In the name of God

1. In the name of God Orthodontics 2 By: Dr Arab

3. Specific causes of malocclusion • Disturbances in embryologic development • Skeletal growth disturbances • Muscle dysfunction • Acromegaly and hemimandibular hypertrophy • Disturbances of dental development • Genetic influences • Environmental influences • Equilibrium theory and development of the dental • occlusion • Functional influences on dentofacial development • Etiology in contemporary perspective • Changing views of etiologic possibilities • Etiology of crowding and malalignment • Etiology of skeletal problems

4. Malocclusion is a developmental condition • Usually, caused not by some pathologic process, but by moderate distortionsof normaldevelopment. result from a complex interaction among multiple factors Occasionally a single specific cause is apparent, as for example, mandibular deficiency secondary to a childhood fracture of the jaw or the characteristic malocclusion that accompanies some genetic syndromes

5. Disturbances in Embryologic Development • Problems that can be traced to embryologic defects are fortunately rare • Defects in embryologic development usually result in death of the embryo • 20% of early pregnancies terminate because of lethal embryologic defects • small number of recognizable conditions that produce orthodontic problems are compatible with long-term survival. • A variety of causes exist for embryologic defects, ranging from genetic disturbances to specific environmental insults • Teratogenes Vs Drugs

7. Skeletal Growth Disturbances A)Fetal Molding and Birth Injuries. • (1) intrauterine molding • (2) trauma to the mandible during the birth B)Childhood Fractures of the Jaw.

8. (1) intrauterine molding • Pressure against the developing face prenatally can lead to distortion of rapidly growing areas. Strictly speaking, this is not a birth injury, but because the effects are noted at birth, it is considered in that category. On rare occasions an arm is pressed across the face in utero, resulting in severe maxillary deficiency at birth • Pierre Robins Sequence: • decreased volume of amniotic fluid fetus' head is flexed tightly against the chest in utero preventing the mandible from growing forward normally • extreme mandibular deficiency at birth • respiratory difficulty at birth • Cleft palate • Do we need early treatment?

11. Birth Trauma to the Mandible No matter what the parents say later, Treacher Collins syndrome or Crouzon's syndrome (see Chapter 3) obviously did not arise because of birth trauma. • Does heavy pressure in the area of the temporomandibular joints could cause internal hemorrhage, loss of tissue, and a subsequent underdevelopment of the mandible?

12. Muscle Dysfunction: Atrophy VS Excessive contraction • The facial muscles can affect jaw growth in two ways • the formation of bone at the point of muscle attachments depends on the activity of the muscle • the musculature is an important part of the total soft tissue matrix • A)Atrophy: • Loss of part of the musculature can occur from • unknown causes in utero • birth injury • most likely results from damage to the motor nerve • result underdevelopment of that part of the face

14. B)Excessive contraction • seen most clearly in torticollis, a twisting • of the head caused by excessive tonic • contraction of the neck muscles on one • side (primarily the sternocleidomastoid) • The result • restrict growth in the same way as scarring after an injury. • facial asymmetry because of growth restriction on the affected side, which can be quite severe • unless the contracted neck muscles are surgically detached • at an early age.

15. C)decrease in tonic muscle activity • occurs in • muscular dystrophy • some forms of cerebral palsy • muscle weakness syndromes • allow the mandible to drop downward away from the rest of the facial skeleton. • Results increased anterior face height • distortion of facial proportions and mandibular form excessive eruption of the posterior teeth • narrowing of the maxillary arch • anterior open bite

17. Acromegaly • caused by an anterior pituitary tumor that secretes excessive amounts of growth hormone • Results: • excessive growth of the mandible(sometimes the mandible is unaffected) • skeletal Class III malocclusion in adult life • mandibular growth accelerates again to the levels seen in AGS • The condylar cartilage proliferates • the excessive growth stops when the tumor is removed or irradiated, the skeletal deformity persists and orthognathic surgery to reposition the mandible is likely to be necessary

19. Hemimandibular Hypertrophy • unilateral excessive growth of the mandible occurs in individuals who seem metabolically normal. Reason is entirely unknown. • Most likely in girls between the ages of 15 and 20 • proliferation of the condylar cartilage is a prominent aspect; so formerly was called condylar hyperplasia • Since the body of the mandible also is affected • hemimandibular hypertrophy now is more accurate • The excessive growth may stop spontaneously, but in severe cases removal of the affected condyle and reconstruction of the area is necessary.

21. Importance of disturbances in early Stages of Development There are five principal stages in craniofacial development ( l ) germ layer formation and initial organization of craniofacial structures (2) neural tube formation and initial formation of the oropharynx (3) origins,migrations, and interactions of cell populations, especially neural crest cells (4) formation of organ systems, especially the pharyngeal arches and the primary and secondary Palates (5) final differentiation of tissues

22. Second stage oropharynx Forth stage pharyngeal arcs Fifth stage neuromuscular structures

23. Disturbance in the first stage (germ layer formation and initial organization of craniofacial structures)fetal alcohol syndrome (FAS) exposure to very high levels of ethanol deficiencies of midline tissue of the neural plate very early in embryonic development maxillary and midface deficiency. Disturbance in the first stage (germ layer formation and initial organization of craniofacial structures)fetal alcohol syndrome (FAS) exposure to very high levels of ethanol deficiencies of midline tissue of the neural plate very early in embryonic development maxillary and midface deficiency.

24. Disturbance in the third stage (neural crest cell origin and migration) • Many of the problems that result in craniofacial anomalies • arise in the third stage of development • severe facial malformations related to the anti-acne drug isotretinoin (Accutane) • Mandibulofacialdysostosis (Treacher Collins' syndrome) • Hemifacialmicrosomia • deformities induced by thalidomide and isotretinoin includes similar to both mandibulofacialdysostosis and hemifacialmicrosomia.

25. Mandibulofacialdysostosis (Treacher Collins' syndrome). excessive cell death (cause unknown) in the trigeminal ganglion secondarily affects neural crest-derived cells generalized lack of mesenchymal tissue Both the maxilla and mandible are underdeveloped Both sides are affected But some degree of asymmetry may be present

27. Hemifacialmicrosomia • Primarily a unilateral always an asymmetrical • characterized by a lack of tissue on the affected side of the face • The external ear is deformed • Both rami of the mandible and relted soft tissues (muscle, fascia) are deficient or missing • arises primarily from early loss of neural crest cells. • Neural crest cells with the longest migration path, those taking a circuitous route to the lateral and lower areas of the face, are most affected, in spite of those going to the centre • midline facial defects including clefts rarely are part of it • Neural crest cells migrating to lower regions are important in the formation • of the great vessels (aorta, pulmonary artery, aortic arch), and they also are likely to be affected. For this reason defects in the great vessels (as in the tetralogy of Fallot) are common in children with hemifacialmicrosomia.

29. spectrum of deformities induced by thalidomide and isotretinoin includes conditions similar to both mandibulofacialdysostosis and hemifacialmicrosomia

30. Disturbance in the forth stage (organ formation) Clefting of the lip, palate, or, less commonly, other facial structures They appear in the locations at which fusion of the various facial processes failed to occur Morphogenetic movements of the tissues are a prominent part of the fourth stage of facial development. A)Cleft lip occurs because of a failure of fusion between median and lateral nasal processes and maxillary prominence, which normally occurs during the sixth week of development. Width of the mouth

32. Disturbance in the third stage (organ formation) Clefting of the lip, palate, or, less commonly, other facial structures B)Cleft palate: Primary palate: occurs because of a failure of fusion between median and lateral nasal processes and the maxillary prominence, which normally occurs during the sixth week of development. accompany of cleft lip and notch in the alveolar process is likely even without cleft of the secondary palate.

34. Disturbance in the fifth stage (final differentiation) • Synostosis syndromes (Apert syndrome, cruzonesyndrom) secondary palatal cleft • Secondary palate: occurs because of a failure of fusion between palatal shelves (from maxillary process) during the Eight week of development 3. bifid uvula • Crouzon's syndrome is the most frequently occurring member characterized by underdevelopment of the midface and eyes that seem to bulge from their sockets • arises because of prenatal fusion of the superior and posterior sutures of the maxilla, along the wall of the orbit. result must be severe underdevelopment of the middle third of the face. The characteristic protrusion of the eyes is largely an illusion • The premature fusion frequently extends posteriorly into the cranium, producing distortions of the cranial vault as well. • intracranial pressure increases. Although the characteristic deformity is recognized at birth, the situation worsens as growth disturbances caused by the fused sutures continue postnatally. Surgery to release the sutures is necessary at an early age.

36. بنام خدا

37. Disturbances of Dental Development • آشنايی با اختلال درتکامل دندان ها • آشنايی با اختلال در در رويش دندان ها • آشنايی با رویش نابجای دندان ها • آشنایی با زود از دست دادن دندان های شيری • اثرات تروما روی دندانها • تاثیرات ژنتیک • تاثیرات محیط

38. اختلال در تکامل دندان ها • همراه با نقایص مادرزادی • عمدتا همراه با ناهنجاری کلاس I دیده می شوند.

39. اختلالات عمده در تکامل دندان ها: • دندانهایی که به طور مادرزادی غایبند • دندانهای بد شکل • دندانهای اضافی • ایجاد تداخل در رویش • از دست دادن زود هنگام دندانهای شیری • جابجایی دندانی ناشی از ضربه

40. دندانهایی که به طور مادرزادی غایبند: • اختلال در مراحل اولیه تشکیل دندان: • Initiation • Proliferation • انواع missing دندانی: • آنودونشیا • الیگودونشیا • هیپودونشیا

41. ارتباط بین حضور دندانهای شیری با دندانهای دائمی: • فقدان دندان شیری لزوم فقدان دندان دائمی • حضور دندان شیری امکان فقدان دندانی دائمی

42. دیسپلازی اکتودرمال

43. Ectodermal dysplasia hypohidrotic type

44. شیوع missing دندانی: • مولرها • ثنایاها • پره مولرها • کانین • معمولا آخرین دندان از هر سری غایب می باشد

45. دندانهای بد شکل و دندانهای اضافه: • اختلال در مرحله morph differentiation • اختلال در مرحله histo differentiation

46. مشکلات مربوط به سایز دندانی • شیوع عدم تناسب سایز دندانهای بالا و پایین در جامعه: • 5% • ترتیب شیوع آنومالی های سایز دندان: • لاترال فک بالا • پره مولرهای دوم فک پایین

47. Disproportionately small /large maxillary lateral incisor

48. آبنورمالیتی های مورفولوژی دندان: • Gemination • Fusion

49. Gemination

50. Fusion