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Factors affecting growth and development.theories of growth.

Sutural and cartilagenous theories.

Dr. Priti Mulimani

FACTORS AFFECTING GROWTH ANDDEVELOPMENT

As thou knowest not the way of the spirit, nor how thebones do grow in the womb of her that is with the child,even so thou knowest not the works of God who makethall.

- Ecclesiastes(11:5)

Classification of factors

1. Intrinsic factors2. Extrinsic factors

VAN LIMBORGH S CLASSIFICATION:1. Intrinsic factors

Local

2. Epigenetic factors GeneralLocal

3. Environmental factorsGeneral

INTRINSIC FACTORS genetic, inherent.EPIGENETIC FACTORS - Indirect genetic control (Proffit)

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- Genetically determined but manifest influence indirectly onassociated structures (Graber)

- The sum total of all biochemical, biomechanical andbiophysical events produced by the functioning of cells,

tissues and organs (Rakosi and Petrovic)Ex. Eye, Brain etc.

EPIGENETIC FACTORSact on products of genome

regulate all developmental processesproduce, regulate & maintain biologic structural complexity

LOCAL EPIGENETIC FACTORS ex MusclesGENERAL EPIGENETIC FACTORS-ex HormonesVARIOUS FACTORS AFFECTINGVARIOUS FACTORS AFFECTING

GROWTH AND DEVELOPMENT-GROWTH AND DEVELOPMENT-pre-natal factorspre-natal factors

Causing INTRAUTERINE GROWTH RETARDATION(IUGR)-

1. Chromosomal abnormalities2. Teratogens a. Infectious agents

b. Physical agents

c. Chemical agentsd. Hormones

MALE MEDIATED TERATOGENESIS

3. Congenital infections- a. Rubellab. CMVc. Toxoplasmosisd. Syphilis

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e. HSV, HIV4. Poor Maternal health- hypertension, renal & cardiac

disease5. Mothers nutritional status/ Socioeconomic status

6. Mothers use of alcohol, cigarettes, drugs etc7. Placental insufficiency8. Multiple births

Developmental anomaliesCLEFT LIP & CLEFT PALATECLEIDOCRANIAL DYSOSTOSISCRANIOFACIAL DYSOSTOSIS (Crouzons disease)MANDIBULOFACIAL DYSOSTOSIS (Treacher-Collins

Syndrome)PIERRE ROBIN SYNDROMEFACIAL HEMIHYPERTROPHYECTODERMAL DYSPLASIA

Natal causesGrowth can be affected by injuries during birth-1. Intrauterine moulding

Arm pressed against the face-maxillary deficiencyHead flexed against the chest-

mandibular deficiency.2. Trauma to mandible during birth process

forceps delivery

Post-natal factors

GENETICS/HEREDITY:

GENERAL EPIGENETIC FACTORS:a. Hormonal factorsb. Neural controlc. General body growth

LOCAL EPIGENETIC FACTORS:

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a. Neurotrophismb. Functionc. Muscles

GENERAL ENVIRONMENTAL FACTORS:a. Nutritionb. Illnessc. Raced. Climate and seasonal effectse. Exercisef. Family size & birth orderg. Psychological disturbance

h. Socioeconomic factorsi. Secular trends

LOCAL ENVIRONMENTAL FACTORS:a. Habits

Genetic / hereditary factorsPotential for growth is genetic.Actual outcome of growth = Genetic potential

+Environmental influences

Advanced rate of maturity in females than males delayingaction of Y- chromosome.

Ex. Klinefelters syndrome (XXY)Individuals with XYYTurners syndrome (XO)

Genetic control seen in-a. body size, shape, deposition of fatb. patterns & rate of growthc. onset of growth events-menarche,

-eruption of teeth,

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-ossification of bones,-beginning of adolescent growth spurt

Genetic studies of physical growth done using-1.TWIN STUDIESSir Francis Galton first scientific analysis of twins & concluded

that it is possible to separate Nurture from Nature.

2. FAMILIAL STUDIES.

a. Parent child study.b. Sibling studies.

TWIN STUDIESLundstrom(1963) conducted a study on 100 pair of twins, half of

which were monozygotic and half were dizygotic.Both skeletal and dental overjets were measured.More variations in the dizygotic than monozygotic.Larger genetic variations for skeletal pattern than dental overjet.

Lauweryns et al summarized a number of twin studies -concluded that 40% of the dental and skeletal variationscan be attributed to hereditary factors.

Familial studiesPARENT-CHILD CORRELATION COEFFICIENTS:Facial skeletal dimensions-0.5Dental characteristics

-maximum for overjet-0.5-minimum for overbite-0.15

Suzuki(1961) - studied 243 Japanese families.-1 parent had anomaly-20% of children affected.-Both parents had anomaly-40% of children were affected.

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Assessment of the transmission of craniofacial characteristicsfrom a study of twins and their siblings when compared to

their parents.

Aims:1.To analyse from the local population the factors affecting

the heritability of craniofacial structures.2.To test the various parameters related to cephalometric &

study model analysis to evaluate the amount of heritabilityof various components of craniofacial structures.

3.To explore the possible application of the findings toclinical situations.

10 pairs of monozygotic twinsZygosity of the samples were determined.2 pairs of dizygotic twins were analysed separately.Analysis was done based on cephalometrics & study models.Direct comparison of the variations was done

RESULTS

1.The twins - similar in large linear measurements & ratios;differ slightly in other measurements in the cephalometricreading,-good co-relation in the study models.

2.Large differences between twins and parents indicating theultimate size of the craniofacial components is difficult topredict.

3.No definite pattern of inheritance could be discerned.

Assessment of the transmission of the craniofacialcharacteristics from a study of monozygotic twins, their

parents & their siblings using conventional cephalometry,FEM cephalometry & model analysis.

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Aim:To test and evaluate the heritability of craniofacial anddental characteristics using FEM analysis in 20 pairs ofmonozygotic twins, their parents and 5 siblings.

results1. Anterior vertical dimensions are under strong

environmental control as compared to horizontalparameters.

2. Twins inherit their genetic pattern more from mother thanfrom father.

Comparison of the soft tissue similarities betweenchildren and their parents and between children

and their older siblings.

Aims :1.To study the degree of correlation of facial soft tissue

structures in a profile perspective between parents andoffspring and the control group.

2.To asses the degree of similarity between youngchildren in an age group at which orthodontic treatmentis usually started with their older siblings who havecompleted growth.

The study comprised of 30 families,11families had 2daughters and 11 families had 2 sons for comparison.

Comparison based on- cephalometric tracing, profilephotographs.

RESULTS:

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1.Strong genetic control in the transmission of soft tissuefacial characteristics.

2.Forecasting of the childs nose, lips and position of chincan be done by comparing with that of the adult sibling.

Experimental studyVan Limborgh s study on chick embryo Intrinsic genetic information necessary for tissue

differentiation.Primary Genetic control Initial features.Secondarily- inductive local feedback & inner communication

mechanisms between cells & tissues.

Review article -ajo-dojune 2004

Growth & Development : Heredity & Mechanical ModulationsJeremy Mao, Hyun-Duck NahGoals:1. Synthesize current knowledge of bone & cartilage of

craniofacial skeletal lineage2. Explore effective means of mechanical stresses to

communicate with bone & cartilage cells.

discussion3 cell lineages primarily involved osteogenic,

chondrogenic, fibrogenic common progenitor ofmesenchymal cells.

Behaviour of all cells controlled by genes.Genes regulated by environmental cues including

mechanical stimuli.Combined approaches of genetics, bioengineering &

quantitative biology.Bottom-up approach instead of top-down approach.

summaryFacial dimension inheritance POLYGENIC, not Mendelian

If Mendelian inheritancenumerous environmental influences

great change in underlying genetic features

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inherited features undetectableFace not under rigid genetic control impossible to predict

features of children from cephalometric data of parents.

If both parents are alike with respect to a particular trait, thechances of sibiling showing that particular trait are more.

If one parent is unlike the other with respect to a particulartrait the chances of the sibling showing either trait vary.

Hormonal factorsHORMONES

LOCAL GENERAL(ENDOCRINE)Ex.Acetyl choline NON-SPECIFIC SPECIFIC

Secretin (all body cells) (target organs)ex. Growth hormone ex.ACTH

Thyroid hormones LH, FSHInsulin

Endocrine glands

Hormones affecting growthGrowth HormoneThyroid HormonesParathyroid HormoneCalcitoninInsulinAdrenocortical hormones

Growth hormone/ somatotropinSecreted by-

ACTIONS

Protein synthesis synthesis & secretionLipolysis of IGFProtein breakdownUse of glucose for ATP production

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Increases size & number of cellsConverts chondrocytes into osteogenic cellsDeposition of proteins by chondrocytic and osteogenic cells

IGF- INSULIN-LIKE GROWTH FACTORSSmall protein hormonesPreviously called SomatomedinsStructure & function similar to insulin; growth-promoting

effects more potentGH- release of IGF by cells of liver, muscle, cartilage, bone

etcAct through blood (endocrine) or locally (autocrine /

paracrine)Increased amino acid entry in cells, prevent protein

breakdown - increased cell growth & multiplication

Pituitary gigantism, dwarfism & acromegalyThyroid hormones

(t3 and t4)Regulate 1. O2 & BMR

2. Cellular metabolism3.GROWTH & DEVELOPMENT-- G & D of brain- No. & size of neurons- Myelinization of axons

Hypothyroid- retarded growthCRETINISM

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Parathyroid hormoneIncreases serum Ca-1. Rapid phase Ca & PO4 absorption from bone matrix

around osteocytes & osteoblasts- Osteolysis2. Slow phase- activation & formation of new osteoclasts3. Promotes formation of 1,25 dihydroxycholecalciferol in

kidneysIncreases Ca absorption & reabsorption

calcitoninSecreted by C-cells / parafollicular cells of thyroid.Antithesis of PTH.Decreases serum Ca-1. Immediate effect - decreases osteolytic effect of

osteocytic membrane2. Prolonged effect - decreases new osteoclast formationEffect negated by PTH - except in

- children- Pagets disease

insulinFirst isolated from pancreas by Banting & Best in 1922Hormone associated with Energy AbundancePeripheral uptake of glucose by cellsGlycogenesisLipogenesisProtein synthesisGlycogenolysis, neoglucogenesis

Adrenocortical hormones-GLUCOCORTICOIDS

Stimulate Gluconeogenesis

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Decreased glucose utilization by cellsDecreased cellular proteinIncreased liver & plasma proteinsMobilization of fatty acids

Anti-allergic, anti-inflammatoryDecreased immunity

Cushings syndromeRole in growth

Physiological levels (10-9 M) -promote DNA synthesis,

-mesenchymal cell growth-with other hormones/ growth factors- controls stages of

palatogenesisIncreased levels Cleft palate-inhibition of mesenchymal cell proliferation-interference with protein production

Adrenal androgensWeak male sex hormone, converted to testosteroneDevelopment of male sex organs in fetal life & early

childhoodMild effect in females throughout life

Growthfactors

Neural controlNeural growth centre in HypothalamusKeeps children on genetically determined growth curves

At birth- body size limited to accommodate birth process.After birth- children destined to become large experience

burst of early growth during first 2 years.

General body growthCo-relation exists between adult physique & developmental

events

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Variations in rate of growth of different somatotypesEx. tall women mature laterFacial dimensions spurt at

about the same time as stature

Period of growth modificationneurotrophismDefinition:Interaction between nerves and other cells which initiate or

control molecular modifications in other cells.- Guth (1969)

Nervous control of skeletal growth, assumedly bytransmission of a substance through the axons of thenerves. - Moyers

DIRECTINDIRECT

TYPES OF NEUROTROPHISM1. Neuromuscular Trophism2. Neuroepithelial Trophism3. Neurovisceral TrophismEffects of NEUROMUSCULAR TROPHISM :a. Muscle developmentb. Muscle denervation-reinnervation

c. Cross-innervationd. Control of genetic activity

MUSCLE DEVELOPMENT:

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Embryonic myogenesis independent of neural innervationNeural innervation Myoblast stage of differentiationi.e. until then Neurotrophic control (Studitsky et al 62)

MUSCLE DENERVATION-REINNERVATIONAutotransplanted minced muscle fragments reform into afunctional muscle if supplied by a motor nerve

CROSS-INNERVATION:Respective nerves of fast-slow muscle pair cutFree ends implanted in the other muscle fast muscles

become slow & vice-versa

Changes in speed resulting from nerve cross-union arebrought about by a neural influence which has a directeffect on the contractile material itself, therebydetermining intrinsic speed of contraction. Close(1969)

CONTROL OF GENETIC ACTIVITY:Regenerating nerves may exert direct control on synthesis of

DNA, RNA & protein in regenerating tissues (Dresden,Thornton).

Qualitatively different myosin in cross-innervated muscle-new species of protein produced by nerve influence ofgene expression in muscle cell.

Neuroepithelial trophismIn regions of sensory loss- skin lacks usual ability to

withstand trauma. Healing slow unless regeneration ofnerve occurs.

In amphibians- subepidermal grafts of neural tissuestimulate epidermal mitosis (Overton).

LIMB REGENERATION- epithelial activity must occur first forlimb regeneration requires neural innervation (Singer &Craven).

Maxillary & Mandibular hypoplasia intra-oral & intra-nasalsensory deficits (Henkin).

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Evidence against neurotrophic theoryGutmann complete differentiation of some myotubes to

muscle fibres can occur without neural innervation;though very slowly & occasionally

In vitro- aneurogenic limb with fully developed musclesexperimentally produced in amphibians- peripheral tissuesmay produce & utilize their own trophic substances.

If motorneurons sectioned & related muscles reinnervated muscle tissue reforms & grows before recovery of neuronalconductive function.

FunctionRole of function is the primary factor in control of

craniofacial growth- Moss Functional Matrix TheoryAbsence of normal function gross distortion of bony

morphology ex. TMJ ankylosis, aglossia, NM disorders etc.Malfunctions cause compensatory abnormal growthEx. Altered nasorespiratory function, tongue-thrusting.

Wolffs Law- internal architecture of bone representsexternal stresses.

musclesFormation of bone at the point of muscle attachment

depends on muscle activityMusculature imp. part of total soft-tissue matrix whose

growth carries jaws downwards & forwards.Loss of part of musculature underdevelopment of that part

of face

Excessive muscle contraction restricts growth ex.Torticollis.

Functional equilibrium

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There should be a balance between the forces of the tongueand compensating action of lips & cheeks musculature toallow the jaws & dentition normally.

Deleterious patterns of muscles behavior produce-

Perverted osseous growth.Tooth malpositions.Disturbed breathing.Difficulty in speech.Upset balance of facial musculature.Psychological problems.

nutrition

Proteins ( 9 essential amino acids), carbohydrates, fats.Ca, PO4, Mg, Mn, F, Vit D bone & toothFe- Hb formationVit A- activities of osteoblasts & osteoclastsVit B complex- DNA formation & cell maturationVit C- collagen formationOxygen cardiac anomalies stunted growthUndernutrition- accentuates normal differential growth of

body tissuesTeeth- bone- soft tissues

Effects of malnutritionDelays growth, adolescent spurtAffects size of body parts, proportions & chemistryQuality & texture of tissues bone & teethIf period of malnutrition short catch-up growthGirls better buffered against malnutriton & illness.

illnessMinor childhood illnesses not much effectSerious, prolonged, debilitating illnesses marked effectDisease increased cortisone decreased GH.Cartilage cell growth stopped temporarilyLines of arrested growth- on X-rays, teeth.Catch up growth brings child back on predetermined

genetic curve

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raceRacial differences-climatic, nutritional or socioeconomic.Gene pool differences North American blacks ahead of

whites in skeletal maturity at birth & for at least first 2 yrs

of life.Calcification & eruption of teeth 1 yr earlier than whites.

Climate & seasonal effectsCold climates- increased adipose tissue.

Increased height in spring than autumn.Increased weight - in autumn than spring.Growth in height & eruption of teeth more at night than

day.Fluctuations in hormone release.

Family size & birth orderFirst-born children weigh less at birth, ultimately less

stature ; higher I.Q.Sizes, maturation, intelligence of individuals- no correlation

with size of family.

EXERCISEEffects on linear growth not proved.

Development of motor skills, in muscle mass, fitness,general well-being.

Psychological disturbancesPsychological abuse adversly affects growth- accidental

discovery in 1948 by German physician.Ht. & wt. gain of children in 2 German orphanages for 1 yr.Orphanage governed by harsh headmistress grew less in

ht. & wt. though 20% extra calories.

Inhibition of growth hormone.Catch-up growth.

Socioeconomic factorsFavorable socioeconomic status--larger-different type of growth

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-variation in timing of growthPositive relationship associated with socioeconomic class ;

not family income.As our society becomes more affluent, how long will we get

bigger & mature earlier ?Secular trends15 yr-old boys now are approximately

5 inches taller than 15 yr-old boyswere 50 yrs ago.

Children grow at a faster rate but stopgrowing sooner.

Adolescent growth spurt earlierbut not accentuated.

Earlier total ht. reached at 25 yrs of age ; now at 20.i.e. secular trend more marked in children than in total adultht.

Progressive advancement in timing of menarche.

habitsHabits are learned patterns of muscle contraction of a very

complex nature.1. Thumb-sucking2. Tongue-thrusting

3. Mouth-breathingThumb-sucking

Mandible positioned in a downward manner to accommodatethe interposed thumb- causing increased eruption ofposterior teeth.

Tongue is lowered which decreases the pressure on theupper posterior teeth.

Imbalance between tongue & cheek pressures.Cheek pressure increased as buccinator muscle contracts

during suckling

Tongue-thrustingTongue thrust is forward placement of

the tongue between the anterior teeth

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& against the lower lip duringswallowing- Schneider (1982).

Tongue thrusting results due to lack of anterior seal.Skeletal openbite

Steep mandibular plane.Increased anterior facial height.

Mouth-breathingBreathing through the mouth alters equilibrium of the jaws &

teeth.Lowering of the mandible & tongue & extension of the head

is seen.

Adenoid facies-separated lips, small nose, nostrils poorlydeveloped, pout in the lower lip, vacant facial expression.

Greatest change occurred in the dentition and the sagittaldepth of the nasopharynx in the first year.

Mandibular plane angle diminished by 4 degrees (gradual

change).Results were statistically significant but no large

measurement differences facial height only 3 mm largerin adenoidectomy group.

ORTHOPEDIC FORCESMILWAUKEE BRACE THERAPY

Non dental application of orthopaedic forceThere are adjustable steel supports transferring stress

directly from the chin and occiput to the iliac crest.Maxilla and mandible may be deformed by growth guidance

procedures aimed at the endochondral spine.

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If we could first know where we are & whither we aretending, we could better judge what to do & how to do it.

- Abraham Lincoln

referencesT.M. Graber Orthodontics: Principles & Practice, III Ed.Proffit Contemporary Orthodontics, III Ed.Moyers Handbook of Orthodontics, IV Ed.Bishara Textbook of Orthodontics, I Ed.Enlow Essentials of Facial Growth, I Ed.

Tortora Principles of Anatomy & Physiology, VIII Ed.Guyton & Hall Textbook of Medical Physiology, IX Ed.

8. Sadler- Langmans Medical Embryology, VIII, Ed.

9. Craniofacial Growth Series Monograph 3 (ControlMechanisms in Craniofacial Growth Edited byMcNamara)

10. Craniofacial Growth Series Monograph 21(Craniofacial Morphogenesis & Dysmorphogenesis Editedby Vig & Burdi)

11. James A. McNamara jr. Influence of respiratory patternon craniofacial growth. The Angle Orthodontist. 1981; vol-51, no-4

12. Anders Lundstrom- Nature vs nurture in dentofacialvariation- Eu J ortho. 1984;

13. Katherine W. L. Vig- Nasal obstruction and facial growth:The strength of evidence for clinical assumptions. Am JOrthod. 1998; 113: 603-7.

14. Dr. Chitra Prasad- An assessment of the transmission ofcraniofacial characteristics from a study of twins and their

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siblings when compared to their parents. MDSDissertation Feb-1999.

15. Dr. Mallikarjun Prasad- An assessment of thetransmission of craniofacial characteristics from a study

of monozygotic twins, their parents and siblings usingconventional cephalometry, FEM cephalometry and modelanalysis. MDS Dissertation Sept-2002.

16. Dr. Siju M. George- A comparison of soft tissue similaritycorelation between children and parents with the same

corelation between children and their older siblings- Aprofile view photographic study. MDS Dissertation Mar-2002.

.FACTORS AFFECTING GROWTH AND DEVELOPMENT

- case reports

Functional appliance therapy in conjunction withgrowth hormone treatment. A case report

-T. I. Davies & P. H. W. Rayner- Br. J of Orthod 1995;22: 361-5.

Intro:TURNERS SYNDROME 45 XOIncidence 1:2000 female births

Features:

Low birth weightOedema of hands & feet in neonatal period.Co-arctation of aortaShort statureOvarian dysgenesis Primary amenorrhoeaMicrognathia

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Growth-promoting effect of HGH in children with retarded

growth but normal normal pituitary pituitary growthhormone secretion also.Growth hormone deficient children 0.5 IU/Kg/week

Turners 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 patientwith 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 analysisAt age 10.8yrs Ht.-128.7 cm.2nd centile for normal, 75th centile for Turners syndrome

Skeletal age= chronological age.

Combined Pituitary function test- partial growth hormone deficiency

HGH (Gentotropin)- 2 IU subcutaneously- 6 times/wk.After 3 mths.- ht.-132.1 (128.7)HGH- dose inreased to 3 IU.

Ethinyloestradiol- 2 g dailyAfter 9 mths.- ht.-139.2 cm ; HGH 4 units

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Class II Div. 1 14 mm overjetClass II Skeletal base Retrognathic mandible.No history of habits, well-aligned arches.Andresen activator 8 mths after commencement of GH

therapy mandibular advancement2nd appliance- after 6 mths into treatment complete overjetreduction.

Active treatment completed after 10 mths (12.5 yrs) continued in retention phase.

Avg. daily wear 18 hrs; Retention phase 8 hrs.

RESULTS: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.

Conclusion:HGH & etinyloestradiol needed to induce pubertal growth

spurt in Turners syndrome.Without hormone administration successful orthodontic

treatment unlikely, especially in an active treatment periodof 10 mths.

Orthodontic treatment with growth hormone therapy in agirl of short stature

- Chung-Ju Hwang & Jung-Yul Cha-AJO-DO July 2004; 126:118-26

SHORT STATURE:Ht below 5th percentile for age

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Lower limit of normal for ht. at 3rd or 4th percentile for age.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 controversial.

All linear measurements of facial structures smallerDisproportionate growth in cranial base structures & jaws-

facial 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 GrowthHormone (HGH) therapy on craniofacial complex.

Case:

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 features.Slow post-natal growth, body ht. std. deviation score less

than -2.Skeletal age- 7.5yrs.

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High mandibular angleClass III dental maloclusionSkeletally retrognathic mandible

Ant. Crossbite (-2 mm overjet), openbite, constrictedmaxillary arch- buccal edge bite, incompetent lips, mildanterior crowding, midline deviation.

Treatment:HGH (Eutropin) 2 IU/m2 s.c. 6 times/week.HGH increased to 3 IU/m2 & then to 5 IU/m2 (4th yr)RPE & facemask (8 mths) crossbite correction.Upper plate with anteroposterior screw for 3 mths.

After 15 mths spring-loaded posterior occlusal bite blockappliance on mandibular dentition with chincup- verticaldiscrepancy.

28th mth- Cl. III molar, anterior- edge-to-edge

After 3 yrs, 7 mths fixed appliance.Cl III elastics- edge-to-edgeVertical elastics on anteriors overbite.Continuous chincup- pt. uncooperative.

Results:Increase in ht.-

10 cms (24 mths); 7.3 cms(3rd yr); 5.2cms(4th yr)Intermaxillary elastics

increased mandibular plane angle,clockwise rotation of mandible,extrusion of maxillary molars.

Dental corrections achieved- poor profile.

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Discussion:HGH therapy affects growth of mandible more than growth

of maxilla.Amount & pattern of growth during HGH administration

unpredictableHGH therapy rarely affects dental maturity.Further research on effect of HGH- craniofacial growth &

tooth movement during orthodontic therapy.