Specific causes of malocclusion

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  • Underdevelopment of lateral orbital and zygomatic areas.
  • Facial asymmetry is always seen. Cause is loss of neural crest cells during migration. Cells with longest migration path are most affectedNCCs migrating to lower regions are responsible for the development of major vessels (pulomonary artery, aortic arch, aorta) and therefore they are also affected by failure of migration. For this reason, defects in great vessels is common in children with craniofacial malformation.
  • Usually accompanied by a cleft palate because the restriction on displacement of the mandible forces the tongue upward and prevents normal closure of palatal shelves.
  • Not a syndrome with defined cause.Because pressure against the face would not be present after birth, there is possibility of normal growth thereafter and perhaps a complete recovery
  • Muscular dystrophy ,cerebral palsy ,muscle weakness syndromes lead :to increased anterior facial height.distortion of facial proportions & mandibular form.excessive eruption of the posterior teethnarrowing of the maxillary arch.anterior open bite.
  • Specific causes of malocclusion

    1. 1.  A malocclusion is an incorrect relationship between the maxilla (upper arch) and the mandible (lower arch), or a general misalignment of the teeth.
    2. 2.  Malocclusion is said to result due to the following factors occurring alone or in combination: 1. Specific causes of malocclusion 2. Genetic influences 3. Environmental influences
    3. 3.  Disturbances in embryologic development  Growth disturbances in fetal period  Progressive deformities in childhood  Disturbances arising in adolescence  Disturbances of dental development
    4. 4. Defect in embryologic development usually . result in death of the embryo Although most defects are of genetic origin, effects from environment are also important Chemicals and other agents capable of producing embryologic defects are called teratogens.
    5. 5. Stages of Embryonic Craniofacial Development Stage Time in humans (post-fertilization) Related syndromes Germ layer formation and Initial organization of structures Day 17 Fetal alcohol syndrome (FAS) Neural tube formation Day 18-23 Anencephaly Origin, migration and interaction of cell populations Day 19-28 Craniofacial microsomia Mandibulofacial dysostosis Limb abnormalities Formation of organ systems Primary palate Secondary palate Day 28-38 Day 42-45 Cleft lip and/or palate, other facial clefts Cleft palate Final differentiation of tissues Day 50-birth Achondroplasia Synsostosis syndromes (e.g. crouzon’s)
    6. 6.  FAS can be traced to the very early first and second stages of craniofacial development.  Occurs due to deficiencies of midline tissue of the neural plate very early in embryonic development caused by exposure to very high levels of ethanol.  Although extreme intoxication is required, the resulting facial deformity and developmental delay occur frequently enough to be implicated in many cases of mid-face deficiency.
    7. 7.  Most craniofacial anomalies are related to neural crest cell origin and migration.  Since most structures of the face are derived from migrating neural crest cells, interferences with their migration produce facial deformities
    8. 8.  Altered development of cells derived from neural crest cells has also been implicated inTreachers- Collins syndrome  It is characterized by generalized lack of mesenchymal tissue
    9. 9.  Formerly called hemifacial microsomia is characterized by a lack of development in lateral facial areas.  Typically there is deformation of external ear and ramus of the mandible alongwith associated soft tissues.
    10. 10.  Most common congenital defect involving the face and jaws  Exactly where these clefts appear is determined by the locations at which fusion of various facial processes fail to occur
    11. 11.  Occurs during the final stage of facial development  Arises due to prenatal fusion of the superior and posterior sutures of maxilla along the wall of the orbit.  Characterized by severe underdevelopment of midface and eyes that seem to bulge from their sockets.
    12. 12.  Pressure against the developing face prenatally can lead to distortion of rapidly growing areas.  For instance, an arm may be pressed across the face in utero, resulting in severe maxillary deficiency at birth.  Occasionally, a fetus’ head is flexed tightly against the chest in utero, preventing the mandible from growing forward normally.  Result is an extremely small mandible at birth.
    13. 13.  Extreme mandibular deficiency at birth  Reduced volume of the oral cavity can lead to respiratory difficulty at birth  One-third of the patients have a cartilage forming defect alongwith pierre robin syndrome, this is known as Stickler syndrome.
    14. 14.  Use of forceps to assist in delivery might damage either or both of temporomandibular joints.  Heavy pressure in the area ofTMJ can cause internal hemorrhage, loss of tissue and a subsequent underdevelopment of the mandible.
    15. 15.  Childhood fractures of the jaw  Muscle dysfunction
    16. 16.  Condylar neck is particularly vulnerable and fracture of this area is relatively common  Condylar process tends to regenerate well after early fractures.  Problem arises when the more severely affected side lags behind in growth or scarring aroundTM joint restricts translation of condyle.
    17. 17. Facial muscles can affect jaw growth in two ways: 1.Formation of bone at points of muscle attachment depends upon muscle activity 2.musculature is an important part of the total soft tissue matrix whose growth normally carries the jaw downward and forward
    18. 18.  Loss of part of musculature is most likely to result from damage to motor nerve  Result is underdevelopment of that part of face with a deficiency of both soft and hard tissues  Excessive muscle contraction can also restrict growth  Conversely, a major decrease in tonic muscle activity allows the mandible to drop downward
    19. 19. Occasionally, unilateral excessive growth of the mandible occurs in metabolically normal individuals. Proliferation of condylar cartilage is a prominent feature. Release of excessive amounts of growth hormone from an anterior pituitary gland tumor resulting in excessive growth of mandible.
    20. 20.  Congenitally missing teeth  Malformed and supernumerary teeth  Traumatic displacement of teeth
    21. 21.  Results from disturbances during the initial stages of formation of a tooth, that is, initiation and proliferation. Total absence of teeth absence of many but not all teeth absence of only a few teeth
    22. 22.  Abnormalities in tooth size and shape result from disturbances during the morphodifferentiation stage of development.  Most commonly malformed tooth is maxillary lateral incisor
    23. 23.  Supernumerary teeth also result from disturbances during the initiation and proliferation stages of dental development  Most common supernumerary tooth appears in the maxillary midline and termed as mesiodens.  Presence of an extra tooth disrupts normal occlusal development  Multiple supernumerary teeth are associated with Cleidocranial dysplasia, a congenital syndrome.
    24. 24.  Trauma to teeth during their formative phase occurs very commonly in children.  Trauma to primary tooth displaces the underlying permanent tooth bud.  If trauma occurs during the stage of crown formation, a permanent tooth with defective crown is formed.  If trauma occurs after the completion of crown, the crown is displaced relative to the root.

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