Etiological basis of malocclusion theories /certified fixed orthodontic courses by Indian dental academy


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  • Specifically this means to the orthodontist that nature harmonizes the dental structures according to facial type. He cannot impose preconceived ideas of facial form and beauty on structures whose foundation is built for something else, Call it human engineering or whatever you wish, but this predominance of the morpho-genetic pattern profoundly influences orthodontic objectives and therapeutic results
  • This does not mean that the musculature has created the maxillary protrusion and mandibular retrusion in the Class II malocclusion, and the maxillary retrusion and mandibular protrusion in a Class III malocclusion. It may have accentuated the deformation by virtue of its adaptive functional activity. Class III malocclusions, by contrast, the lower lip is redundant and often hypofunctional. During deglutition the tongue lies lower in the mouth, but the tip reaches up and contacts the vermilion border of the upper lip as it drops partly behind the lower incisors. The oral seal is thus effected by tongue and upper lip. The lower lip may curl slightly on itself, with an increase in the depth of the mentolabial sulcus. Even in less severe maxillary deficiency cases or mandibular prognathism, the tongue posture is still low in the mouth. There is some tongue protrusion as the anterior portion curls back on itself to achieve a lingual dento-alveolar contact.
  • Thus, the original malocclusion may have been the result of a hereditary pattern, but this has been made worse by the compensatory malposition and malfunction of the associated musculature. Unfortunately, this becomes a vicious circle. The greater the overjet, the more habitual the interposition of the lower lip nestled between the labial aspect of the mandibular incisors and the lingua! aspect of the maxillary incisors.
  • Duration of the habit beyond early childhood is not the only determinari Equally important are at least two other considerations. The frequency of habit during the day and night affects the end-result. The child who su* sporadically or just when going to sleep is much less likely to do any dai than one who constantly has his finger in his mouth. The intensity of the hab! is important. In some children the sucking can be heard in the next room, perioral muscle function and facial contortions are easily visible. In others the thumb habit is little more than a passive insertion of the finger in the mouth with no apparent buccinator activity. If the forefinger is a favorite digit, more damage may be expected with the dorsal surface of the finger resting fulcrum, like on the lower incisors than with the palmar surface hooked over the same teeth, with the tip of the finger innocuously placed in the floor of the mouth The finger itself may show the effects of the habit
  • Etiological basis of malocclusion theories /certified fixed orthodontic courses by Indian dental academy

    1. 1. MALOCCLUSION THEORIES INDIAN DENTAL ACADEMY Leader in continuing dental education
    2. 2. Introduction  1. 2. There is general agreement that an individual’s occlusal status is described by two major characteristics: The relationship of the teeth within each arch to a smoothly curving line of occlusion ( alignment ), and The pattern of occlusal contacts between maxillary and mandibular teeth in the transverse, anteroposterior, or vertical planes of space (occlusion). It is difficult to implicate a single major cause for malalignment or malocclusion.
    3. 3.  Rather than having specific "causes," as do some diseases, malocclusions are usually clinically significant variations from the normal range of growth and morphology. Etiologic factors contribute to the variance more often than they simply "cause" it. The primary etiologic sites of malocclusion are (a) the craniofacial skeleton, (b) the dentitions, (c) the orofacial neuromusculature, and (d) other "soft tissues" of the masticatory system, (excluding muscle).
    4. 4. Incidence of Malocclusion The most prevalent type of malocclusion in deciduous dentitions is anterior open bite tied with tongue thrust & finger habits. Class II division 1 was next common.  In mixed dentitions, crowding was most common, & mandibular retrusion is the next common.  In permanent dentitions, Class II, Division 1 & crowding were equally distributed. 
    5. 5. Prevalence Brunelle JA et al J Dent Res 1996.     Angle I Normal: 30% Angle Class I Malocclusion: 50% Angle Class II Malocclusion: 20% Angle Class III Malocclusion: <1% Horizontal Plane: Vertical Plane: • Posterior Cross • Open Bite (≥ 0 mm):< 3% Bite :9.1% • Vertical Deep Bite (≥5 mm): 16 %
    6. 6. Racial Differences:     Asian: increased Angle III prevalence Afro-American: 10% anterior open bite,increased Angle III Northern European: increased prevalence of vertical deep bite,increased prevalence Angle II Hispanic: increased severe Angle II
    7. 7.  In homogeneous racial groupings the incidence of malocclusion seems relatively low. In certain areas of the world for example, some of the Philippine Islands malocclusion is almost nonexistent Population groups there are relatively pure genetically, and the occlusion of the natives "normal."
    8. 8.  A study was done by Stockard, C. R. (1932) on the genetics of modified endocrine secretion and associated form pattern among dog breeds. Proc. Sixth Internat. Cong. Genetics,.  Results : gross deformities were seen after crossbreeding of dogs. Racial crossbreeding may emulate these experiments to a degree.  Conclusion :Where there has been a mixture of racial strains the incidence of jaw size discrepancies and occlusal disharmonies is significantly greater.
    9. 9. Chung, Niswander and Runck (1971) studied the effect of intermixing of European, Japanese and Chinese races with native Polynesians of Hawaii, on the malocclusion in their descendents. Their study showed that the effect of inter racial crosses on malocclusion is additive rather than multiplicative. No independent inheritance of discrete morphologic characteristics like tooth and jaw sizes.
    10. 10. Systems of classification  The first useful orthodontic classification of malocclusion was given by Angle (1890s). Angle’s postulate was that the upper 1st molar were the key to occlusion and that the upper & the lower molars should be related so that the mesiobuccal cusp of the upper molar occludes in the buccal groove of lower molar.
    11. 11. Angle’s classification     Normal occlusion - Normal (Class I) molar relationship, teeth on line of occlusion Class I malocclusion - Normal (Class I) molar relationship teeth crowded, rotated, etc. Class II malocclusion -Lower molar distal to upper molar, relationship of other teeth to line of occlusion not specified Class III malocclusion-Lower molar mesial to upper molar, relationship of other teeth to line of occlusion not specified
    12. 12. CLASS I Molar and Jaw Relationship CLASS II Molar and Jaw Relationship CLASS III Molar and Jaw Relationship
    13. 13. Simon’s method  One of the best classification efforts has been made by Simon, using the gnathostatic approach and orienting the dentition to anthropometric landmarks in an attempt to better show the actual relationship of the dentition in the face. Simon took the suggestion made by Bennett in 1912 that malocclusions be categorized in three planes.
    14. 14.
    15. 15. Ackerman Profitt’s Classification
    16. 16. Classifications of etiology of malocclusion According to Dockrell (1) Heredity; (2) Developmental causes of unknown origin; (3) Trauma; (4) Physical agents; (5) Habits; (6) Disease; and (7) Malnutrition
    17. 17. The primary etiologic sites of malocclusion are (a) the craniofacial skeleton, (b) the dentitions, (c) the orofacial neuromusculature, and (d) other "soft tissues" of the masticatory system,(excluding muscle).
    18. 18. Dockrell’s Equation  Causes ACT Times Tissues PRODUCING Results ON SOME PREDISPOSING PRENATAL SOME EXCITING OR POSTNATAL 1.Heridity 2.Developmental causes of unknown origin 3.Trauma 4.Physical agents 5.Habits 6.Disease 7.Malnutrition 1.Continuous OR Intermittent 2.May act at different age levels. May be following SOME PRIMARILY SOME SECONDARILY 1.Neuromuscular tissue 2.Teeth 3.Soft tissue other than muscles or a combination of these 1.Malfunction . 2.Malocclusion. 3.Osseous dysplasias.
    19. 19.  McCoy and Shepard(1956) a) Direct(determining) b) Indirected(predisposing)
    20. 20. GRABER'S CLASSIFICATION  GENERAL FACTORS 1. Heredity 2. Congenital 3. Environment  a: Pre-natal [trauma, maternal diet, German measles, maternal metabolism etc.,.]  b. Post natal [birth injury, cerebral palsy, T.M.J.injury.] 4. Pre-disposing metabolic climate and disease  a.Endocrine imbalance  b.Metabolic disturbances  c.Infectious diseases 5. Dietary problems (nutritional deficiency)
    21. 21. 6. Abnormal pressure habits and functional aberrations a.Abnormal sucking. b.Thumb and finger sucking c.Tongue thrust and tongue sucking d.Lip and nail biting e.Abnormal swallowing habits [improper deglutition] f. Speech defects g. Respiratory abnormalities [mouth breathing etc.,.] h. Tonsils and adenoids i. Psychogenic tics and bruxism 7. Posture 8. Trauma and accidents
    22. 22. GRABER'S CLASSIFICATION  LOCAL FACTORS 1. Anomalies of number: Supernumerary teeth, Missing teeth [congenital absence or loss due to accidents, caries, etc.] 2. Anomalies of tooth size 3. Anomalies of tooth shape 4. Abnormal labial frenum : mucosal barriers 5. Premature loss of deciduous teeth
    23. 23. 6. Prolonged retention of deciduous teeth 7. Delayed eruption of permanent teeth 8. Abnormal eruptive path 9. Ankylosis 10Dental caries 11Improper dental restoration
    24. 24. MOYER'S CLASSIFICATION 1 Heredity a.Neuromuscular System b.Bone c.Teeth d.Soft Parts 3.Trauma a.Prenatal trauma and birth injuries b.Postnatal trauma 4. Physical agents a.Premature extraction 2.Developmental defects of of primary teeth unknown origin b. Nature of food
    25. 25. 5.Habits a. Thumb sucking and finger sucking b. Tongue thrusting c. Lip sucking and lip biting d. Posture e. Nail biting f. Other habits 6.Diseases a.Systemic diseases b.Endocrine disorders c.Local diseases i.Nasopharyngeal diseases and disturbed respiratory function ii.Gingival and periodontal disease iii.Tumors iv Caries 7.Malnutrition
    26. 26. WHITE AND GARDINER'S CLASSIFICATION B.Preeruption abnormalities A. Dental base abnormalities 1. Abnormalities in position of developing tooth germ 1. Antero-posterior 2. Missing teeth malrelationship 2. Vertical malrelationship 3. Supernumerary teeth and teeth abnormal in form 3. Lateral mairelationship 4. Prolonged retention of 4. Disproportion of size deciduous teeth between teeth 5. Large labial frenum and basal bone 6. Traumatic injury 5. Congenital abnormalities
    27. 27. C. Post-eruption abnormalities 1. Muscular a. Active muscle force b. Rest position of musculature c. Sucking habits d. Abnormalities in path of closure 2. Premature loss of deciduous teeth 3. Extraction of permanent teeth
    28. 28. Salzman’s Classification Prenatal Postnatal Developmental A. General B. Local Functional A. General B. Local Environmental Or Acquired A. General B. Local
    29. 29. Salzman’s classification Prenatal 1.Genetic: Dentofacial anomalies may or may not be in evidence at birth. 2. Differentiative – a. General: affect the body as a whole b. Local: affect the face, jaws, and teeth 3 Congenital a. General or constitutional b. Local or dentofacial
    30. 30.  Postnatal 1. Developmental A. General a. Birth injuries b. Abnormalities of relative rate of growth in different body organs c. Hypo or hypertonicity of muscles d. Endocrine disturbances e. Nutritional disturbances f. Childhood diseases that affect the growth pattern g. Radiation
    31. 31. B. Local a. Abnormalities of the dentofacial Complex (1) Birth injuries of the head, face and jaws (2) Micrognathia or macrognathia (3) Microglossia or macroglossia (4) Abnormal frenum labil (5) Facial hemiatrophy b. Anomalies of tooth development (1) Delayed or premature eruption of the deciduous or permanent teeth (2) Delayed or premature shedding of deciduous teeth. (3) Ectopic eruption (4) Impacted teeth (5) Aplasia of teeth
    32. 32.  Functional 2. Local A. Malfunction of forces exerted A. Muscular hyper- or by the inclined planes of the hypotonicity. cusps of the teeth B. Endocrine disturbances B. Loss of force caused by failure of proximal contact of teeth C. Neurotrophic C. Temporomandibular disturbances articulation disturbances 1. General D. Nutritional deficiencies E. Postural defects F. Respiratory disturbances, mouth breathing. D. Masticatory and facial muscular hypo- or hyperactivity E. Faulty masticatory function, (during tooth eruption).
    33. 33. Environmental Or Acquired. 1. General A. Disease B. Nutritional disturbances (during tooth formation). C. Endocrines. D.Metabolic disturbances E.Trauma. Accidental injuries F.Radiation 2. Local A. Disturbed forces of occlusion B. Early loss of deciduous teeth C. Prolonged retention of deciduous teeth D. Delayed eruption of permanent teeth E. Loss of permanent teeth F. Periodontal diseases G. Temporomandibular articulation disturbances H, Infections in the oral cavity I. Pressure habits J. Traumatic injuries, fractures of jaws
    34. 34.  Equilibrium Theory first given by Weinstein.S et al A O 1963 revisited by William R Proffit A O 1978 states that Equilibrium theory, as applied in engineering, that an object subjected to unequal forces will be accelerated and thereby will move to a different position in space .It follows that if any object is subjected to a set of forces but remains in the same position, those forces must be in balance or equilibrium. From this perspective, the dentition is obviously in equilibrium, since the teeth are subjected to a variety of forces but do not move to a new location under usual circumstances. Even when teeth are moving, the movements are so slow that a static equilibrium can be presumed to exist at any instant in time.
    35. 35. Equilibrium components Four major primary factors 1. Intrinsic forces by tongue & lips 2. Extrinsic forces: Habits (thumb-sucking, etc) Orthodontic appliances. 3. Forces from dental occlusion 4. Forces from the periodontal membrane.
    36. 36. .
    37. 37. 25 After a paralytic stroke in this patient, the side of the tongue rested A large portion of die cheek has been lost because of a against the mandibular left posterior teeth. A, Intraoral view; B, casts tropical infection. The out­ward splaying of die teeth when mounted on an articulator. The extreme displacement of teeth in this adult the restraining force of the check :s lost illustrates the effect resulted from the increased tongue pressure, altering the equilibrium. of a change in equilibrium. (From Moss JP, Picton DCA: (Courtesy Dr. T. Wallen.) Arch OralBiol 12:1313­1320, 1967.)
    39. 39. Heredity    Two Facts 1.For each individual there is a basic pattern or blueprint for dentofacial development , not really which may be masked but not really changed. (unless by surgery). 2.Racial and familial characteristics repeat
    40. 40. Inheritance and Malocclusion Familial occurrence of Class II division 2 has been documented in several published reports including twin and triplet studies e.g. Korkhaus (1930), Markovic (1992), Peck et al. (1998). Markovic (1992) carried out a clinical and cephalometric study of 114 Class II division 2 malocclusions (48 twin pairs and six sets of triplets)
    41. 41.   Of the monozygotic twin pairs, 100 per cent demonstrated concordance for the Class II division 2 malocclusion, while almost 90 per cent of the dizygotic twin pairs were discordant. This is strong evidence for genetics as the main etiological factor. Genetic influence is probably Autosomal dominant with incomplete penetrance and variable expressivity.
    42. 42.   It could also be explained by a Polygenic model with a simultaneous expression of a number of genetically determined morphological traits acting additively rather than being the effect of a single controlling gene for the entire occlusal malformation. Controversy regarding the etiology arises from a failure to appreciate the synergistic effects of genetics and environment.
    43. 43.  The most famous example of a genetic trait passing through several generations is the pedigree of the so called Hapsburg jaw.( Hungarian /Austrian dual monarchy)  Strohmayer (1937) concluded from pedigree analysis of the Hapsburg family line that the mandibular prognathism was transmitted as an Autosomal dominant trait.
    44. 44. King Charles II of Spain who had a Hapsburg jaw.
    45. 45. Heritability of craniofacial skeletal dimensions and tooth-based occlusal variables      Craniometric measures have higher heritabilities than occlusal variables of tooth position. Mild occlusal relationship problems may be largely environmental, while the more severe ones probably have a stronger genetic component. A number of cranio-facial features are under polygenic control. Mesiodistal dimensions of teeth are strongly influenced by genetic determinants. All teeth have about the same amount of heritability. MZ twins show greater concordance in tooth morphology than DZ twins.
    46. 46. Affected by Heredity According to Lundstrom. A – (1949).  Tooth size  Arch length and width  Height of the palatal vault  Crowding or spacing of teeth.  Overbite and overjet  Position and configuration of muscles  Tongue size and shape  Character of the oral mucosa, frenum size,shape & position.
    47. 47. Heredity also plays a role in:            Facial asymmetries Macrognathia and micrognathia Macrodontia and microdontia Oligodontia and anodontia Tooth shape variations (peg-shaped lateral incisors. Carabeli's cusps,mamelons, etc.) Cleft palate and harelip Frenum diastemas Deep overbite Crowding and rotation of teeth Mandibular retrusion Mandibular prognathism
    48. 48.  Robert S. Corruccini,, and Rosario H. Yap Potter: AJO-DO, 1980. Genetic variance and heritability were estimated for a series of arch and occlusal traits in sixty twins using recently developed methods that are unbiased by variance heterogeneity between zygosities. Heterogeneity was demonstrated for 20 of the 40 traits, suggesting considerable amounts of hidden environmental determinance. Toothdisplacement means differed between monozygotes and dizygotes, indicating bias in that trait's genetic variance analysis.
    49. 49. Significant heritability could not be demonstrated for overbite, overjet, buccal segment relation, total tooth displacement, and occlusal discrepancies in arch shape.  Arch size, individual tooth displacement scores, and cross-bite show significant genetic variance, averaging only about 36 percent of the total variance of these traits. 
    50. 50. Jedidiah R. Gass, Manish Valiathan, Hemant K. Tiwari, Mark G. Hans, and Robert C. Elston, (AJODO 2003) to estimate familial correlations and heritability to evaluate familial aggregation patterns of maxillary midline diastemas. The sample consisted of 30 extended families: 15 black, 14 white and 1 mixed race. Family data were collected with a 7-question survey.
    51. 51. In all, the sample of 430 subjects consisted of 220 females, 210 males, 99 nuclear families, 534 sibling pairs, 422 avuncular pairs, 318 grandparent pairs, and 27 cousin pairs. Data were analyzed. Heritability was found to be 0.32 ± 0.14 in the white sample and 0.04 ± 0.16 in the black sample. The preliminary results suggest a possible genetic basis for maxillary midline diastema and a greater role of environmental factors in the black sample than in the white sample.
    52. 52.   A study was done by Lisa King et al ( AJODO 1993 ) to estimate heritabilities of skeletodental variables. Of only that portion of the adolescent population receiving comprehensive orthodontics. Initial treatment records of 104 pairs of siblings were studied, all of whom subsequently received full-banded treatment. In this selected series of overt malocclusions, heritability estimates for craniometric variables were significantly lower than in a comparable series of adolescents with naturally occurring good occlusions, whereas heritability estimates for occlusal variations (e.g., rotations, crossbites, displacements) were significantly higher.
    53. 53.    This indicates the clinical perception that siblings often present with similar malocclusions. They propose that the substantive measures of intersib similarity for occlusal traits reflect similar responses to environmental factors common to both siblings. That is, given genetically influenced facial types and growth patterns, siblings are likely to respond to environmental factors (e.g., reduced masticatory stress, chronic mouth breathing) in similar fashions. Malocclusions appear to be acquired, but the fundamental genetic control of craniofacial form often diverts siblings into comparable physiologic responses leading to development of similar malocclusions.
    54. 54.  Hasund and Sivertsen ( A O – 1971) point out the sexlinked nature of facial width and dental arch shape. Females demonstrate a positive correlation the wider the face, the wider the arch. Unless we can change cranial and facial superstructures and reorient bony trabeculae, stress trajectories and supporting pillars and buttresses, along with their muscle attachments, we cannot significantly alter the hereditary pattern determinant that furnishes the blueprint for arch form, arch size, arch shape, etc.
    55. 55.  According to Pruzhansky (1959), the individual never fully realizes the genetic pattern in postnatal life. Human potentialities are determined by the genotype, but their manifestation depends on environment. With the exception of identical twins, no two persons have the same genotype.
    56. 56. Examples of Congenital Defects      Clefts of the lip and palate Cerebral Palsy Crouzons syndrome Cleido-Cranial Dysostosis Cranial Synostosis
    57. 57. Craniosynostoses  The sutures ( or lines of fusion ) between the bones of the cranium are the areas across which the skull expands as growth occurs. Craniosynostosis describes the premature fusion of skull sutures. Those which particularly affect skull shape are the coronal, sagittal and lamboid sutures.
    58. 58.  It is the constraint on neurocranial growth by prematurely closed sutures that results in the characteristic shape. Head shape depends on which sutures are prematurely synostosed, the order in which they synostose, and the timing at which they synostose. As a general rule, growth restriction occurs at right angles to the fused suture with compensatory expansion in the same direction as the fused suture.
    59. 59. Crouzon Syndrome  Autosomal dominant with almost complete penetrance  Considerable variability of cranial form depending upon the sequence and degree of sutural synostosis. The most characteristic type is represented by the premature closing of the lamboid and coronal sutures resulting in an abnormally high, peaked or conically shaped skull.
    60. 60.
    61. 61.  Malformations of the face lend the disease its characteristics. The face is flattened, sometimes concave.
    62. 62.  Protrusion of the eyeballs is a constant, cardinal sign and is often quite marked.
    63. 63.   Wide-set eyes may be present Nasal root is flat, the dorsum and the nostrils are wide
    64. 64.  Because of recession of the maxillary bone, there is the impression of protruded mandible despite the fact that the latter is normal or even reduced in size.
    65. 65.  Orally, the dental arch may be V-shaped. The palate is usually higharched and narrow
    66. 66. Apert’s Syndrome   Autosomal dominant. High infant mortality.Advanced male parental age consistently noted. The occiput is flat and not clearly demarcated from the plane of the back of the neck. The forehead is steep, high and flat. Temporal bulging is evident
    67. 67.  Osseous and / or cutaneous syndactyly of hands and feet
    68. 68.  Downward slanting of the eyes with a drooping of the upper eyelids
    69. 69.  The mouth remains open in the shape of an isosceles triangle. The upper lip is retracted. The cheeks are rounded while the dangling lower lip juts out.
    70. 70.  Class III malocclusion
    71. 71. Treacher-Collins Syndrome (Mandibulofacial Dysostosis)  The term “ dysostosis refers to a malformation of individual bones either singly or in combination, but it is not a generalized skeletal disorder. Thus, mandibulofacial dysostosis is limited to facial structures.  Autosomal dominant trait.
    72. 72.   Varying degrees of hypoplasia of the mandible, maxilla, and zygoma. Sagging lower eyelid
    73. 73. Cleiocranial Dysplasia    Autosomal dominant inheritance. Penetrance is high, although expressivity may be low requiring careful examination to establish proper diagnosis. Sagitally diminished cranial base and transverse enlargement of the cranium, resulting in a large head. Facial bones and paranasal sinuses are hypoplastic giving the face a small and short appearance
    74. 74.  Orally, delayed eruption of secondary dentition, supernumerary teeth, more frequent caries, and malformed teeth or roots. The cause of delayed or failed eruption of the teeth has been associated with lack of cellular cementum. Dentigerous cysts
    75. 75.  Partial to complete aplasia of clavicles, which allows the patient to oppose the shoulders. Severely sloped and hypermobile shoulders
    76. 76. Cleft lip & palate
    77. 77. The literature on tooth formation in children with cleft lip and/or palate is reviewed by Reijo Ranta, (AJODO 1986.) 1. The upper lateral incisor is the most susceptible to injury in the area of cleft in both deciduous and permanent dentitions. This tooth is affected in most instances, even in the cases of microforms of the cleft lip. 2. The prevalence of hypodontia increases strongly with the severity of cleft. More teeth are congenially missing from the upper jaw than from the lower jaw; however, in the permanent dentition both jaws are affected.
    78. 78. 3. Very high prevalence of hypodontia are observed in connection with the Van der Woude syndrome associated with cleft and with the Pierre Robin anomaly. 4. Hypodontia is similarly prevalent in subjects with isolated cleft palate with and without a positive family history of clefts. 5.Asymmetric formation of the contralateral teeth is a milder form of hypodontia. 6. The prevalence of asymmetrically developing pairs of teeth is far more common in children with clefts than in children with normal palates or lips.
    79. 79. 7. In the permanent dentition the timing of tooth formation is delayed in children from all cleft groups compared to noncfeft children. The delay lengthens (with increasing severity of cleft) from 0.3 to 0.7 years and is similar in all permanent teeth in both jaws. 8. In children with hypodontia, the delay is still more severe. As the child becomes older, the delay may increase. 9. The size of the permanent teeth is smaller than in non cleft children and the metric asymmetry of the crown or root size is apparent in both jaws.
    80. 80. 10. Enamel defects and abnormalities in shape and size of both deciduous and permanent teeth are far more common in children and fetuses affected with cleft than in normal subjects. These abnormalities occur in both jaws. 11. Dental abnormalities in number, size, shape, timing of formation, eruption, and the cleft itself seem to have a common cause in most instances. The postnatal environmental factors nutrition, infections, and surgical treatment may have an effect only on enamel defects and, perhaps, in some instances, on agenesis of the permanent teeth
    81. 81. Cerebral Palsy.      Cerebral palsy is a paralysis or lack of muscular coor­dination attributed to an intracranial lesion. It is most commonly considered to be the result of a birth injury. Effects of this neuromuscular disorder may be seen in the integrity of the occlusion . Unlike cleft palate, where there are abnormal structures, the tissues are quite normal but the patient, because of his comparative lack of motor control, docs not know how to use them properly. Varying degrees of abnormal muscular function may occur in mastication, deglutition, respiration and speech. The uncontrolled or aberrant activities upset the muscle balance that is necessary for the establishment and maintenance of a normal occlusion.
    82. 82.  TORTICOLLIS. The farreaching effects of abnormal muscle forces are visible also in torticollis, or "wry neck." The foreshortening of the sternocleidomastoid muscle can cause profound changes in the bony morphology of the cranium and face. Torticollis provides an example of the thesis that in a struggle between muscle and bone, bone yields. Bizarre facial asymmetries with uncorrectable dental maloccluslons may be created if this problem is not treated fairly early.
    83. 83.  a. b. c. d. e. f. Congenital Syphilis - Abnormally shaped teeth and malposed teeth are considered characteristic disease phenomena Hutchinson’s incisors. Mulberry molars Enamel deficiencies. Extensive dental decay. The maxilla may be smaller in size relative to maxilla. Anterior crossbite.
    84. 84.  a. b. c. Maternal Rubella infection : Dental Hypoplasia. Retarded eruption of teeth. Extensive caries.
    85. 85. ENVIRONMENT Prenatal Influence –  Uterine posture,  fibroids of the mother,  amniotic lesions,  maternal diet and metabolism,  drug-induced deformities (thalidomide),  possible injury or trauma and  German measles
    86. 86. Intrautcrinc moulding, showing probable intrauterine posture distortion & assymetry in view. But may be temporary.
    87. 87. Phocomelia
    88. 88. Paulo Frazãoa and Paulo Capel Narvai (AJODO 2006) The aim of their study was to assess the severity of occlusal disorders in Brazilian adolescents, 12 and 18 years old, and to investigate associations between occlusal disorders and demographic, socio-environmental, and clinical variables. Secondary data from a cross-sectional study, including 13,801 dental occlusion status records from a sample randomly selected from public and private schools in 131 cities in the state of São Paulo, Brazil, were analyzed.
    89. 89. Results: The mean DAI score for the sample was 24.33 (SD 7.54), and 16.5% of the subjects had DAI scores of 30 or more (severe or very severe malocclusion). The rate of DAI 31 was significantly higher among 12-yearolds, nonwhites, public-school students, those from smaller municipalities, those without fluoridated tap water, and those with a CI 51%, a DMFT score 4 at age 12 years, or a DMFT score 6 at age 18 years. At age 18, fewer subjects had DAI scores 30; the components responsible for this reduction were spacing in at least 1 incisal segment, midline diastema 1, and anterior maxillary overjet 4. Conclusion: Some socio-environmental factors are associated with severity of malocclusion in adolescents.
    90. 90. Postnatal Influence.   Birth Forceps delivery  Another possibility, is the delivery-induced deformation of the upper jaw. Obstetricians frequently insert the forefinger and middle finger into the baby's mouth to ease passage through the birth canal. Because of the plasticity of the maxillary and premaxillary region, temporary deformation is quite likely and permanent damage may result  Accidents Extensive scar tissue 
    91. 91. Birth Injury 8 year old girl
    92. 92. Extensive scar tissue
    93. 93. Milwaukee brace
    94. 94. PREDISPOSING METABOLIC CLIMATE AND DISEASE Exanthematous fevers  Diseases like Poliomyelitis which have paralytic effect  Endocrinopathies (pituitary and parathyroid disturbances) 
    95. 95. Acromegaly  In acromegaly, which is caused by an anterior pituitary tumor that secretes excessive amounts of growth hormone, excessive growth of the mandible may occur, creating a skeletal Class III malocclusion in adult life . Often (but not always sometimes the mandible is unaffected) mandibular growth accelerates again to the levels seen in the adolescent growth spurt, years after adolescent growth was completed. The condylar cartilage proliferates, but it is difficult to be sure whether this is the cause the mandibular growth or merely accompanies it. Although the excessive growth stops when the tumor is removed irradiated, the skeletal deformity persists.
    96. 96. Hemimandibular Hypertrophy     Occasionally, unilateral excessive growth of mandible occurs in individuals who seem metabolic normal. Aetiology - entirely unknown. It is more likely in girls between the ages of 15 and 20yrs, but may occur as early as age 10 or as late as the early 30s . Formerly was called condylar byperplasia.
    97. 97. Achondroplasia     Achondroplasia is rare in humans, but it does occur, and it produces the expected changes. Clinical Features short limbs, the cranial base does not lengthen normally because of the deficient growth at the synchondroses, the maxilla is not translated forward to the normal extent, and a relative midface deficiency occurs. In a number of relatively rare genetic syndromes like achondroplasia, influences on the form of the face, jaws, and teeth can be discerned, but those cause only a small percentage of orthodontic problems.
    98. 98. DIETARY PROBLEMS (NUTRITIONAL DEFICIENCY)  Disturbances such as rickets, scurvy and beri beri can produce severe malocclusions. (Main problem is the upseting of the dental developmental timetables. The resultant premature loss prolonged retention, poor tissue health and abnormal eruptive paths mean malocclusion).
    99. 99.   Muscle Dysfunction The facial muscles can affect jaw growth in two ways. First, the formation of bone at the point of muscle attachments depends on the activity of the muscle; second, the musculature is an important part of the total soft tissue matrix whose growth normally carries the jaws downward and forward. Loss of part of the musculature can occur from unknown causes in utero or as a result of a birth injury, but is most likely to result from damage to the motor nerve (the muscle atrophies when its motor nerve supply is lost). The result would be underdevelopment of that part of the face
    100. 100.
    101. 101.
    102. 102. Abnormal muscle activity  In Class III malocclusions, the lower lip is impotent, while the upper lip is quite active as it lengthens and is drawn against the maxillary incisors and alveolar process by the contracting buccinator mechanism.
    103. 103.  In the Class II, Division I malocclusion, the lower lip is constantly forcing the premaxillary segment upward and outward against a hypotonic, flaccid, relatively functionless upper lip. If there is a negative overbite (open bite), the tongue may actually assist in this deformation.
    104. 104. Habits Duration Frequency Intensity
    105. 105.  ORAL HABITS S U C K I N G ME C H A N I S M      Coordinated Reflex Nourishment Security/Warmth Prevalence – 60% Persistency
    106. 106. Note collapse of cheeks and bottle due to vacuum created during excessive sucking.
    107. 107.
    108. 108. EXCESSIVE digit sucking can set up abnormal forces on the oral cavity and surrounding structures.
    109. 109. Labbok / Hendershot 1987 • Principle finding - the longer the duration of breastfeeding, the lower the incidence of malocclusion. • Bottle feeding leads to a habit of forward tongue thrusting and a weakened development of the orbicularis muscles. • There is a significant decrease in tongue thrusting with an increased duration of breastfeeding .
    110. 110. Thumb sucking   Incidence & Damage – Kjellgren, in a study of 167 thumb suckers, found 87 per cent with a malocclusion; Popovitch, in the Burlington study, reported 52 per cent of the 689 children from 3 to 12 years of age with malocclusion that could be attributed to oral habits.
    111. 111.  Gesell and Ilg of Yale's Child Development Laboratory contend that finger sucking is perfectly normal at one stage of a child's development. They concur with this opinion and feel that most finger sucking and tongue sucking habits, which may be considered normal for the first year and a half of life, will disappear spontaneously by the end of the second year with proper attention to nursing. For the first three years of life, damage to the occlusion is confined largely to the anterior segment. This damage is usually temporary, provided the child starts with a normal occlusion.
    112. 112.  The original morphology is quite important because there is much controversy over the damage that may result from finger and thumb sucking habits, because some of damaging consequences of the habit are similar to the characteristics of a typical hereditary pattern type of Class II , Division I malocclusion, it is easy to assume that the retrognathic mandible, prognathic premaxillary segment, deep overbite, flaccid upper lip, high palatal vault and narrow dental arches are the result of finger sucking.
    113. 113.   There is clinical evidence that deglutitional maturation is retarded in confirmed finger suckers. The finger habit in duration and intensity may be relatively innocuous (perhaps at bed time only) but the tongue thrust continues to adapt to the morphology and the, tongue does not drop back, hump up or spread out.
    114. 114. More damage may be expected with the dorsal surface of the finger resting fulcrum
    115. 115. Ogaard B, Larsson E, Lindsten R Pacifiers A J O D O 1994. • Positive association between pacifiers use and posterior cross bite and reduced upper arch width. • Probable mechanism – Sucking activity in the cheeks – Reduced palatal support as the tongue takes a lower position
    116. 116. Peter H. Lam et al (AJODO 1999) to determine if condylar position in children with functional unilateral crossbites was different from that found in children with Class I noncrossbite malocclusions. Mandibular asymmetry in children with functional unilateral posterior crossbite was also compared to that of a Class I noncrossbite group. It was revealed that the mandibles of children in the functional unilateral posterior crossbite group exhibited asymmetry in both anteroposterior and transverse dimensions when compared with the Class I noncrossbite group (P < .05).
    117. 117. These asymmetries were the result of a functional deviation of the mandible that was present in all subjects in the crossbite group. This deviation was manifested occlusally by a Class II subdivision on the crossbite side as indicated from the study model analysis (P < .05). Examination of condylar position as evidenced by horizontally corrected tomograms demonstrated a large standard deviation, resulting in an inability to detect any significant differences within or between groups at both T1 and T2 (P > .05).
    118. 118. Chang Liua et al Angle Orthodontist,, 2007 To evaluate the morphological and histological responses of the glenoid fossa to mandibular lateral shift in growing rats. It is suggested that the mandibular lateral shift causes asymmetry in the position and size of the glenoid fossa and that this phenomenon can be related to different bilateral directional new bone formation in the posterior region.
    119. 119. Etiological Basis of Malocclusion:theories & contemporary view Presented by- Dr.Neelesh Shah Done Under The Guidance OfProfessor.Ashima.Valiathan B.D.S {Pb}, D.D.S, M.S{U.S.A} Director of P.G studies Department of Orthodontics, Manipal College Of Dental Sciences, Manipal. Part-2
    120. 120. Habits  Tongue thrust habit
    121. 121.  A case report by Valiathan A. & Shaikh.S. (J I OS 1998;31:53-57) showed the effect of an abnormally large tongue in producing the spaces similar in appearance to primate spaces. A 28 year male patient of south Indian origin was presented with a chief complain of proclination of upper anterior teeth along with spacing between the same. His face was fairly symmetrical with convex facial profile, prominent nose, acute nasolabial angle and incompetence of lip. An additional lateral ceph was taken following the administration of radio- opaque contrast medium to highlight the dorsum of tongue and related soft tissue. Based on detailed examination of the tongue dimension, tongue volume, electromyographic activity and force exerted by the tongue, it was concluded that excessively large volume tongue and dimension produce excessive force which possibly causes the malocclusion.
    122. 122. Wallen, T. R.: Vertically directed forces and malocclusion: A new approach. J. Dent. Res., 1974.  Studies by Wallen (1974) indicate that vertically directed pressures during swallowing actually are less in patients with anterior open bite than in patients with normal vertical relationships .If the tongue pressures were greater in the open bite patients than in the normal occlusion patients, it would be easy to understand how the tongue was preventing eruption.
    123. 123.   Birte Melsen et al A O April, 1987 to evaluate the relationships between swallowing pattern and mode of respiration and different malocclusion traits. Considering malocclusion, it was observed that the frequency was higher among children swallowing without tooth contact, and that this was especially pronounced when a tongue thrust was involved. The malocclusion traits most affected by the swallowing pattern were the sagittal discrepancies.
    124. 124.  The frequencies of both distal and mesial molar occlusion were higher, as were the frequencies of extreme maxillary overjet and mandibular overjet. Children with a tongue thrust also had a slightly higher frequency of openbite, although only 9.8% of the subjects exhibited lack of incisal overlap. In the transverse plane, both groups with a swallowing anomaly exhibited an higher frequency of crossbite. Comparing children with nasal respiration with mouth breathers, the latter category exhibited a higher frequency of distal occlusion, openbite, crossbite, and crowding.
    125. 125. Conclusions - Tongue-thrust swallowing is more detrimental to occlusal development than teeth-apart swallowing. Respiration pattern may influence the development of the transverse relationship, resulting in development of crossbite. The influence of deviation in swallowing and respiratory pattern depends on the interaction between genetic and environmental factors. The isolated effect of change in respiratory and swallowing pattern is still to be elucidated.
    126. 126.  A study by Dr.Ashima Valiathan & Padmapriya C V was done on tongue volume & tongue force exerted during swallowing to evaluate their effect on the dentition. cephalometric findings of the study group were compared with normal cases as well as togue volume & pressure were measured. The results showed an increase in tongue pressure of 33 cN compared to 20.5 cN in control group & also an increase in the occurance of mouth breathing & tongue & lip habits in the study group.Thus in the complex etiology of bimaxillary protrusion,environmental factors in the form of various habits & excessive tongue force play an important role.
    127. 127. Lischer’s drawing
    128. 128.  John J. Warren Samir E. Bishara, (A J O D O 2002) to determine the association between the duration of nutritive and nonnutritive sucking behaviors and various occlusal characteristics in the primary dentition. The results indicated no relationship between duration of breast-feeding during the first year of life and any dental arch or occlusal parameters. The study found that prolonged pacifier habits resulted in changes to the dental arches and the occlusal parameters that were different from the effects of digit sucking.
    129. 129.  In addition, some changes in the dental arch parameters and occlusal characteristics (eg, prevalence of posterior crossbite and increased amount of overjet) persisted well beyond the cessation of the pacifier or digit habit , the results suggest that current recommendations for discontinuing these habits may not be optimal in preventing habit-related malocclusions.
    130. 130. Lip sucking
    131. 131. Arm sucking
    132. 132.  Posture
    133. 133. Yocheved Ben-Bassat et al (AJODO 2006) Patients with idiopathic scoliosis have asymmetric features of malocclusion compared with a random population. Carsten Lippold et al (AO 2006) Significant correlations could be obtained with respect to the facial axis and the lordotic angle, the facial axis and the pelvic inclination, the inner gonial angle and the lordotic angle, the inner gonial angle and the pelvic inclination, the mandibular plane angle and the lordotic angle, the mandibular plane angle and the pelvic inclination, as well as the facial depth and the pelvic inclination
    134. 134.  Beni Solow et al (AO, 1977) demonstrated a relationship between the craniocervical angulation (the way the head is carried on the neck) and both facial proportions and dentoalveolar proportions. The farther the head is carried forward on the neck, the more likely the face is to be long vertically, and vice versa. There are corresponding differences in dentoalveolar morphology relating to head posture. For instance, the more the head is held forward, the more likely it is that upper dentoalveolar height will be increased, especially in its basal portion. Forward head posture also correlates strongly with a steep occlusal plane.
    135. 135. John R. C The postural basis of malocclusion: A philosophical overview (AJODO 2004). Our current environment and diet are dramatically different from those of our ancestors of 30,000 years ago when malocclusion was rare; no evidence suggests that there has been a significant change in our genes since then. This questions all hypotheses that are based on the longheld belief that most malocclusions are inherited. There is strong scientific, logical, and clinical evidence to suggest that the weak muscles and open mouth postures that are now endemic in our society can cause increased vertical growth, whereas parafunction of the tongue, lips, and cheeks is known to displace both the teeth and their supporting bone. Such a malocclusion would be a postural deformity.
    136. 136. Perverse oral postures have proved difficult to measure, diagnose, and treat, and, in these circumstances, we should perhaps be guided by basic research in preference to clinical evidence. The tropic premise seems the best fit of the hypotheses that have been considered, and no evidence appears to disprove it. It suggests that environmental factors disrupt resting oral posture, increasing vertical skeletal growth and creating a dental malocclusion, the occlusal characteristics of which are determined by inherited muscle patterns, primarily of the tongue.
    137. 137.    Bengt Ingerval Urs Thuer ( AO 1988). To measure maxillary cheek pressures in the molar area, at the teeth and high in the buccal sulcus, in both natural and extended head positions, with teeth at rest and in function. In the rest position, the pressure on the alveolar process was greater than that on the teeth, and at both locations it was slightly greater with the head extended than in the natural position. The pressures on the teeth did not vary noticeably with head position or among rest, chewing, or swallowing; but the pressure on the alveolar process during chewing was greater with the head extended then in the natural position.
    138. 138.  Local factors
    139. 139. GRABER'S CLASSIFICATION  LOCAL FACTORS 1. Anomalies of number: Supernumerary teeth, Missing teeth [congenital absence or loss due to accidents, caries, etc.] 2. Anomalies of tooth size 3. Anomalies of tooth shape 4. Abnormal labial frenum : mucosal barriers 5. Premature loss of deciduous teeth
    140. 140. 6. Prolonged retention of deciduous teeth 7. Delayed eruption of permanent teeth 8. Abnormal eruptive path 9. Ankylosis 10Dental caries 11Improper dental restoration
    141. 141. Missing Teeth (4) Muller,T.P et al (J.A.D.A,1970) The order of frequency of absence tooth is : Maxillary & Mandibular third molars. Maxillary lateral incisors. Mandibular second premolar. Mandibular incisor. (5) Maxillary second premolar.   (1) (2) (3)
    142. 142.      Anodontia - the total absence of teeth Oligodontia - atleast 6 teeth are missing Hypodontia - the absence of only a few teeth. Anodontia or oligodontia , is usually associated with an usual but mild systemic abnormality, ectodermal dysplasia . Occasionally, oligodontia occurs in a patient with no apparent systemic problem or congenital syndrome.
    143. 143. Supernumerary or extra teeth      Disturbances during - initiation and proliferation stages. The most common supernumerary tooth appears in the maxillary midline and is called a mesiodens. Gupta L.D etal 1970 They may form prior to birth or as late as 10 -12 years of age. When it erupts at an advanced age “a third set of teeth” In few cases Supernumerary lateral incisors; Extra premolars appear; Fourth & third molars may be present
    144. 144.  A.Hall & A.Onn (JO 2006) showed 4 cases in which delayed formation & late eruption of supernumerary teeth in the mandible occurred in patients with history of supernumerary formation in the premaxillary region. In all cases the premaxillary supernumeraries prevented eruption of the associated permanent incisors & they concluded that an opportune time for further radiographic review old young adult with history of previous supernumerary teeth may be around 16 – 18 years when assessment of the third molars is often desirable .
    145. 145. Malformed Teeth      Disturbances during - morphodifferentiation stage (some carry over) histodifferentiation stage. The most common abnormality is a variation in size, maxillary lateral incisors and second premolars. About 5 % of the total population have a significant tooth size discrepancy because of disproportionate sizes of the upper and lower teeth. Fusion Gemination.
    146. 146.   As dietary habits in humans adapt from a hunter/gatherer to a refined food culture evolutionary selection pressures are tending to reduce tooth volume, which is manifested in the 3rd molar , 2nd premolar and lateral incisor “fields” ( Butler's Field Theory ) Clinical evidence suggest that congenital absence of teeth and reduction in tooth size are related. example hypodontia and hypoplasia of the maxillary lateral incisors present simultaneously.
    147. 147.   Douglas R. Crosby et al (A J O D O 1989 ) Occurrence of tooth size discrepancies among different malocclusion groups The results showed that there was no significant difference in the incidence of tooth size discrepancies among malocclusion groups, there was a large number of tooth size discrepancies in each group. Therefore it is suggested that Bolton's tooth size analysis be performed before initiation of orthodontic treatment.
    148. 148. Abnormal Labial Frenum  At birth the frenum is attached to the alveolar ridge, with fibers actually running into the lingual interdental papilla. As the teeth erupt and as alveolar bone is deposited, the frenum attachment migrates superiorly with respect to the alveolar ridge. Fibers may persist between the maxillary central incisors and in the Vshaped intermaxillary suture ,attaching to the outer layer of the periosteum and connective tissue of the suture.
    149. 149.           As Faustin Weber has noted, the diastema may be due to other factors, the following list should be eliminated as possible causative factors: microdontia, macrognathia, supernumerary teeth (especially a mesiodens), peg laterals, missing lateral incisors, heavy occlusion against the lingual surfaces of the maxillary incisors, habits such as thumb sucking, tongue thrust, lip biting or lip sucking, and midline cysts.
    150. 150.    Existence of a heavy fibrous frenum does not always mean that spacing is present. Frequently during the course of orthodontic therapy the interposed fibers will atrophy, making a frenectomy unnecessary “Blanche test" At 10 to 12 years of age no demonstrable change at the maxillary central inderdental papilla.
    151. 151.   Where there is a heavy fibrous frenum that may be contributory, however, a "blanching" of the tissue just lingual to the maxillary central incisors can be noted. This usually means that the fibrous attachment still remains in this area. The difficulty lies in establishing whether this fibrous attachment is "causative" or "resultant" or whether it is primary or secondary to such problems as excessive overbite, local habits, tooth size discrepancy. The hereditary component is a major factor in persistent diastemas.
    152. 152.
    153. 153. Jedidiah R. Gass, Manish Valiathan, Hemant K. Tiwari, Mark G. Hans, and Robert C. Elston, (AJODO 2003) to estimate familial correlations and heritability to evaluate familial aggregation patterns of maxillary midline diastemas. The preliminary results suggest a possible genetic basis for maxillary midline diastema and a greater role of environmental factors in the black sample than in the white sample.
    154. 154. Interference with Eruption.     For a permanent tooth to erupt, the overlying bone as well as the primary tooth roots must resorb . Factors that obstruct eruption Supernumerary teeth, Sclerotic bone, and Heavy fibrous gingiva . All of these interferences are present in cleidocranial dysplasia. The multiple supernumerary teeth contribute an element of mechanical interference. Children with this condition have a defect in bone resorption, and the gingiva is quite heavy and fibrous.
    155. 155.  In patients with less severe interferences with eruption, delayed eruption of some permanent teeth contributes to malocclusion only when other teeth drift to improper positions in the arch.
    156. 156. Ectopic Eruption.      Cause - Malposition of a permanent tooth bud . Most likely seen with - Maxillary first molars If the eruption path of the maxillary first molar carries it too far mesially at an early stage, the permanent molar is unable to erupt. The mesial position of the permanent molar leads crowded arch. Ectopic eruption of other teeth is rare but can result in transposition of teeth or bizarre eruption positions. Other teeth especially , maxillary canines , usually is due the eruption path altered by a lack of space.
    157. 157.
    158. 158. Sune Ericson etal (A O 2001) The Dental Follicle in Normally and Ectopically Erupting Maxillary Canines: A Computed Tomography Study The dental follicles of the ectopically erupting canines were, on average, wider than those of the normally erupting canines.
    159. 159.  Sheldon Peck, Leena Peck, Matti Kataja, (AO 1994) Palatal displacement of the maxillary canine tooth is a positional variation thought generally to develop as a result of local factors, such as retained deciduous canines, anomalous permanent lateral incisors, or dental crowding. From analysis of available evidence, the PDC positional anomaly appears to be a product of polygenic, multifactorial inheritance.
    160. 160. Adrian Becker (AO 1995) 1.Their conclusion does not contradict the possibility that environmental factors may give rise to palatal displacement of canines generated by genetic anomaly of the adjacent teeth. 2.The buccally displaced canine finds itself similarly environmentally compromised by the different factor of crowding which leads to its characteristic buccally ectopic guidance pattern. 
    161. 161. 3.(a) Canines that are transposed with the premolar. (b) Others that have erupted ectopically, high in the buccal sulcus and in the absence of crowding , (c) Certain palatal canines whose root apex is located markedly distant from their designated site, may all be labeled as genetically controlled with a fair degree of confidence.
    162. 162. 4. In between these clearly defined entities there exists a “gray area” in which it is probable that the etiology of the individual displaced teeth may be linked to a combination of circumstances that obey premise number 1 and premise number 2, to varying degrees. The guidance theory cannot provide the complete answer to the etiology of the palatally displaced canine. Were this so, we would find PDC every time there was an anomalous or missing lateral incisor. Equally, it may not yet be discounted out of hand and certainly not on the basis of the evidence provided in the article in question.
    163. 163. Early Loss of Primary Teeth  When a unit within the dental arch is lost, the arch tends to contract and the space to close. At one time, this space closure was attributed entirely to mesial drift of posterior teeth, which in turn was confidently ascribed to forces from occlusion. Although a mesially directed force can accompany occlusion, it probably is not a major factor in closure of spaces within the dental arches.
    164. 164.   Thomas E. Southard, Rolf G. Behrents, and Elizabeth A. Tolley – A J O DO 1989 to design and develop instrumentation to measure the anterior component of occlusal force generated by a single tooth under a known axial load. An additional objective was to quantify the distribution and dissipation of this force as it progressed anteriorly. The distribution and dissipation of the anterior component of the occlusal force anteriorly approximated an exponential decay function.
    165. 165.  The contemporary view is that mesial drift is a phenomenon of the permanent molars only. The major reason these teeth move mesially when a space opens up is their mesial inclination , so that they erupt mesially as well as occlusally.
    166. 166. Leeway space  In the mandibular arch the combined width of the deciduous canine, first deciduous molar and second deciduous molar is on the average of 1.7 mm greater on each side than the permanent successors. In the maxillary arch this "leeway" space averages only 0.9 mm because of the greater size of the permanent canine and first and second premolar teeth. This space differential is necessary to allow for the occlusal adjustment and final alignment of the incisors and a settling in of the occlusion as the terminal plane relationship is corrected.
    167. 167.    Experimental data suggest that, occlusal forces rather than causing mesial drift, actually retard it.( i.e. : permanent molar is likely to drift mesially more, rapidly in the absence of occlusal contacts than if they are present) Mesial drift of the permanent first molar after a primary second molar is lost prematurely can significantly contribute to the development of crowding in the posterior part of the dental arch. This has been a significant cause of crowding and malalignment of premolars. If a primary canine or first molar is lost prematurely on only one side, the permanent teeth drift distally only on that side, leading to an asymmetry in the occlusion as well as a tendency toward crowding.
    168. 168. When a primary first molar or canine is lost prematurely, there is also a tendency for the space to close. This occurs primarily by distal drift of incisors, not by mesial drift of posterior teeth The impetus for distal drift appears to have two sources:  Force from active contraction of transseptal fibers in the gingiva, and pressures from the lips and cheeks.  The pull from transseptal fibers probably is the more consistent contributor to this space closure tendency, whereas lip pressure adds a variable component. 
    169. 169. Ibrahim Yavuz et al (A J O D O) 2006 Effects of early loss of the permanent first molars on 3rd molars Early loss of the permanent first molars might have an accelerating effect on the development of the third molar on the extraction side compared with the contra lateral teeth. Therefore, emergence of the third molars on the extraction side might be hastened, and these teeth might erupt earlier than the contra lateral teeth.
    170. 170. ABNORMAL ERUPTIVE PATH    This is usually a secondary manifestation of primary disturbance. With a hereditary pattern of severe crowding and totally inadequate space to accommodate all the teeth, deflection of the erupting tooth may be merely an adaptive response to the conditions present Because of the presence of a super­numerary tooth, retained deciduous tooth or root fragment, or possible bony barrier, a physical barrier often influences the direction of eruption, setting up an abnormal path as a result.
    171. 171. ANKYLOSIS      Accidents or trauma, certain endocrine conditions and congenital diseases like cleidocranial dysostosis predispose an indivdual to ankylosis Ankylosis or partial ankylosis is encountered relatively frequently during the 6 to 12year age period. Ankylosis is probably due to an injury Submerging of the offending tooth is seen. In actuality, the other teeth are erupting and the ankylosed tooth is not The contiguous teeth often migrate into the space, effectively locking the tooth in the process.
    172. 172. Traumatic Displacement of Teeth Dental trauma can lead to the development of malocclusion in three ways: (1) Damage to permanent tooth buds from an injury to primary teeth (2) Drift of permanent teeth after premature loss of primary teeth, and (3) Direct injury to permanent teeth. 
    173. 173.  1. 2. Trauma to a primary tooth can displace the permanent tooth bud underlying it. There are two possible results. If the trauma occurs while the crown of the permanent tooth is forming, enamel formation will be disturbed and there will be a defect in the crown of the permanent tooth. (Turner’s Tooth ). If the trauma occurs after the crown is complete, the crown may be displaced relative to the root. Root formation may stop, leaving a permanently shortened root or root formation continues, but the remaining portion of the root then forms at an angle to the traumatically displaced crown .( Dilacerated root )
    174. 174. DENTAL CARIES    Caries, which leads to the premature loss of a deciduous or permanent tooth, subsequent drifting of contiguous teeth, abnormal axial inclination, over eruption, bone loss, etc. Loss of arch length due to a series of proximal carious lesions that are unrepaired . Immediate and correct anatomic restoration should be made of all teeth as a preventive orthodontic procedure.
    175. 175. Effect of proximal caries on. arch length. Great care must be exercised in maintaining the mesio-distal dimension through proper restoration of tooth Contours and the contact relationship.
    176. 176. IMPROPER DENTAL RESTORATIONS      Overextended proximal restorations irregular mandibular incisors . Snap ligature concept (super-tight mesial and distal contacts) Too tight a contact causes elongation of either the tooth being restored or approximating teeth, creates functional prematurities and severely strains the canine-lateral contact .With more than one restoration in a segment placed with "snap-ligature" precision, the arch length is increased that leads to break in the continuity of the arch. Gutta-percha filling left in occlusion or the slightest bit high has plunger-like action of the rubberoid mass. Mechanical separation also encourages increase of arch length as the dentist strives for a tight contact
    177. 177. An increase in arch length through improper restoration of one or more carious proximal surfaces may result in the creation of broken contacts, rotations, cross-bite conditions and functional prematurities.
    178. 178. Conclusion  Malocclusion can occur due to number of possible causes. It can be caused by either genetic factors or by environmental factors. Comprehensive Orthodontic management involves identification of the possible etiologic factors & an attempt to eliminate the same. Although it may not be possible to eliminate the cause in most cases of malocclusion it nevertheless is of value in preventive & interceptive orthodontic procedure where a possible malocclusion is prevented or intercepted by timely removal of the cause .
    179. 179. References 1. Weinstein.S et al :On an equilibrium theory of tooth position. A O 1963;33: 1 -26. 2. Proffit . W .R Equilibrium Theory Revisited : Factors Influencing Tooth Position A O 1978;48:175 – 86. 3. Wallen, T. R.: Vertically directed forces and malocclusion: A new approach. J. Dent. Res., 1974.53:1015-1022. 4. Robert S. Corruccini,, and Rosario H. Yap Potter Genetic analysis of occlusal variation in twins : AJODO, 1980;44(140 - 154):
    180. 180. 5. Ashima Valiathan. Malocclusion and Genetics. JIOS 1976, vol 8, no 1; 29-33. 6. Gass J, Valiathan M, Tiwari H, Hans M, Elston R.Familial correlations and heritability of maxillary midline diastema AJODO 2003 123 (1):35-39. 7. Chung C, Niswander J. Genetic and epidemiologic studies of oral characteristics in Hawaiian schoolchildren V. J Dent Res 1975;54:324-29 8. Peck S, Peck L, Kataja M. The palatally displaced canine as a dental anomaly of genetic origin. Angle Orthod 1994;64:249-56.
    181. 181. 9. Valiathan A. and Sameer H Shaikh. (J Ind Ortho Soc 1998;31:53-57) 10. Moyers, R. E.: Handbook of Orthodontics. 3rd ed. Chicago, Year Book Medical Publishers,Inc., 1972. 11. Reijo Ranta A review of tooth formation in children with cleft lip/palate, (AJODO, 1986;90: 11-18,.) 12. Ben-Bassat Y,Yitschky M ,Kaplan L,Brin I Occlusal patterns in patients with idiopathic scoliosis.. AJODO. 2006 ;130(5):629-33.
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    191. 191. Thank you Leader in continuing dental education