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Growth & development in orthodontics   /certified fixed orthodontic courses by Indian dental academy
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Growth & development in orthodontics /certified fixed orthodontic courses by Indian dental academy

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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.


Indian dental academy provides dental crown & Bridge,rotary endodontics,fixed orthodontics,
Dental implants courses.for details pls visit www.indiandentalacademy.com ,or call
00919248678078

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  • Pressure against rapidly growing areas leads to distortion <br /> Arm pressed against the face-maxillary deficiency <br /> Head flexed against the chest-mandibular deficiency. <br /> Pressure against rapidly growing areas leads to distortion <br /> Arm pressed against the face-maxillary deficiency <br /> Head flexed against the chest-mandibular deficiency. <br /> Pressure against rapidly growing areas leads to distortion <br /> Arm pressed against the face-maxillary deficiency <br /> Head flexed against the chest-mandibular deficiency. <br />

Growth & development in orthodontics   /certified fixed orthodontic courses by Indian dental academy Growth & development in orthodontics /certified fixed orthodontic courses by Indian dental academy Presentation Transcript

  • Factors affecting growth and development. theories of growth. Sutural and cartilagenous theories. www.indiandentalacademy.com 1
  • INDIAN DENTAL ACADEMY Leader in continuing dental education • www.indiandentalacademy.com • www.indiandentalacademy.com 2
  • FACTORS AFFECTING GROWTH AND DEVELOPMENT “ As thou knowest not the way of the spirit, nor how the bones do grow in the womb of her that is with the child, even so thou knowest not the works of God who maketh all.” - Ecclesiastes(11:5) www.indiandentalacademy.com 3
  • Classification of factors  1. Intrinsic factors 2. Extrinsic factors  VAN LIMBORGH’S CLASSIFICATION: 1. Intrinsic factors Local 2. Epigenetic factors General Local 3. Environmental factors General www.indiandentalacademy.com 4
  •  INTRINSIC FACTORS – genetic, inherent.  EPIGENETIC FACTORS – - Indirect genetic control (Proffit) - Genetically determined but manifest influence indirectly on associated structures (Graber) - The sum total of all biochemical, biomechanical and biophysical events produced by the functioning of cells, tissues and organs – (Rakosi and Petrovic) Ex. Eye, Brain etc. www.indiandentalacademy.com 5
  • EPIGENETIC FACTORS act on products of genome regulate all developmental processes produce, regulate & maintain biologic structural complexity LOCAL EPIGENETIC FACTORS –ex Muscles GENERAL EPIGENETIC FACTORS-ex Hormones www.indiandentalacademy.com 6
  • VARIOUS FACTORS AFFECTING GROWTH AND DEVELOPMENTpre-natal factors Causing INTRAUTERINE GROWTH RETARDATION (IUGR)1. Chromosomal abnormalities 2. Teratogens – a. Infectious agents b. Physical agents c. Chemical agents d. Hormones ‘ MALE – MEDIATED TERATOGENESIS’ www.indiandentalacademy.com 7
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  • 3. Congenital infections- a. Rubella b. CMV c. Toxoplasmosis d. Syphilis e. HSV, HIV 4. Poor Maternal health- hypertension, renal & cardiac disease 5. Mother’s nutritional status/ Socioeconomic status 6. Mother’s use of alcohol, cigarettes, drugs etc 7. Placental insufficiency 8. Multiple births www.indiandentalacademy.com 10
  • Developmental anomalies  CLEFT LIP & CLEFT PALATE  CLEIDOCRANIAL DYSOSTOSIS  CRANIOFACIAL DYSOSTOSIS (Crouzon’s disease)  MANDIBULOFACIAL DYSOSTOSIS (Treacher-Collins Syndrome)  PIERRE ROBIN SYNDROME  FACIAL HEMIHYPERTROPHY  ECTODERMAL DYSPLASIA www.indiandentalacademy.com 11
  • Natal causes Growth can be affected by injuries during birth1. Intrauterine moulding  Arm pressed against the face -maxillary deficiency  Head flexed against the chestmandibular deficiency. 2. Trauma to mandible during birth process – forceps delivery www.indiandentalacademy.com 12
  • Post-natal factors  GENETICS/HEREDITY:  GENERAL EPIGENETIC FACTORS: a. Hormonal factors b. Neural control c. General body growth  LOCAL EPIGENETIC FACTORS: a. Neurotrophism b. Function www.indiandentalacademy.com c. Muscles 13
  •  GENERAL ENVIRONMENTAL FACTORS: a. Nutrition b. Illness c. Race d. Climate and seasonal effects e. Exercise f. Family size & birth order g. Psychological disturbance h. Socioeconomic factors i. Secular trends  LOCAL ENVIRONMENTAL FACTORS: www.indiandentalacademy.com a. Habits 14
  • Genetic / hereditary factors  Potential for growth is genetic.  Actual outcome of growth = Genetic potential + Environmental influences  Advanced rate of maturity in females than males – delaying action of ‘Y’- chromosome.  Ex. Klinefelter’s syndrome (XXY) Individuals with XYY Turner’s syndrome (XO) www.indiandentalacademy.com 15
  •  Genetic control seen ina. body size, shape, deposition of fat b. patterns & rate of growth c. onset of growth events-menarche, -eruption of teeth, -ossification of bones, -beginning of adolescent growth spurt www.indiandentalacademy.com 16
  •  Genetic studies of physical growth done using1.TWIN STUDIES Sir 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. www.indiandentalacademy.com 17
  • TWIN STUDIES  Lundstrom(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. www.indiandentalacademy.com 18
  •  Lauweryns et al summarized a number of twin studies - concluded that 40% of the dental and skeletal variations can be attributed to hereditary factors. www.indiandentalacademy.com 19
  • Familial studies  PARENT-CHILD CORRELATION COEFFICIENTS: Facial skeletal dimensions-0.5 Dental 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. www.indiandentalacademy.com 20
  • Assessment of the transmission of craniofacial characteristics from 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 heritability of various components of craniofacial structures. 3.To explore the possible application of the findings to clinical situations. www.indiandentalacademy.com 21
  •  10 pairs of monozygotic twins  Zygosity 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 www.indiandentalacademy.com 22
  • RESULTS 1.The twins - similar in large linear measurements & ratios; differ slightly in other measurements in the cephalometric reading, -good co-relation in the study models. 2.Large differences between twins and parents indicating the ultimate size of the craniofacial components is difficult to predict. 3.No definite pattern of inheritance could be discerned. www.indiandentalacademy.com 23
  • Assessment of the transmission of the craniofacial characteristics from a study of monozygotic twins, their parents & their siblings using conventional cephalometry, FEM cephalometry & model analysis. • Aim: To test and evaluate the heritability of craniofacial and dental characteristics using FEM analysis in 20 pairs of monozygotic twins, their parents and 5 siblings. www.indiandentalacademy.com 24
  • results 1. Anterior vertical dimensions are under strong environmental control as compared to horizontal parameters. 2. Twins inherit their genetic pattern more from mother than from father. www.indiandentalacademy.com 25
  • Comparison of the soft tissue similarities between children 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 and offspring and the control group. 2.To asses the degree of similarity between young children in an age group at which orthodontic treatment is usually started with their older siblings who have completed growth. www.indiandentalacademy.com 26
  •  The study comprised of 30 families,11families had 2 daughters and 11 families had 2 sons for comparison.  Comparison based on- cephalometric tracing, profile photographs. RESULTS: 1.Strong genetic control in the transmission of soft tissue facial characteristics. 2.Forecasting of the child’s nose, lips and position of chin can be done by comparing with that of the adult sibling. www.indiandentalacademy.com 27
  • Experimental study Van 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. www.indiandentalacademy.com 28
  • Review article -ajo-do june 2004 Growth & Development : Heredity & Mechanical Modulations – Jeremy Mao, Hyun-Duck Nah Goals: 1. Synthesize current knowledge of bone & cartilage of craniofacial skeletal lineage 2. Explore effective means of mechanical stresses to communicate with bone & cartilage cells. www.indiandentalacademy.com 29
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  • discussion  3 cell lineages primarily involved – osteogenic, chondrogenic, fibrogenic – common progenitor of mesenchymal 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. www.indiandentalacademy.com 32
  • summary  Facial dimension inheritance – POLYGENIC, not Mendelian  If Mendelian inheritance numerous environmental influences great change in underlying genetic features inherited features undetectable  Face not under rigid genetic control – impossible to predict features of children from cephalometric data of parents. www.indiandentalacademy.com 33
  •  If both parents are alike with respect to a particular trait, the chances of sibiling showing that particular trait are more.  If one parent is unlike the other with respect to a particular trait the chances of the sibling showing either trait vary. www.indiandentalacademy.com 34
  • Hormonal factors HORMONES LOCAL GENERAL(ENDOCRINE) Ex. Acetyl choline NON-SPECIFIC Secretin (all body cells) ex. Growth hormone Thyroid hormones SPECIFIC (target organs) ex. ACTH LH, FSH Insulin www.indiandentalacademy.com 35
  • Endocrine glands www.indiandentalacademy.com 36
  • Hormones affecting growth 1. Growth Hormone 2. Thyroid Hormones 3. Parathyroid Hormone 4. Calcitonin 5. Insulin 6. Adrenocortical hormones www.indiandentalacademy.com 37
  • Growth hormone/ somatotropin  Secreted by-  ACTIONS INDIRECT     DIRECT Protein synthesis synthesis & secretion Lipolysis of IGF Protein breakdown Use of glucose for ATP production  Increases size & number of cells  Converts chondrocytes into osteogenic cells 38 www.indiandentalacademy.com  Deposition of proteins by chondrocytic and osteogenic
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  • IGF- INSULIN-LIKE GROWTH FACTORS  Small protein hormones  Previously called ‘ Somatomedins’  Structure & function – similar to insulin; growthpromoting effects more potent  GH- release of IGF by cells of liver, muscle, cartilage, bone etc  Act through blood (endocrine) or locally (autocrine / paracrine)  Increased amino acid entry in cells, prevent protein breakdown - increased cell growth & multiplication www.indiandentalacademy.com 40
  • Pituitary gigantism, dwarfism & acromegaly www.indiandentalacademy.com 41
  • Thyroid hormones (t3 and t4)  Regulate – 1. O2 & BMR 2. Cellular metabolism 3.GROWTH & DEVELOPMENT- G & D of brain - No. & size of neurons - Myelinization of axons www.indiandentalacademy.com 42
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  •  Hypothyroid- retarded growth  CRETINISM  Hyperthyroid- excessive growth, early maturity of bones, short height eventually. www.indiandentalacademy.com 44
  • Parathyroid hormone  Increases serum Ca1. Rapid phase – Ca & PO4 absorption from bone matrix around osteocytes & osteoblasts- Osteolysis 2. Slow phase- activation & formation of new osteoclasts 3. Promotes formation of – 1,25 dihydroxycholecalciferol in kidneys  Increases Ca absorption & reabsorption www.indiandentalacademy.com 45
  • calcitonin  Secreted by C-cells / parafollicular cells of thyroid.  Antithesis of PTH. Decreases serum Ca1. Immediate effect - decreases osteolytic effect of osteocytic membrane 2. Prolonged effect - decreases new osteoclast formation  Effect negated by PTH - except in - children www.indiandentalacademy.com - Paget’s disease 46
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  • insulin  First isolated from pancreas by Banting & Best in 1922  Hormone associated with ‘Energy Abundance’  Peripheral uptake of glucose by cells  Glycogenesis  Lipogenesis  Protein synthesis  Glycogenolysis, neoglucogenesis www.indiandentalacademy.com 48
  • SYNERGISTIC ACTION WITH GROWTH HORMONE ON GROWTH www.indiandentalacademy.com 49
  • Adrenocortical hormonesGLUCOCORTICOIDS  Stimulate Gluconeogenesis  Decreased glucose utilization by cells  Decreased cellular protein  Increased liver & plasma proteins  Mobilization of fatty acids  Anti-allergic, anti-inflammatory  Decreased immunity www.indiandentalacademy.com 50
  • Cushing’s syndrome www.indiandentalacademy.com 51
  • Role in growth  Physiological levels (10-9 M) – -promote DNA synthesis, -mesenchymal cell growth -with other hormones/ growth factors- controls stages of palatogenesis  Increased levels – Cleft palate -inhibition of mesenchymal cell proliferation -interference with protein production www.indiandentalacademy.com 52
  • Adrenal androgens  Weak male sex hormone, converted to testosterone  Development of male sex organs in fetal life & early childhood  Mild effect in females throughout life www.indiandentalacademy.com 53
  • Growth factors www.indiandentalacademy.com 54
  • Neural control  Neural growth centre – in Hypothalamus  Keeps 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. www.indiandentalacademy.com 55
  • General body growth  Co-relation exists between adult physique & developmental events  Variations in rate of growth of different somatotypes  Ex. tall women mature later  Facial dimensions spurt at about the same time as stature  Period of growth modification www.indiandentalacademy.com 56
  • neurotrophism Definition: “Interaction between nerves and other cells which initiate or control molecular modifications in other cells.” - Guth (1969) “Nervous control of skeletal growth, assumedly by transmission of a substance through the axons of the nerves.” - Moyers DIRECT INDIRECT www.indiandentalacademy.com 57
  • Neurotrophic substances pass, utilising the processes of axoplasmic transport, from their sites of synthesis in the neural cell body to the innervated tissues. www.indiandentalacademy.com 58
  • TYPES OF NEUROTROPHISM 1. Neuromuscular Trophism 2. Neuroepithelial Trophism 3. Neurovisceral Trophism Effects of NEUROMUSCULAR TROPHISM : a. Muscle development b. Muscle denervation-reinnervation c. Cross-innervation d. Control of genetic activity www.indiandentalacademy.com 59
  • MUSCLE DEVELOPMENT:  Embryonic myogenesis – independent of neural innervation  Neural innervation – Myoblast stage of differentiation  i.e. until then – Neurotrophic control (Studitsky et al ’62) MUSCLE DENERVATION-REINNERVATION  Autotransplanted minced muscle fragments – reform into a functional muscle if supplied by a motor nerve www.indiandentalacademy.com 60
  • CROSS-INNERVATION:  Respective nerves of fast-slow muscle pair cut  Free ends implanted in the other muscle – fast muscles become slow & vice-versa  “Changes in speed resulting from nerve cross-union are brought about by a neural influence which has a direct effect on the contractile material itself, thereby determining intrinsic speed of contraction.” Close(1969) www.indiandentalacademy.com 61
  • 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 of gene expression in muscle cell. www.indiandentalacademy.com 62
  • Neuroepithelial trophism  In regions of sensory loss- skin lacks usual ability to withstand trauma…. Healing slow unless regeneration of nerve occurs.  In amphibians- subepidermal grafts of neural tissue stimulate epidermal mitosis (Overton).  LIMB REGENERATION- epithelial activity must occur first for limb regeneration – requires neural innervation (Singer & Craven).  Maxillary & Mandibular hypoplasia – intra-oral & intra-nasal sensory deficits (Henkin). www.indiandentalacademy.com 63
  • Presence of taste bud depends on intact innervation (Jeppsson) Gustatory nerve section- degeneration of taste buds & adjacent epithelium. www.indiandentalacademy.com 64
  • Evidence against neurotrophic theory  Gutmann – complete differentiation of some myotubes to muscle fibres can occur without neural innervation; though very slowly & occasionally  In vitro- aneurogenic limb with fully developed muscles experimentally produced in amphibiansperipheral tissues may produce & utilize their own trophic substances.  If motorneurons sectioned & related muscles reinnervated – muscle tissue reforms & grows before recovery of neuronal conductive function. www.indiandentalacademy.com 65
  • Function  Role of function is the primary factor in control of craniofacial growth- Moss’ Functional Matrix Theory  Absence of normal function – gross distortion of bony morphology ex. TMJ ankylosis, aglossia, NM disorders etc.  Malfunctions cause compensatory abnormal growth  Ex. Altered nasorespiratory function, tongue-thrusting.  Wolff’s Law- internal architecture of bone represents external stresses. www.indiandentalacademy.com 66
  • muscles  Formation of bone at the point of muscle attachment depends on muscle activity  Musculature – 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. www.indiandentalacademy.com 67
  • Functional equilibrium  There should be a balance between the forces of the tongue and compensating action of lips & cheeks musculature to allow the jaws & dentition normally.  Deleterious patterns of muscles behavior produce1. Perverted osseous growth. 2. Tooth malpositions. 3. Disturbed breathing. 4. Difficulty in speech. 5. Upset balance of facial musculature. 6. Psychological problems. www.indiandentalacademy.com 68
  • nutrition  Proteins ( 9 essential amino acids), carbohydrates, fats.  Ca, PO4, Mg, Mn, F, Vit D – bone & tooth  Fe- Hb formation  Vit A- activities of osteoblasts & osteoclasts  Vit B complex- DNA formation & cell maturation  Vit C- collagen formation  Oxygen – cardiac anomalies – stunted growth  Undernutrition- accentuates normal differential growth of body tissues www.indiandentalacademy.com  Teeth- bone- soft tissues 69
  • Effects of malnutrition  Delays growth, adolescent spurt  Affects size of body parts, proportions & chemistry  Quality & texture of tissues – bone & teeth  If period of malnutrition short – “catch-up growth”  Girls better buffered against malnutriton & illness. www.indiandentalacademy.com 70
  • illness  Minor childhood illnesses – not much effect  Serious, prolonged, debilitating illnesses – marked effect  Disease increased cortisone decreased GH.  Cartilage cell growth stopped temporarily  Lines of arrested growth- on X-rays, teeth.  Catch up growth – brings child back on predetermined genetic curve www.indiandentalacademy.com 71
  • race  Racial 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. www.indiandentalacademy.com 72
  • Climate & seasonal effects  Cold 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. www.indiandentalacademy.com 73
  • Family size & birth order  First-born children – weigh less at birth, ultimately less stature ; higher I.Q.  Sizes, maturation, intelligence of individuals- no correlation with size of family. EXERCISE  Effects on linear growth not proved.  Development of motor skills, in muscle mass, fitness, general well-being. www.indiandentalacademy.com 74
  • Psychological disturbances  Psychological 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. www.indiandentalacademy.com 75
  • Socioeconomic factors  Favorable socioeconomic status-larger -different type of growth -variation in timing of growth  Positive relationship associated with socioeconomic “class” ; not family income.  As our society becomes more affluent, how long will we get bigger & mature earlier ? www.indiandentalacademy.com 76
  • Secular trends  15 yr-old boys now are approximately 5 inches taller than 15 yr-old boys were 50 yrs ago.  Children grow at a faster rate but stop growing sooner.  Adolescent growth spurt earlier but 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 adult ht.  Progressive advancement in timing of menarche. www.indiandentalacademy.com 77
  • habits  Habits are learned patterns of muscle contraction of a very complex nature. 1. Thumb-sucking 2. Tongue-thrusting 3. Mouth-breathing www.indiandentalacademy.com 78
  • Thumb-sucking Begins at birth and outgrown by 3-4 years. Through sucking child obtains- nutrients, feelings of euphoria, sense of security and feeling of warmth. Maxillary constriction- not due to negative pressure. www.indiandentalacademy.com 79
  •  Mandible positioned in a downward manner to accommodate the interposed thumb- causing increased eruption of posterior teeth.  Tongue is lowered which decreases the pressure on the upper posterior teeth.  Imbalance between tongue & cheek pressures.  Cheek pressure increased as buccinator muscle contracts during www.indiandentalacademy.com suckling 80
  • Tongue-thrusting  Tongue thrust is forward placement of the tongue between the anterior teeth & against the lower lip during swallowingSchneider (1982).  Tongue thrusting results due to lack of anterior seal.  Skeletal openbite  Steep mandibular plane.  Increased anterior facial height. www.indiandentalacademy.com 81
  • Mouth-breathing  Breathing through the mouth alters equilibrium of the jaws & teeth.  Lowering of the mandible & tongue & extension of the head is seen. www.indiandentalacademy.com 82
  •  ‘Adenoid facies’-separated lips, small nose, nostrils poorly developed, pout in the lower lip, vacant facial expression.  James Mcnamara- caused complete nasal obstruction in primates using silicon plugs.  Found downward & backward rotation of mandible & increased lower facial height.  Linder- Aronson studied 41 children who underwent adenoidectomies- 5 years.  34 children who switched to oral respiration compared with 54 normal children. www.indiandentalacademy.com 83
  •  Greatest change occurred in the dentition and the sagittal depth 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 larger in adenoidectomy group. www.indiandentalacademy.com 84
  • ORTHOPEDIC FORCES MILWAUKEE BRACE THERAPY  Non dental application of orthopaedic force  There 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. www.indiandentalacademy.com 85
  • “If we could first know where we are & whither we are tending, we could better judge what to do & how to do it.” - Abraham Lincoln www.indiandentalacademy.com 86
  • references 1. T.M. Graber – Orthodontics: Principles & Practice, III Ed. 2. Proffit – Contemporary Orthodontics, III Ed. 3. Moyers – Handbook of Orthodontics, IV Ed. 4. Bishara – Textbook of Orthodontics, I Ed. 5. Enlow – Essentials of Facial Growth, I Ed. 6. Tortora – Principles of Anatomy & Physiology, VIII Ed. 7. Guyton & Hall – Textbook of Medical Physiology, IX 87 www.indiandentalacademy.com Ed.
  • 8. Sadler- Langman’s Medical Embryology, VIII, Ed. 9. Craniofacial Growth Series – Monograph 3 (Control Mechanisms in Craniofacial Growth – Edited by McNamara) 10. Craniofacial Growth Series – Monograph 21 (Craniofacial Morphogenesis & Dysmorphogenesis– Edited by Vig & Burdi) 11. James A. McNamara jr. –Influence of respiratory pattern on craniofacial growth. The Angle Orthodontist. 1981; vol-51, no-4 12. Anders Lundstrom- Nature vs nurture in dentofacial variation- Eu J www.indiandentalacademy.com ortho. 1984; 88
  • 13. Katherine W. L. Vig- Nasal obstruction and facial growth: The strength of evidence for clinical assumptions. Am J Orthod. 1998; 113: 603-7. 14. Dr. Chitra Prasad- An assessment of the transmission of craniofacial characteristics from a study of twins and their siblings when compared to their parents. MDS Dissertation Feb-1999. 15. Dr. Mallikarjun Prasad- An assessment of the transmission of craniofacial characteristics from a study of monozygotic twins, their parents and siblings using conventional cephalometry, FEM cephalometry and model analysis. MDS Dissertation Sept-2002. www.indiandentalacademy.com 89
  • 16. Dr. Siju M. George- A comparison of soft tissue similarity corelation between children and parents with the same corelation between children and their older siblings- A profile view photographic study. MDS Dissertation Mar-2002. www.indiandentalacademy.com 90
  • ….FACTORS AFFECTING GROWTH AND DEVELOPMENT - case reports www.indiandentalacademy.com 91
  • Functional appliance therapy in conjunction with growth hormone treatment. A case report -T. I. Davies & P. H. W. Rayner - Br. J of Orthod 1995;22: 361-5. Intro: TURNER’S SYNDROME – 45 XO Incidence – 1:2000 female births Features: 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 6. Micrognathia www.indiandentalacademy.com 92
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  •  Growth-promoting effect of HGH – in children with retarded growth but normal normal pituitary pituitary growth hormone secretion also.  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. www.indiandentalacademy.com 94
  • 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. www.indiandentalacademy.com 95
  •  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 µg daily  After 9 mths.- ht.-139.2 cm ; HGH – 4 units www.indiandentalacademy.com 96
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  •  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 overjet reduction.  Active treatment completed after 10 mths (12.5 yrs) – continued in retention phase.  Avg. daily wear – 18 hrs; Retention phase – 8 hrs. www.indiandentalacademy.com 98
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  • 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. www.indiandentalacademy.com 101
  • Conclusion:  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. www.indiandentalacademy.com 102
  • 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 SHORT STATURE:  Ht below 5th percentile for age  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. www.indiandentalacademy.com 103
  •  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. www.indiandentalacademy.com 104
  • 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.  www.indiandentalacademy.com Skeletal age- 7.5yrs. 105
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  •  High mandibular angle  Class III dental maloclusion  Skeletally retrognathic mandible  Ant. Crossbite (-2 mm overjet), openbite, constricted maxillary arch- buccal edge bite, incompetent lips, mild anterior crowding, midline deviation. www.indiandentalacademy.com 110
  • 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 block appliance on mandibular dentition with chincupvertical discrepancy.  28th mth- Cl. III molar, anterior- edge-to-edge www.indiandentalacademy.com 111
  •  After 3 yrs, 7 mths – fixed appliance.  Cl III elastics- edge-to-edge  Vertical elastics on anteriors – overbite.  Continuous chincup- pt. uncooperative. www.indiandentalacademy.com 112
  • 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. www.indiandentalacademy.com 113
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  • Discussion:  HGH therapy affects growth of mandible more than growth of maxilla.  Amount & pattern of growth during HGH administration unpredictable  HGH therapy rarely affects dental maturity.  Further research on effect of HGH- craniofacial growth & tooth movement during orthodontic therapy. www.indiandentalacademy.com 119
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