Concepts of growth and development / orthodontic courses /certified fixed orthodontic courses by Indian dental academy

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  • DEVELOPMENT OF FACE
  • These sex hormones are released into the blood stream causing development of secondary sexual characteristics and accelerated growth of genitals. Also there is an increase in general body growth and decrease in lymphoid tissue.
  • The sex hormones stimulates cartilage to grow faster causing adolescent growth spurt, at the same time they also cause a increase in skeletal maturation this is the rate at which cartilage is transformed into bone. If the acceleration in maturation is faster then acceleration in growth it leads to cartilage getting used up faster then it is replaced, leading to growth completion.
  • When a number of bones are united to function as a single cranial component is termed as “ macro skeletal unit” e.g.endocranial surface of the calvarium

Transcript

  • 1. CONCEPTS OF GROWTH ANDDEVELOPMENT INORTHODONTICS INDIAN DENTAL ACADEMY Leader in Continuing Dental Education www.indiandentalacademy.com
  • 2. CONTENTS• INTRODUCTION• DEFINITION• PHYSIOLOGY OF GROWTH• FACTORS AFFECTING GROWTH AND DEVELOPMENT• PATTERN OF GROWTH• VARIABILITY OF GROWTH• TIMING OF GROWTH
  • 3. CONTENTS• MODES OF GROWTH• CHARACTERISTICS OF GROWTH• SITES AND TYPES OF GROWTH• THEORIES OF GROWTH CONTROL• METHODS OF STUDYING GROWTH• METHODS OF COLLECTING DATA• BIBILOGRAPHY
  • 4. THE MOBILE MASK IN FRONT OFHUMAN BRAIN BEGAN TO ATTRACTOUR ATTENTION WHEN WE WEREBABIES AND CONTINUES TO FASCINATEUS AS LONG AS WE LIVE W. K. GREGORY, OUR FACE FROM FISH TO MAN
  • 5. WITHIN THE TEXT OF THE CRANIOFACIAL EMBRYOLOGY,WE COME ACROSS TWO TERMS GROWTH & DEVELOPMENT.WHAT DOES THE TERM GROWTH IMPLIES TO US ?CHANGE IN MAGNITUDE.DOES IT EXPLAIN TO HOW FAR IT HAPPENS ?WHY SHOULD IT HAPPEN IN A PREDETEMINEDDIRECTION ?
  • 6. TO UNDERSTAND THIS ,THE MORE DESCRIPTIVE & EXPLANATORY TERM DEVELOPMENT IS ADDED. DEVELOPMENT CONNOTES A MATURATIONAL PROCESS INVOLVINGPROGRESSIVE DIFFERENTATION AT THE CELLULAR & TISSUE LEVELS,THERE BYFOCUSING ON THE ACTUAL BIOLOGICAL MECHANISM THAT ACCOUNTS FOR OVERALL GROWTH.
  • 7. DEFNITION:GROWTH DEVELOPMENT
  • 8. DEFINITION GROWTH• GROWTH IS AN INCREASE IN SIZE -“TODD”• THE SELF MULTIPLICATION OF LIVING SUBSTANCE -“HUXLEY”• THE INCREASE IN SIZE,CHANGE IN PROPORTION AND PROGRESSIVE COMPLEXITY -“KROGMAN”
  • 9. • ENTIRE SERIES OF SEQUENTIAL ANATOMIC AND PHYSIOLOGICAL CHANGES TAKING PLACE FROM THE BEGINNING OF PRENATAL LIFE TO SENILITY “MERIDTH”• QUANTATIVE ASPECT OF BIOLOGIC DEVELOPMENT PER UNIT OF TIME. “MOYERS”• CHANGE IN ANY MORPHOLOGICAL PARAMETER WHICH IS MEASUREBLE “MOSS”
  • 10. DEFNITION: DEVLOPMENT • DEVELOPMENT MEANS PROGRESS TOWARDS MATURITY. “TODD” • ALL THE NATURALLY OCCURING UNIDIRECTIONAL CHANGES IN THE LIFE OF AN INDIVIDUAL FROM ITS EXISTENCE AS A SINGLE CELL TO ITS ELABORATION AS A MULTIFUNCTIONAL UNIT TERMINATING IN DEATH. “MOYERS”
  • 11. DEFINITIONS OFDEVELOPMENT ACC TO PROFITT INCREASEIN COMPLEXITY
  • 12. • ACC TO CARLSON: DEVELOMENT IS A LIFE LONG PROCESS THAT ENCOMPASSES ALL OF THE STRUCTURAL AND FUNTIONAL CHANGES THAT TAKES PLACE FROM CONCEPTION THROUGH MATURITY.
  • 13. NEGATIVE GROWTH• GENERALLY WE EQUATE GROWTH WITH ENLARGEMENT BUT THERE ARE INSTANCE IN WHICH GROWTH RESULTS IN DECREASE IN SIZE.• EXAMPLE: THYMUS GLANDS AFTER PUBERTY. THEREFORE GROWTH MAY RESULT IN INCREASE OR DECREASE IN SIZE, CHANGE IN FORM OR PROPORTION, COMPLEXITY , TEXTURE.
  • 14. HusbandTowife
  • 15. HOW DO WE GROW? (AN OVER VIEW ON PHYSIOLOGY)• CONTINOUS INTER ACTION BETWEEN ENDOCRINE AND SKELETAL SYSTEMS• MOST OF THE HARMONES INVOLVED• KEY FACTOR IN ENDOCRINE GROWTH ACCESS IS HUMAN GROWTH HARMONE (HGH) BY SOMATOTROPIC CELLS IN Ant.PITUTARY.• RELEASE OF (HGH ) REGULATED BY HYPOTHALAMIC HARMONES HGH-RELEASING AND HGH- INHIBITORY HARMONES.
  • 16. BASIC CONCEPTS OF GROWTHPHYSIOLOGY OF GROWTHPITUITARY GLAND OR HYPOPHYSIS – 1CMDIAMETER, 0.5 – 1gm IN WEIGHTLIES IN SELLA TURSICA AND IS CONNECTED TOHYPOTHALAMUS BY PITUITARY STALKPITIUTARY GLAND ANTERIOR PITUITARY OR ADENOHYPOPHYSIS POSTERIOR PITUITARY OR NEUROHYPOPHYSISANTERIOR PITUITARY RELEASES 6 IMPORTANTPEPTIDE HARMONES-GH, ACTH, FSH, LH, PROLACTIN
  • 17. GROWTH HARMONE : PROTEIN IN NATURE WITH MOL WT 21500FUNCTIONSMETABOLIC: INCREASES SYNTHESIS OF PROTEINS, INCREASES MOBILIZATION OFLIPIDS, CONSERVATION OF CARBOHYDRATESBONE : DIFFERENTIATION AND DEVELOPMENT OF BONE CELLS INCREASES GROWTH OF SKELETON( LENGTH AND THICKNESS)PARTICULARLY MEMBRANOUS BONES SUCH AS JAW BONES AND SKULL BONESBECOME THICKERGH HAS INDIRECT EFFECT ON BONES LIVER SOMATOMEDINGH EFFECT ON BONES IGF-1 SOMATOMEDIN C IGF-2 ACTS ON BONE AND CAUSES GROWTH
  • 18. HYPOTHALAMUS GHRH , GHIH SOMATOSTATIN ALSO SECRETED BY DELTA CELLS OF ISLETS OF LANGERHANS (PANCREAS) INHIBITIONSTIMULATION OFANTERIOR PITUITARY GH WHICH ACTS ON LIVER, TISSUES SOMATOMEDIN FEED BACK INHIBITION
  • 19. PHYSICAL GROWTHAND DEVELOPMENT PRENATAL POSTNATAL PRENATAL GROWTH: MOST CRUCIAL IN DETERMINING A CHILDS GROWTH AND FUTURE WELL BEING SINCE GROWTH IS AT ITS FASTEST DURING THIS TIME PRENATAL PERIOD – 18 TO 22 WEEKS OF GESTATION (BODY LENGTH) PEAK VELOCITY FOR HEIGHT – 34 WEEKS GESTATION GREAT RATE OF GROWTH OF FETUS COMPARED WITH THAT OF A CHILD IS LARGELY DUE TO CELLULAR PROLIFERATION .
  • 20. Physiology of growth (an over view)• HGH ACTS ON LIVER AND PRODUCES SOMATOMEDIN (SMD) WHICH STIMULATES CARTILAGE TO DIVIDE AND SYNTHESIZE CARTILAGE MATRIX• DESPITE EPISODIC SWINGS IN HGH LEVELS, SMD ACTIVITY TENDS TO REMAIN CONSTANT AS ITS HALF-LIFE IS LONGER THAN HGH
  • 21. Physiology of growth(an over view)• SMD ACTIVITY IS LOW IN PROTIEN- CALORIE MALNUTRITION• EXESSIVE GLUCOCORTICOIDS SUPRESS SMD GENERATION AND REDUCED SMD ACTIVITY IS ASSOCIATED WITH ESTROGEN ADMISTRATION
  • 22. Physiology of growth(an over view)• SKELETAL MATURATION IS CONTROLLED BY: -THYROXINE -ADRENAL STERIODS -GONADAL STEROIDS• EXCESS OF THESE ACCLERATES MATURATION AND DEFACIENCY CAUSES DELAY• DURING PUBERTY SEX STEROIDS AND HGH PRODUCE PUBERTAL GROWTH SPURT.
  • 23. Principles of growth and development 1. Bone grows by adding new bone on one side of bony cortex and taking it away from the other side, due to which bone drift occurs. 2. The inner and outer surface of the bone are covered with mosaic type appearance of growth fields, which can be resorbtive or depository. If it is resorbtive on one side it will be depository on other.
  • 24. 3. Bone has periosteal and endosteal layer if one is resorbtive then other will be depository.4. The control of growth is done by the soft tissue matrix present around the bone. The blueprint of the design construction and growth of the bone lies in the composite of muscles, tongue, lips, connective tissue, nerves, blood vessels, airways etc.
  • 25. 5. The various sites of growth do not show a same rate of growth activity.6. Remodeling is a basic part of growth process.7. Growth process leads to primary or secondary displacement.
  • 26. FACTORS AFFECTINGGROWTH AND DEVELOPMENT • 1. HEREDITY. • 2. NUTRITION. • 3. ILLNESS. • 4. RACE. • 5. SOCIO ECONOMIC FACTOR. • 6. FAMLY SIZE AND BIRTH ORDER. • 7. EXCERSIZE. • 8. ADULT PHYSIQUE. • 9. CLIMATE AND SEASONAL FACTORS. • 10. PSYCOLOICAL DISTURBANCES • 11. ENDOCRINE FACTORS
  • 27. HEREDITY: (genetic control)- Genetic control on size of parts, rate of growth and onset of growthevents.E.g.: teeth eruption, ossification of bones, adolescent growth spurt.NUTRITION:-Malnutrition delays growth and affect size of body parts. i.e. bodyproportions, body chemistry, quality and texture of tissues.E.g. teeth, bones.During short periods of mal nutrition growth slows and with return ofgood nutrition growth takes place fast.ILLNESS:Minor childhood illness does not have much effect. Prolonged seriousillness have marked effect on growth.
  • 28. Race :• Most of the differences are due to climatic, nutritional or socioeconomic• North American blacks are ahead of whites in skeletal maturity at birth up to 2 yrs of age and is associated with advanced motor behavior. Calcification & eruption is 1 yr earlier in blacks. Socio Economic factors: •Is directly related to size of the baby •Child living in favorable condition tend to be larger, display different types of growth & show variation in timing of growth when compared with disadvantaged children.
  • 29. Family size and birth order :• Size of individuals, maturation levels and intelligence can be correlated with the size of family.• First born children tend to weigh less at birth, ultimately achieve less stature and higher IQ. Exercise: Favors development of motor skills, increase in muscle mass and fitness. Adult physique: correlates with developmental events. Taller women tend to mature late.
  • 30. Climate & seasonal factors:• There is general tendency for those living in cold climate have greater proportion of adipose tissue.• Skeletal variations are associated with the climatic conditions Psychological disturbances : Children experiencing stressful conditions display an inhibition of Growth Hormone. Catch up growth is seen when the stress on them is removed.
  • 31. Endocrine Factors :• Males exhibit a more rapid growth for 3 – 6 months after birth.• This is due to presence of testosterone in serum of male infants in first few post- natal months.• This acceleration is again found after puberty that is during adolescence.
  • 32. PATTERN OF GROWTHProportionality of growth at a point of time and also changes inthis proportionality over a period of time. At 3rd month of intra uterine life: Head: 50%of total body length. At birth: Head: 39% of total body length Legs: 30% of total body length Adults:“Cephalo Caudal gradient of growth” Head: 12% of total body length “Scammon” Legs: 50% of total body length.
  • 33. SCAMMON’S GROWTHCURVE 1) NEURAL TISSUE : 90% BY 6 YRS 96%BY 10 YRS 2) LYMPHOID TISSUE : 100% BY 7 YRS 3)SOMATIC TISSUES : Slow during child hood & accelerates at puberty 4)GENITAL TISSUES : • Accelerates rapidly -on Set of puberty
  • 34. VARIABILITY OF GROWTH• Indicates the degree of difference between two growing individuals, in all planes of space including the all important time.• Everyone is not alike in the way that they grow.• Difficult but clinically important to decide an individual is normal or away from the normal range.• Evaluate deviation from usual pattern and express variability quantitatively.
  • 35. VARIABILITY OF GROWTHCharts to assess Height and Weight: Boys: Girls: 1. To evaluate the present growth status of individuals 2. To follow the growth over a period of time
  • 36. Variability in growth occurs inseveral waysFrom normal variationFrom influences out side the normal experience E.g.: Serious illnessFrom Timing effects
  • 37. TIMING OF GROWTH •Timing of Developmental events is largely under genetic control yet altered by environment. •Sex related differences in timing of growth phenomena. •Physique related difference. e.g. taller one’s mature late.• BIOLOGICAL CLOCK SET DIFFERENTLY FOR DIFFRENT INDIVIDUALS
  • 38. TIMING OF GROWTH Growth is not a steady and uniform process.• There are four growth spurts : 1. At birth. 2.1 yr. after birth. 3.Pre pubertal growth spurt. • 6-7 yrs. in females. • 7-9 yrs. in males. 1. Adolescent growth spurt. • 11-13 yrs. in females. • 14-16 yrs. in males.
  • 39. Pre pubertal Growth Spurt • Occurs due to production of sex hormones from adrenal gland at the age of around 6 yrs. In the form of a weak androgen (Dihydroepiendosterone). • This activation is therefore also referred to as adrenarche. • In girls more amount of hormones are released hence is more prominent than in boys.
  • 40. Adolescent Growth Spurt• Initiation occurs in the brain. Hypothalamus releases releasing factor from neuroendocrine glands. Via cytoplasmic transport Base of the hypothalamus near pituitary Via capillaries pituitary Ant.. pituitary releases pituitary gonadotropins Stimulates endocrine cells in adrenal gland and sex glands to produce sex hormones
  • 41. IN MALES: In testes : - Sertoli cells produce testosterone - Leydig cells produce estrogen In adrenal cortex: -Male and female sex hormones are produced. IN FEMALES: In ovaries: -Estrogen is produced initially and then progesterone. In adrenal cortex: -Male and female sex hormones are produced.
  • 42. sex hormones blood streamdevelopment of GENERAL BODY decrease in secondary GROWTH lymphoid sexual tissue characteristicsgrowth of genitals
  • 43. Timing of puberty makes a difference in ultimate body size. The earlierthe puberty the smaller will be the bodysize.
  • 44. sex hormones cartilage to grow Increases the rate at which cartilage is transformed into bone increase in skeletal maturationadolescentcomplete Growth growth spurt This maturation occurs faster in females hence they have a shorter stature.
  • 45. Clinical significance of growth spurts• Differentiate normal or pathologic growth changes• Treatment of skeletal discrepancies is advantageous if carried out in mixed dentition• Pubertal growth spurt offers the best time for treatment direction and management• Orthoganthic surgery should be performed after growth ceases.• Arch expansion is carried out during maximum growth period.
  • 46. CATCH UP GROWTHGrowth in man is very carefully regulatedprocessChildren are meant to achieve a certain heightdetermined in large part by genetic factorsIf growth is interrupted by acutemalnutrition/illness and this is then correctedthen child catches up his/her original growth.This increased velocity of growth followingcorrection of adverse circumstances istermed catch up growth
  • 47. CRITICAL PERIODS - SMITH.D.W, BIERMAN.E.L The biologic ages of man• The stage that an individual has reached at a particular time may be referred to as Biologic or Maturational age• During these periods of rapid change and differentiation, developing tissues and organs are most susceptible to humoral and environmental insults leading to growth deficiency and resultant malformations, referred to as Critical periods
  • 48. CRITICAL PERIODSBrain cells have been formed by 6 months of age and so it ishighly susceptible to produce growth deficiency disorders duringfetal and early infancy life.Bone and cartilage cells continue to divide till 15-20 years of age.Hence skeletal system is susceptible during prenatal andthroughout childhood and adolescence
  • 49. MODES OF GROWTHAt the cellular level there are onlythree possibilities of growth • HYPERTROPHY • HYPERPLASIA • EXTRA CELLUAR MATERIAL SECRETION
  • 50. NATURE OF THE SKELETAL GROWTH• INTERSTITIAL GROWTH:Combination of hyperplasia and hypertrophy and secretion of extra cellular material can also accompany. e.g.: ALL SOFT TISSUES & UNCALCIFIED CARTILAGES• DIRECT (OR) SURFACE OPPOSITION:formation of new cells in periosteum, extra cellular material secreted, get mineralized and new bone formed. e.g.: BASAL PART OF THE SKULL,TRUNK & LIMBS
  • 51. CHARECTERISTICS OFBONE GROWTH • INTRAMEMBRANIOUS OSSIFICATION Transformation of mesenchymal connective tissue into membranous sheets to osseous tissue EX: CALVARIUM, CLAVICLES BODY OF MANDIBLE SPINAL PROCESS OF VERTEBRA PART OF PELVIS • ENDOCHONDRAL OSSIFICATION Conversion of hyaline cartilage prototype into bone EX: TUBULAR BONE CUBOID BONES BASE OF SKULL VERTEBRAL BODIES PART OF PELVIS
  • 52. GROWTH MOVEMENTS (Boneremodeling)CORTICAL DRIFT:Growth movement towards the depository surface by a combination of resorption and depositionDISPLACEMENT:Movement of the whole bone as a unit - PRIMARY Displacement in conjunction with its own growth - SECONDARY Displacement of bone as result of growth and enlargement of adjacent bone.
  • 53. SITES & TYPES OF GROWTH INTHE CRANIOFACIAL COMPLEXCRANIO FACIAL COMPLEX ISDIVIDED INTO FOUR AREAS 1)CRANIAL VAULT 2)CRANIAL BASE 3)NASOMAXILLARY COMPLEX 4)MANDIBLE
  • 54. CRANIAL VAULTFLAT BONES FORMED BY INTRAMEMBRANEOUS OSSIFICATIONGROWTH PROCESS IS ENTIRELY THERESULT OF PERIOSTEAL ACTIVITY ATTHE SURFACES OF BONEREMODELLING AND GROWTH ATSUTURESCONTOUR IS BY REMODELLING ININNER AND OUTER SURFACESFONTANELLAE FUSE IN ADULT LIFE
  • 55. CRANIAL BASEINITIALLY BY CARTILAGETRANSFORMED LATER BYENDOCHONDRAL OSSIFICATIONCENTERS OF OSSIFICATION:BASI OCCIPITALSPHENOIDETHMOIDCARTILAGE IN BETWEEN CENTERSIS SYNCHONDROSIS
  • 56. NASO MAXILLARY COMPLEX ENTIRELY BY INTRAMEMBRANEOUS OSSIFICATION BY APPOSITION OF BONE AT THE SUTURES MAXILLA MOVES DOWN WARDS AND FORWARDS RELATIVE TO CRANIUM.
  • 57. NASOMAXILLARY COMPLEXBY SURFACE REMODELLINGBONE RESORBTION ANTERIORLY
  • 58. “ENLOW’S” CARTOON REPRESENTATIONSURFACE REMODELLING OF BONE IN OPPOSITEDIRECTION TO THAT IN WHICH IT IS BEINGTRANSLATED BY GROWTH OF ADJACENT STRUCTURES
  • 59. NASOMAXILLARY COMPLEX REMODELLING OF PALATAL VAULTBONE REMOVED FROMNASAL FLOOR AND ADDEDIN THE ROOF OF MOUTHRESULTING DOWNWARDAND FORWARD MOVEMENTAND ALSO WIDENING
  • 60. MANDIBLEENDO CHONDRAL AND PERIOSTEALACTIVITYCONDYLE AS AN EXCEPTION, THE REST ISBY SURFACE APPOSITION ANDREMODELLING.PRINCIPLE SITES ARE POSTERIOR SURFACEOF RAMUS,CONDYLAR AND CORONOIDPROCESSES
  • 61. MANDIBLEThe height of the mandible is byendochondral ossification at the condyleaccompanied by surface remodeling.The chin moves downwards andforwards but as a growth site chin isalmost in active.Grows longer by apposition of new boneon the posterior surface of ramus andlarge quantities of bone resorbed fromanterior surface of ramus.
  • 62. “ALTHOUGH WE APPEAR TO HAVE A FAIRLY CLEAR IDEA OF HOW THE FACES GROWS. AND OF WHERE IT GROWS, WE HAVE LITTLE IDEA OF WHY IT GROWS… WE DO NOT FULLY UNDERSTAND THE FACTORS WHICH CONTROL THE AMOUNT AND DIRECTION OF GROWTH”. MILLER - 1982
  • 63. THEORIES OF GROWTH CONTROL• 1) GENITIC THEORY• 2)SUTURAL DOMINANCE THEORY - SICHER• 3)CARTILAGENOUS THEORY - JAMES SCOTT (1950)• 4)THE FUNCTIONAL MATRIX THEORY - MELVIN MOSS (1962)• 5)VAN LIMBORGH’S THEORY - VAN LIMBORGH (1970)
  • 64. THEORIES OF GROWTHCONTROL• ENLOW’S EXPANDING “V” PRINCIPLE• ENLOWS COUNTER PART PRINCIPLE -ENLOW• SERVO SYSTEM THEORY -CHARLIER & PETROVIC(1967) -STUTZMANN &PETROVIC (1970)
  • 65. SUTURAL DOMINANCE THEORY SICHER -1952 CARTILAGE SUTURES AND PERIOSTIUM PLAY A SIGNIFICANT ROLE IN CONTROL OF THE GROWTH OF SKULL.POINTS OPPOSING :- EXTIRPATION OF FACIAL SUTURES HAS NO APPRECIABLE EFFECT ON DIMENSION- SUTURAL GROWTH HALTED BY MECHANICAL FORCES EVIDENCING THAT SUTURE DOES NOT HAVE INDEPENDENT GROWTH POTENTIAL ( KOSKI, 1968) - MICROCEPHALAY AND HYDROCEPHALAY RAISED DOUBTS ONINTRENSIC GENETIC STIMULUS OF SUTURES
  • 66. CARTILAGENOUS THEORY JAMES SCOTT-1950INTRNSIC GROWTH CONTROLLING FACTORS WEREPRESENT ONLY IN THE CARTILAGE AND PERIOSTEUMAND THE SUTURES BEING SECONDARY. NASAL SEPTAL CARTILAGE IS PACEMAKER IN NASOMAXILLARY COMPLEX
  • 67. CARTILAGENOUS THEORY….• Mandible considered as diaphysis of a long bone, bent into horse shoe shape with a cartilage constituting, half an epiphyseal plate at the ends represented by condyles.
  • 68. EXPERIMENTAL STUDIESFOVOURING THE THEORYTO TEST THE IDEA THAT CARTILAGE SERVE ASTRUE GROWTH CENTER. 1. TRANSPLANTATION OF CARTILAGE IN A NEW LOCATION OR IN CULTURE 2. EVALUATION OF THE EFFECT ON GROWTH BY REMOVING CARTILAGE AT EARLY STAGE OF LIFE.TRANSPLANTATION RESULTS: •NOT ALL SKELETAL CARTILAGE ACTS THE SAME •EPIPHYSEAL PLATE OF LONG BONES, CARTILAGE FROM SPHENOID AND CARTILAGE FROM NASAL SEPTUM APPEARED CAPABLE OF ACTING AS GROWTH CENTERS. •ALMOST NO GROWTH WAS OBSERVED ON CONDYLAR CARTILAGE TRANSPLANTATION.
  • 69. EXPERIMENTAL STUDIES FOVOURING THE THEORY THE IDEA IS THAT IF REMOVING A CARTILAGENOUS AREA STOPS OR DIMINISHES GROWTH, PERHAPS IT REALLY WAS AN IMPORTANT CENTRE FOR GROWTH. SEPTAL CARTILAGESEGMENT OF NASAL CARTILAGE REMOVED AT 8YRS OF AGEREMOVED IN A GROWING RABBIT. DUE TO TRAUMA MOST OBSERVERERS CONCLUDED THAT THE SEPTAL CARTILAGE DOES HAVE SOME INNATE GROWTH POTENTIAL.
  • 70. POINTS IN FAVOUR OF THETHEORY:1. IN MANY BONES CARTILAGE GROWTH OCCURS, WHILE BONE MERELY REPLACES IT.2. TRANSPLANTED EPIPHYSEAL PLATE CONTINUES TO GROW IN NEW LOCATION INDICATES THE INNATE GROWTH POTENTIAL OF THE CARTILAGE.3. NASAL SEPTAL CARTILAGE ALSO SHOWED INNATE GROWTH POTENTIAL ON BEING TRANSPLANTED TO ANOTHER SITE.4. EXPERIMENTS ON RABBITS INVOLVING REMOVAL OF NASAL SEPTAL CARTILAGE DEMONSTRATED RETARDED MID-FACE DEVLOPMENT. BUT…..
  • 71. SOME AUTHORS ARGUE THAT SURGERY ITSELFAND THE ACCOMPANYING INTERFERENCE WITHBLOOD SUPPLY TO THE AREA, NOT THE LOSS OFTHE CARTILAGE, CAUSE FOR THE GROWTHDEFICIENCY.AS RECENTLY AS THE 1960s IT WAS STATED THAT CONDYLAR FRACTURES, AT AN EARLY AGE LEAD TO SEVERE GROWTH DISTRUBANCES. THIS MAY BE DUE TO , THE CONDYLAR FRAGMENT IS PULLED AWAY FORM ITS ORIGINAL LOCATION BY THE LATERAL PTERIGOID MUSCLE AND GET RESORBED OVER A PERIOD OF TIME. AND SO THE GROWTH DISTURBANCE. BUT….
  • 72. “Gillhums-moe and Lund” in their studies conducted scandinavian children, only 15 to 20% suffered fromreduction of growth after condylar #s.“THEY DEMONSTRATED THAT AFTER THE #OF MANDIBULAR CONDYLE IN A CHILD ,THERE WAS AN EXCELLENT CHANCE THATTHE CONDYLAR PROCESS WOULDREGENERATE TO OPPROXIMATELY ITSORIGINAL SIZE”.“THEY ALSO EXPLAINED THAT A NEW CONDYLEREGENERATES DIRECTLY FROM THE PERIOSTEUMAT THE SITE OF FRACTURE”.
  • 73. It appears that epiphyseal cartilages,nasal septal cartilage (to a lesserextent) and cranial base synchondrosesprobably act as independently growingcenters. Transplantation experiments nor experiments in which condyle is removed lend any support to the idea that the condylar cartilage is an important growth centre.
  • 74. Functional Matrix Hypothesis(Moss’ Hypothesis-1968) “The functional matrix is primary and the presence, size, shape, spatial position, and growth of any skeletal unit is secondary, compensatory, and mechanically obligated to changes in the size, shape, spatial position of its related functional matrix”PROFESSOR MEVLIN L MOSS
  • 75. Functional Matrix Hypothesis (Moss’ Hypothesis) “The origin, development and maintenance of all skeletal units are secondary, compensatory and mechanically obligatory responses to temporally and operationally prior demands of related functional matrices.”
  • 76. The functional cranial component isdivided into two: • Functional Matrix • Skeletal Unit.•All the tissues, organs and spaces comprise thefunctional matrix•Skeletal matrix comprises the skeletal unit.
  • 77. Skeletal unit:• All skeletal tissues associated with a single function are called “skeletal unit”. E.g. bone, cartilage and tendinious tissue.When a bone is comprised of several contiguous skeletal units,they are termed as “micro- skeletal units”.Maxilla and Mandible are comprised of number of such Micro-Skeletal Units.e.g. Mandible: alveolar,angular,condylar,gonial,mental,coronoidand Basal skeletal units.Maxilla: Orbit, Pneumatic,, palatal micro skeletal units.
  • 78. Types of Functional Matrix1. Periosteal matrix 2. Capsular matrix(e.g., muscles, blood vessels, (e.g., brain, oral cavity)nerves and glands) Passive growthAct directly on skeletal units No depositionDeposition and resorption No resorptionAffect size and/or shape Affect location
  • 79. Craniofacial Growth Active growth process 1) Sutural growth Growth 2) Bone remodeling 3) Cephalic cartilage growthActive growth (Periosteal) +Passive growth (Capsular) Passive growth process = 1) The growth of neural, Total growth orbital, CSF, and other masses and real substances 2) The expansion of oro- naso- pharyngeal and other functioning spaces
  • 80. He theorizes that growth of faceoccurs as response to functional needsand neurotrophic influences, and ismediated by the soft tissue in whichthe jaws are embedded. The soft tissues grow, and both bone and cartilage react.
  • 81. • The growth of cranium is a direct response to the growth of the brain.• Pressure exerted by the growing brain separates the bones at sutures, and new bone passively fills in at these sites .e.g. Microcephaly & Hydrocephaly are explanatory.
  • 82. • Enlarged eye or small eye causes a corresponding change in the orbital cavity.• Moss theorizes that major determinant of growth of maxilla and mandible is enlargement of nasal and oral cavities, which grow in response to functional needs.• Absence of normal function would have wide-ranging effects.
  • 83. • Resulting loss of condyle in condylar # does not impede mandibular growth.• Children in whom a growth deficit occurs, may be due to interference with normal function.• Mandibular Ankylosis.• Infection or trauma in the TMJ, leading to scarring causes mechanical restriction, thus impeding the growth .
  • 84. Illizarow: 1950• Demonstrated that bone can be induced to grow at surgically created sites by a method called Distraction osteogenesis.“If cuts were made throughthe cortex of any bone, theycould be lengthened byapplying graduated traction(.5-1.5mm/day) after initialcallus formation (7 days).Large amounts of new bonecan be formed in between thecut segments”.
  • 85. Distraction osteogenesis is now a days widely used in lengthening Arms or legs by several centimeters.In 1992, McCarthy et al, reported the firstclinical cases of mandibular lengtheningby gradual distraction.Molina et al, reported mandibularelongation by distraction as a farewell tomajor osteotomies. Reconstruction of mandibular and maxillary defects, treating patients with “hemi facial microsomia” is done now a days by distraction osteogenesis.
  • 86. Mouth breathing children tend to havehigher mandibular inclination and morevertical growth. These findings supportthe influence of the breathing mode incraniofacial development. Fernanda Campos Rosetti Lessa,etal Otorrinolaringol. V.71, n.2, 156-60, mar./apr. 2005
  • 87. Obliterative osteogenesis occurred in the inter nasal suture (synostosis) in the group of rats with reduced masticatory function. Thus, it seems that masticatory function may influencesuture closure. Christer Engström, Stavros Kiliaridis and etal The European Journal of Orthodontics 1986 8(4):271-279; doi:10.1093/ejo/8.4.271 © 1986 by European Orthodontic Society
  • 88. Van limborgh’s theory: 1970He explained the process of growth and development in a view that combines all the three theories.He suggested five factors which controls growth. 1. Intrinsic genetic factor 2. Local epigenetic factor 3. General epigenetic factor 4. Local environmental factor 5. General environmental factor
  • 89. Intrinsic genetic factor :They are genetic control of the skeletal units themselvesLocal epigenetic factor :Bone growth is determined by genetic control originating from adjacentstructures like brain, eyes etcGeneral epigenetic factor:They are genetic factors determining growth from distant structures. E.g.sex harmones, growth harmones. Etc.Local environmental factors:They are non-genetic factors from local external environment. e.g. habits,muscle force. etc.General environmental factors: They are general non-geneticinfluences such as nutrition, oxygen. Etc.
  • 90. Views expressed by van limborghsummsrised as:• Chondro cranial growth is mainly controlled by intrinsic genetic factors.• Desmocranial growth is controlled by any few intrinsic factors• Cartilagenous parts of the skull must be growth centers.
  • 91. Views expressed by van limborghsummsrised as: • Sutural growth is controlled by influences originating from skull cartilages and from other adjacent skull structures. • Periosteal growth largely depend upon growth of adjacent structures. • Sutural and periosteal growth are additionally governed by local non-genetic environmental influence.
  • 92. ENLOWS’S “V” PRINCIPLE: Many facial bones or parts of bones have a “V” shaped pattern of bone growth. “V” pattern of growth occurs in: - Base of the mandible - Ends of long bones - Mandibular body - Palate. etc.Bone deposition occurs on the inside of the wide endV and resorption on the outer side
  • 93. Enlow’s counter partprinciple:• Growth of any given facial or cranial part relates to other structural and geometric counter parts in the face and cranium.• There are regional relationships throughout the whole face and cranium.• If each regional part and its counter part enlarge to the same extent balanced growth occurs
  • 94. Enlow’s counter part principle:• Imbalances in the regional relationships are produced by differences in: - Amounts of growth between counterparts- Directions of growth between them- Time of growth between them.
  • 95. Different parts and their counterparts:• NASOMAXILLARY COMPLEX – ANTERIOR CRANIALFOSSA• HORIZONTAL DIMENSION OF – MIDDLECRANIAL FOSSA• PHARYNGEAL SPACE• MIDDLE CRANIAL FOSSA – BREADTH OF RAMUS• MAXILLA – MANDIBLE• BONY MAXILLA – CORPUS OF MANDIBLE• MAXILLARY TUBEROSITY – LINGUAL TUBEROSITY
  • 96. SERVO SYSTEM THEORY : Charlier and Petrovic 1967, stutzmann and petrovic-1970 • The influence of the Somatomedin complex (STH) on growth of primary cartilages like: - Epiphyseal cartilage of long bones - Cartilage of nasal septum - Spheno occipital synchondrosis - Lateral cartilagenous mass of ethamoid - Cartilage between body and greater wing of sphenoid has a cybernetic form of command.
  • 97. SERVO SYSTEM THEORY :The influence of thesomatomedin complex on thegrowth of secondary cartilageslike condylar, coronoid, angularcartilage of mandible, cartilageof mid-palatal suture, someother cranio facial sutures andprovisional callus during bonefracture repair comprises notonly direct but also someindirect effects on the cellmultiplication. With condylar , coronoid & angular cartilages, these indirect effects corresponds to regional and local factors involving primarily neuro muscular mechanisms relative to postural adjustment.
  • 98. Methods of studying growth:• 1) MEASUREMENT APPROACH : Technique for measuring living animals including Humans, so that measurement itself does not harm the animal, and it is available for additional measurements another time. CRANIOMETRY ANTHROPOMETRY CEPHALOMETRIC RADIOGRAPHY• 2)EXPERIMENTAL APPROACH: This approach manipulates in the some way. The subject is available for a detailed study that may be destructive. And so done in only in Non- Human species. VITAL STAINING (JOHN HUNTER) AUTO RADIOGRAPHY RADIO ISOTOPES IMPLANT RADIOGRAPHY (VJORK&COWORKERS)
  • 99. OTHER METHODS: • 1)NATURAL MARKERS - NUTRIENT CANALS - TUBERCULAE • 2)COMPARITIVE ANATOMY • 3)GENETIC STUDIES
  • 100. Craniometry:• Involves measurement of skull found among human skeletal remains.• Can be made on dry skulls.• Such a growth study can only be cross sectional. Anthropometry :•Involves measuring skeletal dimensions on living individualsby using soft tissue points overlying these bony landmarks.•Measurements can be made on both dry skull as well as livingindividuals, where the thickening of soft tissue is alsoconsidered.•Study is longitudinal, where in the growth of an individual canbe followed directly over a period of time with repeatedmeasurement without damaging subject.
  • 101. Cephalometric Radiography :• This technique depends on placement of an individual in a cephalostat so that the head can be precisely oriented and controlled magnification can be made.• Combines the advantage of both cranio and anthropometry• Bony measurements as seen on the radiograph can be made over a period of time for the same individual.• Dis-advantage: produces only two dimensional representation of two dimensional structure making it impossible to make all measurements
  • 102. Vital staining: originated by John hunter in 18 th centuary• Growth is studied by observing the pattern of stained mineralized tissues after the injection of the dyes into the animal. E.g. Alazarin was used for vital staining studies in animals.• The gamma emitting isotope can be used to detect areas of rapid bone growth in humans.
  • 103. Auto radiography:• Technique in which film emulsion is placed over a thin section of tissue containing radio active isotope and then is exposed in dark by radiation.• After the film is developed, the location of the radiation that indicates where growth is occurring can be observed by looking at the tissue section through the film.
  • 104. Radio isotopes:• These elements were injected into tissues which get incorporated in the developing bone and act as in vivo marker.• These can be later detected by tracing down the radioactivity they emit. The radio isotopes used are:• Technetium – 33• Calcium – 45• Potassium – 32.
  • 105. Implant Radiographyused by : Bjork and co-workers• Inert pins made of titanium are inserted in bone anywhere in the skeleton including face and jaw.• These pins are biocompatible super-imposing radiographs (cephalograms in case of face) on the implants allow precise observation of both changes in position of bone relative to another and changes in external contour of the individual bone.
  • 106. METHODS OF COLLECTINGGROWTH DATA• LONGITUDINAL STUDIES INVOLVES GATHERING DATA OF GIVEN INDIVIDUAL OVER A PERIOD OF TIME AT REGULAR INTERVALS * ADVANTAGES AND DISADVANTAGES• CROSS SECTIONAL STUDIES OBSERVATIONS AND MEASUREMENTS MADE OF DIFFERENT SAMPLES STUDIED AT DIFFERENT PERIODS * ADVANTAGES
  • 107. TYPES OF GROWTH DATA• 1)OPINION From experienced person, but not reliable scientifically when better sources available.• 2)OBSERVATION all or none phenomenon• 3)RATINGS AND RANKINGS a standard conventionally accepted scale for classification.• 4)QUANTITATIVE MEASURMENTS - DIRECT DATA - INDIRECT DATA - DERIVED DATA
  • 108. Genes in growth and development Hox genes: {homeobox genes}:they are an excellent example of molecular studies as applied to craniofacial embryogenesis is homeoboxgenes These were first discovered in fruitfly [drosophila} research and subsequent similar genes were aslo discovered in other organisms
  • 109.  This high similarity of genes in which more than 400 have been indentified in human ,fly underlines the universality of basic biologic templates from which developmental mechanisms evolve A recentlu developed hox genes 7 8 9 is expressed in range of neural crest derived tissues and areas of putataive epithelial mesenchymal interactions during embryogenesis
  • 110. Growth factors in growth and development They are mitigenic polypeptides tht influence cell differntiation and morphogenesis Three imp growth fators are TGF-BETA EGF FGF
  • 111. TGF-BETA IT IS IMP GROWTH FACTOR IN EMBRYOGENESIS IT IS MAINLY USEFUL IN CHEMOTACTIC PROLIFERATION APOPTOSIS CONTROL THE EDEVELOPMENT AND MAINTANENCE OF MOST TISSUES
  • 112.  TGF BETA SIGNALLING PATHWAY ACTS MAINLY BY PHOSPORELATION OG SMAD PROTIENSBY SERINE AND THREONINE KINASE THEY REGULATE SPECIFICATION OF CRANIAL NEURAL CREST CELLS THEY PLAY MAJOR ROLE IN DEVELOPMENT AND MAINTANENCE AFFECTING BOTH CARTILAGE AND BONE METABOLISM IT AFFECTS BOTH OSTEOBLATS AND OSTEOCLASTS
  • 113. The FGF signalling pathway plays crucialrole in development of craniofacialskeletogenesis, synchondrosis regulation,lacrimal and salivary gland formation,myogenesis and even tooth formationX Nie,K Luukko, P KettunenOral Diseases(2006) 12,102-111
  • 114. FGF PATHWAY FGF CONSTITUTE LARGE FAMILY OF POLYPEPTIDE GROWTH FACTORS THERE SIGNALLING PATHWAY IS THROUGH RECEPTOR TYROSINE KINASE THEY HELP IN APOTOSIS CELL SURVIVAL CHEMOTAXIS CELL ADHESION CELL MIGRATION CELL DIFFERNTIATION AND PROLIFERATION
  • 115. REFERENCES INTRODUCTION TO CRANIOFACIAL BIOLOGY BY DAVID S CARLSON ESSENTIALS OF MEDICAL PHYSIOLOGY BY DICKSON AND TORTORA ESSENTIAL PEDIATRICS BY GHAI DENTISTRY FOR CHILD AND ADOLESCENT BY MC DONALD EIGHTH EDITION CONTEPORARY ORTHODONTICS 3RD EDITION BY WILLIAM R PROFITT MOYERS TEXT OF ORTHODONTICS 3 EDITION STEWARTS TEXT OF PEDIATRIC DENTISTRY
  • 116. CONCLUSION JUST AS THE CLINICIAN NEEDS THE MEDICAL HISTORY TO MAKE A LOGICAL DIAGNOSIS,SO TO THE GROWTH AND DEVELOPMENT OF FACE IS ESSENTIAL FOR A LOGICALEXPLANATION OF ANY STRUCTURAL AND
  • 117. REFERENCES:• PEDIATRIC DENTISTRY• -REY E STEWART CONTEMPORARY ORTHODONTICS• -WILLIAM R PROFIT –3 rd EDITION• ORTHODONTICS PRINCIPLES AND PRACTICE• -GRABER T.M –3 rd EDITION• HAND BOOK OF ORTHODONTICS• -ROBERT E MOYERS-4 th EDITION
  • 118. REFERENCES:Christer Engström, Stavros Kiliaridis and etalThe European Journal of Orthodontics 1986 8(4):271-279Fernanda Campos Rosetti Lessa,etal Otorrinolaringol. V.71, n.2, 156-60, mar./apr. 2005X Nie,K Luukko, P KettunenOral Diseases(2006) 12,102-111
  • 119. THANK YOU