Theories of growth00000000000000000000000.pptx

l

1. THEORIES OF GROWTH

2. INTRODUCTION MECHANISM OF BONE GROWTH EVOLUTION OF THEORIES BONE REMODELLING THEORY BRASH (1930) GENETIC THEORY A. BRODIE (1941) SUTURAL HYPOTHESIS SICHER AND WEINNMAN (1952) CARTILAGINOUS THEORY/ SCOTT HYPOTHESIS FUNCTIONAL MATRIX THEORY MELVIN MOSS (1960S) ENLOW’S PRINCIPLES COMPOSITE HYPOTHESIS VON LIMBORGH NEUROTROPHIC THEORY SERVO SYSTEM THEORY REFERENCES CONTENTS

3. PROFFIT Growth usually refers to an increase in size and number MOSS Change in any morphological parameter which is measurable KROGMAN Increase in size, change in proportion and progressive complexity TODD Growth refers to increase in size MOYERS Growth is the quantitative aspect of biologic development and is measured in units of increase per units of time, for instance, inches per year or grams per day JX HUXLEY The self multiplication of living substance GROWTH

4. DEVELOPMENT

5. Apposition ( Deposition) Resorption Growth Site Growth Centre Cortical drift Displacement

6. Remodeling Bone changes in shape and size by two basic mechanisms, bone deposition bone resorption. The process of bone deposition + resorption is called bone remodeling . Addition of new bone to the bony surfaces by osteoblastic activity is called Apposition (deposition) usually represented by "+" sign. The removal of bone by osteoclastic activity is called Resorption usually represented by "- ve " sign.

7. Backward movement of the ramus of the Mandible The mandible grows longer by: apposition of new bone on the posterior surface of the ramus. Resorption of bone from the anterior surface of the ramus

8. GROWTH SITE GROWTH CENTER A site where actual growth or its effects occurs but that is not genetically controlled, eg : sutures of the maxilla and cranium The location at which independent (genetically controlled) growth occurs, eg : synchondroses, epiphyseal plates All growth sites are not growth centers All growth centers are the growth sites They do not control overall growth of the bone They control overall growth of the bone They do not have independent growth potential They have independent growth potential When transplanted on other sites, they do not grow When transplanted, they can grow independtly They are affected by external influence They are mainly affected by functional needs They do not lead to growth of whole bone, but only some part of the bone. They lead to growth of major parts of the bone. GROWTH FIELD

9. Cortical drift Cortical drift and displacement provides means of growth movement in craniofacial development. The cortical plate can be relocated by simultaneous apposition and resorption process occurring on the opposing periosteal and endosteal surface. Such a combination of deposition and resorption resulting in a growth movement towards a depositing surface has been described as cortical drift by Enlow (1963). If bone deposition & resorption on either side of a bone are equal thickness of the bone remains constant. If more bone is deposited on one side & less bone resorbed on the opposite side thickness of the bone increases

10. It is the movement of the whole bones as a unit. Displacement can be of two types: ■ Primary displacement or translation : displacement of the bone as a result of its own growth. For eg ; maxilla grows with deposition of bone at the tuberosity region. The formation of new bone at its posterior end results in pushing of the maxilla against the cranial base displacement of the maxilla in a forward and downward direction. Displacement

11. ■ Secondary displacement or translocation : This is the dislacement of the bone resulting from the pull or push of the growth of the peripheral structures or an adjacent bone. For eg , the growth of the cranial base pushes the entire maxilla in forward and downward direction. This displacement is passive in nature.

12. Early Concepts of Craniofacial Growth During the latter part of the 19th century and the middle third of the 20th century, the field of craniofacial biology witnessed development of a series of four or five relatively distinct, sequentially arranged, and competing theories of craniofacial growth. Each of these theories supported to explain the essential elements of craniofacial growth by focusing essentially on a particular factor as being the primary mechanism determining craniofacial growth and form. Studies by Sir John Hunter in the 18th century on the growth of the jaws and eruption of the dentition represent the first scientific research on craniofacial growth. This line of research using vital dyes continued throughout the late 19th and early 20th centuries primarily to study the nature of bone growth in general

13. The various theories of growth are: • Bone remodelling theory Brash (1930) • Genetic theory A. Brodie (1941) • Sutural hypothesis Sicher and Weinnman (1952 ) • Cartilaginous theory/ Scott Hypothesis/ Nasal Septum Theory/ Nasocapsular Theory • Functional matrix theory Melvin Moss (1960s) Enlow ’s V Principle Enlow’s Counterpart Principle Composite hypothesis Von Limborgh Neurotrophic process in orofacial growth (Moss 1971) • Servo system theory Alexandre Petrovic (1970s) Theories of growth

14. Bone remodelling theory of Craniofacial Growth Brash (1930) Introduction of vital staining method by John Hunter helped Brash to postulate the first general theory the "bone remodeling theory". This theory concluded that bone grows only by interstitial growth . The three fundamental tenets of this theory are: 1. Bone grows only by apposition at the surfaces. 2. Growth of jaws takes place by deposition of bone at the posterior surfaces of the maxilla and mandible. This is described as " Hunterian growth ".

15. 3. Calvarium grows through bone deposition on the ectocranial surface of the cranial vault and resorption of bone on the endocranial surface Bone remodeling theory postulated that the craniofacial skeletal growth takes place by bone remodeling selective deposition and resorption of bone at its surfaces.

16. The Genetic Theory (A. Brodie—1941) The genes determine and control the whole process of craniofacial growth. The field of genetics consists of two principle areas of interest: " Transmission genetics " is characterized by statistical approach and involved only in explaining possible method of transmission. It did not explain about genes or its characteristics. Weisman-19th century introduced the concept of " germ plasm “, determinant of traits that is transmitted from parents to offspring is present in the cytoplasm of the gametes. Mendel- introduced the term " Pangene " to describe the germ plasm. Bateson introduced the term “ genetics ”(1909)

17. Johnson used the term " gene " to the presumed unit of heredity. Limitation- Transmission genetics could not explain all the changes taking place in craniofacial growth. As the genetic theory failed to explain so many occurrences on craniofacial growth, the focus shifted from transmission genetics to molecular genetics. 2. Developmental and molecular genetics

18. The Sutural Hypothesis/Sutural Dominance Theory (Sicher and Weinnman)—1952 Introduction S utures, cartilages and periosteum are growth centers like the epiphysis of long bones and all responsible for facial growth and were assumed to be under intrinsic genetic control Essence of the Theory According to Sicher , the sutures are the primary determinants of craniofacial growth. The craniofacial skeleton enlarges due to the expansible forces exerted by the sutures as they separate.

19. The primary event in sutural growth is the proliferation of the connective tissue which between the two bones. CRANIAL VAULT primary growth of bone at the sutures, which forces the bones of the vault away from each other. MANDIBLE intrinsically determined growth of the cartilage of the mandibular condyle, which pushes the mandible downward and forward. MAXILLA bone growth within the various maxillary sutures produces pushing of the bone which results in forward and downward movement of maxilla.

20. It was believed that the stimulus for bone growth is tension, produced by the displacement of bones.

21. Growth of the midface takes place via intrinsically determined sutural expansion of the circummaxillary suture system, which forces the midface downward and forward.

22. Evidences against Sutural Theory • Trabecular pattern in the bones at the suture change with age, indicating the changes in the direction of growth. It cannot be accepted that sutures will have the necessary information for altering growth. • Subcutaneous auotransplantation of the zygomaticomaxillary suture in the guinea pigs has not been found to grow • Extirpation of facial sutures has no appreciable effect on the dimensional growth of the skeleton • Shape of sutures have been found to depend on functional stimulus (Moss & Salentejin , 1969). • Closure of suture appears to be extrinsically determined (Moss ML). • Sutural growth can be halted by mechanical force like clips placed across the sutures ( Leitunen , 1956).

23. Scott Hypothesis/Nasal Septum Theory/ Cartilagenous Theory/ Nasocapsular Theory James H Scott, proposed the nasal septum theory as the single and unified theory of craniofacial growth. Essence of Theory According to the theory, sutures play little or no direct role in the growth of the craniofacial skeleton (Sutures are considered as merely passive , secondary and compensatory sites of bone formation and growth.) but cartilage and periosteum play primary role in craniofacial growth. Scott felt that cartilagenous development was under tight genetic control and they continued to dominate postnatal facial growth also.

24. MANDIBLE Mandible can be viewed as a diaphysis of a long bone, bent into a horseshoe shape with the epiphyses removed He explained the mandibular condyle cartilages as growth centers for the growth of mandible as it “pushes” the mandible downward and forward.

25. CALVARIA (BASE AND VAULT) "Synchondrosis" in the cranial base is the primary cartilage for the calvaria growth and sutures of cranial vault are secondary. These two factors are involved in the calvarian growth.

26. MIDFACE( NASOMAXILLARY COMPLEX ) - Nasal Septum Theory Scott concluded that nasal septum is mostly active and vital (PACEMAKER) for craniofacial growth both prenatally and postnatally The anteroinferior growth of the nasal septal cartilage which is buttressed against the cranial base "pushes" the midface downward and forward

27. Evidences Supporting the Theory Two kinds of experiments have been carried out to test the idea that cartilage can serve as a true growth center. Transplanting cartilage epiphyseal plate of a long bone is transplanted- continue to grow in a new location or in culture, indicating that these cartilages do have innate growth potential. spheno -occipital synchondrosis of the cranial base - grows when transplanted, but not as well. mandibular condyle- little or no growth was observed when transplanted

28. Evaluation of the effect on growth of removing cartilage at an early age. One individual in whom the entire septum was removed at age 8 after an injury.

29. Evidences Against the Theory • Moss and Bloonberg (1968), Brigit Thilander (1970)found only slight deformity after extirpation of septal cartilage. They concluded that septal cartilage provides only mechanical support for the nasal bonesand is not a primary growth center. • Melson (1977) stated that downward sliding of vomer in relation to anterosuperior part of nasal septum takes place throughout craniofacial development making it unlikely that cartilaginous septum could push the maxillary complex forward as suggested by Scott. • It can be argued that the surgery itself and the accompanying interference with blood supply to the area, not the loss of the cartilage, cause the growth changes.

30. Functional Matrix Hypothesis (FMH)— Melvin Moss Introduction The concept that "form follows function" was first proposed by Vander Klaaw (1948-52). Functional matrix theory is actually an extension of this concept. Melvin Moss and his co-workers developed the form and function concept into the "functional matrix hypothesis". Essence of the Theory Functional matrix hypothesis maintains that apart from initiating the process of development, heredity and genes play no active role in growth of skeletal Structures.

31. Definition Functional matrix hypothesis claims that the origin,growth and maintenance of all skeletal tissues and organs are always secondary compensatory and obligatory responses to temporally and operationally prior events or processes that occur in specifically related nonskeletal tissues, organs or functioning spaces (functional matrices) Functional Cranial Component The totality of all the skeletal structures, soft tissues and functioning spaces (nasal, oral, etc.) necessary to carry out a specific function is collectively called a "functional cranial component”

32. Acts directly on the Macroskeletal unit Cause changes in size and shape of bone by apposition and resorption Effects active growth/ Transformation Acts indirectly on the Macroskeletal unit Cause changes in spatial position of skeletal units Effects passive growth/ Translation Maxilla Mandible eg : alveolar, gonial,condylar,angular unit of Mandible

33. Periosteal matrix The periosteal matrix corresponds to the immediate local environment. Examples of periosteal matrices include muscles,blood vessels, nerves, teeth etc. These matrices act directly and actively on adjacent skeletal units. All periosteal matrices act homogenously by means of osseous deposition and resorption. The net effect of periosteal matrix is to alter the form and relative position of that particular microskeletal unit.

34. The capsular matrix ■ The capsular matrix is defined as the functional matrix that encloses functioning cavities/spaces/organs. ■ Examples NEUROCRANIAL CAPSULE- brain and covering layers, aponeurosis, dura mater, skin,skin and dura mater. OROCRANIAL CAPSULE - oropharynx, nasopharynx, the skin and mucosa form the covering encloses oral, nasal and pharyngeal spaces. Other examples are orbital capsule, otic capsule , etc. ■ The capsular matrix unlike periosteal matrix acts indirectly and passively in total on all these microskeletal units producing a secondary translation of whole macroskeleton in space. ■ Capsular matrices do not act by the processes of resorption and deposition.

35. All the skeletal tissues associated with a single function is called the 'skeletal unit’ The skeletal unit may be comprised of bone, suture, cartilage, synchondrosis and tendinous tissue, etc. MICROSKELETAL UNIT The skeletal unit (bone) is made up of several small contiguous skeletal units MACRO SKELETAL UNIT When adjoining portions of a number of microskeletal units work to carry out a single cranial component. Thus, macroskeleton is composed of small micro skeletal units Eg : Cranial vault is a macroskeleton with numerous microskeletons of anatomically different bones. Skeletal unit

36. Evidences Supporting the Theory Growth of the cranial vault is a direct response to the growth of the brain. Pressure exerted by the growing brain separates the cranial bones at the sutures, and new bone passively fills in at these sites so that the brain case fits the brain. W hen the brain is very small, the cranium is also very small, and the result is microcephaly. An enlarged eye or a small eye will cause a corresponding change in the size of the orbital cavity. In this instance, the eye is the functional matrix. bone can be induced to grow at surgically created sites by the method called distraction osteogenesis Ilizarov discovered in the 1 950s that if cuts were made through the cortex of a long bone of the limbs,the arm or leg then could be lengthened by tension to separate the bony segments. segments are separated at a rate of 0.5 to 1 .5 mm per day Teeth act as functional matrix for the alveloar bone

37. An enlarged eye or a small eye will cause a corresponding change in the size of the orbital cavity. In this instance, the eye is the functional matrix. bone can be induced to grow at surgically created sites by the method called distraction osteogenesis Ilizarov discovered in the 1 950s that if cuts were made through the cortex of a long bone of the limbs,the arm or leg then could be lengthened by tension to separate the bony segments. segments are separated at a rate of 0.5 to 1 .5 mm per day

38. ENLOW’S V PRINCIPLE A most useful and basic concept in facial growth is the V principle. Many facial and cranial bones, or parts of bones, have a V-shaped configuration(funnel shape in three diemensions ). Bone deposition - inner side of the V Resorption - outside surface . Due to this, the bone moves in the direction towards the wide end of 'V.’ Simultaneously deposition takes place at the ends of the two arms of the 'V,' resulting in its widening.

39. Most of the craniofacial bones including mandible- base of the mandibular body, coronoid, condylar process, maxilla and palate grow on an expanding “ V”principle . Deposition occur on the palatal periosteal surface and resorption occurs on the side of nasal floor in this way ,palate expands on the lateral direction and also move downward.

40. The counterpart principle of craniofacial growth states that events (growth) in any one region of the skull necessarily influence the growth in others. functional equilibrium is maintained According to this, the growth of any given craniofacial structure is related specially to certain other structural and geometric counterpart in the craniofacial complex. A dimensionally balanced growth occurs when each regional part and its particular counterpart enlarge to the same extent. ENLOW’s Counterpart principle

41. There are number of counterparts, which are situated in the craniofacial region. Few of them are: ■ Nasomaxillary complex v/s anterior cranial fossa ■ Middle cranial fossa and breadth of ramus are counterparts ■ Maxillary arch v/s mandibular arch.

42. Van Limborgh’s Theory Van Limborgh put forward a multifactorial theory in 1970’s as a compromise between the existing popular three theories of growth. He accepts functional matrix theory of Moss, supports some aspects of sutural theory of sicher and also genetic involvement.

43. 1.Intrinsic genetic factors: they are the genetic factors inherent to the craniofacial skeletal tissues. 2.Local epigenetic factors(Capsular matrix) : these are genetically determined influences originating from the adjacent structures and spaces such as brain,eyes etc. 3.General epigenetic factors : these are originating from growth hormones. 4. Local environmental factors: ( periosteal matrix) : these are local nongenetic influences from external environment.Example : muscle force local external pressure(habit). 5.General environmental factors: general nongenetic influences from external environment. Example: oxygen supply nutrition. Van Limborgh : 5 controlling factor of growth

44. This was proposed by Behrents in 1970. This theory states that the nerve impulse involving axoplasmic transport has direct growth potential. It also has an indirect effect on the osteogenic growth by influencing soft tissue growth. The different types of neurotrophic mechanisms are: 1. Neuroepithelial trophism 2. Neurovisceral trophism 3. Neuromuscular trophism Neurotrophism

45. Neuroepithelial Trophism Epithelial growth is normally controlled by the release of neurotrophic substances by the nerve synapses. Lack of this neurotrophic process causes abnormal epithelial growth , orofacial hypoplasia and malformation etc , i.e., the tissues and epithelium become atrophic when they are deinnervated since the nerves have a neurotrophic effect in sustaining healthy growth. Neuromuscular Trophism At the myoblast stage of differentiation, the embryonic myoblasts establishes neural innervation without which further myogenesis usually cannot continue.

46. Neurovisceral Trophism The periosteal matrices genetically determine the apparent localized neurotrophically controlled genomes. The attributing factors that form the basis of the neuro-visceral tropism, e.g., the salivary glands, fat tissue and other organ, regulate the embedded passive position of the skeletal units. The degree to which neurovisceral control has altered the casual change indicates the dominance of the homeostatic control of genome.

47. The last major theory of craniofacial growth to emerge, the servosystem theory, was developed by Alexandre Petrovic 1974 , a physician-scientist interested in the extrinsic and intrinsic hormonal factors that affect cartilage growth. Craniofacial growth is controlled by a series of changes occurring in craniofacial skeleton and dentition, which in turn start a feedback mechanism, to stimulate further growth changes to occur. 1970s: Servosystem Theory of Craniofacial Growth (Petrovic)

48. Most simply, the servosystem theory is characterized by the following two principal factors: (1) the hormonally regulated growth of the midface and anterior cranial base, which provides a constantly changing reference input via the occlusion, and (2) the rate-limiting effect of this midfacial growth on the growth of the mandible. While growth of the mandibular condyle and of the sutures may be affected directly and indirectly by systemic hormones, growth of these structures is clearly more compensatory and adaptive to the action of extrinsic factors, including local function as well as the growth of other areas of the craniofacial complex. Growth of the primary cartilages of the craniofacial complex, such as the cranial base and nasal septum, was influenced significantly less by local epigenetic factors and more by STH-SOMATOMEDIAN COMPLEX

49. as the midface grows downward and forward under the primary influence of the cartilaginous cranial base and nasal septum, mediated by the endocrine system the maxillary dental arch is carried into a slightly more anterior position. This causes a minute discrepancy between the upper and lower dental arches proprioceptors within the periodontal regions and temporomandibular joint perceive even a very small occlusal discrepancy and tonically activate the muscles responsible for mandibular protrusion- LATERAL PTERYGOID MUSCLE acts directly on the cartilage of the mandibular condyle and indirectly through the vascular supply to the temporomandibular joint, stimulating the condyle to grow .

50. Finally, the effect of the muscle function and responsiveness of the condylar cartilage is influenced both directly and indirectly by hormonal factors acting principally on the condylar cartilage and on the musculature. This entire cycle is continuously activated as a servomotor as long as the midface-upper dental arch continues to grow and mature and appropriate extrinsic, hormonal, and functional factors remain supportive .

51. Whetten and Johnston (1985) used a bilateral condylotomy model in young rats to test the extent to which direct muscle traction can alter the rate of condylar growth and removed the lateral pterygoid muscle unilaterally. They found no difference in condylar growth between the two sides. Das, Myer and Sicher (1980) found that the occlusion remained unaffected in condylectomy studies. DRWABACKS

52. References 1.Proffit's Contemporary Orthodontics, Elsevier India. 3/E; 2000 2. Graber TM. Orthodontics: Principles and Practice, 3rd ed., WB Saunders; 1988. 3. Moyers E. Handbook of Orthodontics, 4th ed. Year Book Medical Publishers, Inc.; 1988. 4. Limborgh J Van. A new view on the control of the morphogenesis of the skull. Acta Morph Need Scand 1970;8:143-60. 5. Enlow OH, Hans MG. Essentials of Facial Growth, Philadelphia, Saunders; 1996. 6. Moss M, Salentijn L. The Primary role of functional matrices in facial growth. AmJ Ortho 1969;5:566-77. 7. Moss ML. Neurotrophic processes in orofacial growth. J Dent Res 1971;50:1492-1494. 8.Baume LJ. Principles of cephalofacial development revealed by experimental biology. Am J Orthod 1961;47:895-8. 9 . Behrents and Johnston. Influence of the trigeminal nerve on facial growth and development. AJO, 1984;199-206.

53. Thankyou