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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
  2. 2. INDIAN DENTAL ACADEMY Leader in continuing dental education
  3. 3. Contents Introduction System Of Classification Orthodontic Equation Primary Etiologic Sites General Factors Local Factors Conclusion
  4. 4. The beginning of wisdom is to call things by their right names. An old Chinese proverb The origin of all sciences is in the desire to know causes and the origin of all false science and imposture is in the desire to accept false causes rather than none or which is the same thing in the unwillingness to acknowledge our own ignorance. Burke and Edinburgh Phrenologist
  5. 5.
  6. 6. Introduction Etiology of malocclusion is the study of its causes. Recognition and elimination of the etiological factors is important so that one can prevent and correct the malocclusion and obtain a permanent result. Etiologic factor contribute to the variance more often than they simply “cause” it.
  7. 7. Current level of etiologic researchinherited pattern is polygenic.
  8. 8. Based on a multifactorial system with additive polygenesis and threshold effect – in order to become a distinctive factor in the phenotype, the inherited bundle of genes can be ‘‘tipped over the edge’’ for instance by environmental factors. Jorgensen 1966
  9. 9. Interaction b/w Hereditary factor and Exogenous influences
  10. 10. Systems Of Classification Inherited and Congenital Causes Acquired causes Indirect or predisposing Causes Direct or determining causes Various classification proposedWhite and Gardiner’s Classification Salzmann’s Classification Moyer’s Classification Graber’s Classification Proffit’s Classification
  11. 11. White and Gardiner’s Classification A. Dental Base Abnormalities 1.Antero-posteror Malrelationship 2.vertical Malrelationships 3.Lateral Malrelationships 4.Disproportion of size b/w teeth and basal bone 5.Congenital abnormalities
  12. 12. B. Pre-Eruption Abnormalities 1.Abnormalities in the position of developing tooth germ 2.Missing Teeth 3.Supernumerary Teeth and Teeth abnormal in form 4.Prolonged retention of Deciduous teeth 5.Large Labial Frenum 6.Traumatic Injury
  13. 13. C. Post-Eruption Abnormalities 1.Muscular Forces: a.Active Muscle Forces-Swallowing b.Rest Position of the Musculature c.Sucking habits d.Abnormalities of path of closure 2.Premature Loss of Deciduous teeth 3.Extraction of Permanent Teeth
  14. 14. Salzmann’s classification Prenatal 1.Genetic:transmitted by genes. may or may not be at birth. 2.Differentiative: a.General or Constitutional: whole body b.Local or dentofacial: face, jaws & teeth 3.Congenital:hereditary or acquired exist at birth
  15. 15. Postnatal A.Developmental General Local a.Abnormalities in relative rate of growth. b.Hypo/hypertonicity of muscles. c.Childhood diseases, nutritional,Endocrine,& metabolic disturbance d.Radiation/Radiotherapy. a.Birth injuries. b.Micro / macrognathia c.Micro/macroglossia. d.Abnormal labial frenum. e.Facial hemiatrophy. f.Anomalies of tooth development & eruption.
  16. 16. B.Functional Local General a.Muscular hyper or hypotonicity. b.Neurotropic disturbances. c.Postural defects of the tongue and jaws. d.Masticatory and respiratory disturbances. a.Premature loss or prolonged retention of deciduous teeth. b.Loss of proximal contact. c.Temporomandibular articulation disturbance. d.Muscular hypo or hyperactivity
  17. 17. C.Environmental or Acquired General Local a.Diseases can affect the a.Eruption anomalies dentofacial tissue b.Premature loss or directly or indirectly. prolonged retention of deciduous teeth. b. Radiation. c.Loss of permanent teeth. d.Periodontal disease e.Harmful dentofacial pressure habits. f.Trauma g.Infection i.Temporomandibular disturbance.
  18. 18. Moyer’s Classification Heredity Developmental defects of unknown origin. Trauma a.Prenatal trauma &Birth injuries b.Postnatal trauma. Physical agents a.Premature extraction of primary teeth b.Nature of food
  19. 19. Habits a.Thumb sucking and finger sucking b.Tongue thursting c.lip sucking & Lip biting d.Posture e.Nail biting f.Other habits Disease a.systemic b.Endocrine disorder.
  20. 20. c.Local disease -nasopharyngeal diseases & disturbed respiratory function. -gingival & Periodontal disease -tumors -Caries Malnutrition
  21. 21. Proffit’s Classification Specific causes1.Disturbances in embryologic development. 2.Skeletal growth disturbances a.Fetal molding & birth injuries. b.Birth trauma to the mandible. c.Childhood fracture of the jaw. 3.Muscle dysfunction. 4.Acromegaly & hemimandibular hypertrophy.
  22. 22. 5.Disturbances in dental development. a.Congenitally missing teeth. b.Malformed teeth. c.Supernumerary teeth. d.Interference with eruption. e.Ectopic eruption. f.Early loss of primary teeth. g.Traumatic displacement of teeth Genetic Influences
  23. 23. Environmental Influences 1.Equilibrium Theory & Development of the Dental Occlusion. a.Equilibrium effect on the Dentition -tooth contacts during mastication & swallowing. -soft tissue pressure of lip,cheek & swallowing. -external pressure like Habits & orthodontics. -Intrinsic pressures like PDL fibers & Gingival fibers. b.Equilibrium effects of Jaw size & shape
  24. 24. 2.Functinal influences on Dentofacial developmenta.Masticatory function -Function & Dental arch size -Biting force & Eruption b.Sucking & Other Habits c.Tongue thrusting d.Respiratory pattern
  25. 25. Graber’s Classification General Factors 1.Heredity 2.Congenital Defectss -Cleft palate -Torticolis -Cleidocranial dysostosis -Cerebal palsy -Syphilis
  26. 26. 3.Environment a.Prenatal b.Postnatal -Trauma -Birth injuries -Maternal Diet -cerebral Palsy -Maternal metabolism -TMJ injury. -German measles. 4.Predisposing Metabolic Climate & Disease a.Endocrine Imbalance b.Metabolic Disturbances c.Infectious Diseases 5.Dietary Problems -Nutritional Deficiency
  27. 27. 6.Abnormal Pressure habits & Functional aberration a.Abnormal suckling b.Thumb & Finger sucking c.Tongue Thrust & Tongue sucking d.Abnormal swallowing habits f.Speech defects g.Respiratory abnormalities h.Tonsils & Adenoids i.Psychogenic Tics & bruxism. 7.Posture 8.Trauma & Accidents
  28. 28. Local Factors 1.Anamolies of number a.Supernumerary Teeth b.Missing Teeth 2.Anamolies of Tooth Size 3.Anamolies of Tooth Shape 4.Abnormal Labial frenum; Mucosal barriers 5.Premature Loss.
  29. 29. 6.Prolonged Retention 7.Delayed Eruption of Permanent teeth 8.Abnormal Eruption Path 9.Ankylosis 10.Dental Caries 11.Improper Dental Restorations.
  30. 30. Orthodontic Equation [ Dockrell’s Classification ] Causes Act at Times On Tissues Producing Results
  31. 31. Primary Etiologic Sites Neuromuscular System Bone of the facial skeleton The Teeth The Soft parts excepting muscles
  32. 32. Hereditary / Genetic factors in malocclusion Strong influence of inheritance on facial features- obvious at a glance. The Hapsburg jaw- prognathic mandible. Two pertinent questions asked on the inherited influences are1. Is malocclusion often caused by inherited characteristics? 2.How much of these inherited characteristics is modified by the pre & postnatal environment?
  33. 33. Sir Francis Galton – first scientific analysis of twins & concluded that it is possible to separate ‘Nurture’ from ‘Nature’. The best way to find out about genetic basis in malocclusion is by using1.Twin studies (difficult to obtain samples). 2.Familial studies. a.Parent child study (less comprehensive). b.Sibling studies (more comprehensive).
  34. 34. Twin studies: Lundstrom(1963) conducted a study on 100 pair of twins,half of which were monozygotic and half were dizygotic. Both skeletal and dental overjets were measured Conclusions More variations in the dizygotic than monozygotic. Larger genetic variations for skeletal pattern than dental overjet. Indicates dentoalveolar compensation.
  35. 35. Lauweryns et al(1993) summarized a number of twin studies and concluded that 40% of the dental and skeletal variations that lead to malocclusion can be attributed to hereditary factors. The use of twins in dentofacial genetic research Lauweryn I,Carels C,Vlietinck R AJODO 1993;103:33-38
  36. 36. Familial Studies: Parent-Child corelation co-efficient  Facial skeletal dimension-0.5  Dental characteristic -maximum for overjet-0.5 -minimum for overbite-0.15
  37. 37. Suzuki(1961)studied 243 Japanese families.  1 parent had anomaly-20% of children affected.  Both parents had anomaly-40% of children were affected.
  38. 38. Bolton & Brush Growth study(conducted on siblings between 1930s & 1970s).  Harris & Johnson concluded that-heritability of craniofacial characters was high but dental was low.  Heritability estimates for skeletal characters increases with age but for dental characters decreased-indicates environmental contribution. Heritability of craniometric & occlusal variables: A longitudinal sib analysis. Edward F Harris & Michelle G.Johnson AJO-DO 1991;99:258-68
  39. 39. Harrs has shown that the craniofacial skeletal pattern with class II malocclusion is heritable & there is high resemblance of skeletal pattern in their siblings. He concluded that the genetic basis for their resemblance is polygenic.
  40. 40. Genuine Class II malocclusion in three brother
  41. 41. Litton etal (1970) in their sibling study have reported Class III malocclusion to be heritable trait that is polygenic in nature. A genetic study of ClassIII malocclusion Litton SF,Ackerman LV, Isarcson RJ AJO-DO 1970;58(6) 565-577
  42. 42. Hereditary mandibular prognathism
  43. 43. Malocclusion could be produced by inherited characteristics in two major ways:  Disproportion between the size of the jaw and size of the teeth.  Disproportion between size and shape of the upper and lower jaw. More independently these characteristics are inherited more likely is the disproportion .
  44. 44. Studies done to find out if tooth & jaw size discrepancy is due to independent inheritance. Stockard’s study on cross-bred dogs (1930s) • Observations  Dramatic malocclusions did occur more from jaw discrepancies than from tooth-size- jaw-size discrepancy.  This seemed to confirm that independent inheritance of facial characteristics could be a major cause of malocclusion
  45. 45. Study was misleading as many breeds of small dogs carry genes for Achondroplasia.
  46. 46. Studies using out breeding in human populations.  In primitive human populations- malocclusions less frequent since characterised by genetic isolation & uniformity.  Tooth-size jaw-size discrepancies were infrequent.  Where out breeding occurs incidence of malocclusion greatly increased.  This seemed to show that the independent inheritance could be a major cause of malocclusion.
  47. 47. Hawaiian melting-pot study, Chung et al.  One of the best investigations to examine the hypothesis of independent inheritance of tooth & jaw characteristics.  Hawaii-homogenous Polynesian population.  Large scale migration by Europeans, Chinese, Japanese-Heterogeneous modern population.  High prevalence of malocclusion would be expected in this population but not so.
  48. 48. The prevalence of malocclusion though higher than in the original population was only additive rather than multiplicative. Ex.10% of Chinese who had Cl III if mated with 10% of Polynesians with crowded teeth, the offspring seemed to have 10% prevalence of each characteristic. Conclusion that can be drawn from this study is if malocclusion is inherited, the mechanism is not the independent inheritance of discrete morphological characteristics like tooth & jaw sizes.
  49. 49. Lundstrom made an intensive analysis of several characteristics & found the followingHeredity significant1.Tooth size. 2.Width & length of arch. 3.Height of the palate. 4.Crowding & spacing. 5.Degree of sagittal overbite/overjet. Heredity probable1.Position and conformation of perioral musculature to tongue size and shape. 2.Soft tissue peculiarities(character and texture of mucosa, frenum size, shape and position.)
  50. 50. Heredity also plays an important role in the foll. conditions1.Congenital deformities. 2.Facial asymmetries. 3.Macro/micrognathia. 4.Macro/microdontia. 5.Oligodontia & anodontia. 6.Tooth shape variations. 7.Cleft-lip/palate. 8.Frenum diastemas. 9.Deep overbites. 10.Crowding & rotation of teeth. 11.Mandibular retrusion. 12.Mandibular prognathism.
  51. 51. Clinical implications Heredity can affect the orthodontic treatment as seen by the following examples1.Class II malocclusion caused due to habit much easily corrected than one due to genetic causes. 2.Class III malocclusion mostly due to mandibular prognathism(genetic) as against maxillary retrusion. The greater the genetic component, the worse the prognosis for a successful outcome by means of orthodontic intervention.
  52. 52. Congenital malformations 1.Single gene abnormality Genetic disorder 2.Chromosomal disorders 3.Multifactorial disorder- Genetic +environment 4.Disorder cause by Teratogens NG & E 5.Disorders of unknown etiology
  53. 53. Autosomal Dominant Disorder Treacher collins syndrome Achondroplasia Crouzon Disease [cranio facial dysostosis] Cleido cranial dysostosis Marfan syndrome Dentinogenesis imperfecta Hemifacial microsomia [goldenhar syndrome] Basal cell nevus syndrome Neuro fibromatosis
  54. 54. Autosomal Recessive Disorders Cerebro-Costo-mandibular syndrome [micrognathia with Pierre Robin Syndrome] Bloom syndrome [with Skin lesion]Maxillary hyperplasia Stickler symdrome Nagar Aerofacial dysostosis.
  55. 55. Multi Factorial Inheritance Cleft Lip and Palate Disease with which we deal malocclusion, Dental Caries, Periodontal disease which are multifactorial triats.
  56. 56. Disorder Caused By Teratogens A group of congenital malformation caused by maternal exposure to teratogens [malformation inducing] agents during pregnancy. The best known teratogenic agents are Viruses [Rubella], heavy dose natural irradiation and maternal exposure to various chemical substances. Heavy alcohol consumption during pregnancy.
  57. 57. Teratogens affecting dentofacial development Contemporary Orthodontics: William R Proffit
  58. 58. Cleft Lip And Palate Cleft Palate can defined as a furrow in the palatal vault or Breach in continuity of palate. Most commonly seen congenital deformity at the time of birth. Incidence of cleft of the lip & palate varies from 1 in 500 to 1 in 2500 of live births,depending on geographic origin, racial & ethnic background & socioeconomic status.
  59. 59. Both dental & skeletal components affected. More common in maxilla-damage to profile due to maxillary deficiency. Influenced byType of surgery. Type of deformity. Timing of intervention.
  60. 60. Etiology of cleft Fogh & Anderson – Genetic in origin Bhatia – Either by single mutant gene or by number of genes . Bixler – 1.Probably polygenic. 2.Monogenic or syndromic. Various environmental factor. -Alcohol [Munger et. al 1996] -Maternal illness & smoking [Werler et. Al 1990]
  61. 61. Classification of cleft lip & palate Veau’s classification[1931] Group I: Soft palate Group II: Hard & soft palate Group III: Comp. Unilateral cleft Group IV: Comp. bilateral cleft
  62. 62. Kernahan & Stark’s classification Cleft of pri. Palate only a. Unilateral - Complete - Incomplete b. Median - Comp.[ premaxilla absent] - Incomplete[PM rudiment] c. Bilateral - Complete - Incomplete Cleft of sec. palate only - Complete - Incomplete - Submucous
  63. 63. Cleft of pri. & sec. palate a. Unilateral - Complete - Incomplete b. Median - Complete - Incomplete c. Bilateral - Complete - Incomplete
  64. 64. Schuchardt & Pfeifer symbolic classification
  65. 65. Kernahan’s Striped Y Classification
  66. 66. Millard’s modification of the striped Y
  67. 67.
  68. 68. Problems associated with CL & CP Dental Esthetics. Speech & hearing. Psychology.
  69. 69. Dental problem Congenitally missing teeth [U LI ] Mobile premaxilla Anterior & post. Cross bite Ectopically erupting teeth Impacted teeth Supernumerary teeth
  70. 70. Poor alignment – poor oral hygiene Multiple decayed teeth Periodontal complications Enamel hypoplasia & microdontia Protruding premaxilla Deep bite Spacing / crowding
  71. 71.
  72. 72. Speech & hearing Speech depends on timing of palatal surgery. Velopharngeal sphincter dysfunction.
  73. 73. The term Cleft Palate Speech include: Abnormal nasal resonance Abnormal nasal airflow Altered laryngeal voice quality Nasal or facial grimace Atypical consonant production McWilliam etal 1990, Trost-Cardemone 1990, Sell etal 1994 Wyatt etal 1996
  74. 74. Clinical significance Surgically repaired with excellent cosmetic & functional result Best operated bfore the pt. is 1 mth old. 3 mths - CL , 18 mths – CP Physical & psychological effect of CP on pt. are considered Eating & drinking are difficult because of regurgitation of food & liquid through the nose Speech problem is serious & tends to increase mental trauma suffered by the pt.
  75. 75. Cliedocranial dysplasia Hereditary – important cause of malocclusion Unilateral/bilateral absence of clavicles. Delayed closure of cranial sutures. High, narrow,arched palate and actual cleft palate appears to be common. Maxillary retrusion. Mandibular protrusion. Retarded eruption of permanent teeth Retained deciduous teeth. Multiple impacted supernumerary teeth
  76. 76.
  77. 77. Ectodermal Dysplasia Specific syndrome characterised by a congenital dysplasia of one or more ectodermal structures manifested primarily by hypohydrosis, hypotricosis & hypodontia. X-linked recessive mendelian character. EDSs may manifest in association with midfacial defect- CL &CP.
  78. 78. Light very thin hair Underdeveloped eye brows Broad nose Ridge like lip configuration Pronounced mentolabial sulcus. Underdevelopment of middle face & lower facial height
  79. 79. Frontal bossing ,Collapsed middle third face & Spare hair on the Scalp Anodontia or oligodontia. Growth of jaw is normal. Alveolar process does not developreduced vertical dimensionprotuberant lips. High Palatal arch & CP.
  80. 80. Mandibulofacial Dysostosis [Treacher Collins-Franceschetti Syndrome] Encompasses a group of closely related defects of the head & face. Hereditary or familial in pattern.
  81. 81. Clinical manifestations Antimongoloid palpebral fissures with a coloboma of the outer portion of the lower lids & deficency of the eyelashes. Hypoplasia of facial bone. Malformation of external ear. Macrostomia, high palate & abnormal position & malocclusion of teeth. Blind fistulas b/w the angle of the ears & angle of mouth. Facial cleft and deformity. Micrognathia & Openbite. Characteristic facies of patient-Birdlike or Fishlike
  82. 82. Craniofacial Dysostosis [Crouzon Disease] Autosomal dominant pattern. Mutation of FGFR-2 gene. Early synostosis of the sutures. Facial deformities is observed at birth. AP diameter is smaller than transverse Wide face & hypoplastic maxilla producing pseudoprognathism. Deviation of nasal septum, narrowed ant nare & wide beaked nose Mimicks frog face. Upper lip is shortened & cleaved. Impair vision & earing. Malocclusion, malposed teeth & dysplasia noted.
  83. 83. Craniofacial Dysostosis Cranial & facial deformities. Hypoplasia of maxilla. Mandibular prognathism. High-arched palates & clefts.
  84. 84. Pierre Robin Syndrome May/may not be genetic. Characterised by- Cleft Palate, Micrognathia,Glossoptosis. Primary defect in the mandible. U or V shaped hard & soft palate. Respiratory difficulty due to epiglottic obstruction.
  85. 85. Achondroplasia Caused by mutations in the gene for FGFR-3[fibroblast growth factor receptor] Characteristic form of dwarfism. Disease begins in utero. 80% of affected infants are still born. Maxilla retruded & mand prognathism. Midfacial hypoplasia & prominent fore head.
  86. 86. Achondroplasia
  87. 87. Down’s Syndrome First described by John Langdon Down in 1866. Form of mental retardation. Somatic abnormalies due to number of chromosomal aberrations. Three Cytogenetic variants: Trisomy-21 Trisomy-18 Trisomy-13 Small head,flat face,depressed nasal bridge, flat occiput & broad short neck. Small slanting eyes with epicanthal folds, open mouth, frequent prognathism & sexual underdevelopment.
  88. 88. Down Syndrome
  89. 89. Protrusion of tongue [macroglossia] with difficulty in eating & speaking. Scrotal teeth Hypoplasia of maxilla. Delayed tooth eruption, partial anodontia, enamel hypoplasia, jevinile periodontitis & Clept lip or palate. Fissuring & thickening of lips & angular Cheilitis are frequent.
  90. 90. Stickler Syndrome Autosomal dominant connective tissue disorder. Greater b/w families rather than with in families. Manifest as three main groups- the Eyes , Joints & facial appearance. At birth only features of pierre Robin sequence. The facial appearance at birth –mid face hypoplasia, flat nasal bridge,anteverted nares & prominent eyes.
  91. 91. Syphilis Caused by treponema palladium. Classified as Congenital & Acquired. Congenital syphilis is transmitted to offspring only by an infected mother. Manifest variety of lesions including frontal bossae, short maxilla, high palatal arch, saddle nose, mulberry molars, Higoumenakis’s sign [ irregular thickening of the sternoclavicular portion of clavicle], protruberance of mandible.
  92. 92. Hutchinson’s triad: - hypoplasia of incisor & molar teeth -eight nerve deafness -Interstitial Keratitis. Malocclusion frequently observed is open bite & lack of development of maxilla.
  93. 93. Environmental factors Skeletal growth disturbancesFetal moulding and birth injuries Injuries apparent at birth : 1.Intra uterine moulding [prenatal] 2.Trauma to mandible during the birth process [postnatal]
  94. 94. Prenatal Intrauterine moulding: Pressure against rapidly growing areas leads to distortion Arm pressed against the facemaxillary deficiency Head flexed against the chest-mandibular deficiency.
  95. 95. Decreased amniotic fluid-small mandible-cleft palate results due to upward displacement of tongue. Catch-up growth occurs when pressure is released except when cartilage is affected-Stickler syndrome
  96. 96. Rubella [German Measles] Caused by togavirus which spread by droplet infection. When the disease occurs in women during the first trimester of pregnancy, the offspring has a high incidence of congenital defects such as blindness, deafness, & cardiovascular abnormalities. Occasionally can cause enamel hypoplasia high carious incidence & delayed eruption of deciduous teeth.
  97. 97. Post-Natal Birth injuries 1.Trauma to mandible Most mandibular deformities-due to congenital anomalies-but thought to be due to birth trauma. Forceps delivery –TMJ damage. 2.Vogelgeschist: development ankylosis of TMJ,may be due to birth injury.
  98. 98. Childhood Fractures of the jaw  Mandible more common than the maxilla.  Condylar neck is vulnerable.  75% of these fractures –normal growth occurs.  Asymmetric growth due to injury to the soft tissue matrix –scarring restricts the growth.  Management of fractures very critical-early immobilisation.
  99. 99. Muscular trauma  Part of soft tissue matrix responsible for bone growth.  Malocclusion can be caused by, a.Decreased tone of the muscles-due to muscular dystrophy,or loss of motor nerve supply-muscle atrophy b.Excessive muscle contraction-torticollis or scaring after a injury.
  100. 100. Cerebral Palsy Cerebral palsy is a paralysis or lack of muscular co-ordination attributed to an intracranial lesion. Result of birth injuries. Effect of this neuromuscular disorder may be seen in the integrity of occlusion. Varying degree of abnormal muscular function may occur in mastication, deglutition, respiration and speech.
  101. 101. Predisposing metabolic Climate And Disease Endocrine imbalance. Hypopituitarism:  Dwarf  Delayed eruption of permanent teeth and delayed shedding of primary teeth.  Crowding due to smaller arch size.  Mandibular growth more affected than maxilla.
  102. 102. Hyperpituitarism: Gigantism-large teeth and jaws. Acromegaly-occurs after growth and ossification is complete. Lips thick,tongue enlarged,shows scalloping. Accelerated condylar growth-large mandible. Teeth tipped buccally due to large tongue.
  103. 103. Hypothyroidism: Delayed eruption. Abnormal resorption pattern. Retained deciduous teeth. Malposed teeth-deflected from eruption path. Gingival disturbances. Hyperthyroidism: Early shedding and eruption Atrophy of alveolar bone.
  104. 104. Nutritional Deficiency Disturbances in the developmental timetable. Rickets, scurvy and beri-beri can produce severe malocclusions. Premature loss of teeth /Prolonged retention. Abnormal eruptive path. Poor tissue health Poor absorption-hormonal /enzymatic deficiency. Decreased fluoride intake-loss of teeth due to caries-malocclusion.
  105. 105. Abnormal Pressure Habits And Functional Aberration EQUILIBRIUM THEORY If an object is acted upon by a set of forces but remains in the same position, then the forces must be in balance. Dentition is in equilibrium. Movement occurs when equilibrium is disturbed.
  106. 106. 4 PRIMARY FACTORS IN EQUILIBRIUM: 1.Intrinsic forces of tongue and lips. 2.Extrinsic forces-habits &orthodontic appliances. 3.Forces from dental occlusion. 4.Forces from periodontal membrane.
  107. 107. Equilibrium effects on the dentition. 1.Intrinsic forces -Tongue Vs. Lip. Duration of force more important than the magnitude. Chewing force - heavy. Periodontal ligament -shock absorber. Force maintained longer -pain is felt. Heavy but intermittent force no change in tooth position.
  108. 108. Forces from lips, cheek and tongue- lighter but act for a longer duration. Capable of causing tooth movement. Since no tooth movement occurs-forces are in equilibrium. Electronic measurement showed- pressures are unequal.
  109. 109. Study by Walter Straub(1950)- clinical observation. Tongue and lip pressures during swallowing varied among individuals. Did not correlate with the position of the teeth. The tongue and lip pressures were never balanced. Tongue pressure several times higher during swallowing. Thought lip pressure acts for longer time but was disproved. Concluded that incorrect swallowing – major cause of anterior open bite & incisor protrusion.
  110. 110. Lear & Moorrees studied tongue and lip pressures. Tongue and lips pressures measured over a 4 hour period and projected over 24 hours. In the 24 hour period, summary of tongue and lip pressures are close to the equilibrium. Total tongue and lip pressures still imbalanced. Other forces must be considered, if equilibrium is to be explained.
  111. 111. 2.Extrinsic forces: Pressure habits & orthodontic appliances. a.Orthodontic treatment causing tooth movement interferes with the equilibrium. b.Same can be concluded about habits. c.Extrinsic forces effective only when duration exceeds 6 hours.
  112. 112. Factors affecting equilibrium in the vertical direction: 1.Tongue & lips. 2.Forces of occlusion. 3.Forces of eruption.
  113. 113. Studies by Wallen- to find if tongue pressure leads to anterior open bite: 1.Tongue pressure in patients with anterior open bite less than persons with normal vertical relationships. 2.Due to relatively high position of the incisors the tongue doesn’t contact them during swallowing.
  114. 114. 3. Forces from dental occlusion: Attachment apparatus effective hydrodynamic damping system. The occlusal forces influence vertical position of teeth. Maximum force of 100kg or more sustained for fraction of a second. Vertical position of teeth when changed can alter the rest position of the mandible. Extrusion of molar teeth rotates the mandible downward & backward & intrusion causes the mandible to move to a closed position. These changes mediated by proprioceptors in the periodontal ligament.
  115. 115. Forces of eruption: Eruptive force moves the tooth through the bone. Remains active till tooth has come into occlusion. Extraction of antagonist restarts the eruption process again. Studies show eruptive force generated in the periodontal membrane rather than the root apex. Strain gauge pressure transducer shows the eruptive force can be between 2 to 10gms
  116. 116. Biting forces & Eruption: Patients with deep / openbite show infra/supra eruptive posterior teeth – how much a tooth erupts depends on how much force is placed on it. Studies to find if long faced persons have lower maximum biting force & short faced persons have high biting forces were done. Swallowing, chewing & maximum biting forces were evaluated.
  117. 117. 3 groups measured were- children with long faces, children with normal faces & long faced adults. All 3 groups had less biting forces than normal adults. Difference in occlusal forces arises at puberty -when the normal faced individual gains muscle strength. Tendency towards long face before the difference in force appears- difference is than the cause. an effect rather
  118. 118. 4. Forces from the periodontal membrane: Form an important part in stabilizing teeth. Though the tongue & lip pressure are unequal postulated that periodontal ligament maintains teeth in stable position. Pathological migration – break down of periodontal ligament. Final position of teeth influenced by two factors1.Resting positions of lip, cheek & tongue. 2.Metabolic activity within the periodontal membrane
  119. 119. Abnormal Habits All habits are learned patterns of muscle contraction of a very complex nature. Habits such as normal lip action and mastication-stimulants for normal growth, Undesirable habits –malocclusion.
  120. 120. Duration not the only determinant but frequency & intensity affect the end result. The trident of habit factors.
  121. 121. Deleterious habitual patterns of muscles behavior produce: 1.Perverted osseous growth. 2.Tooth malpositions. 3.Disturbed breathing. 4.Difficulty in speech. 5.Upset balance of facial musculature. 6.Psychological problems.
  122. 122. Thumb/Finger sucking One of the most important factors in producing and maintaining malocclusion. Begins at birth and outgrown by 3-4 years.
  123. 123. Finger sucking from birth to 4 years: Suckling mechanism –most important exchange with the outside world. Through suckling child obtainsnutrients, feelings of euphoria, sense of security and feeling of warmth.
  124. 124. Time of appearance of digital suckingFirst few weeks- feeding problems. During the eruption of teeth- Teething device. Older children- release of emotional tensions. THEORIES FOR NON-NUTRITIVE SUCKING: 1. Classical Freudian theory(1905) Orality of the infant related to pregenital organisation. Sexual activity not separated from taking of nourishment. Abrupt stopping of habit leads to substitution by other antisocial tendencies.
  125. 125. 2.The learning theory- Davidson(1967) Association of non-nutritive sucking with pleasurable feelings like hunger. 3. The oral drive theory- Sears and Wise (1982) Strength of the oral drive is proportional to how long a child continues to feed by suckling. Thumb sucking is due to the oral drive and not the result of frustration of weaning. Agrees with the Freudien theory- suckling increases the erotogenesis of the mouth.
  126. 126. Studies done to evaluate feeding pattern: Children fed had less thumb sucking habit than children whose feedings were widely separated. Non-thumb suckers took a longer time to feed. Digital sucking related to inadequate sucking activity. Benjamin did a series of experiments with monkeys and found – less thumb sucking in those in whom the nutritive suckling experience is less Thumb sucking is an expression of a need to suck – associated thumb-sucking with primary reinforcing aspects of feeding. Thumb sucking – reflex common to all mammalian infants.
  127. 127. Studies done to evaluate psychological aspects: Thumb sucking result of inadequate attention. Manifestation of feeling of insecurity. Should be screened for underlying psychological disturbances. Psychological consultation needed when trying to break the habit. Studies in the university of Alberta disproved the above facts.
  128. 128. This study was done with 66 children divided into 6 groups. a. Control group. b. Psychologic treatment. c. Palatal arch only. d. Palatal arch & psychological treatment. e. Palatal crib only. f. Palatal crib reinforced by psychological treatment. Children who suck their thumbs failed to demonstrate any consistent psychological difference from the control group.
  129. 129. Results support the theory that digital sucking is a simple learned habit. No support for interpretation of thumb sucking as a symptom of psychological disturbance. Orthodontic intervention failed to produce any increase in alternative or substitute undesirable behaviour. Palatal crib with spurs was most effective and associated habits like hair-twisting, fondling, disappeared with finger habits.
  130. 130. Palermo- thumb-sucking arises out of a progressive stimulus & reward reaction; spontaneously disappears unless becomes an attention getting mechanism. Eysenek- learning theory regards neurotic symptoms as simple learned habits; no neurosis underlying the symptom but the symptom itself. Various theories of non-nutritive digit sucking are not completely incompatible. Findings support the learning theory – associated with prolonged nutritive sucking.
  131. 131. Classification of Sucking Habits 1.O’Brien (1996) Nutritive sucking habit – breast feeding/bottle feeding. Non-nutritive sucking habit – thumb / finger sucking, pacifier sucking. 2.Subtelny (1973) – 4 grades of thumb sucking Type A 50% of children – whole digit is placed inside the mouth. Pad of the thumb presses against the palate. Maxillary & mandibular anterior contact is maintained
  132. 132. Type B 13-24% of children. Thumb is placed without touching the palate. Maxillary & mandibular anterior contact is maintained. Type C 18% of the children. Thumb is placed just beyond the first joint. Contacts the hard palate. Contacts only the maxillary incisors. Type D 6% of the children. Tip of the thumb inside the mouth.
  133. 133. Digit Sucking & Malocclusion. Large percentage of children practicing digit sucking but little correlation with malocclusion. Sucking habits in primary dentition – little or no long term effects. Habits persist beyond the time that the permanent teeth erupt - malocclusion occurs. Characterized by flared & spaced maxillary incisors, lingually positioned lower incisors, anterior open bite, narrow upper arch. Rarely due to finger pressure alone, assistance from perioral musculature.
  134. 134. Burlington Orthodontic Research Center – Popovitch & Thompson report.  High association of abnormal sucking habits with malocclusion. Cook measured forces of thumb sucking:  Three distinct patterns of force application during sucking.  All forces sufficient to displace teeth & deform growing bone.
  135. 135. How does malocclusion actually occur?  When thumb / finger placed between the teeth – positioned at an angle.  Presses lingually against the lower incisors & labially against the upper incisors.  There can be variation depending on which teeth are contacted.  Duration of the sucking is most important.  Child who sucks vigorously but intermittently does not displace incisors but when continuous light pressure is applied – malocclusion results.
  136. 136.  Anterior open bite – Combination of thumb sucking & interference with normal eruption.  Excessive eruption of posterior teeth & impedes eruption of incisors.  Mandible positioned in a downward manner to accommodate the interposed thumbcausing increased eruption of posterior teeth.  Direct impediment of incisor eruption.  Maxillary constriction- not due to negative pressure.
  137. 137. Imbalance between tongue & cheek pressures. Tongue is lowered which decreases the pressure on the upper posterior teeth. Cheek pressure increased as buccinator muscle contracts during suckling.
  138. 138. Constricted maxillary arch least likely to correct spontaneously. When maxillary arch expanded, incisor protrusion & anterior open bite improves spontaneously. No use beginning orthodontic therapy till habit is stopped.
  139. 139. Tongue Thrusting Often associated with thumb sucking. Tongue thrust is forward placement of the tongue between the anterior teeth & against the lower lip during swallowing- Schneider (1982). Normal swallow – the teeth are in occlusion, lips lightly closed, the tongue held against the palate behind the anterior teeth.
  140. 140. CLASSIFICATION OF TONGUE THRUST SWALLOW: 1.Simple tongue-thrust swallow – Normal teeth together swallow. Associated with digit sucking habit. Needed to maintain anterior seal.
  141. 141. 2. Complex tongue thrust swallow. Associated with chronic nasorespiratory distress, mouth-breathing, tonsillitis or pharyngitis. Inflamed tonsils produce pain due to encroachment of the root of the tongue. Reflex drop of mandible – separating the teeth & provides more room for the tongue to thrust - assuming a more comfortable position.
  142. 142. In chronic mouth breathers - large freeway space due to dropping of the mandible & protrusion of the tongue – adequate airway. Jaws held apart during swallow – tongue remains in a protracted position.
  143. 143.  Studies by Melsen et al showed tongue thrust swallow & teeth apart swallow favor development of disto-cclusion, maxillary overjet & openbite.  Tongue thrust a misnomer – Proffit.  Swallowing not a learnt behavior but is integrated & controlled physiologically at subconscious levels.
  144. 144. Mature adult swallow develops at 3 years of age, in majority of people seen by the age of 6 yrs. Only brain damaged children retain a true infantile swallow. Transition stage characterized by muscular activity which brings the lips together, separates the posterior teeth & there is forward protrusion of the tongue. Delayed normal swallow transition associated with previous history of sucking habit
  145. 145.  Upper incisor protrusion or anterior open bite – Difficult to seal the mouth by bringing lips together.  Bringing the tongue forward – a successful maneuver to form an anterior seal.  Too short a duration to have impact on the tooth position-1 second.  Total swallows per day approx.-1000.
  146. 146. Tongue thrust swallow present in children with good anterior occlusion. Due to stoppage of sucking habit & where the open bite is closing – tongue position persists for a while. Tongue thrusting seen in two circumstances1. Children with normal occlusion passing through the transition stage. 2. Where there is an anterior openbite or protracted anterior teeth. Tongue thrusting result of malocclusion not the cause.
  147. 147. Tongue Posture & Tongue Size  TONGUE POSTURE:  Tongue thrust swallowing – short duration to have impact on tooth position.  If posture of tongue is forward resting for long duration effects tooth position.
  148. 148. TONGUE SIZE: Macroglossia can lead to proclination of anteriors & anterior openbite. Aglossia/Microglossia can lead to crowding and lingual inclination of teeth.
  149. 149. Skeletal openbite Steep mandibular plane. Increased anterior facial height. Tongue thrusting results due to lack of anterior seal.
  150. 150. Respiratory Pattern Respiratory needs – Primary determinants of the jaw & tongue. Breathing through the mouth alters equilibrium of the jaws & teeth. Lowering of the mandible & tongue & extension of the head is seen.
  151. 151. Effects of mouth-breathing: -Increase in facial height. -Supraeruption of posterior teeth. -Rotation of mandible downwards & backwards. -Open bite anteriorly. -Increase in overjet. -Pressures from stretched cheeks – narrow maxillary arch.-Posterior crossbite . &class II malocclusion.
  152. 152. Causes leading to mouth breathing: Chronic respiratory obstruction. Mechanical obstruction. Size of the nostril. Pharyngeal tonsils or adenoids (adenoid facies). Greater effort required to breath through the nose – tortuous nasal passages. Partial blockage of the nose leads to resistance of airflow – person shifts to mouth breathing
  153. 153. Studies to Find Association of Respiratory Pattern & Craniofacial Growth. D’Arcy Thompson – ‘Form of an object is its diagram of forces’. Methods to evaluate nasal obstruction: 1.Clinical tests- fogging of mirror, movement of cotton wisps. 2.Cephalometric Radiographs. 3.Rhinomanometric tests
  154. 154. 1. CLINICAL STUDIES OF RESPIRATORY OBSTRUCTION: Classic example – ‘adenoid facies’ Characterized by separated lips, small nose, nostrils poorly developed, pout in the lower lip, vacant facial expression. All patients with this facial characteristics are not mouth breathers. a. Case- children with nasal obstruction- downward & backward rotation of mandible. Subsequent growth increases lower facial height.
  155. 155. b. Howard reviewed 500 patients.  159 patients classified as mouth breathers.  59% - normal occlusion.  14% with Class II malocclusion.  27% with Class III / Class I malocclusion. c. Linder – Aronson & Backstrom compared facial types & type of occlusion in nose breathers and mouth breathers.  Greater nasal resistance – children with long narrow faces & high narrow palate.  No direct correlation between mouth breathing & type of occlusion - particularly overbite / jet.
  156. 156. d. James A. McNamara Jr. – Preliminary analysis of skeletal & dental characteristics of 40 patients. Tonsil & adenoid study (children’s hospital Pittsburgh). Prospective study – Each subject met 1 criterion (at least) for adenoidectomy. Recurrent otitis media. Nasal obstruction due to large adenoids. Both.
  157. 157. Classified as surgical/non-surgical groups. Lateral radiographs analyzed77% - Class I molar relation. 13% - Class II molar relation. 10% - Class III molar relation. On an average – excessive anterior facial height & steep mandibular plane (31.5°) was characteristic. 4 patients – steep mandibular plane, 4 fell within normal limits. Results indicate craniofacial relationships with mouth breathing are variable & associated with no. of facial patterns.
  158. 158. . Fields et al-compared respiratory modes of normal and long-faced subjects using respirometric studies. 1/3rd of the long-faced individuals have less than 50% nasal respiration and none of the normal-faced individuals have such low values. Most of the long faced individuals are predominantly nasal breathers.
  159. 159. Nasal impairment may contribute to long –face but not the sole and major cause. Multifactoral nature of association between nasal obstruction and facial growth. Conclusion of clinical studies: Relationship exists between upper respiratory obstruction & configuration of craniofacial structures for a given individual. No specific pattern can be directly co-related with mouth-breathing
  160. 160. 2. EXPERIMENTAL STUDIES OF RESPIRATORY OBSTRUCTION: James Mcnamaracaused complete nasal obstruction in primates using silicon plugs. Found downward & backward rotation of mandible & increased lower facial height. b. Harvold Miller – Classical studies in young rhesus monkey. Latex plugs inserted into the nasal passages – forcing to breathe through the mouth. Gradual adaptation from nasal to oral respiration.
  161. 161. Some animals positioned mandibles downward & backward. Some, rhythmically lowered and raised the mandibles. Some positioned the mandible downward & forward. Morphological changes – Soft tissue changes occurred first – notching of upper lip & grooving of the tongue. Moderate skeletal changes in animals who lowered mandible for each breath
  162. 162. Dramatic changes In mandibular morphology –at the gonial region and chin in animals which maintained lowered mandibular posture. Distance from nasion to chin increasedlowering of mandible. Distance from nasion to hard palate increased –downward displacement of maxilla.
  163. 163. Lower border of the mandible became steeper, increase in gonial angle. The ramus height maintained its normal relation – masticatory muscles attaching the ramus to the skull are unaffected. Conclusions: Every animal adapted to the environmental insult with unique neuromuscular adaptation. Occlusal effects variedRotation of the mandible in a posteroinferior direction – Class I skeletal open bite or Class II malocclusion. Maintained more anterior position of mandible – Class III malocclusion. Total nasal obstruction- rare in human beings.
  164. 164. 3. STUDIES FOR ADAPTATIONS FOLLOWING REMOVAL OF NASAL OBSTRUCTIONS: Linder- Aronson studied 41 children who underwent adenoidectomies- 5 years. 34 children who switched to oral respiration compared with 54 normal children. Significant group mean difference found initially. Greatest change occurred in the dentition and the sagittal depth of the nasopharynx in the first year.
  165. 165. Mandibular plane angle diminished by 4 degrees (gradual change). Results were statistically significant but no large measurement differences – facial height only 3 mm larger in adenoidectomy group.
  166. 166. Solow & associates studied relationship of craniofacial angulations & nasal respiratory resistance. 2 months after adenoidectomy – 2% reduction in the craniocervical angulation & position of the head in relation to true vertical. Bushey-Compared lateral cephalograms –pre and post surgically.  Found no relationship between linear measurements of the adenoids and nasal respiration.
  167. 167. Research leads to 2 opposing principles: Total nasal obstruction – highly likely to alter the pattern of growth & lead to malocclusion. Majority of individuals with long face pattern of deformity have no evidence of nasal obstruction & must have some other etiological factor as the principle cause.
  168. 168. Roles of the Muscles in Producing Class I, II & III Malocclusion Class I malocclusion – Muscle function usually normal & in a state of balance. Class I open bite – exception – attributable to thumb/finger sucking or abnormal swallow or both. Displacement of maxillary incisors labially results in tongue thrusting to ‘close off’ the oral cavity – accentuation of open bite occurs.
  169. 169. Tongue thrusting enhances as lips become hypotonic & no longer contact. Mouth breathing aggravated as tonsils & adenoids are larger at this stage.
  170. 170. If maxillary incisors are very proclined – cushions to the lingual aspect of maxillary incisors making them more proclined. Mentalis activity increases – puckering of the skin with each swallow. Tongue drops lower in the mouth – no longer approximates the palate
  171. 171.  Disturbance of the equilibrium – narrowing of the maxillary arch.  Over eruption of the posterior teeth because lateral portion of tongue do not overlay occlusal surfaces of posterior teeth.  Interocclusal space eliminated.  Crossbite occurs – leading to mandibular displacement. • Though malocclusion not entirely caused by the finger habit, it was the first assault on the integrity of the dentition. • Compensatory tongue & lip activity resulted in significant deforming mechanism.
  172. 172. Class II Div. 1 malocclusion: Change in the muscle function – requisite. Proclination of anterior teeth leads to excessive overjet. Lip sucking habit develops – hypertrophic lower lip. Incisors move further labially – no resistance from hypotonic functionless upper lip. Lower incisors pushed lingually by abnormal mentalis activity. Lower tongue position – Narrowing of the maxillary arch.
  173. 173. Class II Div. 2 malocclusion:  Muscle function usually normal.  Tongue occupies the interocclusal space – increases interocclusal clearance.  Interferes with eruption & accentuate curve of spee.  Due to lingual inclination, excessive interocclusal clearance & infraocclusion of posterior teeth – forced retrusion of mandible occurs.  TMJ problems can arise.
  174. 174. ‘Forced retrusion’- controversial. Swann (1954)-functional displacement of mandible when teeth are occluded. Ricketts (1955),Jarabac(1963),Graber(1969)-also agreed that there was a displacement of mandible posteriorly and superiorly. Recent studies have challenged this concept.
  175. 175. Gianelly (1989)-studied 19 asymtomatic subjects with no overjet,deep bite and upright incisors against 21 Cl II subjects with normal overbite,overjet and interincisal angulations. Concluded that condylar positions in both groups were essentially centered. Demisch(1992)-concluded that-if there is distal positioning of the mandible,it would spontaneously reposition anteriorly on treatment. As this phenomenon not noticedmandible not displaced posteriorly.
  176. 176. Assessment of the condylar position in class II div 2,using the mandibular position indicator-30 subjects. Conclusions: 1.Although no particular predisposition to condylar retrusion,it is seen in (uni/bilatrelly)in more than 50% of cases. 2.No association between condylar retrusion and overjet, overbite and incisal inclinations. 3.Significant association between mandibular size and condylar retrusion.
  177. 177. Class III malocclusion: Abnormal muscle function is seen. Upper lip – short but not hypotonic. Lower lip hypertrophic & redundant – passive during deglutition. Upper lip shows greater activity during swallowing. Tongue lies low in the floor of the mouth – constricted maxillary arch. Interocclusal space – small or absent
  178. 178. Lip-Sucking & Lip-Biting  May be seen on its own or associated with thumb sucking.  Mandibular lip mostly involved.  Results in labioversion of maxillary teeth.  Open bite & linguoversion of mandibular incisors.
  179. 179. Nail-Biting Seen in high strung & nervous children. Symptom of social & psychologic maladjustment. Often mentioned to cause malposition but rarely does. Marked increase in children after 6 year of age. Clinical examination of the incisor teeth in finger-nail biters indicate that the habits is responsible for openbite & rotation of the mandibular incisor.
  180. 180. Clenching & Bruxism Is rhythmic contraction of the masticatory muscle – side to side grinding & gnashing of teeth during sleep. Imp factor psycological or emotional tension. Initiated local factors-cusp interference loose teeth, high filling…
  181. 181. Effect on Dentition Reduction in the length of the crown. Esthetic concern arises from excessive wear in anterior region. Wear in posteriors-Inter proximal spacing & food impaction. Generalised wear of teeth-reduced facial vertical dimension or mandibular overclosure.
  182. 182. Posture  Frequently suggested that poor posture can lead to malocclusion.  Stooping with chin on the chestmandibular retrusion.  Child resting head on hand or sleeping on arm or fist- possible development of malocclusion.  May accentuate existing malocclusion.  Role as primary etiological factor to be proved conclusively.
  183. 183. Appliances Leading to Malocclusion Milwaukee Brace – Given in the treatment of scoliosis. Holds the head in extended position. Constant pressure on the mandible – causes malocclusion. Plaster castsUsed to stabilize cervical vertebrae can produce similar effects.
  184. 184. Accident or Trauma Undiscovered traumatic experiencessignificant in malocclusion.  Eruptive abnormalities.  Abnormal resorption.  Loss of vitality. Both prenatal trauma & postnatal injuries- Dentofacial deformity:
  185. 185. Prenatal trauma Intrauterine pressure or trauma during delivery-Hypoplasia of mandible. Asymmetry Postnatal Trauma Fracture of jaws &teeth. Habits may produce ‘microtrauma’. TMJ-impaired growth & functionasymmetry & TMD.
  186. 186. REFERENCES Robert E. Moyers- Handbook of Orthodontics- 4th ed Salzmann. J. A- Orthodontics in daily practice- 4th ed William R. Proffit- Contemporary Orthodontics- 3rd ed T. M. Graber- Orthodontics- Principles and practice T. C. White, J. H. Gardiner, B. C. LeightonOrthodontics for dental students. Shobha Tandon- Text book of pedodontics Shafer, Hine and Levy- A text book of oral pathology- 4th ed
  187. 187. Thank you Leader in continuing dental education