Etiology of malocclusion 1/certified fixed orthodontic courses by Indian dental academy


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Etiology of malocclusion 1/certified fixed orthodontic courses by Indian dental academy

  1. 1. ETIOLOGY OFETIOLOGY OF MALOCCLUSIONMALOCCLUSION INDIAN DENTAL ACADEMYINDIAN DENTAL ACADEMY Leader in continuing dental educationLeader in continuing dental education
  2. 2. Etiology-Etiology- Etia – causeEtia – cause Logy – ScienceLogy – Science Scientific study of the causeScientific study of the cause Malocclusion-Malocclusion- Malocclusion can be defined as a significant deviation from what is defined as normal or ideal’s occlusion. IntroductionIntroduction
  3. 3. IntroductionIntroduction  The term “ NORMAL OCCLUSION “ is arbitrary but is generally accepted to be class I molar relationship with good alignment of all teeth.
  4. 4. IntroductionIntroduction  Many components are involved in normal occlusion. Most important are 1. The size of maxilla 2. The size of the mandible (both ramus and body) 3. The factors which determine the relationship between the two skeletal bases such as cranial base and environmental factors 4. Arch form 5. Size and morphology of the teeth 6. No. of teeth present 7. Soft tissue morphology and behavior, lips, tongue and peri-oral musculature
  5. 5.  The understanding of a disease is incompleteThe understanding of a disease is incomplete without total knowledge of its causation.without total knowledge of its causation.  Without knowledge of etiology neither prophylaxis norWithout knowledge of etiology neither prophylaxis nor specific treatment is possiblespecific treatment is possible IntroductionIntroduction
  6. 6.  Malocclusion is a major developmental problem.Malocclusion is a major developmental problem.  Kelly and Harvey report that only 9% of American youthsKelly and Harvey report that only 9% of American youths aged 12 to 17 years have virtually classic normalaged 12 to 17 years have virtually classic normal occlusion and that orthodontic treatment wouldocclusion and that orthodontic treatment would measurably improve the occlusion of 55% of themeasurably improve the occlusion of 55% of the adolescent population.adolescent population.  The high prevalence is a major heath care concern, andThe high prevalence is a major heath care concern, and it is only natural to be interested in the causes ofit is only natural to be interested in the causes of malocclusion.malocclusion. IntroductionIntroduction
  7. 7. Epidemiology of malocclusionEpidemiology of malocclusion Proffit WR; 3rd ed.
  8. 8.  Prevalence of malocclusion is higher in developed countriesPrevalence of malocclusion is higher in developed countries as compare to developing compare to developing countries.  Indians have more tendency for class II malocclusion.Indians have more tendency for class II malocclusion.  Netherlands, and Kenyans have more tendency for class IIINetherlands, and Kenyans have more tendency for class III malocclusion.malocclusion. Epidemiology of malocclusionEpidemiology of malocclusion
  9. 9.
  10. 10.  The prevalence of malocclusion among Indian childrenThe prevalence of malocclusion among Indian children has been reported to be as low ashas been reported to be as low as 19.6% in Punjab19.6% in Punjab byby Miglani D.S. et al inMiglani D.S. et al in 19651965 and as high asand as high as 90% in Delhi90% in Delhi byby Sidhu S.S. inSidhu S.S. in 1968.1968. Epidemiology of malocclusion inEpidemiology of malocclusion in IndiaIndia
  12. 12.
  13. 13. The Orthodontic Equation:  The orthodontic equation elaborated.(from Dockrell R: classifying etiology of malocclusion. Dent Rec 1952; 72:25.)
  14. 14. Skeletal Crossbite  Occlusal relationship seems correct on the patients left side, crossbite on the right side.  Mandibular prognathism  Patients face shows that the cross bite is primarily the result of an osseous dysplasia.
  15. 15. Muscular Or Functional Crossbite  Midline do not coincide, half the mandibular denture is outside the maxillary denture.  Removal of the occlusal interferences in the primary teeth enabled muscles to return the mandible to its proper position and to a proper occlusion.
  16. 16. Dental Type CrossbiteDental Type Crossbite  Mandibular and maxillary bases are harmonious with each other, midline coincide, crossbite is localized in the right central incisor region.  Due to tipping of individual teeth
  17. 17. CLASSIFICATION OF ETIOLOGY OF MALOCCLUSION  Classification will help the clinician in identifying situation which they can either prevent or intervene, thus avoiding the severity of malocclusion.  The various classification proposed are: 1. White and Gardiner’s classification. 2. Salzmann’s classification. 3. Moyer’s classification. 4. Graber’s classification.
  18. 18. White & Gardiner’s Classification: This was one of the first attempts to classify malocclusion. A. Dental Base Abnormalities: 1. Anterio-posterior mal-relationship. 2. Vertical mal-relationship 3. Lateral mal-relationship 4. Disproportion of size between teeth and base bone. 5. Congenital abnormalities.
  19. 19. White & Gardiner’s Classification: B. PRE-ERUPTION ABNORMALITIES: 1. Abnormalities in position of developing tooth germs. 2. Missing teeth. 3. Supernumerary teeth with teeth abnormal in form. 4. Prolonged retention of deciduous teeth. 5. Large labial frenum. 6. Traumatic injury.
  20. 20. White & Gardiner’s Classification: C. POST-ERUPTIVE ABNORMALITIES: 1. Muscular: i. Rest position of musculature. ii. Active muscle force. iii. Sucking habits. iv. Abnormalities in path of closure. 2. Premature loss of deciduous teeth. 3. Extraction of permanent teeth
  21. 21. A. PRENATAL: 1. Genetic: malocclusion transmitted by genes, may or may not be evidence at birth. 2. Differentiative: malocclusion that are inborn, engrafted on the body in the prefunctional embryonic developmental stage, can be subdivided into— i. General or constitutional: effect the body as a whole. ii. Local: effect the face, jaws and teeth only. 3. Congenital: can be hereditary or acquired but existing at birth. Salzmann’s Classification:
  22. 22. B. POSTNATAL: 1. DEVELOPMENTAL: i. GENERAL DEVELOPMENTAL: a. Abnormalities of relative rate of growth in dentofacial region b. Hypo or hypertonicity of muscles which influence dentofacial development and function. c. Childhood diseases, nutritional, endocrine, and other metabolic disturbances that affect dentofacial growth d. Radiation and radiotherapy of mother or fetus which can produce orofacial clefts and cephalic and dental abnormalities in the offspring Salzmann’s Classification:
  23. 23. B. POSTNATAL: ii. LOCAL DENTOFACIAL: a. Birth injuries of the head, face, jaws b. Micrognathia or macrognathia c. Microglossia or macroglossia d. Abnormal frenum labii e. Facial hemiatrophy f. Anomalies of tooth development and eruption Salzmann’s Classification:
  24. 24. 2. FUNCTIONAL: i. GENERAL: a. Muscular hyper or hypotonicity b. Neurotrophic disturbances c. Postural defects of the tongue and jaws d. Masticatory and respiratory disturbances ii. LOCAL: a. Premature loss or prolonged retention of deciduous teeth b. Loss of proximal contact following tooth loss c. Temporomandibular articulation disturbances d. Muscular hypo or hyperactivity Salzmann’s Classification:
  25. 25. 3. ENVIRONMENTAL OR ACQUIRED: i. GENERAL a. Diseases can affect the dentofacial tissues directly or indirectly b. Radiation ii. LOCAL: a. Eruption anomalies b. Premature loss or prolonged retention of deciduous teeth c. Loss of permanent teeth d. Harmful dentofacial pressure habits e. Trauma f. Infection g. Temporomandibular disturbances h. Periodontal disease Salzmann’s Classification:
  26. 26. Prenatal Postnatal Genetic Differentiative congenital Developmental Functional Environmental Salzmann’sSalzmann’s diagrammatic representation of the interdependence of thediagrammatic representation of the interdependence of the etiologic factors in malocclusionetiologic factors in
  27. 27. MOYER’S CLASSIFICATION: Moyer’s lists seven causes and clinical entities. 1. Heredity 2. Development defect of unknown origin 3. Trauma a) Prenatal trauma and birth injuries b) Post natal trauma 4. Physical agents 5. Habits
  28. 28. 6. Diseases a) Systemic disease b) Endocrine disorder c) Local disease i. Nasopharyngeal diseases and disturbed respiratory function ii. Gingival and periodontal diseases iii. Tumors iv. Caries 7. Malnutrition MOYER’S CLASSIFICATION:
  29. 29. GRABER’S CLASSIFICATION: Divide the etiologic factors into two groups: General factor Local factor
  30. 30. 1. Heredity (the inherited pattern) 2. Congenital defect: cleft palate, torticollis, cleidocranial dysostosis, cerebral palsy, syphillis,etc. 3. Environment : -prenatal ( trauma, maternal diet, maternal metabolism, German measles) -postnatal ( birth injury, cerebral palsy, TMJ injury) 4. Predisposing metabolic climate and disease Endocrine imbalance Metabolic disturbance Infectious diseases GRABER’S CLASSIFICATION:GRABER’S CLASSIFICATION: GENERAL FACTORS
  31. 31. 5. Dietary problem ( nutritional deficiency ) 6. Posture 7. Trauma and accident 8. Habits  Abnormal suckling  Thumb and finger sucking  Tongue thrusting  Lip and nail biting  Abnormal swallowing habits (improper deglutition)  Mouth breathing  Speech defects  Bruxism GRABER’S CLASSIFICATION:GRABER’S CLASSIFICATION: GENERAL FACTORS
  32. 32. 1. Anomalies of number -supernumerary teeth -missing teeth 2. Anomalies of tooth size 3. Anomalies of tooth shape 4. Abnormal labial frenum; mucosal barriers 5. Premature loss of deciduous teeth 6. Prolonged retention of deciduous teeth GRABER’S CLASSIFICATION:GRABER’S CLASSIFICATION: LOCAL FACTORS 7. Delayed eruption of permanent teeth. 8. Abnormal eruptive path. 9. Ankylosis. 10. Dental caries. 11. Improper dental restoration
  33. 33. General Factors HEREDITY:  Transmission of character from one generation to theTransmission of character from one generation to the otherother - Joseph Adam – 1847- Joseph Adam – 1847  There is a definite genetic determinant that influences the ultimate accomplishment of dentofacial morphology.  These genetic determinants may be modified by prenatal and postnatal environment, by physical entities, by pressures, abnormal habits, nutritional disturbances and idiopathic phenomena.
  34. 34. Mode of inheritance-Mode of inheritance- Mendelian inheritance-Mendelian inheritance-  Autosomal recessiveAutosomal recessive  Autosomal dominantAutosomal dominant  X linked and Y linked conditions.X linked and Y linked conditions. General Factors HEREDITY:
  35. 35. Autosomal recessive inheritance-Autosomal recessive inheritance-  Traits that are manifest only when mutations are present in bothTraits that are manifest only when mutations are present in both copies of gene are recessive traits.copies of gene are recessive traits.  If a gene causing a recessive trait is on one of the autosomes, theIf a gene causing a recessive trait is on one of the autosomes, the trait is autosomal recessive.trait is autosomal recessive.  Autosomal recessive trait tend to occur more frequently in isolatedAutosomal recessive trait tend to occur more frequently in isolated populations or in cases of consanguinity.populations or in cases of consanguinity.  The parents of affected individuals are usually unaffected.The parents of affected individuals are usually unaffected.  Recurrences between siblings are common.Recurrences between siblings are common. General Factors HEREDITY:
  36. 36.  Seen in both males and females in equal numbers.Seen in both males and females in equal numbers.  The chance of having an affected child is 25% for eachThe chance of having an affected child is 25% for each pregnancy resulting from mating between two heterozygouspregnancy resulting from mating between two heterozygous carriers of an autosomal recessive condition.carriers of an autosomal recessive condition.  The other possibilities are 50%that a child will be a carrier of aThe other possibilities are 50%that a child will be a carrier of a single copy of the mutation and 25% that the child will besingle copy of the mutation and 25% that the child will be noncarrier.noncarrier.  This is because each parent has an approximately equalThis is because each parent has an approximately equal probability of passing on either the normal or abnormal allele.probability of passing on either the normal or abnormal allele. General Factors HEREDITY:
  37. 37. Autosomal dominant inheritance-Autosomal dominant inheritance-  In autosomal dominant disorders, heterozygous individuals have aIn autosomal dominant disorders, heterozygous individuals have a recognizable phenotype.recognizable phenotype.  Homozygous individuals also show the phenotype, but may be moreHomozygous individuals also show the phenotype, but may be more severely affected.severely affected.  Pedigrees will frequently show that parent is affected.Pedigrees will frequently show that parent is affected.  Trait is transmitted by an affected person to half his children on anTrait is transmitted by an affected person to half his children on an averageaverage  The number of affected males and females is approximately equalThe number of affected males and females is approximately equal  Two affected individuals may have affected and unaffected childrenTwo affected individuals may have affected and unaffected children since each parent would have one normal and one abnormal genesince each parent would have one normal and one abnormal gene General Factors HEREDITY:
  38. 38. X-linked inheritance-X-linked inheritance-  Refers to conditions caused by genes on the X chromosome.Refers to conditions caused by genes on the X chromosome.  Many X-linked recessive conditions and a few X-linkedMany X-linked recessive conditions and a few X-linked dominant conditions.dominant conditions.  If a mutation occurs in an X-linked recessive gene, a female isIf a mutation occurs in an X-linked recessive gene, a female is likely to have mild or no effects, because female inherit twolikely to have mild or no effects, because female inherit two copies of X chromosome.copies of X chromosome.  A male who inherits the gene is likely to be more severelyA male who inherits the gene is likely to be more severely affected because he has only one copy of a geneaffected because he has only one copy of a gene General Factors HEREDITY:
  39. 39.  Affected males pass the gene to 100% of theirAffected males pass the gene to 100% of their daughters.daughters.  There is no father-to-son transmission because fathersThere is no father-to-son transmission because fathers do not give an X chromosome to their not give an X chromosome to their sons. General Factors HEREDITY:
  40. 40. X linked dominant inheritance-X linked dominant inheritance-  It is rare with a few disorders.It is rare with a few disorders.  Characterized by having all the daughters of affectedCharacterized by having all the daughters of affected males inherit the disorder.males inherit the disorder.  Sons of affected males never inherit the disorder,Sons of affected males never inherit the disorder, because they receive the Y chromosome from the father.because they receive the Y chromosome from the father.  Affected females can transmit the disorder to offspring ofAffected females can transmit the disorder to offspring of both sexes.both sexes. General Factors HEREDITY:
  41. 41. Multifactorial inheritance-Multifactorial inheritance-  Some human disorders result from an interaction ofSome human disorders result from an interaction of multiple genes with environmental influences.multiple genes with environmental influences.  Cleft lip and palate demonstrate a multifactorialCleft lip and palate demonstrate a multifactorial inheritance.inheritance. General Factors HEREDITY:
  42. 42. General Factors HEREDITY:  A strong influence of inheritance on facial features such as tilt of nose , shape of the jaw and look of the smile are familial tendencies.  Certain types of malocclusion run in families. The HAPSBURG JAW , the prognathic mandible of German royal family is the best known example
  43. 43. General Factors HAPSBURG JAWHAPSBURG JAW
  44. 44. Facial type of the offspring probably is heavily influenced by heredity. There are three general types of head shapes- •Brachycephalic or broad round heads •Dolichocephalic or long narrow heads •Mesocephalic or a shape in between the brachycephalic and the dolichocephalic Hereditary Influence on Facial Type: General Factors
  45. 45. General Factors
  46. 46. Hereditary influence on the growth and developmental pattern:  As ultimate morphogenetic pattern has a strong hereditary component, the accomplishment of that pattern is also at least partially under the influence of heredity.  For example, a child patient is very slow in losing his deciduous teeth and the eruption of permanent teeth is equally slow. General Factors
  47. 47. Heredity and specific dentofacial morphologic characteristics:  Heredity has role in the accomplishment of specific dentofacial attributes.  Lundstrom concluded that heredity could be considered significant in determining the following characteristics: 1.Tooth size. 2.Height of the palate. 3.Width and length of the arch. 4.Crowding and spacing of teeth. 5.Degree of sagittal overbite (overjet) General Factors
  48. 48.  Hereditary influence on Race:  Facial and Dental characteristics of different races is influenced by heredity.  In homogenous 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. General Factors
  49. 49.  Hereditary influence on Race:  Where there has been a mixture of racial strains the incidence of jaw size discrepancies and occlusal disharmonies is significantly greater.  Professor Stockard produced gross deformities with his crossbreeding of dogs. General Factors
  50. 50. Breeding experiment with animal by Professor Stockard  Crossbred dogs (Boston terrier and collie) and recorded the interesting effects on body structure.  Offspring might have the Collie’s long, pointed lower jaw and the terrier’s diminutive upper jaw.
  51. 51. Breeding experiment with animal by Professor Stockard  Demonstrated that severe malocclusions could be developed by crossing morphologically different breeds, more from jaw discrepancies than from tooth size – jaw size imbalances.  Confirm that independent inheritance of facial characteristics could be the major cause of malocclusion and the rapid increase in malocclusion was probably the result of increased outbreeding.
  52. 52.  These dog experiments turned out to be misleading, because many breeds of small dogs carry the gene for achondroplasia. Most of the malocclusions produced in Stockard’s breeding experiments can be explained not on the basis of inherited jaw size but by the extent to which achondroplasia was expressed in that animal. So these experiments have been severely criticized on the basis that the gene for achondroplasia is likely to have contributed. General Factors
  53. 53. Achondroplasia Deficient growth of cartilage in the cranial base Autosomal dominant trait Rare in humans In humans; short limbs, deficient maxillary translation, relative midface deficiency General Factors
  54. 54.  Results of out breeding in human populations casts doubt on the hypothesis that independently inherited tooth and jaw characteristics are a major cause of malocclusion.  The best data are from investigations carried out in Hawaii by Chung et al.  Hawaii had a homogenous Polynesian population – large scale migration to the islands by European, Chinese, Japanese and many other racial and ethnic group resulted in heterogeneous modern population. General Factors
  55. 55.  Tooth size, jaw size and jaw proportions were all rather different for the Polynesian, Oriental, European contributors.  If tooth and jaw characteristics were inherited independently, a high prevalence of severe malocclusion would be expected in this population.  The prevalence and the types of malocclusion in the current Hawaiian population, thought greater than the prevalence of malocclusion in the original population, do not support this concept.  The effect of interracial crosses appear to be additive than the multiplicative. General Factors
  56. 56. Twin Study  The classic way to determine to what extent a characteristic is determined by inheritance is to compare monozygotic twins (identical) with dizygotic twins (fraternal).  Studies of this type are limited because it is difficult to established zygosity and confirm that environments were in fact the same for both members of a twin pair.  Lauweryns et al ; concluded that 40% of dental and facial variation that lead to malocclusion can be attributed to hereditary factor.
  57. 57. Classical Method Is To Study FamilyClassical Method Is To Study Family Members:Members:  The other classic method of estimating the influence of heredity is to study family members by observing similarity and differences between father-child, mother-child, and sibling pairs.  For most measurements of facial skeletal dimensions (i.e. length of the mandible), correlation coefficients for parent- child pairs are about 0.5 .  For dental characteristics, the parent – child correlations are lower, ranging from a maximum of nearly 0.5 for overjet to a minimum of 0.15 for overbite.
  58. 58. Classical Method Is To Study FamilyClassical Method Is To Study Family Members:Members:  When parent-child correlation are used to assist in predicting facial growth, errors are reduced  It indicates hereditary influence on these dimensions. - Suzuki A, Takahama Y, 1991(AJODO,99:1991)
  59. 59. Heritability of craniofacial characteristics between parents and offspring Nakasima et al.found high correlation co-efficient values between parents and their offspring in the class II and class III malocclusion groups suggesting a strong familial tendency in the development of these malocclusions.  The genetic effects of determining the craniofacial form of offspring by the father were equivalent to those by the mother, but daughters were more affected by parents than were sons because of this finding they suggested a major influence of X-linked genes from 0.5 to 0.9. (By BerglindJohanndottir et al.) AJODO Vol. 127, Feb 2005) General Factors
  60. 60. Heritability of craniofacial characteristics between parents and offspring cont…  Fernex et. al.(1967) found boys to show more similarities to their parents than girls. Facial skeletal structures were more frequently transmitted from mother to sons than from mother to daughters.  Hunter et. al. (1970) found genetic correlation to be strongest between father and children, especially in mandibular dimensions. There was a significant relation in facial height between mother and their offspring's. (BJO Vol.26 NO.3, Sep. 1999) General Factors
  61. 61.  For skeletal characteristics, the heritability estimates increased with increasing age, for dental characteristics, the heritability estimates decreased, indicating an increase in environmental contribution to the dental variation. ( Harris EF, Johnson MG, AJO vol.99,1991) General Factors
  62. 62.  The influence of inherited tendencies is particularly strong for mandibular prognathism  The one third of the group of children who presented with severe class III malocclusion had a parent with the same problem (Litton SF, Ackerman LV, Isaacson RJ,AJO Vol. 58, 1970)  The long face pattern seems to be the second most likely type of deformity to run in families. General Factors
  63. 63.  It is logical to assume that heredity plays a part in the following conditions. 1. Congenital deformities. 2. Facial asymmetries. 3. Macrognathia and micrognathia. 4. Macrodontia and microdontia. 5. Oligodontia and anodontia. 6. Tooth shape variations (peg-shaped lateral incisors, carabelli’s cusps, mamelons etc). General Factors
  64. 64. 7. Cleft palate and harelip. 8. Frenum diastemas. 9. Deep overbite. 10.Growing and rotation of teeth. 11.Mandibular retrusion 12.Mandibular prognathism. General Factors
  65. 65. Congenital Defects Cleft lip & Palate- Cleft lip and palate can be defined as a “a furrow in the lip and palatal vault”. It may be defined as a “breach in continuity of lip and palate General Factors
  66. 66. Etiology- Heredity  According to Bhatia the possible modes of transmission are either by a single mutant gene producing a large effect, or by a number of gene (polygenic inheritance) each producing a small effect together, create this condition.  According to Fogh-Andersen slightly less than 40 % of the cleft lip cases with or without cleft palate are genetic in origin where as slightly less than 20% of the isolated cleft palate cases appear to be genetically derived. Cleft lip & Palate Cont..  Clefts usually have a strong genetic relationship.  About 1/3 or 1/2 of all cleft palate children have a familiar history of this deformity.
  67. 67. Environment: Teratogens, radiation, dietary deficiency  Teratogens are:  Aspirin – cleft lip and palate  Cigarette smoke (hypoxia) – cleft lip and palate  Dilantin – cleft lip and palate  Valium- cleft lip and palat  Rubella virus Etiology Cleft lip & Palate Cont..
  68. 68. Environment Radiations such as X-rays, gamma rays are capable of producing clefts in fetus during pregnancy. Dietary deficiency- such as folic acid deficiency can produce clefts Etiology Cleft lip & Palate Cont..
  69. 69. Etiology MULTIFACTORIAL ETIOLOGY:  Recent studies have shown that the etiology of cleft lip and palate cannot be attributed solely to either genetic or environmental factors. It seems to involve more than one factor.  Multi-factorial inheritance theory implies that many contributory risk genes interact with one another and the environment, resulting in a defect in the developing fetus  Unless a person is genetically susceptible, the environment factors may not by themselves cause clefts Cleft lip & Palate Cont..
  70. 70. Incidence:  Cleft lip & palate are common congenital malformations.  The reported incidence of clefts of the lip and palate from 1 in 500 to 1 in 2500 live births depending on geographic origin, racial and ethnic backgrounds and socioeconomic status.  Asian populations have the highest frequencies, often at 1 in 500 or higher, with Caucasian populations intermediate, and African-derived populations the lowest at 1 in2500  In the USA, one child in every 700 live births is afflicted. Cleft lip & Palate Cont..
  71. 71. Incidence:  Unilateral cleft accounts for nearly 80% of all cleft seen.  While bilateral clefts account for remaining 20%.  Among the unilateral clefts, clefts involving the left side are more common.  Male patients show a higher incidence of cleft lip with and without palate.  Female patients suffer from isolated cleft palate more. Cleft lip & Palate Cont..
  72. 72. Cleft lip & Palate Cont..
  73. 73. Categories of Clefts: 4 general categories 1. Involving the lip and alveolus. 2. Involving the lip and palate. 3. Palate alone is affected . 4. Submucous cleft palate. Cleft lip & Palate Cont..
  74. 74. Clefts of the lip and alveolus:  May be complete, extending from the vermilion border to the floor of the nose or it may be incomplete.  May be unilateral or bilateral.  Drillien, estimated that the incidence of bilateral clefts of the lip is 3.6%, while that of unilateral clefts of the lip is 96.4%.  According to Fogh-Anderson, the incidence of complete bilateral cleft of the lip is only 1% of all individuals with cleft lip with or without a cleft palate.. (AJODO,1985,JULY) Cleft lip & Palate Cont..
  75. 75. Clefts of the lip and alveolus:  The effect of the cleft of the lip and alveolus on the growth of the premaxilla varies.  With cleft lip only and no alveolar clefts, the continuity of the palatal bone helps maintain the maxillary arch form and relationship.  When the cleft of the lip extends to involve the primary palate, the premaxilla protrudes to different degrees because of absence of the restraining influence of the lip and the lack of continuity of the bony palate. (AJODO,1985,JULY) Cleft lip & Palate Cont..
  76. 76. Clefts of the lip and alveolus:  Nasal alar cartilage on the side of the cleft is displaced and flattened.  The tip of the nose is deviated towards the non cleft side. Cleft lip & Palate Cont..
  77. 77. Unilateral Cleft of the lip and alveolus Bilateral Cleft of the lip and alveolus Cleft lip & Palate Cont..
  78. 78. Cleft lip and cleft palate:  May be complete or incomplete.  May be unilateral or bilateral.  In a complete unilateral cleft of the lip and palate, a direct communication exists between the oral and nasal cavities on the side of the palate where the cleft is situated. Cleft lip & Palate Cont..
  79. 79. Cleft lip and cleft palate  In a complete bilateral cleft lip and palate both nasal chambers are in direct communication with the oral cavity.  Premaxilla projects considerably forward from the facial aspect of the maxilla.  Anteriorly progressive constriction of the upper dental arch (Omar Gabriel da Silva Filho and et al,1998 Aug, AJODO)  Significantly longer maxillary dental arch, which is attributed to the premaxillary anterior projection. (Omar Gabriel da Silva Filho and et al,1998 Aug, AJODO) Cleft lip & Palate Cont..
  80. 80. BCLP patients tend to have-BCLP patients tend to have-  Smaller mandiblesSmaller mandibles  Mandible showed a vertical growth pattern, with anMandible showed a vertical growth pattern, with an increased mandibular plane inclinationincreased mandibular plane inclination  Increase in lower anterior facial height.Increase in lower anterior facial height.  These are mandibular morphologic characteristics thatThese are mandibular morphologic characteristics that are also found in unilateral CLP and isolated CP.are also found in unilateral CLP and isolated CP. (AJODO,1998,AUG) Cleft lip & Palate Cont..
  81. 81. Complete unilateral cleft lip and palate Incomplete unilateral cleft lip and palate Cleft lip & Palate Cont..
  82. 82. Complete bilateral cleft lip and palate Incomplete bilateral cleft lip and palate Cleft lip & Palate Cont..
  83. 83. Isolated Cleft palate:  Neither the lip nor the alveolar process is involved.  The cleft may involve only the soft palate or both the soft and hard palates but never the hard palate alone.  In some, cleft is limited to the uvula or to the uvula and soft palate.  In others it may extend into the hard palate.  In the extreme form, the cleft palate may extend anteriorly as far as the nasopalatine foramen. Cleft lip & Palate Cont..
  84. 84. Isolated Cleft palate:  When the cleft involves a considerable portion of the hard palate, the nasal chambers are in direct communication with the oral cavity.  The outline of the cleft may be wide or narrow, pyriform or V- shaped.  With wide cleft that extend to a considerable degree into the hard palate– excessively wide dental arches result.  In such instances the mandibular dental arch may be in complete lingual relation to the maxillary arch. Cleft lip & Palate Cont..
  85. 85. Cleft of the uvulae Cleft of the soft palate and uvulae Isolated cleft of the hard and soft palate Cleft lip & Palate Cont..
  86. 86. Submucous Cleft palate: The classic triad of diagnostic signs is the 1. Bifid uvula 2. Partial muscle separation in the midline with an intact mucosal surface. 3. Midline notch in the posterior edge of bony palate. Cleft lip & Palate Cont..
  87. 87. Submucous Cleft palate Cleft lip & Palate Cont..
  88. 88. The problems associated with cleft lip and/ palate patients: DENTAL:  Multiple missing teeth (most commonly the maxillary lateral incisor).  Mobile premaxilla.  Anterior &/ posterior cross-bites.  Ectopically erupting teeth. Cleft lip & Palate Cont..
  89. 89. The problems associated with cleft lip and/ palate patients: DENTAL:  Impacted teeth.  Supernumerary teeth.  Poor alignment of the teeth often predisposes to poor oral hygiene.  Multiple decayed tooth. Cleft lip & Palate Cont..
  90. 90. Cleft palate with congenital absence of lateral incisor in cleft area and three missing second premolars. Cleft lip & Palate Cont..
  91. 91. The problems associated with cleft lip and/ palate patients: ESTHETIC:  The patients with un-repaired clefts are badly disfigured.  Even following the closure of the cleft, the maxilla remains under-developed with compromised esthetics.  Deformity of the normal nasal architecture is commonly seen in individuals with cleft lips. Cleft lip & Palate Cont..
  92. 92. The problems associated with cleft lip and/ palate- PYSCHOLOGICAL:  The disfigurement caused by the condition is enough to cause psychological stress for the patient and the family. Cleft lip & Palate Cont..
  93. 93. The problems associated with cleft lip and/ palate patients: SPEECH & HEARING:  Cleft lip and palate are sometimes associated with disorders of the middle ear which may affect hearing.  Since speech is learnt by the art of imitation, if hearing is compromised so it the speech.  Also if the maxilla is underdeveloped the space for the tongue gets decreased and the speech is likely to get affected. Cleft lip & Palate Cont..
  94. 94. Other Congenital Defects Although cleft lip and palate is the most common congenital defects to be of concern to the dentist as far as creation of malocclusion is concerned, but some problems such as- Cerebral palsy Torticollis Cleidocranial dysostosis Congenital syphilis Congenital Defects Cont..
  95. 95. Cerebral Palsy:  Cerebral palsy is a paralysis or lack of muscular co- ordination attributed to an intracranial lesion.  It is most commonly considered to be the result of a birth injury.  CP is also caused by a broad group of development, genetics, metabolic, infectious, ischemic and other acquired etiology.  CP is often associated with epilepsy, abnormality with speech, vision. Congenital Defects Cont..
  96. 96. Cerebral Palsy:  Effects of this neuromuscular disorder may be seen in the integrity of the occlusion.  The uncontrolled or aberrant activities upset the muscle balance that is necessary for the establishment and maintenance of the normal occlusion. Congenital Defects Cont..
  97. 97. Torticollis: Twisting of the head caused by excessive tonic contraction of the neck muscles on one side (primary sternocleidomastoid). The fore-shortening of the sternocleidomastoid muscle can cause profound changes in the bony morphology of the cranium and face. Congenital Defects Cont..
  98. 98.  Bizarre facial asymmetries with uncorrectable dental malocclusion because of growth restriction on the affected side, may be created if this problem is not treated fairly early. Preoperative TorticollisPreoperative Torticollis Postoperative TorticollisPostoperative Torticollis Congenital Defects Cont..
  99. 99. Torticollis: Other physical pictures of Torticollis 1. Plagiocephaly (generally visible as a mild flattening of the occiput on one side and the forehead on the opposite side). 2. Misalignment of the eyes. 3. Asymmetry of the ears. 4. Depression on the side of the neck under the ear. 5. Flattening of the mandible. 6. Upward tilting of the lower jaw and gum line. 7. Limited movement of the neck. Congenital Defects Cont..
  100. 100.  Cleidocranial Dysplasia:  Congenital disease of unknown etiology which is often but not always hereditary.  Transmitted as an autosomal dominant trait.  It is characterized by abnormalities of the skull, teeth, jaws and shoulder girdle as well as by occasional stunting of the long bones. Congenital Defects Cont..
  101. 101.  Cleidocranial Dysplasia:  Delayed ossification of the skull, excessively large fontanelles and delayed closing of the sutures.  The fontanelles may remain open until adulthood but the sutures often close with interposition of wormian bones.  Bossing of the frontal, parietal and occipital regions give the skull a large globular shape with small face.  Characteristic skull abnormalities – “ Arnold Head” . Congenital Defects Cont..
  102. 102.  Cleidocranial Dysplasia:  Sagittal suture is characteristically sunken, giving the skull a flat appearance.  Paranasal sinuses are underdeveloped and narrow.  The head is brachycephalic.  Complete to partial absence or even a simple thinning of one or both clavicles is seen. Congenital Defects Cont..
  103. 103.  Cleidocranial dysplasia: • High, narrow, arched palate, and actual cleft palate appears to be common. •The maxilla is underdeveloped in relation to the mandible. •Prolonged retention of the deciduous teeth and subsequent delay in eruption of the permanent teeth. •The roots of the teeth are often somewhat short and thinner than usual and may be deformed Congenital Defects Cont..
  104. 104.  Cleidocranial dysplasia:  There is absence or paucity of cellular cementum on the roots of the permanent teeth and this may be related to the failure of eruption so frequently seen.  Unerupted supernumerary teeth are common. These are most prevalent in the mandibular premolar and incisor areas.  Partial anodontia has also been recorded but is rare. Congenital Defects Cont..
  105. 105. Cleidocranial dysplasia
  106. 106. Prolonged retention of deciduous teeth. Supernumerary Teeth Cleidocranial dysplasia
  107. 107. Highly vaulted and narrow palate Cleidocranial dysplasia
  108. 108.  Congenital (Prenatal) Syphilis:  It is transmitted to the offspring only by an infected mother and is not inherited.  Persons with congenital syphilis manifest a great variety of lesions, including • frontal bossae • Short maxilla • High palatal arch • Saddle nose • Mulberry molars • Relative protuberance of mandible Congenital Defects Cont..
  109. 109. • Rhagades • Pathognomonic of the disease is the occurrence of Hutchinson’s triad -Hypoplasia of the incisor and molar teeth. -Eighth nerve deafness -Interstitial keratitis Congenital (Prenatal) Syphilis: Congenital Defects Cont..
  110. 110. Environment Prenatal Postnatal (Intrauterine molding, maternal diet, maternal metabolism, Trauma, German measles etc.) (Birth injury, TMJ injury etc). General FactorGeneral Factor
  111. 111. Prenatal Influence:  The role of prenatal influences on malocclusion is probably very small.  Intrauterine molding pressure against the developing face prenatally can lead to distortion of rapidly growing areas.  Eg. On rare occasions an arm is pressed across the face in uterus, resulting in severe maxillary deficiency at birth. General FactorGeneral Factor
  112. 112. Prenatal Influence:  Occasionally a fetus head is flexed tightly against the chest in uterus, preventing the mandible from growing forward normally.  The result is an extremely small mandible at birth, usually accompanied by the cleft palate because the restriction on the displacement of the mandible forces the tongue upwards and prevents normal closure of the palatal shelves. Intrauterine molding Distortion and Asymmetry General FactorGeneral Factor
  113. 113. Prenatal Influence:  Extremes mandibular deficiency at birth is the Pierre Robin syndrome.  Characterized by 1. Cleft palate 2. Micrognathia 3. Glossoptoptosis General FactorGeneral Factor  The combination of micrognathia and glossoptosis can lead to respiratory difficulty.  Because the pressure against the face that caused the growth problem would not be present after birth, one would predict normal growth thereafter.  So early aggressive treatment to lengthen the mandible should be avoided.
  114. 114. Prenatal Influence: Severe mandibular deficiency in Pierre Robin Syndrome General FactorGeneral Factor
  115. 115. Prenatal Influence:  So, although abnormal fetal posture have caused marked cranial or facial asymmetries that are apparent at birth, but after the first year of life most of these have disappeared. Thus, the deformity is temporary.  Maternal nutritional disturbances such as folic acid deficiency can produce malocclusions.  Minor injury to the mother is unlikely to affect the child, since the fetus is well cushioned by the amniotic fluid.  German measles cause gross congenital deformities including malocclusion. General FactorGeneral Factor
  116. 116. Prenatal Influence:  Certain chemical (teratogens) , taken during pregnancy, causes gross congenital deformities including malocclusion.  The time of exposure is important concept for teratogen, as certain stages of embryonic & fetal development are more vulnerable than others.  In general, the embryonic stage (first trimester) is more vulnerable than the fetal period (second & third trimester). General FactorGeneral Factor
  117. 117. Thalidomide provides a classic example. The critical period of exposure is during organogenesis from the 35th-48th day after the last menstrual period. The malformations is linked to the time of exposure:35-37 days-no ears,39-41 days-no arms,41-43days- no uterus,45-47 days-no tibia,47-49 days-triphalangeal thumbs. Prenatal Influence: General FactorGeneral Factor
  118. 118. Some of the known teratogens are- 1)Thalidomide- Embryo is most vulnerable in the first trimester. It was use to treat morning sickness but is not used anymore. Thalidomide produced malformations limited to limbs, ears, cardiovascular system,& gut musculature.  Abnormal development of long bones, typically the upper limbs were more severely involved than the lower limbs.  Phocomelia, polydactyly, syndactyly, oligodactyly were all reported.  Cleft palate could be a complication. General FactorGeneral Factor
  119. 119. 2)Hydantoins(Phenytoin & Trimethadione)- It is anticonvulsant drug. Hydantions have been associated with Foetal hydantoin syndrome. The clinical features include wide anterior fontanelle, ocular hypertelorism, depressed nasal bridge, cleft lip & cleft palate. General FactorGeneral Factor
  120. 120. 3)Folic acid antagonists(Aminopterin & Methotrexate)- •Aminopterin is an antifolic drug,is used as a abortifacient. •Surviving fetuses of such abortion attempts are grossly malformed. •Malformation include facial anomalies(cleft palate,high arched palate, micrognathia, ocular hypertelorism, external ear anomalies), intrauterine growth retardation & mental retardation. General FactorGeneral Factor
  121. 121. 4)Isotretinoin(13-cis-retinoic acid)- It is a synthetic vitamin A derivative,prescribed for severe cystic acne. A pattern of anomalies termed Retinoic acid embryopathy has been associated with isotretinoin exposure in pregnancy. The clinical features include craniofacial anomalies micrognathia, flat nasal bridge, cleft lip& palate). General FactorGeneral Factor
  122. 122. 5)Carbamazepine- •It is a anticonvulsant drug. •Exposure to carbamazepine produces malformations similar to those described with the foetal hydantoin syndrome. General FactorGeneral Factor
  123. 123. 6)Alcohol- •The fetal alcohol syndrome General FactorGeneral Factor
  124. 124. Full expression of this syndrome occurs with chronic daily ingestion of at least 2 grams alcohol / kg(eight drinks / day). Alcohol is teratogen that affects the central nervous system& central nervous system is sensitive to teratogens throughout the entire pregnancy. So alcohol,at any time during the pregnancy,has the potential to cause birth defects. This is why alcohol consumption should be avoided entirely during pregnancy. General FactorGeneral Factor 6)Alcohol-
  125. 125. Birth Injury:  In some diffficult birth, the use of forceps to the head to assist in delivery might damage either or both the temporomandibular joints.  At one time this was a common explanation for mandibular deficiency.  But, in light of contemporary understanding, the condylar cartilage is not as easy to blame underdevelopment of the mandible.  So injury to the mandible during a traumatic delivery appears to be rare and unusual cause of facial deformity. General FactorGeneral Factor Postnatal Influence
  126. 126. Birth Injury:  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.  Due to the plasticity of the maxillary and premaxillary region, temporary deformation is quite likely and permanent damage may result. General FactorGeneral Factor Postnatal Influence
  127. 127. General FactorGeneral Factor  Accidents:  The falls and impacts of childhood can fracture jaws just like other parts of the body.  The condylar neck of the mandible is particularly vulnerable.  Fortunately, the condylar process tends to regenerate well after early fractures. 75% of children with early fractures of the mandibular condylar process have normal mandibular growth, therefore do not develop malocclusions.  When a problem does arise following condylar fracture, it usually is asymmetric growth, with the previously injured side lagging behind. Postnatal Influence
  128. 128. Deficient growth on the affected side after fracture of the left condylar process
  129. 129. General FactorGeneral Factor  Extensive Scar tissue: Eg. From a burn, may also produce malocclusions. Postnatal Influence
  130. 130. Predisposing metabolic climate and disease Endocrine Imbalance Metabolic disturbances Infectious Diseases (Poliomyelitis etc.) General FactorGeneral Factor
  131. 131. General FactorGeneral Factor ENDOCRINE DISTURBANCES: PITUITARY PROBLEMS:  A few workers have studied the relation of the pituitary gland to dental development, notably Schour and Van Dyke and Baume, Becks and associates. Working with rats, they found that after hypophysectomy there was a – progressive retardation of eruption of the incisor tooth which eventually ceases to erupt. – The tooth attained only about 2/3rd normal size and showed a distortion of form. – When an extract of the anterior lobe of the pituitary was injected into the hypophysectomized rats, the eruption rate of the incisor tooth returned to normal.
  132. 132. General FactorGeneral Factor ENDOCRINE DISTURBANCES: PITUITARY PROBLEMS: Baume and his associates injected thyroxin into hypophysectomized animals, either alone or with purified growth hormones. Their findings led them to the following explanation. – The pituitary gland influence eruption not only with its thyrotropin but also with its growth hormones. – The effect of thyroxin on dental growth and development are different from those of the pituitary growth hormone. – Thyroxin is the factor which stimulates the eruption movements and tooth size but it has little influence on alveolar growth. – Growth hormones on the other hand spur dental as well as alveolar growth.
  133. 133. General FactorGeneral Factor ENDOCRINE DISTURBANCES: PITUITARY PROBLEMS: Hypopituitarism: Two basic manifestations of hypopituitarism-  Dwarfism in children  Simmonds’ disease in adults
  134. 134. General FactorGeneral Factor Hypopituitarism:  Under-secretion of growth hormone before epiphyseal plate closure resulting in Pituitary Dwarfism.  In pituitary dwarfism, there is diminutive but well- proportioned body.  Supporting structures are retarded in growth.  The osseous development of mandible is more retarded than maxilla.
  135. 135. General FactorGeneral Factor Hypopituitarism:  The dental arch is smaller than normal and therefore cannot accommodate all the teeth, so that a malocclusion develops.  In pituitary dwarfs the eruption rate and shedding time of the teeth are delayed.  Clinical crown appears smaller than normal because even though eruption does occur, it is not complete.  The roots of teeth are shorter than normal in dwarfism.
  136. 136. General FactorGeneral Factor Hyperpituitarism:  An increase in the number of granules in the acidophilic cells or an adenoma of the anterior lobe of the pituitary is associated with gigantism or acromegaly  If the increase occurs before the epiphyses of the long bones are closed, gigantism results.  If the increase occurs later in life i.e. after epiphyseal closure, acromegaly develops.
  137. 137. General FactorGeneral Factor Hyperpituitarism:  Gigantism is characterized by a general symmetric overgrowth of the body.  Some persons with this disturbance attaining a height of over 8 feet.  The teeth in gigantism are proportional to the size of the jaws and rest of the body.  The roots may be longer than normal.
  138. 138. General FactorGeneral Factor Hyperpituitarism:  Acromegaly, results in enlarged hands, feet, an enlarged skull and mandible along with soft tissue enlargement.  Excessive growth of mandible, creating a skeletal class III malocclusion.
  139. 139. General FactorGeneral Factor Hyperpituitarism:  The lips become thick.  The tongue also becomes enlarged and shows indentations on the sides from pressure against the teeth.  The teeth in the mandible are usually tipped to the buccal or labial side, owing to the enlargement of the tongue.
  140. 140. General FactorGeneral Factor Hyperpituitarism:  Multiple root resorptions may be seen.
  141. 141. General FactorGeneral Factor THYROID PROBLEMS: Hypothyroidism:  If hypothyroidism occurs in infancy and childhood, cretinism results.  If it occurs in the adult, myxedema results.
  142. 142. General FactorGeneral Factor Hypothyroidism:  The cretinism leads to mental defects, retarded somatic growth, generalized edema.  Skeletal growth in the cretin is characteristically more inhibited than the soft tissue growth.  As a result of this disproportionate rate of growth, the soft tissues are likely to enlarge excessively, giving the cretin the appearance of an obese and short child.
  143. 143. General FactorGeneral Factor Hypothyroidism:  The cretin or acutely hypothyroid dwarf has - -Thick neck -Shorter extremities -Thick lips -Large protruding tongue  But the pituitary dwarf is harmoniously proportioned.  In both intances dentition is delayed, with deciduous teeth still present
  144. 144. Hypothyroidism
  145. 145. Large tongue in cretinism, may contribute to the development of mandibular prognathism by causing the mandible to be positioned forward at all times Hypothyroidism
  146. 146. General FactorGeneral Factor Hypothyroidism: Myxedema is characterized by • Lower metabolic rate • Slowed heart rate • Decreased cardiac output • Decreased mental activity • Increased weakness • Increased weight • Depressed growth of hair and scaliness of skin • Facial edema • Increase blood cholesterol
  147. 147. General FactorGeneral Factor Hypothyroidism:  The orofacial findings in myxedematous patients are apparently limited to the soft tissues of the face and mouth.  Lips, nose, eyelids are edematous and swollen.  The tongue is large and edematous, frequently interfering with speech.
  148. 148. General FactorGeneral Factor THYROID PROBLEMS: Hyperthyroidism: Boothby and Plummer described two fundamental different type of hyperthyroidism – Exophthalmic goiter (Grave’s disease) characterized by diffused hyperplasia of the thyroid and by eye signs. – Toxic adenoma, in which hyperfunction originates in a benign tumor of the thyroid gland.
  149. 149. General FactorGeneral Factor Hyperthyroidism: This is usually manifested as • Increased basal metabolic rate • Increased blood pressure • Increase heart rate • Increased weakness • Intolerance to heat • Increased appetite • Increased weight loss • Nervousness and tremors to the hands • Increased sweating
  150. 150. General FactorGeneral Factor Hyperthyroidism:  In hyperthyroidism shedding of deciduous teeth occurs earlier than normal.  Eruption of the permanent teeth is greatly accelerated.  Alveolar atrophy occurs in advanced cases.
  151. 151.  Increased activity is usually due to an adenoma of one or more of the four parathyroid glands.  Almost all patients with hyperparathyroidism have skeletal lesions, some of which may occur in the skull or jaws.  The skeletal disturbances in hyperparathyroidism vary from vague to roentgenographically characteristic lesions and even gross clinical evidence of bone lesions. General FactorGeneral Factor Parathyroid Hormone Problems: Primary Hyperparathyroidism:
  152. 152. General FactorGeneral Factor Primary Hyperparathyroidism – Three times more common in females than males. – Usually affects people of middle age. – Pathological fracture may be the first symptom of the disease. – Bone pain and joint stiffness are frequent early symptoms. – Occasionally the first sign of the disease may be a giant cell tumor or a cyst of the jaw. – Loss of phosphorus and calcium in this disturbance results in a generalized osteoporosis. – Malocclusion caused by sudden drifting with definite spacing of teeth.
  153. 153. General FactorGeneral Factor Primary Hyperparathyroidism Roentgenographic feature: – Bones of the affected person shows a general radiolucency as compared with those of normal people. – Later, sharply defined round and oval radiolucent areas develop, which may be lobulated. – In the jaws it has been described as having a “ground- glass appearance” – Lamina dura around the teeth may be partially lost. – Pulp calcification
  154. 154. PRIMARY HYPERPARATHYROIDISM Numerous mandibular radiolucencies
  155. 155.  Hyperparathyroidism can also occur secondary to other disorder, the most common being end stage renal disease.  Roentgenographic evidence of bone disease involving the jaws shows Brown tumor and loss of lamina dura. General FactorGeneral Factor Secondary Hyperparathyroidism
  158. 158. General FactorGeneral Factor Hypoparathyroidism:  Caused by elimination of parathyroid glands which may be due to surgical removal or rarely due to congenital absence.  Blood chemistry shows a low concentration of serum calcium and a high concentration of serum phosphorus.  When serum calcium level falls to 6 to 7 mg/dl, tenany develops  Aplasia or hypoplasia of the teeth when hypoparathyroidism developed before the teeth were entirely formed.
  159. 159. General FactorGeneral Factor Sex hormones- •Sex hormones (oestrogen and androgen) play an important role in maintenance of bone volume,a reduction causes osteoporosis. •Sex hormones affect craniofacial bone development. •It has been reported, that the suppression of sex hormone secretion during the pubertal growth phase inhibits craniofacial growth, particulary mandibular growth, and results in reduced craniofacial development European Journal of Orthodontics 28 (2006)
  160. 160. METABOLIC DISTURBANCES:  Acute febrile diseases are capable of affecting not only the general health of the child but might also affect the dentition and its surrounding hard and the soft tissues.  Temporarily they are capable of slowing down growth and may cause delayed tooth eruption.  Usually if the severity and duration is not prolonged the child is able to recoup lost time and catch up growth is possible. General FactorGeneral Factor
  161. 161. INFECTIOUS DISEASES:  Disease with paralytic effect, such as poliomyelitis are capable of producing malocclusions. Osteomyelitis  The adult afflicted with acute suppurative osteomyelitis is usually in severe pain.  The teeth in the area of involvement are loose and sore. General FactorGeneral Factor
  162. 162. INFECTIOUS DISEASES: General FactorGeneral Factor German Measles: (Rubella)  Enamel hypoplasia  A high caries incidence  Delayed eruption of deciduous teeth
  163. 163. Dietary Problems: General FactorGeneral Factor Vitamin A deficiencies-  In the developing tooth that is deficient in vitamin A, the odontogenic epithelium fails to undergo normal histodifferentiation and morphodifferentiation, resulting in the distortion of the shape of the teeth.  Since the enamel forming cells are disturbed, enamel matrix is arrested &/or poorly defined so that calcification is disturbed and enamel hypoplasia results.
  164. 164. General FactorGeneral Factor Vitamin A deficiencies-  Eruption rate is retarded and in prolonged deficiencies eruption ceases.  The alveolar bone is retarded in its rate of formation.  The gingival epithelium becomes hyperplastic & in prolonged deficiencies shows keratinization. This tissue is easily invaded by bacteria that may cause periodontal disease.
  165. 165. General FactorGeneral Factor Vitamin D deficiency:  It is required for normal development of bones and teeth.  Necessary for the absorption of calcium and phosphorus from food in the small intestine.  Deficiency leads to rickets.  Rickets refers to any disorder in the vitamin D –calcium phosphorus axis which results in hypomineralized bone matrix.  Children with rickets shows bowing of the legs.
  166. 166. General FactorGeneral Factor Effects on teeth: • Delayed eruption • Misalignment of teeth • Disturbed calcification of teeth • Higher caries index. Vitamin D deficiency:
  167. 167. Dietary Problems General FactorGeneral Factor Vitamin C  Vitamin C is important for normal development of intercellular ground substances in bone, dentition, and other connective tissues so deficiency of ascorbic acid are associated with disturbances in these tissues.  The characteristic change in the teeth is atrophy and disorganization of the odontoblasts resulting in the production of irregularly laid down dentine with few, irregularly arranged tubules.
  168. 168. Dietary Problems General FactorGeneral Factor Vitamin C  Interdental and marginal gingiva is bright red with a swollen, smooth, shiny surface. In fully developed scurvy the gingiva becomes boggy, ulcerates and bleeds  In severe, chronic cases of scurvy, hemorrhages into and swelling of periodontal membranes occur, followed by loss of bone & loosening of teeth, which eventually exfoliate.
  169. 169. Dietary Problems General FactorGeneral Factor Protein Deficiency:  Overall growth and growth of the jaws were decreased.  Delayed eruption.  The gingiva and periodontal membranes exhibited varying degrees of degeneration.
  171. 171. DEFINATIONDEFINATION It is defined as tendency towards an act that has become a repeated performance, relatively fixed, consistent and easy to perform by an individual.
  172. 172. DEFINATIONDEFINATION According to Moyers, “All habits are learned patterns of muscle contraction of a very complex nature”.
  173. 173. Fins says that habits cause concern because they cause: Oral structural changes: Harm, unbalanced pressures bear upon the immature, highly malleable alveolar ridges and bring about potential changes in position of teeth and occlusion. Behavioral problems Socially unacceptable act.
  174. 174. Classification of HabitsClassification of Habits  Habits in relation to malocclusion perhaps should be classified as: 1.Useful 2.Harmful  Useful Habits: Should include the habits of normal function, such as correct tongue position, proper respiration and deglutition and normal use of the lips in speaking.  Harmful Habits: include all that exert perverted stresses against the teeth and dental arches such as lip biting, lip sucking, thumb sucking.
  175. 175. Classification of HabitsClassification of Habits According to Finn & Sim 1. Compulsive oral habits 2. Non-compulsive oral habits
  176. 176. Classification of HabitsClassification of Habits 1. Compulsive oral habits: • When it has acquired a fixation in the child to the extent that he retreats to the practice of this habit whenever his security is threatened by events which occur in his world. • They express deep-seated emotional needs. • Attempt to correct them may cause increased anxiety.
  177. 177. Classification of HabitsClassification of Habits 2. Non-compulsive oral habits: Habits which are easily added or dropped from the child’s behavior pattern as he matures.
  179. 179. BASIC PHYSIOLOGY OF SUCKING REFLEX:BASIC PHYSIOLOGY OF SUCKING REFLEX:  At birth, the child has a reflex pattern of neuromuscular functions as sucking.  The habit of sucking is a reflex occurring in the oral stage of development and disappears during normal growth between 1 to 31 /2 years.  Even before birth, oral contraction have been observed. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING
  180. 180. There are 2 forms of sucking: • Nutritive form • Non-nutritive form THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING
  181. 181. The nutritive form- Breast & bottle feeding which provides essential nutrients. Breast feeding- • Accomplished by 2 maneuvers-suckling and swallowing. • The milk of lactating mammals are surrounded by smooth muscles, which contracts to force out the milk. • Suckling stimulate the smooth muscle to contract and squirt milk into his mouth. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING
  182. 182. • Suckling consist of small nibbling movements of the lips. • When the milk is squirted into the mouth, it is only necessary for the infant to groove the tongue & allow the milk to flow posteriorly into the pharynx and esophagus. • The tongue, however, must be placed anteriorly in contact with the lower lip, so that milk is deposited on the tongue. • This sequence of events defines as infantile swallow. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING • The suckling reflex and the infantile swallow normally disappear during the first year of life.
  183. 183. BOTTLE FEEDING: • Nipple manufactures have ignored the basic physiology of suckling. • The conventional nipple contacts only the mucous membrane of the lips. • The warmth of association conferred by the breast & the mother’s body is largely lacking & the physiology of suckling is not duplicated. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING
  184. 184. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING BOTTLE FEEDING: •Because of poor design, the mouth is held open more widely & greater demand is made on the buccinator mechanism. •The pumping action of the tongue, the raising & lowering & the rhythmic backward & forward movement of the mandible are reduced. •Suckling becomes sucking.
  185. 185.  Breast-feeding practices contribute in the prevention of malocclusion in addition to decreasing the practice of parafunctional habits. (P R Health Sci J. 2006 Mar)  To provide as close a duplicate of the human breast as possible, a nipple was designed which incited the same functional activity as breast feeding.  The functionally designed latex nipple largely eliminate the objectionable features of previous non-physiologic counterparts. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING
  186. 186. Nonphysiological nursing with a conventional nipple •Mouth is propped open unduly. •Lips seal difficult. •Abnormal muscle pressure are exerted because of excessive opening movement. Nursing action of nuk sauger nipple •Closely simulates natural activity. •Entire perioral areas is able to contact the warm nipple base.
  187. 187.  A minimum of a half hour per nursing interval is recommended.  But no hard & fast rule can be established because some children demand more attention & time, some less depending on individual make up.  Weaning to the cup should be postponed until at least the first birthday.  If nursing is done with the physiologically designed nipple in conjunction with fondling & maternal contact, there is reason to believe that the incidence of prolonged sucking habits will be significantly reduced. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING
  188. 188. NON NUTRITIVE FORM:  Children who neither receive unrestricted breast feeding nor have access to a pacifier may satisfy their need with habits like thumb sucking which ensures a feeling of warmth & sense of security but may be detrimental to their dentofacial development.  Nearly all modern infants engage in some sort of habitual non nutritive sucking- sucking of the thumb, finger or a similarly shaped objects.  Vast majority of infants do so during from 6 months to 2 years or later.  After the eruption of the primary molars during the second year, drinking from a cup replaces drinking from a bottle or continued nursing at the mother’s breast, the number of children who engage in non nutritive sucking diminishes.  Some fetuses have been reported to suck their thumbs in utero.
  189. 189. Recent studiesRecent studies shown thatshown that thumb suckingthumb sucking may bemay be practiced even duringpracticed even during intra uterineintra uterine
  190. 190.  According to Gellin -Thumb sucking is defined as placement of thumb or one or more fingers in varying depths into the mouth.  According to Moyers -Thumb sucking is defined as the repeated and forceful sucking of thumb with associated strong buccal and lip contractions. THUMB SUCKING ANDTHUMB SUCKING AND DIGIT SUCKINGDIGIT SUCKING
  191. 191. Almost all normal children engage in non-nutritive sucking, can lead to malocclusion. As a general rule, sucking habits during the primary dentition years have little if any long term effect.  If these habits persist beyond the time that the permanent teeth began to erupt, however malocclusion occurs. THUMB SUCKING ANDTHUMB SUCKING AND DIGIT SUCKINGDIGIT SUCKING
  192. 192. It is during the transition from the deciduous to the permanent arch that much of the damage takes place.  So during this transition stage that the avoidance of all abnormal pressure habits is of the utmost importance. If a child’s sucking habits persist by the time he/she is 36 to 48 months of age, professional assistance may be warranted to minimize the risk of malocclusion THUMB SUCKING ANDTHUMB SUCKING AND DIGIT SUCKINGDIGIT SUCKING
  193. 193. Oral habits and primary dentition Warren J et al. (JADA 2001,dec) concluded that continuous nonnutritive sucking habits of 48 months or longer produced the greatest changes in dental arch and occlusal characteristics, children with shorter sucking duration also had detectable differences from those with minimal habit duration. • Implications: It may be prudent to revisit suggestions that sucking habits continued to as late as 5 to 8 years of age are of little concern.
  194. 194. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING ETIOLOGY  During the very first weeks of life, thumb sucking are typically related to feeding problems.  To meet the primitive demands like hunger.  Some children suck their thumb as a teething device during the difficult eruption of a primary molar.  Some children use digital sucking for the release of emotional tensions with what they are unable to cope.  Some children suck their thumb as an attention-seeking weapon
  195. 195. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING TRIDENT OF FACTORS Damage to the teeth and investing tissues is dependant on trident of factors that must be recognized and evaluated. i. Duration ii. Frequency iii. Intensity
  196. 196. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING  Duration of the habit beyond early childhood is not the only determinant. Frequency of the habit and intensity of the habit are equally important.  The frequency of the habit during the day and night affects the end result.  The child who sucks sporadically or just when going to sleep is much less likely to do any damage than one who constantly has his finger in his mouth.
  197. 197. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING  The intensity of the habit is important.  In some children the sucking can be heard in the next room. The 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.
  198. 198. EXCESSIVE digit sucking can set up abnormal forces on the oral cavity and surrounding structures.
  199. 199. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGCSUCKINGC Malocclusion characterized by:  Flared and spaced maxillary incisors and lingually positioned lower incisors.  The labially posed upper permanent incisors are particularly vulnerable to accidental fractures.
  200. 200. Afzelius-Alm A,et al, (Swed Dent J. 2004;28)- found that the majority of children with prolonged thumb- sucking have proclined lower incisors rather than retroclined lower incisors. In retroclined lower incisors groups – the angle between the thumb and the lower incisors was significantly smaller. – the thickness of the lower lip significantly thinner than in the group with proclined incisors. – A higher frequency of early loss of deciduous molars was also observed in the group with retroclined incisors. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT CKINGCKING
  201. 201. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING Anterior Open Bite: (Cozza P et al, Am J Orthod Dentofacial Orthop. 2005 Oct) • It is associated by a combination of interference with normal eruption of incisors and excessive eruption of posterior teeth. • When a thumb or finger is placed between the anterior teeth, the mandible must be positioned downward to accommodate it. • The interposed thumb directly impedes incisor eruption. • At the same time, the separation of jaws alters the vertical equilibrium on the posterior teeth and as a result, there is more eruption of posterior teeth than might otherwise have
  202. 202. Anterior Open Bite: • Because of the geometry of jaw, 1mm of elongation posteriorly opens the bite about 2 mm anteriorly, so this can be a powerful contributor to the development of anterior open bite
  203. 203. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING  Narrow upper arch: • Although negative pressure is created within the mouth during sucking, but this is not responsible for the constriction of the maxillary arch. • When the thumb is placed between the teeth the tongue must be lowered, which decreases pressure by the tongue against the lingual of upper posterior teeth. • At the same time cheek pressure against these teeth is increased as the buccinator muscle contracts during sucking. • Cheek pressures are greatest at the corners of the mouth, and this probably explains why the maxillary arch tends to become V-shaped, with more constriction across the canines than the
  205. 205. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING  Unilateral and bilateral cross bites are often associated with finger habits. ( Warren JJ et al. Pediatr Dent. 2005 Nov-Dec))  Flattened mandibular anterior segment: Abnormal mentalis muscle function and lower lip activity serve to flatten the mandibular anterior segment.
  206. 206. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING  Retardation of deglutitional maturation: • Increase in over-jet makes normal swallowing procedures increasingly difficult. • Instead of the lips containing the dentition, during deglutition, the lower lip cushions to the lingual of the maxillary incisors, forcing them farther forward. • Lip muscle aberrations are often assisted by a compensatory tongue thrust during the swallowing act. • So the infantile suckle-swallow continues, or the transitional period is greatly prolonged with a mixture of infantile and mature swallowing
  207. 207. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING  Thumb sucking habit can create a class II malocclusion:.  Thumb-suckers may be found to have a narrower nasal floor and high palatal vault.  The maxillary lip becomes hypotonic and the mandibular lip becomes hyperactive.
  208. 208. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING  Tell-tale callus on the back of the finger or thumb are often present.
  209. 209. THUMB SUCKING AND DIGITTHUMB SUCKING AND DIGIT SUCKINGSUCKING Anterior Open Bite Narrow Constricted maxillary arch Posterior Cross Bite
  210. 210. Tongue Thrusting HabitTongue Thrusting Habit Tongue thrust swallowing defined as placement of the tongue tip forward between the incisors during swallowing.
  211. 211. Tongue Thrusting HabitTongue Thrusting Habit  The term tongue thrust is something a misnomer.  Since it implies that the tongue is forcefully thrust forward.  But individuals who place the tongue tip forward when they swallow usually do not have more tongue force against the teeth than those who keep the tongue tip back.
  212. 212. Tongue Thrusting HabitTongue Thrusting Habit  Swallowing is not a learned behavior, but is integrated and controlled physiologically at subconscious levels.  So whatever the pattern of swallow, it cannot be considered a habit in the usual sense.  Individuals with an anterior open bite place the tongue between the anterior teeth when they swallow while those who have a normal incisor relationship usually do not and it is tempting to blame the open bite on this pattern of tongue activity.
  213. 213. Tongue Thrusting HabitTongue Thrusting Habit Predisposing factors – Associated with history of finger sucking – Associated chronic naso respiratory distress – Mouth breathing – Tonsillitis or pharyngitis – Improper bottle feeding – Macroglossia – Constricted dental arches
  214. 214. Humans show 2 types of swallow pattern: Infantile and neonates swallow Mature/Adult swallow Tongue Thrusting HabitTongue Thrusting Habit
  215. 215. Infantile visceral swallow • Jaws apart, tongue between gum pads • Mandible stabilized by contraction of facial muscles and interposed tongue • Swallow is guided and controlled by sensory interchange between lip and tongue • Active contractions of the musculature of the lips. • Tongue tip brought forward into contact with the lower lip. • Little activity of the posterior tongue or pharyngeal musculature • Forward position of mandible and tongue • Tongue grooved(depressed central position) to steer the liquid into pharynx and esophagus
  216. 216. Mature somatic swallow  Teeth – together (momentarily)  Mandible stabilized by contraction of mandibular elevator muscles  Tongue tip- against palate, above and behind the incisors  Minimum contraction of lips  Appears between 2-4 years in normal
  217. 217. NORMAL SWALLOWING •Incisors are momentarily in contact •Tip of the tongue touches the lingual interdental papillae of maillary arch •Lips are tightly closed together •Dorsum of the tongue closely approximates the palate during swallowing ABNORMAL SWALLOWING •Teeth are often separated •Tongue thrusts forward into the excessive overjet •Dorsum of the tongue drops away from the palatal vault •Instead of the lips creating firm seal,the upper lips remains relative functionless •Mentalis exerts strong forward and upward thrust of lower lip against lingual surfaces of maxillary incisors
  218. 218. Tongue Thrusting HabitTongue Thrusting Habit Classification 1. Simple Tongue Thrust 2. Complex Tongue Thrust
  219. 219. Tongue Thrusting HabitTongue Thrusting Habit Simple tongue thrust swallow (Teeth together swallow) • Teeth are in occlusion as tongue protrudes into open bite • Tongue thrust is present to seal open bite • Well circumscribed open bite • Secure intercuspation • History of digit sucking • Displays contractions of lips, mentalis and mandibular elevators
  220. 220. Tongue Thrusting HabitTongue Thrusting Habit Complex tongue thrust Swallow (Teeth apart swallow) • Teeth apart during tongue thrust • More diffuse open bite • Poor occlusal fit • History of breathing or chronic nasorespiratory diseases • Combined contractions of lip, facial and mentalis muscles. • Lack of contraction of mandibular elevators
  221. 221. Clinical Feature: If the postural position is normal, the tongue thrust swallow has no clinical significance because tongue thrust swallowing simply has too short a duration to have an impact on tooth position. • Pressure by the tongue against the teeth during a typical swallow lasts for approximately 1 second. • A typical individual swallows about 800 times/day while awake but has only a few swallows /hour while asleep. The total/day therefore is usually under 1000. • One thousand seconds of pressure, of course, totals only a few minutes, not nearly enough to effect the equilibrium. Tongue Thrusting HabitTongue Thrusting Habit
  222. 222.  On the other hand, if a patient has a altered resting posture of the tongue, the duration of this pressure, even if very light, could effect tooth position, vertically or horizontally.  Two significant variations from the normal tongue posture can be seen. • Protracted Tongue posture • Retracted Tongue posture Tongue Thrusting HabitTongue Thrusting Habit
  223. 223. There are two forms of protracted tongue posture  Endogenous protracted tongue posture.  Acquired adaptive tongue posture Tongue Thrusting HabitTongue Thrusting Habit
  224. 224. Endogenous protracted tongue posture: • May be a retention of infantile postural pattern. • Some persons, reasons not yet clear, do not change their tongue posture during the arrival of the primary incisors and the tongue tip persists between the incisors. • For the great majority of patients with endogenous protracted tongue posture, the open bite is mild and not a serious clinical problem, but on rare occasions, quite serious open bites are present. Tongue Thrusting HabitTongue Thrusting Habit
  225. 225. Acquired protracted tongue posture • Usually it is the adaptation to enlarged tonsils, pharyngitis, or tonsilitis. • When the acutely inflamed throat (pharyngitis or tonsilitis) is anesthetized, the adaptive protracted posture of the tongue may spontaneously correct to a more normal position. • As long as the precipitating pain mechanism is present, the tongue will posture itself forward, and repositioning of the incisors will not be stable. Therefore, it is best to refer such patients to a physician for correlative therapy. Tongue Thrusting HabitTongue Thrusting Habit
  226. 226. The protracted tongue posture usually results in • Anterior open bite • Proclination of anterior teeth • Contracted upper arch Tongue Thrusting HabitTongue Thrusting Habit
  227. 227. Complex tongue thrust- •Defined as a tongue thrust with a teeth apart swallow. •Combine contractions of the lips, facial, and mentalis muscles, lack of contraction of the elevators. •The open bite associated with it is more diffuse and difficult to define than that seen with a simple tongue thrust. •Indeed, on occasion, complex tongue thrust-thrusters have no open bite at all. •Examination of occlusal casts typically reveals a poor occlusal fit and instability of intercuspation. •The incidence of complex tongue thrusting does not diminish as much with age as does the simple tongue thrust. Tongue Thrusting HabitTongue Thrusting Habit
  228. 228. •Complex tongue thrust are more likely to be associated with chronic nasorespiratory distress, mouth breathing, tonsillitis, or pharyngitis. •When the tonsils are inflamed, the root of the tongue may encroach on the enlarged facial pillars. •To avoid this encroachment, the mandible reflexly drops, separating the teeth and providing more room for the tongue to be thrust forward during swallowing to a more comfortable position. •Pain and lessening of space in the throat precipitate a new forward tongue posture and swallowing reflex. •Melsen et al state that both tongue thrust swallow favor the development of distoocclusion, extreme maxillary overjet and open bite. Tongue Thrusting HabitTongue Thrusting Habit
  229. 229. MOUTH BREATHING HABITSMOUTH BREATHING HABITS ETIOLOGY: • Humans are primarily nasal breathers but everyone breathes partially through the mouth under physiologic conditions. • The most prominent being an increased need for air during exercise. • A rest, minimum airflow is 20-25 L per minute, but heavy mental concentration or even normal conversation lead to increased airflow and transition to partial mouth breathing. • For the average individual there is a transition to partial oral breathing when ventillatory exchange rates above 40-45L/min are reached. • At maximum effort 80 or more L/min of air needed, about half of which is obtained through the mouth.
  230. 230. MOUTH BREATHING HABITSMOUTH BREATHING HABITS • Nasopharyngeal Obstruction if a nose is obstructed, the work associated with nasal breathing increases and at a 3.5-4 cm H-2-0/l/min resistance to nasal airflow, the individual switches to partial mouth breathing.  Chronic respiratory infection  Enlarged tonsils &adenoids  Nasal polyp or tumor  Any mechanical obstruction anywhere within the nasorespiratory system • Anatomic- -short upper lip
  231. 231. MOUTH BREATHING HABITSMOUTH BREATHING HABITS Classification of mouth breathing: Obstructive Habitual Anatomical
  232. 232. MOUTH BREATHING HABITSMOUTH BREATHING HABITS OBSTRUCTIVE MOUTH BREATHERS: Those who have – Increased resistance to or a complete obstruction of the normal flow of air through the nasal passages. – Because of the difficulty of inspiring and expiring air through the nasal passages, the individual is forced to breathe through his mouth. – Obstructive mouth breathing is frequently observed in ectomorphic children who possess long, narrow faces, and nasopharyngeal spaces.
  233. 233. MOUTH BREATHING HABITSMOUTH BREATHING HABITS Habitual mouth breather is an individual who continually breathes through his mouth by force of habit, although the abnormal obstruction has been removed. Anatomical mouth breather is one whose short upper lip does not permit complete closure without undue effort.