Factors effecting growth and development /certified fixed orthodontic courses by Indian dental academy
….FACTORS AFFECTING GROWTH
- case reports
INDIAN DENTAL ACADEMY
Leader in continuing dental education
Functional appliance therapy in conjunction
with growth hormone treatment. A case
-T. I. Davies & P. H. W. Rayner
- Br. J of Orthod 1995;22: 361-5.
TURNER’S SYNDROME – 45 XO
Incidence – 1:2000 female births
1. Low birth weight
2. Oedema of hands & feet in neonatal period.
3. Co-arctation of aorta
4. Short stature
5. Ovarian dysgenesis – Primary amenorrhoea
Growth-promoting effect of HGH – in children with
retarded growth but normal pituitary growth hormone
Growth hormone deficient children – 0.5 IU/Kg/week
Turner’s syndrome- 0.7 – 1.0 IU/Kg/week.
Theoretical side-effects – diabetes mellitus, neoplasias –
acute leukemia, cerebral tumors.
Successful functional appliance treatment- rapid rate of
growth associated with pubertal growth spurt.
Purpose of study:
To highlight benefit of using functional appliance in a
patient with retrognathic mandible with a medical need
for GH, thus providing a predictable growth spurt.
Patient (VW) Female – birth wt.- 2.6 kg.
Diagnosis- oedema, chromosomal analysis
At age 10.8yrs – Ht.-128.7 cm.
2nd centile for normal, 75th centile for Turner’s syndrome
Skeletal age= chronological age.
Combined Pituitary function test- partial growth hormone
HGH (Gentotropin)- 2 IU subcutaneously- 6 times/wk.
After 3 mths.- ht.-132.1 cms (128.7)
HGH- dose inreased to 3 IU.
Ethinyloestradiol- 2 µg daily
After 9 mths.- ht.-139.2 cm ; HGH – 4 units
Class II Div. 1 – 14 mm overjet
Class II Skeletal base – Retrognathic mandible.
No history of habits, well-aligned arches.
Andresen activator – 8 mths after commencement of
GH therapy – mandibular advancement
2nd appliance- after 6 mths into treatment – complete
Active treatment completed after 10 mths (12.5 yrs) –
continued in retention phase.
Avg. daily wear – 18 hrs; Retention phase – 8 hrs.
1 yr. 3 mths. of GH – ht. increased by 10.5 cm; ht.
velocity of 8.4 cms/yr.
Overjet 14 to 2 mm after 10 mths of activator therapy.
Increase in mandibular length – greater than expected.
HGH & etinyloestradiol – needed to induce pubertal
growth spurt in Turner’s syndrome.
Without hormone administration – successful
orthodontic treatment unlikely, especially in an active
treatment period of 10 mths.
Orthodontic treatment with growth hormone
therapy in a girl of short stature
- Chung-Ju Hwang & Jung-Yul Cha
-AJO-DO July 2004; 126:118-26
Ht below 5th percentile for age
Lower limit of normal for ht. at 3rd or 4th percentile for
Growth- less than 4cms/yr after 3yrs. of age.
Skeletal age- 2 yrs behind chronologic age.
Euthyroid, no GH deficiency, no chronic disease.
Treatment of short-statured children with GH –
All linear measurements of facial structures – smaller
Disproportionate growth in cranial base structures & jawsfacial retrognathia.
Proportionately smaller posterior than anterior facial ht.
Steep vertical inclination of mandible.
High incidence of crowding.
Purpose of the study:
To review the characteristics of craniofacial morphology in
children of short stature & the effects of Human Growth
Hormone (HGH) therapy on craniofacial complex.
Girl- 9yrs, 3mths.
Chief complaint- anterior cross-bite.
Ht.- 120.9 cms. Father- 174 cms, Mother- 150 cms.
GH level –normal.
Normal birth wt., no evidence of non-endocrine causes
of short stature, systemic disease or dysmorphic
Slow post-natal growth, body ht. std. deviation score –
less than -2.
Skeletal age- 7.5yrs.
HGH therapy affects growth of mandible more than
growth of maxilla.
Amount & pattern of growth during HGH
HGH therapy rarely affects dental maturity.
Further research on effect of HGH- craniofacial growth
& tooth movement during orthodontic therapy.
Craniofacial biology as “Normal
David S. Carlson
The Structure of Scientific Revolutions – Thomas Kuhn (1970)
“Research firmly based upon one or more past
scientific achievements, achievements that some
particular scientific community acknowledges as
supplying the foundation for its further practice.”
Model or concept
A conceptual scheme that encompasses individual theories and
is accepted by a scientific community as a model and
foundation for further research.
SCIENTIFIC COMMUNITY – group characterized by its
consensus about a paradigm & commitment to relate that
paradigm to the rest of the natural world.
Conflict between scientific communities.
SCIENTIFIC REVOLUTION – Change in paradigm brought
about by inconsistencies within the old scheme or by technologic
developments that permit scientist to ask new questions & gain
Study of craniofacial skeleton with no consideration to
- Anthropologic craniometry
-Racial analysis for socioeconomic
structure of western Europe
Krogman- ‘static approach’
Moss(1982)1. Pre-radiologic phase - craniometry
2. Radiologic phase – no conceptual
Studies based on –
Anatomic intuition & extrapolation from other parts of
body- growth immutable & genetically pre-determined.
Moss- “Classic Triad”
1. Sutures are primary growth sites
2. Growth of the cranial vault occurs only by periosteal
deposition and endosteal resorption.
3. All cephalic cartilages are primary growth centers
under direct genetic control
Genetically determined – so growth pattern invariant.
“norms” or “standards”
Treatment of bones of face ignored – heredity &
Focus on the more plastic dentoalveolar area.
If not alter facial growth – acceptable dental alignment.
Increase in experimental animal research.
Methodologic change- Technological developments:1.
Use of Radioopaque Implants.
In-vivo and In-vitro transplantations.
Conceptual change- too many variations in growth to
be genetically determined; affected by modifying
Mid to late 1950s- PRE-REVOLUTIONARY
The end of 1950’s – 2 approaches within genomic
paradigm (Krogman – 1974) –
1. COMPREHENSIVE APPROACH
2. STRUCTUROFUNTIONAL APPROACH
continued craniometrics with more sophisticated
hardware -radiographs, cephalostats and software
Experimental & analytic
Concentrated more on “cause and effect
Effect of altered or abnormal function on form
The end of 1950’s -genomic paradigm put into question
Periosteal and sutural bone growth - removed from
genomic paradigm - given the status of secondary,
compensatory or adaptive phenomena
Lack of evidence- genomic paradigm remained dominant
Alternative view-“Function” plays a major role continued to gather momentum.
Early 1960s- ‘period of Revolution’.
Development of alternative paradigm mostly
associated with – Melvin Moss
‘Functional Matrix Hypothesis’- some consider it to
be an alternative paradigm itself.
David Carlson- major component of
Daniels & Kremanak – “has probably both stimulated
& inhibited thinking & experimentation. It may be
harmful in thinking.”
“Functional Matrix Hypothesis”- a topic of
theoretical debate involving people likeMoorrees(1972)
Alexander Petrovic and associates(1975)- proposed
the ‘Cybernetic theory’.
2 Paradigms :
1. Genomic--Exists primarily on the strength of the
belief that facial growth and form should be
2. Functional--Includes the Functional Matrix
Hypothesis and its extension-The epigenetic
At present - a confluence of these two
paradigms is seen until a new one is proposed.
Theories of growth
Different theories differ in the location at which
genetic control is established.
3 major theories explaining primary determinant of
craniofacial growth –
Growth site versus growth centre
Cranial growth centers: Facts or fallacies? – Koski
AJO-DO 1968 Aug (566-583)
Growth Centre- site of endochondral ossification with
tissue-separating force, contributing to the increase of
i.e. location at which independent (genetically controlled)
Growth site: regions of periosteal or sutural bone
formation and modeling resorption adaptive to
i.e. merely location at which growth occurs.
Sutural dominance theory
SICHER – studies using vital dyes – sutures caused
much of growth
“….the primary event in sutural growth is the
proliferation of the connective tissue between the two
bones. If the sutural connective tissue proliferates it
creates the space for oppositional growth at the borders
of the two bones.”
Connective tissue in sutures of nasomaxillary complex
& vault – separated bones like synchondrosis &
2 differing views concerning the structure of the
1. Three-layer structure:
- Connective tissue between the two bones - same
as cartilage at the base of the skull, epiphyses, and
articular surfaces of long bones
- "spreading" of the suture, initiated by the proliferation
of the middle layer cells of the sutural tissue.
-"tissue-separating force" in the sutural tissue.
2. Five-layer structure :
-Each bone at the suture has its own two-layer
periosteum covering + opposing surfaces of the
-fifth layer between these periosteal layers - allows for
slight adjustments between the bones during growth
-active proliferating role - layers of the periosteums
of each bone.
Histologic specimens of sutures examined same –
Evidence against sutural theory
1. Subcutaneous autotransplants of the
zygomaticomaxillary suture area in the guinea pig have
not been found to grow – lack of innate growth
2. Growth of sutures – respond to external stimuli.
3. Extirpation of facial sutures - no appreciable effect on
growth of the skeleton.
4. Shape of sutures - depends on functional stimuli
5. Closure of sutures -extrinsically determined.
6. Sites of sutures - not predetermined .
Sutures are growth sites not centres.
Adaptive, compensatory or secondary growth.
Intrinsic growth-controlling factors in cartilage &
Sutures are secondary & dependent on extrasutural
Cartilaginous part of skull must be recognised as primary
centres of growth, with nasal septum being a major
contributor in maxillary growth, per se.
Sutural growth – responsive to synchondrosis
proliferation & www.indiandentalacademy.com factors.
Cranial base synchondroses
Removal of spheno-occipital synchondrosis - results in an
arrest of growth in length of the cranial base .
Pressure & tension – little effect on cartilage.
Intramembranous bone- immediate response.
Endochondral cranial base – lesser response to brain
growth than intramembranous cranial vault.
Primary centres of growth – Sarnat, Burdi, Baume,
Petrovic & others.
Endochondral ossification at the synchondrosesonly a response to external stimuli?
Cartilage- lacks same amount of independent growth
potential as transplants of epiphyseal cartilage under
similar experimental conditions.
Spheno-occipital synchondrosis appears to close
much earlier than is usually stated in the textbooks -11
to 16 years of age
Cranial base – single bone with multiple epiphyseal
Nasal septal cartilage
Scott- primary cartilage in nasal septum – primary
mechanism for growth of nasomaxillary complex.
Latham- ligament extending from nasal septal
cartilage to to anterior premaxillary region –
This is an important relation between midfacial &
nasal septal growth – especially before birth.
Histologic examination - endochondral ossification at the septoethmoidal junction and area of proliferation at the vomeral edge
of the cartilage
In the palatal area - resorption on the nasal side and apposition
on the oral side of the bony palate.
Experimental excision of the nasal septum affects the growth
of the upper face considerably - due to trauma.
Nasal septum - central support for the upper facial area, and its
loss results in a predictable collapse in the area.
Arrhinencephalic 9-month-old child (with the septum
missing) - resorption and apposition processes in the
bony palate normal.
Height of the upper face not greatly affected,
although the sagittal development of the middle third
of the face was retarded
In recent experiments – growth as well in culture as
epiphyseal plate cartilage.
Growth of the condylar cartilage is responsible for the
anteroposterior growth of the mandible- primary growth centre.
Scott- growth of the condylar cartilage enables the
condyle "to grow upwards and backwards so as to
maintain the contact at the temporomandibular joint
as the mandible is carried downwards and forwards by
the growth of the upper facial skeleton."
If the condylar cartilage is transplanted to a relatively
nonfunctional site, such as the subcutaneous or brain
tissue, it does not maintain its structure and does not
behave like the condylar cartilage in situ.
Bilateral condylectomy, congenital absence of the
rami- no appreciable effect on the growth of the rest
of the mandible in humans.