EXTRINSIC AND INTRINSIC FACTORS IN THE ETIOLOGY OF MALOCCLUSION & ITS ROLE IN POST TREATMENT STABILITY : EXTRINSIC AND

D INTRINSIC FACTORS IN THE ETIOLOGY OF MALOCCLUSION & ITS ROLE IN POST TREATMENT STABILITY GUIDED BY: PRESENTED BY: Dr.Mrs.P.V.Hazarey Pallavi Ram Thombare Prof & Guide Pg Student Dept of Orthodontics & Dentofacial Orthopaedics

Slide 2: W. K. Bridgman in 1859 states the proper antagonism of the teeth is of very utmost importance, for if any of the cusps be out of place they disturb equal distribution of forces in biting & tend to produce mischief at the points holding those cusps in their assumed positions Normal occlusion of teeth is supposed to be requisite for normal facial balance which is influenced by soft tissue, underlying bone, occlusion, axial inclination of teeth. The position of the teeth within the jaw and the mode of occlusion are determined by developmental processes that interact with the teeth and associated structures during the periods of formations, growth and postnatal modifications.

NORMAL OCCLUSION: NORMAL OCCLUSION The word occlusion is derived from clusion i.e. close & oc i.e. up. Edward H. Angle in 1907 defined occlusion as being the normal relation of occlusal inclined planes of teeth when the jaws are closed B.S.S.O in 1926 defined it as that occlusion which is within the standard deviation from the ideal

CONCEPTS AND EVOLUTION OF OCCLUSION: CONCEPTS AND EVOLUTION OF OCCLUSION Initially concept was given by E. H. Angle in 1899 . Matthew Cryer questioned Angles concept. Dr P.R. Beggs gave his concept in 1924 of attritional occlusion. To understand the normal occlusion & to differentiate it from malocclusion Lawrence F. Andrews in 1960 - 64 gave the six keys of normal occlusion. Molar relationship Crown angulations mesiodistal tip Crown inclination labiolingual or buccolingual Rotations Spaces Plane of occlusion

WHAT IS MALOCCLUSION: WHAT IS MALOCCLUSION It is a condition where there is departure from the normal relation of the teeth to other teeth in the same arch and to the teeth in the opposing arch. Salzmann says diagnosis of malocclusion is not to be based on subjective, arbitrarily, established criteria or standards, but must take into consideration the genetic endowment, ontogenetic growth & postnatal development of the individual patient. Carabelli in mid of 19 th century was the first to describe abnormal relation of upper & lower dental arches. Angle defined malocclusion of the teeth is but the perversion of their normal relation.

Slide 6: INCIDENCE OF MALOCCLUSION As per the various broad population studies done for the prevalence of malocclusion 20 % of deciduous dentition had malocclusion 39 % of mixed dentition 58 % in permanent dentition No difference noted according to sex.

REVIEW: REVIEW First direct attempt of classification give by Fox in 1803 . Marjolin in 1823 gave direction of dental arches ; prominence, recession, inversion. J.C.F.Mary in 1828 gave the inclination of the teeth; inward, outward, laterally. C.F. Delabarra in 1829 was first to indicate 4 types of bite ; overbite, underbite, edge to edge, cross bite Blandid in 1836 & J.M.A.Schange in 1841 gave the classification as per the number, form, direction & position.

Slide 8: M.S.Cartwright in 1864 gave irregularities of the teeth according to 3 forms of teeth, heredity congenital mechanical Kingsley in 1872 classified the cause of irregularities first by developmental & second as accidental A.Ogston in 1974 classified congenital malformation of the lower jaw Non development of inferior maxilla. Excessive development Congenital smallness of the mandible either both halves / unilateral Congenital dislocation

Slide 9: Most universally used classification was introduced by Edward. H. Angle in 1899 , the basis of Angles classification was his hypothesis that the first molar is the key of occlusion. Simon with suggestion made by Bennet in 1912 categorized malocclusion in 3 planes of space: Horizontal, Vertical & Transverse. Ackermann Proffit recognizing the sagittal orientation & limitations of the angles classification; gave a method of diagrammatic & categorizing malocclusion using the Venn Symbolic Logic Daigram, known as SET THEORY

THE ORTHODONTIC EQUATION: THE ORTHODONTIC EQUATION CAUSE TIME TISSUES RESULT some predisposing prenatal primary following of the three Some existing postnatal secondary or combination. -Heredity continuous/intermittent -neuromuscular -malfunction -Developmental cause -may act at different age -teeth - malocclusion of unknown origin levels -bone and cartilage -osseous dysplasia Trauma -soft tissue other than -physical agents muscles -Habits -Diseases -Malnutrition In an article by Dockrell in 1952 classification of etiology of malocclusion Act at on produce

INTRINSIC FACTORS: INTRINSIC FACTORS

HEREDITY: HEREDITY Offspring inherits few attributes from his parents which are modified by environmental factor, physical entities, pressure, habits, malnutrition, etc. Definite genetic determinant influence dentofacial morphology, thus growth & development has a strong hereditary component. Certain racial & familial characteristics tends to recur. There is a possibility of recapitulation of a hereditary trait from either parent or combination of both parents to produce a characteristic modification.

Slide 13: Heredity with racial influence : certain facial characteristics show racial influence Heredity with facial type: Hasen & Siversten pointed out sex linked nature of facial width & dental arch shape. Female demonstrates positive correlation wider the face wider is the jaw. Heredity influence on growth & development pattern: Growth & development has a strong hereditary influence. Environmental influence modify the hereditary determined pattern. Onset of puberty vary with different races & geographic distribution.

Slide 14: Heredity & specific dentofacial morphology: Lundstrum made an intensive analysis of these characteristics in twin & concluded that heredity could be considered significant in determining the following characteristics: Tooth size Width and length of arch Height of palate Crowding / spacing / rotation of teeth Tooth shape and number Overjet and overbite Inter arch variation in transverse/Sagittal/vertical plane

Slide 15: Frenum Position and confirmation of perioral musculature to tongue size and shape. Soft tissue peculiarities Congenital deformity Facial asymmetry Micrognathia / macrognathia Cleft palate and lip Mandibular prognathism / retrusion

Slide 16: Genetic aberrations make their appearance prenatally / may not be seen until many years after birth. It can be explained as follows as some primary etiological sites: 1. Neuromuscular system: the anomalies with inheriting component are size, position, tonicity, contractility, neuromuscular coordination pattern of facial, oral & tongue musculature. It effects by reflex contraction on bony skeleton & dentition leading to skeletal imbalance. It is not possible to differentiate in the origin of certain habits. There may be various reasons. Some malocclusion are associated with tongue size, lip length, tonicity. 2. Soft tissue other than muscle:

Slide 17: 3. Dentition: Size and shape of the teeth Number of the teeth Primary position of tooth germ and path of eruption. Shedding of deciduous teeth and sequence of eruption Mineralization of the tooth. 4. Skeletal structures: Affected inherently as well as environmentally or acquired congenital malformation. Class III have strong familial tendency. Any pathological condition affecting growth of the jaw affects the dentition Trauma Infection during growing years can affect the jaw growth

CONGENITAL: CONGENITAL Can be identified as early as in 18 20 wks of pregnancy or can be seen immediately after the birth. The aberrations are both inherently & environmentally influenced. The congenital abnormality that can cause malocclusion can be classified as: EXTRINSIC : abnormal state of mother during pregnancy accidents during pregnancy or during birth intra uterine pressure accidental traumatization of the infant by external forces

Slide 19: INTRINSIC : clefts of face and palate macroglossia / microglossia cleidocranial dysostosis malnutrition & endocrinopathies infectious diseases metabolic & nutritional deficiency

Slide 20: Cleft lip and palate: cicatricial bands restrict the horizontal maxillary anterior segmental development Teeth on side of cleft are in lingual crossbites with opposing lowers. Premaxilla displaced anteriorly or due to tight repaired lip pushed posteriorly. Maxillary incisors badly malposed with bizarre axial inclination and teeth frequently jumbled. Maxillary laterals are missing / twined / atypical in shape . Strong forces applied on teeth to correct the malocclusion can lead to early loss of the teeth. Teeth are in good relation to basal bone but entire palatal & alveolar structure is displaced medially.

Slide 21: Cerebral palsy: paralysis/lack of muscular co-ordination attributes to intracranial lesions, considered to be a birth injury. The tissue are normal but lack in motor control with abnormal function in muscle of mastication, deglutition, respiration, speech. Aberrant action upset the muscle balance producing abnormal pressure habits leading to malocclusion. Tortocollis : foreshortening of sterno cleido mastoid muscle change the bony morphology of cranium and face with bizarre facial asymmetry with uncorrective dental malocclusion. Micrognathism : seen with either of jaw mainly associated with congenital heart disease. Maxillary deficiency is due to premaxillary deficiency Mandibular deficiency due to chin with steep mandibular angle.

Slide 22: Cleido cranial dysostosis: its congenital and frequently inheretent. Features are: Absence of clavicle, delayed closure of sutures, maxillary retrusion, mandibular protrusion, retarded eruption of permanent teeth, retained deciduous teeth, roots of permanent are short & thin, supernumerary present. Syphillis: abnormal shaped teeth, malposed teeth like hutchinsons incisors, mulbery molars, enamel deficiency, extensive dental decay, small maxilla, anterior cross bite.

Slide 23: Oligodontia : it is commonly inheriting and congenital III molars are commonly involved. Anodontia: associated with hereditary ectodermal dysplasia Some common reasons of congenital absent teeth are : Heredity Ectodermal dysplasia Localized inflammation / infection Systemic conditions Evolutionary changes in the dentition. Rubella : infection to mother during pregnancy can lead to dental hypoplasia, retarded eruption, extensive caries.

ENDOCRINAL FACTOR: ENDOCRINAL FACTOR Prenatal influence show hypoplasia of tooth while postnatal can retard or hasten the growth but do not distort the direction of the growth. It affect the rate of ossification of bones, time of suture closure, time of eruption of teeth, rate of resorption of roots. Periodontal membrane and gingiva are extremely sensitive to endocrine dysfunction thus affect teeth indirectly.

Slide 25: Features of the endocrinal imbalance are: 1. Hypo thyroidism: Retarded growth with decreased vertical growth of face Anterior open bite tendency Delayed eruption of teeth Maxillary protrusion Spacing of the teeth Over retained deciduous Narrowing of dental arch Abnormal resorption pattern Gingival disturbances

Slide 26: 2. Hyper thyroidism : Accelerated skeletal growth with irregular eruption of teeth Increased vertical facial height Open bite tendency Premature eruption of deciduous 3. Hypo pitutarism: Retarded growth with decrease linear facial measurement and cranial base measures Open bite tendency Delayed tooth eruption Incomplete root formation with incomplete closure of apical foramen

Slide 27: 4. Hyper pitutarism: Accelerated development seen in mandible Accelerated dental development and eruption Enlarged tongue Thick cortical plates 5. Parathyroidism : Accelerated skeletal growth with irregular eruption of teeth Increase vertical facial height Open bite tendency Premature eruption of deciduous Mobility due to loss of cortical bone Interruption of tooth development

METABOIC DISEASE FACTOR: METABOIC DISEASE FACTOR Febrile diseases not only affect health of child but also the dentition and surrounding hard and soft tissue. They are able to sho w decrease growth and delayed eruption of teeth.

EXTRINSIC FACTORS: EXTRINSIC FACTORS

ENVIRONMENTAL: ENVIRONMENTAL PRENATAL INFLUENCE: Cause of malocclusion is due to - Uterine fetal posture, Fibroids of the mother cause facial asymmetries apparent during birth & disappear till 1 st year of life. - Micro mandible / pierre robin syndrome / treacher collin syndrome have tremendous increment of growth largely eliminate the original malformation. - Amniotic lesions - Maternal diet and metabolism - Drug induced deformity e.g. thalidomide - Infections like germen measles - Injury and trauma

Slide 31: POSTNATAL INFLUENCE - Cranial bone slide and mold more than the facial and dental area - High forceps delivery injure the infant with permanent damage to TMJ due to Ankylosis patient show hypo plastic mandible with retarded growth / vogelgesicht. - Malocclusion associated with cerebral palsy attribute to birth injury due to loss of muscle co-ordination - Disabling accidents produce undue pressure on the developing dentition. - Falls lead to condylar fracture & facial asymmetry - Extensive scar tissue restrict the mandibular growth.

DEFICIENCY DISEASE / MALNUTRITION / DIETARY PROBLEMS: DEFICIENCY DISEASE / MALNUTRITION / DIETARY PROBLEMS Malnutrition affect quality of tissue being formed, the rate of calcification Good nutrition plays an imp role in growth & maintenance of good bodily health and hygiene Vitamin deficiency lead to malocclusion by upsetting the dental developmental time table This leads to premature loss of teeth, prolonged retention of teeth, poor tissue health, abnormal eruption pathways Its mainly due to faulty utilization of ingested food, hormonal / enzymatic imbalance, chronic alcoholism.

Slide 33: Protein deficiency delayed eruption Vitamin A deficiency retarded eruption Vitamin B deficiency retarded growth of the bones Vitamin C deficiency bleeding gums, loosening of the teeth Vitamin D deficiency retarded eruption and early loss of deciduous Hyper vitaminosis, vitamin B 12 deficiency, folic acid deficiency cleft lip and palate

INFECTION AND DISEASES: INFECTION AND DISEASES Malocclusion can be secondary to some neuropathies or neuromuscular disorders or it may be a sequel of treatment problem like scoliosis. Systemic: febrile diseases upset the dentitional development time table during infancy and early childhood. It mainly affects the quality rather than the quantity of the dentitional development. Local: Gingival & periodontal diseases Tumors caries

Slide 35: Nasopharyngeal diseases and disturbed respiratory function: There are 3 hypothesis to be considered: Adenoid enlargement leads to mouth breathing resulting in particular type of facial form and dentition. Enlarged adenoids leads to mouth breathing but not influence facial form and type of dentition. Enlarged adenoids in certain types of faces and dentition leads to mouth breathing

The basic assumption is due to compression, tissue atrophy, altered air pressure : Enlarged adenoids obstruct the airway mouth breathing change in tongue, lip and mandibular posture upset the soft tissue balance lead to alter the craniofacial form & malocclusion increase in the anterior facial height narrow & high palate increased lower facial height anterior open bite, posterior cross bite tendency

PHYSICAL AGENTS: PHYSICAL AGENTS Nature of food : In the primitive fibrous food stimulates their muscle to work thus increasing the load of function on the teeth. This type of food produces less caries, great mean arch width, increased wear of occlusal surfaces Now highly refined, soft, pappy modern food plays a role I etiology of malocclusion, as lack of adequate function results in contraction of dental arches, insufficient occlusal wear, absence of occlusal adjustments

TRAUMA AND ACCIDEDNTS: TRAUMA AND ACCIDEDNTS 1. Prenatal trauma / birth injury: Hypoplasia of mandible is caused by intrauterine pressure /trauma during delivery Vegelgesicht: inhibited growth of mandible due to ankylosis in TMJ 2. Trauma at time of delivery : e.g. forcep delivery 3. Postnatal trauma : Occur at any age and affect any region Fracture of jaw and teeth, loss of vitality Habits produce microtrauma if persists for a long time Trauma to TMJ impair growth, function leads to asymmetry, TMJ dysfunction Frequent falls Trauma leads to dilaceration, deformation, displacement, ankylosis. Abnormal resorption pattern, deflect permanent tooth germ.

POSTURE: POSTURE poor posture accentuates existing malocclusion Those who hold their head straight & erect with head placed over the spinal column will almost reflexly hold their chin forward in prefered position Body posture is the summated expression of muscle reflexes & so usually capable of change & correction E.g. abnormal tongue position usually cause open bite a full fledged malocclusion seen in child resting his head on his hands for long period each day, sleeping on his arm, or fist or pillow. a stoop shouldered child with head resting on his chest create his own mandibular retrusion.

HABITS: HABITS All habits are functional abrasion producing forces that are abnormal as produced repeatedly over time thus bring about permanent deformation in musculoskeletal unit. This deformity depends on intensity, duration and frequency of habit. The muscular element is capable of retrained but underlying skeletal structure goes to abnormal proportion. Thus it follows the functional matrix theory. Abnormal pattern interferes with regular pattern of facial growth.

Slide 40: Bone is a plaster tissue responsive to pressure that are continually acting on it. Dynamic role of musculature is apparent. The dentist thinks muscles as a primary masticatory element. An average person eats 3 meals per day, but swallows al the day long, breaths constantly & talks a good part of time. Premature occlusal contacts & compensatory muscle activity during active function produces even greater departure from the normal, which can even change the bony morphology thus accentuating the malocclusion.

Slide 41: 1.POSTURAL RESTING POSITION: It is a sort of balance of extraoral & intraoral muscle forces with the buccal & perioral musculature passively restraining the anterior displacement of the teeth. Lingual pressure are greater but hydraulic effect, tissue mass, cheek elasticity & morphogenetic pattern contributes to a total balance.

Slide 42: BUCCINATOR MECHANISM: It runs posteriorly to pterygomandibular raphe, decussating the fibers of deep constrictor muscles that carry on a round & anchor at pharyngeal tubercle of occipital bone. All facial muscles are intimately related to postvertebral, prevertebral, & cervical musculature, so that a change in one muscle would influence relationship with other muscle. e.g. pattern in class II pattern in class III Thus the musculature dose not create skeletal malocclusion but accentuates the existing deformity by virtue of its adaptive functional activity.

Slide 43: 2. FINGER SUCKING HABIT: According to William James : an acquired habit from psychological point of view is nothing but a new pathway of discharged formed in brain, by which certain incoming current even after tent to escape. Habits is relation to malocclusion are classified into: Useful Harmful According to Dr. E A Barton apart from effect of constantly sucking the foul thumb there is another side which demands consideration. The thumb is a hard body frequently in mouth tends to pull the growing premaxilla forward with upper incisors which projects labially beyond upper lip giving Dents Des Anglais Appearance

Slide 44: FINGER SUCKING FROM BIRTH TO 4 YEARS: New born infant have a relatively well developed suckling mechanism and receives not only nutriment but also a feeling of euphoria, we being, sense of security, feeling of warmth, and being wanted. Lips of infants are sensory organ & pathway to brain is relatively well developed PHILOSOPHY OF SUCKLING: Gum pads are apart tongue brought forward in plunger like fashion tongue & lower lip in constant contact mandible move up & down in rhythm & forward & backward by virtue of flat condylar path as buccinator mechanism alternately contracts & relax. Conventional nipple dose not duplicates the suckling and thus it becomes sucking.

Slide 45: Breast fed babies have less abnormal perioral muscle habit & less retained infantile swallow. Habit continued to 3 years show a temporary damage confined to anterior segment. The damaging features of the habit are similar to characteristics of typical hereditary pattern of class II Div 1 malocclusion. The sequence of total maxillary protrusion to sucking habit with increased pressure from buccinator mechanism activating the pterigomandibular raphe just behind the dentition forcing the teeth anteriorly, with severe openbite, buccal crossbite, protruding maxillary anteriors, mandibular incisor crowding, tongue thrust retained infantile suckle swallow pattern.

Slide 46: ACTIVE FINGER SUCKING HABIT AFTER THE AGE OF 4: Ineffectual badgering attempt to break the habit continues it. The finger sucking is associated with perioral musculature with increased overjet & makes normal swallowing pattern difficult with a class II tendency. As swallowing requires closing off to create a partial vacuum, the lip muscle aberration is assisted by compensatory tongue thrust during swallowing thus retarding deglutition maturation. Finger sucking habit becomes innocuous (only at bed time) but tongue thrust continues to adapt to the morphology. Tongue does not drops back & spread out with abnormal mentalis muscle function while lower lip activity flattens the anterior segment. Fore finger sucking is considered to cause more severe deformation

Slide 47: Effects of digit sucking :- Maxilla : Proclination of maxillary incisors Increased arch length Increased anterior placement of apical base of maxilla with / without midline diastema Increased SNA angle Increased clinical crown length of upper incisors Increased counter clockwise rotation of occlusal plane Decreased width of palate Atypical root resorption of primary central incisors Trauma to anteriors due to their prominence

Slide 48: Mandible: Proclination of mandibular incisors Increased mandibular intermolar width Mandible more distally placed than maxilla Mandibular incisors experience a lingual and apical force Interarch relationship: Decreased interincisal angle Increased overjet & decreased overbite Posterior crossbite & anterior openbite Narrow nasal floor & high palatal vault Uni / bilateral class II occlusion Other effects: Affect psychological health Risk of malpositioning of teeth &jaw lisping

Slide 49: Digit sucking is not directly involved with production of malocclusion Freudian belief holds that an abrupt interference with such a basic mechanism is likely to lead a substitution of such antisocial tendencies. Cook measured the forces of thumb sucking & found 3 distinctly different pattern of force application during sucking utilizing force sufficiently strong to displace the teeth & deform the growing bone. Melson found digit sucking & pacifiers to increase the tendency towards abnormal swallowing.

Slide 50: MUSCLE FACTOR :- Teeth erupt in an environment of functional activity governed by the muscle of mastication, tongue, face. The muscles of tongue, lip, cheeks are important in guiding teeth into their final position, variation in muscle for and function affect the position and occlusion of the teeth. All muscle exert their influence by virtue of their origin and insertion. The muscles have their main origin on basal part of the jaw, so position of jaw affect position and action of muscles which functions on the teeth.

Slide 51: 3. LIPS : 1. Vertical form of the lip: determine the amount of lip pressure on teeth -ideal lip form -lip competency 2. Sagittal form of the lip: determine the position of lip pressure on teeth It is equally possible for the lip activity to produce class II / class III relationships by altering the inclination of the incisor teeth during eruption or to produce class I occlusion on class II / class III skeletal relationship if the skeletal discrepancy is not severe.

Slide 52: Function of the lips:- Modify erupting tooth position Govern the position of incisor teeth Lower lips lead to retroclination of incisors in normal function of swallow, speech, smiling activities The ultimate position of teeth before and after the orthodontic treatment is very much dependent on the lips

Slide 53: In finger sucking the muscle activity accentuates the deformity. Increase in overjet leads to lip incompetence & difficulty in creating negative pressure for normal swallow. Lower lip drops behind the upper incisors & thrust against it with abnormal mentalis muscle activity to affect the closure. Upper lip remains hypotonic, functionless, retracted, and short called as incompetent resting lip posture . To create an anterior lip seal orbicularis oris mentalis muscle complex contracts. Thus the tongue thrust forward to aids in lower lip closing during swallowing Upper lip no longer serve as an effective restraining force, the lower lip teaming with tongue exert a powerful upward & forward vector of force against premaxilla thus enhancing the severity of malocclusion.

Slide 54: This leads to protrusion of maxillary incisors & anterior openbite This cycle repeats during each swallow. Spontaneous drop of finger sucking habit leads to tongue thrust habit. LIP SUCKING: It results due to excessive overjet & difficulty in closing the lips properly during deglutition. It leads to flattening & crowding of lower anteriors with retraction while maxillary incisors forced up & forward. Vermillion border hypotonic & red with flaccid lip & accentuated mentolabial sulcus.

Slide 55: 4. TONGUE In conjugation with lips and cheeks it is the other major guiding force for the erupting teeth. The muscles of the tongue are attached to the inner aspect of the mandible, hyoid bone, palate, styloid process and affect the teeth by virtue of size, resting posture and function. Resting position of the tongue:- is completely with in the dental arches filling the space enclosed by teeth, some times it takes up the adaptive postural position protruded between the teeth to touch the lower lip in order to seal the front of the mouth The essential features of normal swallowing are: Closure of the lips Teeth in light occlusal contact Tongue elevated to the palate Momentary clenching of teeth as food passes into the pharynx

Slide 56: Adaptive swallowing involves tongue between teeth carried out with buccal teeth apart or together. Tooth apart adaptive swallow : tongue positioned between the teeth so does not fill the upper arch both muscle & air pressure in upper arch reduced narrowing of arch & buccal cross bite full vertical development of anterior dento alveolar segment prevented by tongue incomplete overbite. Tooth together adaptive swallow : involves forward positioning of teeth between incisors during swallowing anterior open bite.s

Slide 57: Tongue thrust is a retention of infantile suckling swallow, with eruption of deciduous the tongue does not drops back & continue to thrust Etiology of tongue thrust is : genetically inherent Learned behavior due to improper bottle feeding, tenderness of gums, tonsilitis, upper respiratory tract infection Macroglossia Malocclusion caused by tongue thrust are: Openbite (anterior / posterior) Proclination of upper anterior segment with spacing in canines & incisors. Posterior cross bite due to narrow & constricted maxillary arch.

Slide 58: Mechanism of action of malocclusion caused by tongue: Tongue thrust forward continuously increase in overjet and overbite peripheral position no longer lie on the lingual cusps of buccal segment posterior teeth erupt and gradually eliminate the inter occlusal clearance the postural resting vertical dimension and occlusal vertical dimension becomes the same with posterior teeth in contact all the time leads to bruxism, bilateral narrowing of maxillary arch, as the tongue drops down lower in the mouth providing less support to the maxillary arch cross bites

Slide 59: MOUTH BREATHING: Caused in nasal passage obstruction / inadequacy. Nasal obstruction: Enlarged turbinates : infection leads to hypertrophy of the mucosa causing obstruction Adenoid hypertrophy : blocks the posterior nares leads to mouth breathing. In enlarged tonsils soft palate rest on their upper poles instead of dorsum of tongue thus displace tongue downward & forward causing an open bite posture. Intranasl defect deviate the septum

Slide 60: Altered respiratory pattern mouth breathing alter the posture of head, jaw, tongue alter the equilibrium of pressure of jaw teeth and growth lowers the mandible & tongue extends the face thus face height increases posterior teeth supra erupt mandible rotate down and back increase in overjet and anterior open bite narrow the maxillary arch adenoid face appearance incompetent lips short upper lip proclination and spacing in upper anterior teeth lower lip heavy and everted mandible in distal rotation to maxilla lower anteriors elongate and touch the palatal tissue.

LOCAL FACTOR: LOCAL FACTOR

ANOMALIES IN NUMBER OF TOOTH:: ANOMALIES IN NUMBER OF TOOTH: Heredity plays a strong part & some believe extra tooth as a left over from the primitives. High frequency of extra / missing tooth is associated with congenital deformity e.g. clefts. General pathosis also affect the number of teeth. SUPERNUMERARY TOOTH : they vary in size, shape and location There is no definite time for its development may form prior to birth / as late as at 10 12 years called as third set of teeth Commonly seen in maxilla in between central incisor Many a time they are well formed & so become difficult to identify called as supplementary teeth in premolar region of near lateral incisor

Slide 63: Frequency seen is the mesiodens in midline palatal to maxillary incisors, conical in shape with short root & crown, occasionally fused with right / left central incisors Unerupted becomes generally cystic Some remain out of occlusion so have no deleterious effects & must be left alone. EFFECTS: Lead to deflection / noneruption of permanent central incisor or if they erupt it is in malposed Permanent teeth fail to erupt due to presence of supernumerary teeth, congenital absence, any mucosal barrier Delay the eruption of adjacent teeth Increase the arch perimeter (increase the overjet in maxillary arch & decrease the overjet in mandibular arch ) Crowding in dental arch

Slide 64: MISSING TEETH: Called as partial anodontia / hypodontia Congenitally missing more commonly found than supernumerary. Order of frequently missing tooth Maxillary & mandibular III molars Maxillary lateral incisors Mandibular II premolar Mandibular incisors Maxillary II premolar In congenitally missing tooth size tooth shape deformity is quite frequent Congenitally missing are many a times bilateral e.g. mandibular II premolar Partial / complete anodontia is rare.

Slide 65: Heredity plays a significant role Congenital absence seen commonly in permanent than deciduous When permanent missing roots of deciduous do not sorb In missing maxillary lateral incisor, permanent canine erupt mesial to deciduous canine in space of missing teeth. Teeth are even lost in accidents EFFECTS: Spacing Aberrant swallowing pattern Abnormal tilting & axial inclination The location of adjacent teeth Absence of permanent lead to over retained deciduous teethssssss

ANOMALIES IN TOOTH SISE:: ANOMALIES IN TOOTH SISE: In order to have normal occlusion there must be harmony in tooth size & arch length Called as micro / macrodontia. True microdontia is rarely seen. Largely determined by heredity Microdontia seen with pitutary drawfism while macrodontia with gygantism Greatly vary from individual to individual also within same individual Crowding is major characteristic The width is greater in male than in female, mainly seen in permanent than in deciduous Canine show greater difference than lateral incisors e.g. peg laterals Frequently seen in mandibular premolar region

Slide 67: Developmental aberration are anomalous in shape / fused with neighboring tooth Increase in tooth size lead to crowding decrease in tooth size leads to spacing.

ANOMALIES IN TOOTH SHAPE:: ANOMALIES IN TOOTH SHAPE: Most commonly seen is the peg lateral, small size leads to spacing in anterior segment. Laterals also deform in the congenital clefts Japanese show pronounced cingulum, sharp marginal ridges, well defined boundary to lingual fossa, this all together force the involved tooth labially & prevent normal overbite & overjet Mandibular II premolar show maximum variation with extra lingual cusp thus increasing mesiodistal dimension which reduces the space that the loss of II deciduous teeth provide. Other anomalies are gemination, fusion, concresence, talon cusp, dilaceration, amelogenesis imperfecta, hypoplasia, dens in dente, odontomas, mulberry molars, hutchinsons inciors.

ABNORMAL LABIAL FRENUM: ABNORMAL LABIAL FRENUM labial frenum & midline diastema is a topic of controversy due to incomplete understanding of role of heredity, tooth size, local habits, process of growth & development Spacing in maxillary centrals & thick frenum is a chicken or egg controversy. In the past frenum was needlessly clipped. thus in lack of recognization of habit problems, tooth size discrepancy, congenitally missing teeth, midline supernumerary tooth, clipping of frenum did a little job. Now what exactly is normal? Faustin Waber noted some etiological factors like: Microdontia, macrognathia, supernumerary tooth, peg laterals, missing laterals, heavy occlusal force against the lingual surface of the maxillary incisors, habits, midline cyst.

Slide 70: According to Taylor interincisal spacing close without any interference Existence of heavy fibrous frenum dose mot always mean spacing, during ortho treatment frenum get atrophy. Frenum migrates superiorly enough at the age of 10 12 years Heredity plays an important role. Age Incedence of daistema 6 97% 6 7 88% 10 11 48 % 12 18 7 %

PREMATURE LOSS OF PRIMARY TOOTH: PREMATURE LOSS OF PRIMARY TOOTH The primary are considered as space saver for permanent. If primary tooth lost before crown formation completion & root formation begin of permanent, bone reform atop it thus delay the eruption adjacent teeth drift in space. Caries play an important role in decreasing the arch length by decreasing the mesiodistal dimension. Rate of loss of space is related to extraction age in maxilla but not in mandible e.g. loss of first primary molars in maxilla block out permanent cuspids while loss of maxillary II primary molar tends to impact the II premolar. Molar & canine occlusal relationship is significantly affected by premature loss of primary molars in either arches

Slide 72: Loss of PRIMARY INCISORS is of less concern but its loss before permanent erupt drifting of most distal teeth malocclusion. Loss of PRIMARY CUSPIDS matter of great concern as permanent canine erupt late in maxilla & if lost before permanent central & lateral erupt permanent spacing seen in anterior segment with labioversion of canine erupting due to no space. In mandible early loss lingual tipping of anteriors with abnormal mentalis muscle activity. Loss of FIRST PRIMARY MOLAR permanent canine & I permanent molar move mesially I premolar not displaced as it is narrow mesiodistally. In mandible II primary molar shift forward at the time permanent molar is erupting

Slide 73: Loss of SECOND PRIAMRY MOLAR first permanent molar drift forward & rotates mesiolingually II premolar, canine shift distally as it is wider mesiodistally the space get occupied with permanent canines incisors alter midline canine erupt with no space to occupy. In mandible II premolar is last to erupt block out the teeth loss of tooth substance is more important than the whole teeth as it establish occlusal relationship & in maintenance of arch perimeter Loss of ONE OR MORE PRIMARY TOOTH drifting with loss of posterior support when mandible held in position to provide some sort of adaptive occlusal function result in crossbite affects TMJ, musculature, growth of facial bone, final position of permanent teeth Loss of PERMANENT TOOTH upset physiological functioning break mesiodistal contact shift

Slide 74: According to Dewey after loss of primary molars the drifting of permanent molar the factors related were 1. Leeway space more drift occurred in arches with less leeway space. 2. Cusp height high cusp height prevent drifting 3. Age when the primary teeth were lost great loss occur when primary molars lost before eruption of the permanent Abnormal order lead to shift & loss of space This will shorten the arch length, crowding, tip the contagious teeth, over erupt the opposing teeth, cause further periodontal problem Periapical pathology of primary teeth hasten the eruption of successors due to loss of bone & increased vascularity

PROLONGED RETENTION & ABNORMAL ERUPTION OF DECIDUOUS TEETH: PROLONGED RETENTION & ABNORMAL ERUPTION OF DECIDUOUS TEETH ETIOLOGY : Absence of underlying permanent successor Hypothyroidism Ankylosed deciduous tooth that fail to resorb Non vital deciduous EFFECTS: Deflection in path of eruption Cross bite due to palatal eruption Impaction of permanent as its last tooth to erupt, space occupied by deciduous canine is less, premolar migrate mesially leaving limited space for canine, longest path of eruption its the only tooth to erupt after root completion. Prolong retention lead to break in contact, rotations

Slide 76: Any mechanical interference deflect an erupting permanent tooth If the roots of deciduous not resorbed , permanent successor withheld from eruption & defect into malocclusion Some children are precocious & loss teeth early while other very slow, both the patterns are normal Gonadotropis hormone accelerates the dental development Early maturation lead to crowding Medicines like cortisone, steroids, metabolic, climatic, endocrinal balance alter the pattern. Many a times fragments of root remain n alveolar process that do not resorb but deflect the permanent tooth.

DELAYED ERUPTION OF PERMANENT TOOTH: DELAYED ERUPTION OF PERMANENT TOOTH heredity plays an important role Hpothyroidism leads to absence of permanent, presence of supernumerary, deciduous root pieces road blockers, mucosal barrier, eruption force not vigorous, bony crypt, premature loss of deciduous, early loss of deciduous lead to flaring & spacing which decrease the space available for the permanent Odontomas, cyst, fibroma, tumor delay or malpose the teeth Ankylosed deciduous teeth Congenitally missing succedenous teeth

ANKYLOSIS: ANKYLOSIS Called as partial anodontia, with union of roots and bone, occur at the age of 10 12 years Due to injury to periodontal membrane, or if it get perforated, any bony bridge forms joining lamina dura & cementum. Occur at buccal or lingual aspect. If left can cover the mucosa deflect / block the tooth. Accidents, trauma, endocrinal conditions, congenital diseases, cleidocranial dysostosis , certain infections, in case of apisectomy.

ABNORMAL ERUPTIVE PATHWAY: ABNORMAL ERUPTIVE PATHWAY Each tooth travel a distinct path till it erupts. But it can deviate due to Tooth bud displaced from its ideal location Presence of supernumerary odomtomas, cyst, tumors Unresorbed / retained deciduous tooth or root fragment True arch length discrepancy or excess tooth material Heredity cause crowding due to less space. A blow, mechanical interference by ortho treatment, early class II treatment restrict the maxilla posteriorly so II molar erupt into crossbite or impacted. Ectopic eruption mainly due to arch length deficiency e.g. maxillary II deciduous molar Most commonly maxillary canine is in abnormal position.

DENTAL CARIES:: DENTAL CARIES: Premature loss of deciduous or permanent drifting of adjacent teeth abnormal axial inclination over eruption bone loss loss of arch length crowding tilting of teeth, supra eruption. IMPROPER DENTAL RESTORATION: Improper proximal restoration gingival inflammation, loss of periodontal membrane attachment, mobility in tooth Tight contacts lead to elongation of teeth, tilting. Cross bite occur due to poorly placed restorations Mechanical separation, large restorations, unnecessarily increases the arch length Under contoured proximal restoration decreases arch length while over contoured occupy the space left out by deciduous Premature contact functional shift of mandible

BRUXISM / CLENCHING:: BRUXISM / CLENCHING: It was described by Marie in 1907 . Called as psychogenic or idiopathic functional aberration Contraction of masticatory muscle, rhythmic side to side grinding, gnashing of teeth during sleep cause malocclusion EFFECTS Deep bite Malposed dental unit, Tooth mobility Non functional pattern of occlusal wear Pulp exposure Fracture of crown & root Muscular facial pain, tired ness, hypertrophy, incordination Locking of jaw, deviation TMJ pain and dysfunction

Slide 82:

ETIOLOGY: GENERAL Psychogenic Environmental, heredity Nervous tension High strung person, excited children, athletes Nutritional deficiency, hyperthyroidism, Infections, GIT disturbances, enzymatic imbalance, Pubertal growth spurt Nocturnal : due to increased negative pressure in tympanic cavity from allergic edema of Eustachian tube mucosa LOCAL Faulty restoration Traumatic occlusal relationship Functionally incorrect occlusion Cyst , faulty eruption of teeth Bruxism cause malocclusion or malocclusion cause bruxism is a chicken or egg controversy

CLASSIFICATION OF ETIOLOGY OF MALOCCLUSION: CLASSIFICATION OF ETIOLOGY OF MALOCCLUSION The proposed classifications are:- 1. Bennets classification 2. The Graber's classification. 3. The Moyer's classification 4. The White & Gardeners classification 5. The Salzmann's classification 6. The McCoy and Shepards classification. 7. The Strangs classif ication 8. Some other classification.

BENNETSS CLASIFICATION: BENNETSS CLASIFICATION Sir Normal Bennet introduced a classification of abnormality of occlusion based on their etiology; Class I : abnormal position of one or more teeth due to local causes. Class II: abnormal formation of a part of whole or either arch due to developmental defects of bone. Class III : abnormal relationship between upper and lower arches, between either arch or facial contour and correlated abnormal formation of the arch.

Graber's Classification: Graber's Classification General -Heredity -Congenital -Environmental Prenatal Postnatal -Predisposing metabolic climate & disease Endocrine imbalance Metabolic disturbances Infectious disease -Dietary problems -Abnormal pressure habits & functional -Posture -Trauma &accident. Local -Anomalies of no. Supernumerary teeth Missing teeth -Anomalies of tooth size. Anomalies of tooth shape -Abnormal labial frenum: mucosal barriers -Premature loss of deciduous teeth -Prolonged retention -Delayed eruption of permanent teeth -Abnormal eruptive path Ankylosis -Dental caries -Improper dental restorations

Slide 86: General factors will always be present producing ideal occlusion or same occlusal variation & usually the major factors are interrelated. The muscles are attached to the jaws & variation in jaw position produces variation in muscle action. Variation in muscle activity alter the relevance of variation in the size of dentition. The local factors are present in isolation or in combination or may superimpose on the adverse effect of one or more of the general factor adding further complication to the occlusion of the teeth. Final form of occlusion & position of teeth exhibit a wide range of variation.

Slide 87: Moyers Classification (1972) :- (causes and clinical entity) 1. Hereditary : a) neuromuscular system b) bone c) teeth d) soft part (other than nerve And muscle) 2. Developmental defects of unknown origin 3. Trauma : a) prenatal / birth injuries- hypoplasia of mandible, position of fetus b) postnatal fracture of jaw, teeth, habits 4. Physical agents: a) premature extraction of primary teeth b) nature of food 5. Habits 6. Diseases :- a) systemic b) endocrinal c) local 7. malnutrition

WHITE AND GARDINERS CLASSIFICATION: WHITE AND GARDINERS CLASSIFICATION A. Dental base abnormality: -AP malrelations Vertical / lateral malrelations Disproportion of size between teeth and basal bone Congenital abnormalities B. Pre eruption abnormalities: -Abnormality in position of developing tooth germ Missing teeth Supernumerary teeth or teeth with abnormal form Prolonged retention of deciduous teeth Large labial frenum Traumatic injury C. Post eruptive abnormalities: - premature loss of deciduous Extraction of permanent Active muscle force Resting position of musculature Suckling habits Abnormalities in path of closure

Slide 89: Salzmanns diagrammatic representation:- ETIOLOGICAL FACTOR OF MALOCCLUSION PRENATAL AND POSTNATAL GENETIC ENVIRONMENTAL DEVELOPMENTAL CONGENITAL FUNCTIONAL DIFFRENTIATIVE DIFFRENTIATIVE

Slide 90: Genetic - transmitted by gene may / may not be present since birth. Differentiative - engrafted on the body during the pre functional embryonic developmental stage. May affect the whole body / only teeth & jaw. Congenita l- may be hereditary / acquired, present since birth Environmental- General : diseases / radiation Local : eruption anomalies premature loss/ prolonged retention of deciduous loss of permanent tooth periodontal diseases & trauma, infections harmful dentofacial pressure habits, TMJ disturbances

Slide 91: Developmental: General- abnormality in relative growth rate in dentofacial region hypo / hyper tonicity of muscles childhood diseases, nutritional, endocrine & metabolic disturbances radiation /radiotherapy to mother or fetus Local- birth injuries macro or micrognathia micro or macro glossia abnormal labial frenum facial hemi atrophy anomaly of tooth development & eruption

Slide 92: Functional : General: hypo / hyper tonicity of muscles neutrotropic disturbances postual defects of tongue and jaw masticatory disturbances Local : premature loss/ prolonged retention of deciduous loss of proximal contacts periodontal diseases & trauma, infections harmful dentofacial pressure habits, TMJ disturbances

Slide 93: According to McCoy & Shepard (1956) - Indirect / predisposing causes:- hereditary congenital defect prenatal abnormalities acute or chronic infections deficiency disease metabolic and endocrinal disturbances - Direct / determining causes :- missing tooth supernumerary tooth transposed teeth malformed teeth abnormal labial frenum

Slide 94: intrauterine pressure sleeping habit posture / pressure abnormal muscular habit malfunctioning muscles premature shedding of deciduous teeth tardy eruption of permanent teeth prolonged retention of deciduous teeth improper dental restoration loss of permanent teeth

STRANGS CLASSIFICATION: STRANGS CLASSIFICATION Heredity Prenatal influence bearing upon malocclusion. 1. Condition of the mother a. Faulty diet. b. Diseases of serious character. c. Traumatism 2. Conditions in Embryo a. Faulty position in utero producing localized Pressure & tissue displacement. b. Injury during development. c. Hare lip & Cleft lip. d. Injury at time of delivery.

Slide 96: Postnatal causes of malocclusion. Intrinsic Premature loss of deciduous The loss of permanent teeth. Prolonged retention of the deciduous teeth. Missing &supernumerary teeth Environmental. Systemic.

Slide 97: One classification refers to:- - Inherited or congenital:- inherited from parents, problems of tooth number and size, congenital deformities, condition affecting the mother during pregnancy, fetal environment. - Acquired :- premature loss and prolonged retention of deciduous teeth, habit abnormal function diet trauma metabolic and endocrinal disturbances

TO SUMMARIZE THE ETIOLOGY OF SOME COMMON MALOCCLUSIONS: TO SUMMARIZE THE ETIOLOGY OF SOME COMMON MALOCCLUSIONS

ETIOLOGY OF CROWDING: ETIOLOGY OF CROWDING Disproportion in arch size and tooth size or arch length discrepancy. Prolonged retention of deciduous teeth. Altered path of eruption. Premature loss of deciduous teeth. Delayed eruption of permanent teeth. Presence of supernumerary teeth. Trauma Localized abnormal size and shape of the teeth e.g. fusion Late horizontal growth of mandible Mesial migration of buccal segment

CAUSES OF SPACING: CAUSES OF SPACING GENERALISED: relative microdotia oligodontia / partial anadontia Large tongue Suckling habits LOCALISED: Missing tooth Undue retention of primary teeth Deleterious sucking habit Premature loss of permanent teeth Localized soft tissue abnormalities

CAUSES OF MIDLINE DIASTEMA: CAUSES OF MIDLINE DIASTEMA - macrognathia - microdontia - Hereditary - racial predisposition - Mild gen. spacing - ugly-duckling stage - Deciduous teeth - congenitally missing Supernumerary teeth - peg laterals - Extraction - ectopic eruption - Midline cystic lesions - RME - Increased over jet - finger sucking - Thumb sucking - tongue thrusting - Abnormal labial frenum - retained deciduous - Palatally erupted lateral incisors - trauma, fibromas - Impacted tooth in midline

CAUSES OF ANTERIOR CROSS BITE: CAUSES OF ANTERIOR CROSS BITE Trauma Arch length discrepancy Retained deciduous teeth Failure of resorption of roots of deciduous upper anteriors. Occlusal prematurities Loss of upper deciduous molars Asymmetric growth of maxilla and mandible

CAUSES OF POSTERIOR CROS BITE: CAUSES OF POSTERIOR CROS BITE Arch length discrepancy Retained deciduous teeth Thumb sucking nasal obstruction Mouth breathing Narrow maxilla.

CAUSES OF ANTERIOR OPEN BITE: CAUSES OF ANTERIOR OPEN BITE Occur during normal closure of development of dentition Disturbances in eruption of teeth and alveolar process (Ankylosis) Mechanical interference with eruption and alveolar growth (finger / thumb sucking / lip sucking habit) Gross osseous dysplasia (micrognathia, mandibular hypertrophy) Soft tissue factor (tongue thrust) Dental factor (failure of alveolar development) Skeletal factor (increased lower facial height, decreased ramal height, increased maxillo mandibular lane angle)

POSTERIOR OPEN BITE: POSTERIOR OPEN BITE lateral tongue thrust ankylosed primary teeth faulty orthodontic treatment primary failure of eruption

CAUSES OF DEEP BITE: CAUSES OF DEEP BITE 1. Skeletal factor: Decreased lower facial height Increased ramal height Low maxillo mandibular plane angle 2. Dental factor: Increased interincisal angle Supra eruption of anterior teeth Under eruption of posteriors 3. Soft tissue factor: Lateral spreading and low tongue posture interferes with nsormal eruption of the posterior teeth High lip line

ETIOLOGY OF MALOCCLUSION: ETIOLOGY OF MALOCCLUSION 1. Class II Div 1: Hereditary Habits 2. Class II Div 2: Low tongue posture High lip line 3. Class III: True class III hereditery Pseudo class III occlusal prematurities early loss of upper deciduous teeth

BIMAXILLARY PROTRUSION: BIMAXILLARY PROTRUSION its a skeletal problem in which both maxilla and mandible have a relationship more forward than normal with respect to cranial base, with large SNA and SNB angle . In true bimaxillary protrusion axial inclination of teeth are normal. While in bimaxillary dental protrusion there is procumbancy of both upper and lower teeth on the basal bone. It is genetically predetermined. Arise from mesial drifting of teeth in both the arches. Commonly seen in negroids, Keralites.

UNFAVORABLE SEQUELAE OF MALOCCLUSION: UNFAVORABLE SEQUELAE OF MALOCCLUSION Depending upon the severity of malocclusion and psychological frame of the patients mind the sequelae can range from mild malocclusion to severe psychological problems: Poor appearance of the patient Predisposition to periodontal disease, dental caries trauma Abnormal muscle function Abnormal oral function resulting from malocclusion Interference to normal growth and development TMJ problems Impacted / unerupted teeth