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Factors effecting growth and development /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. …

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.

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  • 2. INDIAN DENTAL ACADEMY Leader in continuing dental education
  • 3. 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
  • 4.  Growth-promoting effect of HGH – in children with retarded growth but normal 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.
  • 5. 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.
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  • 7.  Combined Pituitary function test- partial growth hormone deficiency  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
  • 8.  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.
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  • 12. 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.
  • 13. 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.
  • 14. 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.
  • 15.  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.
  • 16. 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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  • 20.  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.
  • 21. 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 biteblock appliance on mandibular dentition with chincupvertical discrepancy.  28th mth- Cl. III molar, anterior- edge-to-edge
  • 22.  After 3 yrs, 7 mths – fixed appliance.  Cl III elastics- edge-to-edge  Vertical elastics on anteriors – overbite.  Continuous chincup- pt. uncooperative.
  • 23. 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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  • 29. 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.
  • 31. Craniofacial biology as “Normal Science” David S. Carlson The Structure of Scientific Revolutions – Thomas Kuhn (1970) NORMAL SCIENCE: “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.”
  • 32. paradigm  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.
  • 33.  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 new data.
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  • 36. 1920-1940  Study of craniofacial skeleton with no consideration to function – - 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 change
  • 37.  Studies based on – Comparative anatomy, Craniometrics, Radiographic cephalometrics  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
  • 38. Genomic paradigm  Genetically determined – so growth pattern invariant.  “norms” or “standards”  Treatment of bones of face ignored – heredity & unmodifiable  Focus on the more plastic dentoalveolar area.  If not alter facial growth – acceptable dental alignment.
  • 39. 1940-1960  Increase in experimental animal research.  Methodologic change- Technological developments:1. 2. Autoradiography. 4.  Vital Dyes. 3.  Use of Radioopaque Implants. In-vivo and In-vitro transplantations. Conceptual change- too many variations in growth to be genetically determined; affected by modifying influences Mid to late 1950s- PRE-REVOLUTIONARY
  • 40.  The end of 1950’s – 2 approaches within genomic paradigm (Krogman – 1974) – 1. COMPREHENSIVE APPROACH 2. STRUCTUROFUNTIONAL APPROACH Comprehensive approach:  descriptive  continued craniometrics with more sophisticated hardware -radiographs, cephalostats and software (statistical models).
  • 41. Structurofunctional Approach:  Experimental & analytic  Concentrated more on “cause and effect relationships”  Effect of altered or abnormal function on form
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  • 43.  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.
  • 44. 1960-1980  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 ‘FUNCTIONAL PARADIGM’  Daniels & Kremanak – “has probably both stimulated & inhibited thinking & experimentation. It may be harmful in thinking.”
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  • 46.  “Functional Matrix Hypothesis”- a topic of theoretical debate involving people likeMoorrees(1972) Koski(1972) Wayne Watson(1982) Johnston(1976)  Alexander Petrovic and associates(1975)- proposed the ‘Cybernetic theory’.
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  • 48.  2 Paradigms : 1. Genomic--Exists primarily on the strength of the belief that facial growth and form should be encoded genetically. 2. Functional--Includes the Functional Matrix Hypothesis and its extension-The epigenetic hypothesis  At present - a confluence of these two paradigms is seen until a new one is proposed.
  • 49. Theories of growth  Different theories differ in the location at which genetic control is established.  3 major theories explaining primary determinant of craniofacial growth – 1. Bone 2. Cartilage 3. Soft-tissue matrix
  • 50. Growth site versus growth centre Cranial growth centers: Facts or fallacies? – Koski AJO-DO 1968 Aug (566-583) BAUME: Growth Centre- site of endochondral ossification with tissue-separating force, contributing to the increase of skeletal mass. i.e. location at which independent (genetically controlled) growth occurs.
  • 51. Growth site: regions of periosteal or sutural bone formation and modeling resorption adaptive to environmental influences. i.e. merely location at which growth occurs.
  • 52. 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 & epiphyseal plate
  • 53.  Sicher ascribes equal value – osteogenic tissues, cartilage, sutures & periosteum.
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  • 55.  2 differing views concerning the structure of the sutures– 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.
  • 56. 2. Five-layer structure : -Each bone at the suture has its own two-layer periosteum covering + opposing surfaces of the bones -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 – interpretation different.
  • 57. 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 potential. 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 .
  • 58. CONCLUSION:  Sutures are growth sites not centres.  Adaptive, compensatory or secondary growth.
  • 59. Cartilaginous theory SCOTT’S HYPOTHESIS:  Intrinsic growth-controlling factors in cartilage & periosteum.  Sutures are secondary & dependent on extrasutural influences.  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 & factors. local environmental
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  • 61. 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.
  • 62. Endochondral cranial base – lesser response to brain growth than intramembranous cranial vault. Primary centres of growth – Sarnat, Burdi, Baume, Petrovic & others.
  • 63.  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 plate-like synchondrosis.
  • 64. 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 – SEPTOPREMAXILLARY LIGAMENT.  This is an important relation between midfacial & nasal septal growth – especially before birth.
  • 65.  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.
  • 66.  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.
  • 67.  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.
  • 68. Condylar cartilage  Growth of the condylar cartilage is responsible for the anteroposterior growth of the mandible- primary growth centre.
  • 69.  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.
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  • 71.  Studies involving the use of metallic implants - actual growth of the condyle is sometimes upward and backward and sometimes upward and forward.
  • 73. 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. New Vistas in Orthodontics