction and intensity.
• Analysed mechanics of changes in intermaxillary relations during
growth.

50. Growth rotation
• Mandible can have a forward direction of growth (good growing) or
backward direction of growth (bad growing).
• Bjork gave seven structural signs to find the direction of mandibular
growth.
• These signs are not clearly developed before puberty.

51. Growth rotations

52. Growth rotation
Structural Signs
1. Condylar inclination.
2. Mandibular canal inclination.
3. Lower border of mandible (Antigonial notch).
4. Symphysis inclination.
5. Interincisal inclination.
6. Intermolar angle.
7. Lower face height.

53. Growth rotations

54. Growth rotation

55. Growth modification

56. Growth modification

57. Growth modification

58. Growth modification

59. Growth modification

60. Growth modification
Class III correction
Facemask+RME

63. Assessment of growth
• Observational methods (physical, sexual features, dental age)
• Chart based (height/weight ratio, height-velocity charts, scammon
curve)
• Skeletal methods (CVM)

65. Conclusions