Etiology of malocclusion /certified fixed orthodontic courses by Indian dental academy


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Etiology of malocclusion /certified fixed orthodontic courses by Indian dental academy

  1. 1. Etiology Of Malocclusion INDIAN DENTAL ACADEMY Leader in continuing dental education
  2. 2. Contents % Introduction % Definition of malocclusion % Types of malocclusion % Classification of etiologies of malocclusion % Brief description on various factors % Conclusion
  3. 3. Introduction Comprehensive orthodontic management involves identification of possible etiological factors and an attempt to eliminate the same. Although it may not be possible, it is nevertheless of value in preventive and interceptive procedures. Rather than having specific “CAUSES” as do some diseases, malocclusions are usually clinically significant variations from normal range of growth and morphology. Etiologic factors contribute to the variance, more often than they simply cause it
  4. 4. Definition The arrangement of teeth in a dentition or their relation in the jaws to each other, which is not according to the accepted morphologic configuration of human maxillo- dentofacial complex
  5. 5.  Malocclusions may involve four tissue systems m Teeth m Bones m Muscles m Nerves Malocclusion Groups
  6. 6. m Dental dysplasias m Skeleto dental dysplasias m Skeletal dysplasias Another way to classify malocclusion is to divide them into three groups
  7. 7. Classification Of Etiologic Factors According to Mc coy T Indirect / Pre disposing causes T Direct / Determining causes
  8. 8. Indirect / Pre disposing causes include T Hereditary T Congenital defects T Pre natal abnormalities TAcute / chronic infections and deficiency diseases T Metabolic disturbances T Endocrine imbalance T Unknown causes.
  9. 9. Direct / Determining causes include T Missing teeth T Supernumerary teeth T Transposed teeth T Malposed teeth T Abnormal labial frenum T Intrauterine pressure T Sleeping habits T Posture
  10. 10. T Pressure T Abnormal muscular habits T Malfunctioning muscles T Premature shedding of deciduous teeth T Tardy eruption of permanent teeth T Prolonged retention of deciduous teeth T Loss of permanent teeth T Improper dental restorations
  11. 11. ACCORDING TO MOYERS  Heredity T Neuro muscular system T Bone T Teeth T Soft parts (other than nerve and muscle)  Developmental defects of unknown origin  Trauma T Prenatal trauma and birth injuries. T Post natal trauma.
  12. 12.  Physical agents T Pre natal T Post natal  Habits T Thumb and finger sucking, tongue sucking, lip biting etc  Disease T Systemic diseases T Endocrine diseases T Local diseases Malnutrition
  13. 13. According to Salzmann Salzmann‟s diagrammatic representation of the etiologic factors in malocclusion embodies prenatal and post natal factors. It clearly shows the genetic, differentiative and congenital factors that make up the prenatal elements of causation, which can influence and one or all of the postnatal components- developmental, functional,
  14. 14. According to Graber General Factors Heredity (The inherited pattern) Congenital Defects T Cleft palate T Torticollis T Cleidocranial dysostosis T Cerebral palsy T Syphilis etc.
  15. 15.  Environment T Pre natal Q Trauma Q Maternal diet Q Maternal metabolism Q German measles etc. T Post natal birth injury Q Cerebral palsy Q TMJ injury etc.
  16. 16. Pre disposing metabolic climate and disease T endocrine imbalance T metabolic disturbances T infectious diseases Dietary problems T nutritional deficiency
  17. 17. Abnormal pressure habits and functional aberrations T Abnormal suckling Q Forward mandibular posture Q Non physiologic nursing Q Excessive buccal pressures
  18. 18. T Thumb and finger sucking T Tongue thrust and tongue sucking T Lip and nail biting T Abnormal swallowing habits (improper deglutition) T Speech defects
  19. 19. T Respiratory abnormalities (mouth breathing) T Tonsils and adenoids (compensatory tongue position) T Psychogenic tics and Bruxism T Posture T Trauma and Accidents
  20. 20. Local factors Anomalies of number T Supernumerary teeth T Missing teeth Q Congenital absence or loss due to accidents, caries etc Anomalies of tooth size Anomalies of tooth shape Abnormal labial frenum, mucosal barriers
  21. 21.  Premature loss  Prolonged retention  Delayed eruption of permanent teeth  Abnormal eruptive path  Ankylosis  Dental caries  Improper dental restorations
  22. 22. ACCORDING TO PROFFIT Specific causes T Disturbances in embryologic development (teratogens) T Skeletal growth disturbances Q Intrauterine molding Q Birth trauma to mandible Q Childhood fractures or the jaw T Muscle dysfunction
  23. 23. T Acromegaly and hemi mandibular hyper trophy T Disturbances of dental development Q Congenitally missing teeth Q Malformed and supernumerary teeth Q Interferance with eruption Q Ectopic eruption Q Early loss of primary teeth Q Traumatic displacement of teeth
  24. 24.  Genetic influences  Environmental influences T Equilibrium theory and development of dental occlusion T Functional infuence on dento facial development.
  25. 25. General factors Heredity A child may have facial features that markedly resemble those of his father or mother, or the net result may be a combination of features from each parent. It is also to be noted that, a single gene is not responsible for a particular malocclusion and it may be due to the combined action of different types of Genes Heredity could be considered significant in determining the following characteristics
  26. 26. T Tooth size T Width and length of arch T Height of palate T Crowding and spacing of teeth T Overjet T Position and conformation of perioral musculature to tongue size and shape T Soft tissue peculiarities T Facial asymmetries T Macorgnathia and micrognathia T Macrodontia an microdontia
  27. 27. T Oligodontia and anodontia T Tooth shape variations (peg laterals, Carabellis cusps, mamelons etc) T Cleft palate and hare lip T Diastemas T Deep bite T Rotation of teeth T Mandibular retrusion T Mandibular prognathism
  28. 28. Congenital defects  Cleft lip and palate Congenital defects life cleft lip and palate separately or in combination are among the most frequent congenital deformities of mankind. It is not often possible for the dentist to compensate for residual post surgical abnormalities. In a unilateral cleft, the teeth or one side are usually in lingual cross bite with the opposing lower teeth. Many times the premaxilla is displaced anteriorly, or, because of the tightly repaired lip, the whole pre maxillary structure is forced lingually. The maxillary incisors in this type are badly malposed with bizarre axial inclinations. In the area of cleft, teeth are often jumbled. Maxillary lateral incisors may be missing, atypical in shape or „twinned‟
  29. 29. Cerebral palsy Paralysis or lack of muscular co-ordination due to an intra cranial lesion Complete lack of motor control resulting in abnormal muscular function in masticaction, deglutition, speech and respiration. Abnormal pressure habits lead to malocclusion
  30. 30. Torticollis Shortening of the sternocleido mastoid muscle causing profound changes in the bony morphology of the cranium and the face Characterised by “wry neck” Bizarre facial asymmetries and uncorrectable malocclusions if not treated early
  31. 31. Cleidocranial dysostosis  Maxillary retrusion and possible mandibular protrusion  Retained deciduous teeth  Retarded eruption of permanent teeth  Short and thin permanent teeth roots  Super numerary teeth
  32. 32. Congenital Syphilis  Abnormally shaped teeth
  33. 33.  Pre natal  Post natal Environment
  34. 34. Pre natal Teratogens: Chemical and other agents capable of producing embryologic defects if given at critical time are called teratogens Aminopterin Aspirin Cigarette smoke (hypoxia) Cytomegalovirus Anencephaly Cleft lip and palate Cleft lip and palate Microcephaly, hydrocephaly, microphthalmia Dilantin Ethyl alcohol 6-Mercaptopurine 13-cis Rentinoic acid (Accutane) Cleft lip and palate Central mid-face deficiency Cleft Palate Retinoic acid syndrome: malformations virtually same as hemifacial microsomia, Treacher Collins syndrome Rubella virus Thalidomide Microphthalmia, cataracts, deafness Malformations similar to hemifacial microsomia, Treacher Collins syndrome Toxoplasma Microcephaly, hydrocephaly, microphthalmia X-radiation Valium Vitamin D excess Microcephaly Cleft and palate Premature suture closure
  35. 35. Intrauterine molding  Pressure against the developing face prenatally can lead to distortion of rapidly growing areas. Eg: an arm is pressed across the face in utero resulting in severe maxillary deficiency.  Other factors that may affect are trauma, maternal diet, maternal metabolism and German measles
  36. 36.  Birth trauma  In some difficult births use of forceps to the head to assist in delivary might damage either or both TMJ. Heavy pressure in the area of TMJ could cause internal haemorrhage, loss of tissue and a subsequent under development of the mandible  Childhood fractures: Falls that produce condylar fractures may cause marked facial asymmetries  Extensive scar tissue, from a burn may also produce malocclusions Post natal
  37. 37. Some specific endocrinologic diseases may be potent makers of malocclusion. Diseases with a paralytic effect, such as poleomyelitis are capable of producing malocclusions. Disease with muscle malfunction, such as muscular dystrophy and cerebral palsy also have deforming effects on dental arch Pre disposing metabolic climate and diseases
  38. 38. Hypothyroidism  Abnormal resorption patterns  Delayed eruption pattern  Gingival disturbances  Retained deciduous teeth
  39. 39. Acromegaly Which is caused by an anterior pituitary tumor that secrete excess amounts of GH, excessive growth of mandible may occur, creating a skeletal class III malocclusion in adult life. Also multiple root resorption may be found.
  40. 40. Nutritional deficiency Disturbances such as rickets, scurvy and berry-berry can produce severe malocclusions. Main problem is upsetting of the dental developmental time tables. The resultant premature loss, prolonged retention, poor tissue health and abnormal eruptive paths lead to malocclusion
  41. 41. Non nutritive sucking habits, Includes all sucking habits T Thumb sucking T Finger sucking T Pacifiers etc. Abnormal pressure habits and functional aberrations
  42. 42.  Dento facial changes associated with prolonged non nutritive sucking habits are T Increased proclination of upper incisors T Increased maxillary arch length T Increased clinical crown length of max incisiors T Increased atypical root resorption in primary central incisors
  43. 43. T Increased retroclination of mandibular incisors T Increased overjet T Decreased over bite T Increased unilateral and bilateral class II occlusion T Increased lip incompetence T Tongue thrust T Speech defects, especially lisping
  44. 44. Lip biting T Involves the lower lip which is turned inwards and pressure is exerted on the lingual surfaces of maxillary anteriors T Proclined upper anteriors and retroclined lower anteriors T Hyper trophic and redundant lower lip T Cracking of lips Lip habits
  45. 45. Nail biting  Does not produce gross malocclusion. But minor local tooth irregularities like T Rotation T Wear of incisal edge T Minor crowding.
  46. 46. Tongue thrust  Defined as a condition in which the tongue makes contact with any teeth anterior to the molars during swallowing  It has to be remembered at this time that there is a controversy regarding Tongue thrust as an etiologic factor of anterior open bite. According to Graber and Moyers, Tongue thrust definitely leads to anterior open bite. Proffit contradicts this fully and according to him, it is an already existing anterior open bite that leads to Tongue thrusting habit T Proclination of anterior teeth T Anterior open bite T Bimaxillary protrusion T Posterior open bite in case of lateral Tongue thrust T Posterior cross bite
  47. 47. Mouth breathing Mouth breathing can result in altered jaw and tongue posture which could alter the oro-facial equilibrium there by leading to malocclusion T Long and narrow face T Short and flaccid upper lip. T Contracted upper arch with possibility of posterior cross bite T Increased overjet as a result of flaring of the incisors. T Dryness of the mouth predisposes to caries. T Anterior open bite
  48. 48. Bruxism Grinding of teeth for non functional purposes T Occlusal wear facets T Fractures of teeth and restorations T Mobility of teeth. T Tenderness and hypertrophy of masticatory muscles T TMJ pain
  49. 49. Tongue size as well as function is an important consideration. Aglossia can result in narrowing of the upper dental arch with severely malpositioned teeth and crowding. Where as Macroglossia can lead to widening of dental arches, spacing and open bite.
  50. 50. Anomalies in number of teeth T Super numerary teeth T Missing teeth Local factors
  51. 51. Super numerary teeth The presence of extra tooth obviously has great potential to disrupt normal occlusal development. Early intervention and to remove it is usually required to obtain reasonable alignment and occlusal relationships. Most common-mesiodens.  Also lateral incisors, extra premolars, fourth molars multiple super numerary teeth are found in cleidocranial dysplasia and other congenital deformities like cleft lip and cleft palate
  52. 52. Missing teeth  Congenital absence  Due to accidents / caries  Order of frequency T Max and mandibular 3rd molars T Max laterals T Mandibular 2rd premolars T Mandibular incisors T Maxillary second premolars  Anodontia–complete absence  Oligodontia–congenital absence of many, but not all teeth  Hypodontia – absence of only a few teeth
  53. 53. Quite frequently it has been noted that, one maxillary lateral incisor will be of normal size and configuration while the other is small. Anomalies of size are relatively frequent in the mandibular pre molar area Anomalies of tooth size
  54. 54. Anomalies of Tooth Shape  Most frequent – “Peg Lateral”  Leads to excessive spacing. Anomalies of shape occur as a result of developmental defects like amelogenesis imperfecta, hypoplasia, Gemination, Dens in Dente, Odontomas, Fusions, Congenital syphilitic aberations such as Hutchinson‟s incisors and mulberry molars.
  55. 55. Abnormal labial Frenum  If the frenum is thick, it prevents the closure of diastema (which is normal during mixed dentition prior to the eruption of canines)  In these cases a frenectomy is indicated
  56. 56. Premature loss of deciduous teeth  The early loss of permanent teeth should be considered as a “Malocclusion Maker”  Deciduous teeth not only serve as organs of mastication, but as space savers for permanent teeth. Loss of a deciduous 2nd molar will lead to mesial drift of the 1st permanent molar and blocking of erupting 2nd premolars. In this cases appropriate space maintainers should be given
  57. 57. Prolonged retention and abnormal resorption of deciduous teeth If the roots of the deciduous teeth are not resorbed properly, uniformly or on schedule, the permanent successors may be either withheld from eruption, or they may be deflected into malposition
  58. 58. Delayed eruption of Permanent teeth  Endocrine disorders like hypothyroidism  Presence of supernumerary teeth or deciduous root  Mucosal or Bony barrier
  59. 59. This is usually a secondary manifestation of a primary disturbance T Severe crowding T Super numerary tooth T Retained deciduous tooth / root fragment T Bony barrier T Dentigerous cysts Another form of abnormal eruption is referred as ectopic eruption. Most common form is a permanent tooth erupting through the alveolar process causing resorption on a contiguous deciduous tooth or permanent teeth , rather than its predecessor. Eg; maxillary first molar, causing resorption of maxillary deciduous second molar. Abnormal eruptive path
  60. 60. Ankylosis Ankylosis or partial ankylosis occurs relatively frequently during 6-12 year age period. Ankylosed deciduous teeth should be identified and treated by removal or building up or surgical subluxation along with space maintainers. Permanent teeth can also be found to be ankylosed can be due to T Accidents / trauma T Congenital diseases like cleidocranial dysostosis
  61. 61. Dental caries Dental caries should be considered as one of the local factors causing mal occlusion. Caries which leads to premature loss of a deciduous or permanent tooth may cause drifting, axial inclination, over eruption, bone loss etc.
  62. 62. Improper dental restorations Silver mercury alloy restorations have a tendency to “flow” under pressure. Large proximal restorations change gradually under the assault of occlusal forces, and arch length is increased. This may result in the creation of broken contacts, rotations, crossbite conditions and functional prematurities. Lack of anatomic detail in restoration of cuspal areas of a tooth can permit elongation of opposing tooth. Loose contacts also leads to food packing, teeth tend to move apart and also leads to bone loss
  63. 63. Knowledge about the various etiological factors of malocclusion will help us to plan the various interceptive and preventive orthodontic procedures. It also helps in eliminating the etiological factor if it is of a environmental type. The recognition and reporting of a malocclusion or a condition that could lead to a malocclusion is the most important service that a dentist can provide to his patients. Malocclusion has an important impact on the function and esthetics of the entire dentition. In fact, malocclusion has a detrimental effect on the self esteem of many children, adolescent and adult. If a malocclusion is not recognized by either the dentist or the patient, it cannot be assessed and treated A sound knowledge about the various factors that lead to malocclusion, will definitely help is to render excellent treatment for our patients with good retention and stability Conclusion
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