Theories of growth

orthodontics
dentistry
theories of growth

1. Theories of Growth Department of Orthodontics Presented by- Nikhil C Panicker BDS Final year part 1 Sree Anjaneya Institute of Dental Sciences

2. Contents Introduction Definitions Theories Remodelling theory Genetic theory Sutural theory Cartilaginous theory Functional matrix theory Van Limborgh theory Enlow’s expanding “V” principle Enlow’s counterpart principle Neurotropic theory Servo system theory

3. Introduction The growth of the face is characterized by a number of changes that occur from birth to adult. Studying the normal changes that occur in the facial complex is a very important aspect in orthodontics. This helps to identify and diagnose any existing abnormalities to provide optimal treatment to the patient. The growth pattern of an individual has a strong influence on dentition. Attacking the malocclusion with orthodontic treatment mechanics without knowledge of growth patterns can ultimately affect the treatment results and stability.

4. Definitions related to growth There is no universally accepted definition of growth, various clinicians have defined growth in different ways. “The self multiplication of living substance.”- J S Huxely “Increase in size, change in proportion and progressive complexity.” – Krogman “An increase in size.”- Todd “Quantitative aspect of biologic development per unit time.”- Moyers “Change in any morphological parameter, which is measurable.” – Moss “Growth refers to an increase in size/number.” - Profitt

5. Theories

6. 1. Remodelling theory of craniofacial growth ( Brash) All craniofacial skeletal growth occures exclusively by bone remodelling.

7. 2 . Genetic theory (Brodie) Brodie in 1941 Entire growth process is under the influence of genetic control and is pre- programmed. The role of genetic tissues in growth is controlled by epigenetic influences from other tissue groups and their functional, structural and developmental input signals.

8. 3 . Sutural theory(Weinmann and Sicher) Weinmann and Sicher in 1952. Also known as Sutural Dominance Theory. All bone forming elements ( cartilage, suture and periosteum) are growth centres. These growth centres are primarily under the control of heredity. Sicher believed that craniofacial growth occures at the sutures. Paired parallel sutures that attach the facial areas to the skull and the cranial base region push the nasomaxillary complex downward and forward to pace its growth with the mandible.

9. Against this theory No growth occurring in the area where suture is transplanted Growth at sutures responds to outside influences such as compression and tension Microcephaly Cleft palate

10. 4 . Cartilaginous theory James H Scott (early 1950s) Viewed the cartilaginous sites throughout the skull as primary centres of growth. Sutures play little or no direct role in the development of craniofacial skeleton, but cartilage and periosteum play primary role in craniofacial growth. According to him, intrinsic growth controlling factors are present in the cartilage and periosteum with sutures being only secondary. He concluded that craniofacial regions are dependent primarily on the cartilage and secondarily on sutures.

11. Examples Mandible Mandible can be viewed as a diaphysis of long bone bend in to a horseshoe shape with epiphysis removed He explained mandibular condylar cartilages as growth centres for the growth of mandible as it “pushes” the mandible downward and forward

12. Examples Calvaria (base and vault) “Synchondrosis” in the cranial base is the primary cartilage for the calvaria growth and sutures of cranial vaults are secondary These two factors are involved in the calvarian growth. Midface (nasomaxillary complex) The nasal septal cartilage situated against the cranial base “drives” the midface downwards and forwards.

13. Supporting this theory Transplantation of nasal septal cartilage and epiphyseal cartilage of long bones shows significant growth. This indicates the innate growth potential of the cartilage. Many bones are formed by the endochondral bone formation. Injuries in nasal septum in children resulted in deficient growth of midface.

14. 5. Functional matrix theory of Moss In 1962 Melvin Moss introduced the functional matrix hypothesis in to the orthodontic world. It was developed complimentary to the original concept of functional cranial component by Van der Klaauw (1952). According to this theory, bone growth within the craniofacial skeleton is influenced primarily by function. In short it can be explained as the soft tissues grows and both the bone and cartilage react and are grown in response to the soft tissues.

15. FUNCTIONAL CRANIAL COMPONENT All tissues, organs, spaces, and skeletal parts FUNCTIONAL MATRIX Muscles,glands,nerves, vessels,fat,teeth and the functioning spaces SKELETAL UNIT All skeletal tissues associated with a single function PERIOSTEAL MATRICES Muscles, blood vessels, nerves, glands. Acts directly and actively on related skeletal units thereby bringing about a transformation in their size and shape by bone deposition and resorption CAPSULAR MATRICES Act indirectly and passively on related skeletal units producing a secondary compensatory translation in space Expansion of orofacial capsule within which bone grows. Eg: neurocranial, orofacial Microskeletal units Macroskeletal units

16. Functional matrix and Frankel appliance Frankel appliance works based on the functional matrix theory The functional regulator provides a larger functional matrix than the teeth. The buccinator mechanism will grow and adapt to whichever functional matrix (soft tissue capsule) is present in the mouth. This adaptation occures primarily during growth.

17. 6. Van Limborgh’s Multifactorial theory Van Limborgh in 1970 This theory is conceptual, taking only the positive aspects of Scott’s cartilaginous theory, sutural dominance theory by Sicher and Moss’ functional matrix theory. He suggested 6 factors that controls growth. Van Limborgh lists the essentials of all the three hypothesis.

18. 6 factors that control growth Growth of synchondrosis and endochondrial growth (chondrocranium) is exclusively under the control of intrinsic growth factors. The intrinsic factors controlling intramembraneous growth, i.e., growth at sutures, periosteum (desmocranium) growth to a larger extend are general in nature.

19. Cartilaginous parts of the skull must be considered as growth centres. Sutural growth is controlled by both cartilaginous growth and growth of adjacent structures in the head. Periosteal growth to a large extend depends on growth of adjacent structures. Intramembraneous bone formation is additionally influenced by local non-genetic environmental factors inclusive of muscle forces.

20. The controlling factors judged by Van Limborgh in craniofacial growth Intrinsic genetic factor – genetic factor inherent to the skull tissues Local epigenetic factor – capsular functional matrix General epigenetic factor- originating from distant structure(sex hormone, growth hormone) Local environmental factors- periosteal matrix ( habits, muscle force etc.) General environmental factors- originating from external environment (nutrition, oxygen supply, etc.)

21. 7. Enlow’s ‘V’ Principle of growth Area relocation theory. Most of the facial bones have a ‘V’ shaped configuration. Bone deposition occurs in the inner side of ‘V’ and resorption occurs in the outer 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.

22. 8. Enlow’s counterpart principle It states that growth in any one region of the skull necessarily influence the growth in others. Consequently a functional equilibrium is maintained. Growth of certain skeletal parts in the craniofacial region are related specifically to other structural and geometric counterparts in the face and cranium. A balanced growth occurs if the regional part and counterpart enlarge to the same extend.

23. Imbalances are produced due to variation in: Magnitude of growth between the counterparts. Timing of growth between the counterparts. Directions of growth between the counterparts.

24. Few counterparts Nasomaxillary complex v/s anterior cranial fossa Middle cranial fossa and breadth of ramus are counterparts Maxillary arch v/s mandibular arch Bony maxilla and corpus of mandible are counterparts Maxillary tuberosity v/s lingual tuberosity

25. 9. Neurotrophism Behrents in 1970. It states that the nerve impulse involving the axoplasmic transport has direct growth potential. It also has an indirect effect on osteogenic growth by influencing soft tissue growth.

26. Different types of neurotrophic mechanisms Neuroepithelial trophism Neurovisceral trophism Neuromuscular trophism

27. Neuroepithelial trophism Epithelial growth is normally controlled by release of certain neurotrophic substances by the nerve synapses Lack of this neurotrophic process causes abnormal epithelial growth, orofacial hypoplasia and malformation etc. In short the tissues and epithelium becomes atrophic when they are de innervated since the nerves have a neurotrophic effect in sustaining healthy growth.

28. Neuromuscular trophism At the myoblast stage of differentiation, the embryonic myoblasts establishes a neural innervation without which further myogenesis usually cannot continue.

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

30. 10. Servo System theory Alexander G Petrovic. Explained in a cybernetic language.

31. Growth of primary cartilage The growth of primary cartilage (maxilla) is controlled by somatomedin hormone (STH) complex through a cybernetic command. There are no local feedback loops

32. Growth of secondary cartilage Whereas the growth of secondary cartilage (mandible) by STH complex is by direct or indirect effect on cell multiplication and not by a command. The indirect effect is by the influence of local factors multiplication. Local factors cannot influence primary cartilage

33. Drawbacks The theory places a lot of importance on the condyle as the growth centre. Hence if condylar cartilage is lost subsequent to a fracture, the growth should seize. But this doesn’t happen. The author places a lot of importance on the role of hormones in controlling growth. In all probability they do not have such a large role to play

34. Conclusion Generally growth is irreversible. It is partially true as in the case of increase in length of the body Growth may be reversible as seen in the case of increase in weight of the body. Growth is directly associated with an increase in size and is unidirectional