etiology of malocclusion
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“ETIOLOGY OF MALOCCLUSION”
Presented by—
Hemam Shankar Singh
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CONTENTS
INTRODUCTION
CLASSIFICATION OF ETIOLOGY OF MALOCCLUSION
GRABER’S CLASSIFICATION
CONCLUSION
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INTRODUCTION
FUNDAMENTAL TO UNDERSTANDING MALOCCLUSION IS THE CONCEPT OF `NORMAL OCCLUSION`.
JOHN HUNTER WAS THE FIRST TO DESCRIBE ABOUT NORMAL OCCLUSION.
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• Etiology of malocclusion is the study of its causes.
• Recognition and elimination of the etiological factors is important so that one can prevent and correct the malocclusion and obtain a permanent result.
• Traditionally, any deviation from "ideal occlusion" has represented what Guilford termed mal-occlusion. of course, ideal occlusion rarely exists in nature and so perhaps it is better to call this concept the "imaginary ideal"
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MALOCCLUSION
“An occlusion in which there is mal-relationship between the arches in any of the planes of space or in which there are anomalies in tooth position beyond the limits of normal”
Sameul S. Flitch was the first to classify malocclusion.
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CLASSIFICATION OF ETIOLOGY OF MALOCCLUSION
1. Moyer’s classification2. White and Gardiner’s classification3. Proffit’s Classification4. Graber’s classification
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CLASSIFICATION OF ETIOLOGY OF MALOCCLUSION
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CLASSIFICATION OF ETIOLOGY OF MALOCCLUSION
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HEREDITY
DEVELOPMENTAL DEFECTS OF UNKNOWN ORIGIN
TRAUMA
PHYSICAL AGENTS
HABITS
DISEASES
MALNUTRITION
MOYER’S CLASSIFICATION
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MOYER’S CLASSIFICATIONET
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HEREDITY
1. NEUROMUSCULAR2. BONE3. TEETH4. SOFT PARTS
TRAUMA
1. PRENATAL TRAUMA AND BIRTH INJURIES
2. POSTNATAL TRAUMA
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MOYER’S CLASSIFICATIONET
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PHYSICAL AGENTS
1. PREMATURE EXTRACTION OF PRIMARY TEETH
2. NATURE OF FOOD
HABITS
1. TUMB SUCKING AND FINGER SUCKING
2. TONGUE THRUSTING3. LIP SUCKING AND LIP BITING4. POSTURE5. NAIL BITING6. OTHER HABITS
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MOYER’S CLASSIFICATIONET
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DISEASES
1. SYSTEMIC DISEASES
2. ENDOCRINE DISEASES3. LOCAL DISEASES
i. NASOPHARYNGEAL DISEASES & DISTURBED RESPIRATORY FUNCTION
ii. GINGIVAL &PERIODONTAL DISEASES
iii. CARIESiv. TUMOURS
MALNUTRITION
DEVELOPMENTAL DEFECTS OF UNKNOWN ORIGIN
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WHITE & GARDINER’S CLASSIFICATION
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WHITE & GARDINER’S
CLASSIFICATION
DENTAL BASE ABNORMALITIES
ANTERO-POSTERIOR MALRELATIONSHIP
VERTICAL MALRELATIONSHIP
LATERAL MALRELATIONSHIP
DISPROPORTION OF SIZE BETWEEN TEETH & BASAL BONE
CONGENITAL ABNORMALITIES
PRE-ERUPTION ABNORMALITIES
ABNORMALITIES IN POSITON OF DEVELOPING TOOTH GERM
MISSING TEETH
SUPERNUMERARY TEETH & TEETH ABNORMAL IN FORM
PROLONGED RETENTION OF DCIDUOUS TEETH
LARGE LABIAL FRENUM
TRAUMATIC INJURY
POST-ERUPTION ABNORMALITIES
MUSCULAR1. ACTIVE MUSCLE FORCE2. REST POSITION OF
MUSCULATURE3. SUCKING HABITS4. ABNORMALITIES IN PATH
OF CLOSURE
PREMATURE LOST OF DECIDUOUS TEETH
EXTRACTION OF PERMANENT TEETH
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PROFFIT’S CLASSIFICATIONET
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PROFFIT’S CLASSIFICATION
Genetic Influences
Environmental
Influences
Specific causes
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SPECIFIC CAUSES-1.Disturbances in embryologic development.2.Skeletal growth disturbances
a.Fetal molding & birth injuries.b.Birth trauma to the mandible.c.Childhood fracture of the jaw.
3.Muscle dysfunction.4.Acromegaly & hemi-mandibular hypertrophy.
5.Disturbances in dental development.a.Congenitally missing teeth.b.Malformed teeth.c.Supernumerary teeth.d.Interference with eruption.e.Ectopic eruption.f.Early loss of primary teeth.g.Traumatic displacement of teeth
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• GENETIC INFLUENCES• ENVIRONMENTAL INFLUENCES Functional influences on Dentofacial development- a. Masticatory function b. Sucking & Other Habits c. Tongue thrusting d. Respiratory pattern
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GRABER’S CLASSIFICATIONET
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GRABER’S CLASSIFICATION
GENERAL FACTORS LOCAL FACTORS
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GRABER’S CLASSIFICATIONET
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GENERAL FACTORS
1. HEREDITY
2. CONGENITAL
3. ENVIRONMENTAL
4. PRE-DISPOSING METABOLIC CLIMATE & DISEASES
5. DIETARY PROBLEMS
6. ABNORMAL PRESSURE HABITS & FUNCTIONAL ABERRATIONS
7. POSTURE
8. TRAUMA AND ACCIDENT
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GENERAL FACTORS
3. ENVIRONMENT
a. PRE NATAL
b. POST NATAL
4. PRE-DISPOSING METABOLIC CLIMATE & DISEASES
a. ENDOCRINE IMBALANCE
b. METABOLIC DISTURBANCES
c. INFECTIOUS DISEASES
1. HEREDITY 2. CONGENITAL
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GENERAL FACTORS
5. DIETARY PROBLEMS
7. POSTURE
8. TRAUMA AND ACCIDENT
6. ABNORMAL PRESSURE HABITS & FUNCTIONAL ABERRATIONS
a. ABNORMAL SUCKING b. THUMB & FINGER SUCKING
c. TONGUE THRUST & TONGUE SUCKING d. LIP & NAIL BITING
e. ABNORMAL SWALLOWING HABITS f. SPEECH DEFECT
g. RESPIRATORY DEFECT h. TONSILS & ADENOIDS
i. PSYCHOGENIC TICS & BRUXISM
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LOCAL FACTORS
1. ANOMALIES OF NUMBER2. ANOMALIES OF TOOTH SIZE
3. ANOMALIES OF TOOTH SHAPE 4. ABNORMAL LABIAL FRENUM: MUCOSAL BARRIERS
5. PREMATURE LOST OF DECIDUOUS TEETH 6. PROLONGED RETENTION OF
DECIDUOUS TEETH7. DELAYED ERUPTION OF PERMANENT
TEETH 8. ABNORMAL ERUPTIVE PATH
9. ANKYLOSED10. DENTAL CARIES
11. IMPROPER DENTAL RESTORATION
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GRABER’S CLASSIFICATION-GENERAL FACTORS
HEREDITY-Heredity has for long been attributed as one of the causes of malocclusion- Another reason attributed for genetically determined malocclusion is the
- Racial, ethical & regional inter-mixture
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HEREDITY
-Number of human traits that are influenced by the genes include (according to Lundstrom):
i. Tooth sizeii. Arch dimensioniii. crowding/spacingiv. Abnormalities of tooth shapev. Abnormalities of tooth numbervi. Overjetvii. Inter-arch variationsviii. Frenum
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HEREDITY
-Genuine Class II malocclusion in three brothers
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CONGENITAL DEFECTS
-They are malformations seen at the time of birth-Its causes can be broadly classify as
1. General congenital factors2. Local congenital factors
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CONGENITAL DEFECTS
-General congenital factorsa. Abnormal state of mother during pregnancyb. Malnutritionc. Endocrinopathiesd. Infectious diseasee. Metabolic and nutritional disturbancesf. Accidents during pregnancy and child birthg. Intra-uterine pressureh. Accidental traumatization of the fetus by external forces
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CONGENITAL DEFECTS
-Local congenital factorsa. Abnormalities of jaw development due to intra-uterine
positionb. Clefts of the face and palatec. Macro and microglossiad. Cleidocranial dysostosis
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CONGENITAL DEFECTS
-The following are some of the congenital conditions frequently encountered by orthodontist
a. Clefts of the lip and palateb. Congenital syphilisc. Maternal rubella infectionsd. Cleidocranial dysostosise. Cerebral palsy
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CONGENITAL DEFECTS
CLEFTS OF THE LIP AND PALATECleft Palate can be defined as a furrow in the
palatal vault or Breach in continuity of palate.
Most commonly seen congenital deformity at the time of birth.
Both dental & skeletal components affectedSuch patients exhibit following
Missing Mobile teeth Rotations Cross bite Impacted teeth Supernumerary teeth, etc.
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CONGENITAL DEFECTS
CONGENITAL SYPHILISThe child exhibits one or more of the
following features: Hutchinson’s incisors Mulbery molars Enamel def Extensive dental decay The maxilla may be smaller
in size relative the mandible Anterior cross bite
MATERNAL RUBELLA INFECTIONSMaternal rubella infections duringpregnancy show some features
• Dental hypoplasia• Retarded eruption of
teeth• Extensive caries
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CONGENITAL DEFECTS
CLEIDODOCRANIAL DYSOSTOSISThis is a congenital condition characterizedby unilateral or bilateral, partial orcomplete absence of the clavicle
The patient may exhibit the following features• Maxillary retrusion & possible Mandibular protrusion• Over retained deciduous teeth & retarded eruption of
permanent teeth• Presence of supernumerary teeth• Presence of short & thin roots
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CONGENITAL DEFECTS CLEIDODOCRANIAL DYSOSTOSIS
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ENVIRONMENT
1. PRE-NATAL FACTORS• Fetus is well protected against injuries & nutritional def during pregnancy• But there are certain factors, presence of which can result in abnormal
growth of oro-facial region thereby predisposing to malocclusion Pressure against rapidly growing areas leads to distortionArm pressed against the face- maxillary deficiencyHead flexed against the chest- Mandibular deficiency.Decreased amniotic fluid- small mandible Cleft palate results due to upward displacement of tongue.Growth catches-up when pressure is released except when cartilage is
affected- Stickler syndromeThalidomide – gross congenital deformities including cleft
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ENVIRONMENT
STICKLER SYNDROME
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ENVIRONMENT
Teratogens affecting dentofacial development
Contemporary Orthodontics: William R Proffit
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ENVIRONMENT
2. POST-NATAL FACTORS Birth injuries
i. Trauma to mandible Most mandibular deformities-due to congenital anomalies-but thought
to be due to birth trauma.
ii. Forceps delivery–TMJ damage.iii. Ankylosis: develop ankylosis of TMJ, may be due to birth injury.iv. A high incidence of cross-bite is seen in a group of children who were born
with forceps delivery.v. An increased asymmetric molar occlusion was observed with traumatic breech
delivery.
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ENVIRONMENTvi. A tendency for abnormal dental arch dimension, larger height of the maxilla
and greater length of the mandibular arch was observed to occur as a result of forceps delivery.
vii. Palatal grooves and cleft formation: A prolonged oro-tracheal intubation of pre term infants is seen to be
associated with airway damage, palatal groove formation, defective primary incisors and an acquired cleft palate.
viii. Delayed eruption of primary teeth: Viscardi (1994) found that first primary teeth eruption at the usual chronologic age in healthy premature infants, but eruption may be delayed in premature infants who require a prolonged mechanical ventilation for neonatal illness/or who experience inadequate nutrition
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PREDISPOSING METABOLIC CLIMATE & DISEASE
Hypopituitarism:DwarfDelayed eruption of permanent teeth and delayed shedding of primary
teeth.Crowding due to smaller arch size.Mandibular growth more affected than maxilla.
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PREDISPOSING METABOLIC CLIMATE & DISEASE
Hyperpituitarism:
Gigantism- large teeth and jaws.Acromegaly- occurs after growth and ossification is complete.Lips thick, tongue enlarged, shows scalloping.Accelerated condylar growth-large mandible.Teeth tipped buccally due to large tongue.
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PREDISPOSING METABOLIC CLIMATE & DISEASE
Hypothyroidism: • Delayed eruption.• Abnormal resorption pattern.• Retained deciduous teeth.• Malposed teeth-deflected from eruption path.• Gingival disturbances.
Hyperthyroidism:• Early shedding and eruption• Atrophy of alveolar bone.
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DIETARY PROBLEMS
NUTRITIONAL DEFICIENCY• Disturbances in the developmental timetable.• Rickets, scurvy and beri-beri can produce severe malocclusions.• Premature loss of teeth/Prolonged retention.• Abnormal eruptive path.• Poor tissue health• Poor absorption-hormonal/enzymatic deficiency.• Decreased fluoride intake-loss of teeth due to caries-malocclusion.
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ABNORMAL PRESSURE HABITS AND FUNCTIONAL ABERRATION
EQUILIBRIUM THEORY• If an object is acted upon by a set of forces but remains in the same
position, then the forces must be in balance.• Dentition is in equilibrium.• Movement occurs when equilibrium is disturbed.
4 PRIMARY FACTORS IN EQUILIBRIUM:
1.Intrinsic forces of tongue and lips.2.Extrinsic forces- habits & orthodontic appliances.3.Forces from dental occlusion.4.Forces from periodontal membrane
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POSTURE
Frequently suggested that poor posture can lead to malocclusion. Stooping with chin on the chest- mandibular retrusion. Child resting head on hand or sleeping on arm or fist- possible
development of malocclusion. May accentuate existing malocclusion. Role as primary etiological factor to be proved conclusively.
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ACCIDENT OR TRAUMA
• Undiscovered traumatic experiences- significant in malocclusion. Eruptive abnormalities. Abnormal resorption. Loss of vitality.
• Both prenatal trauma & postnatal injuries- Dentofacial deformity:
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LOCAL FACTORS
ANOMALIES IN NUMBER OF TEETH:
In order to achieve good occlusion, normal number of teeth should be
present. Presence of extra teeth or absence of one or more teeth
predisposes to malocclusion.
Heredity plays a strong part in anomalies in number of teeth.
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LOCAL FACTORS
SUPERNUMERARY TEETH: Teeth that are extra to the normal complement are termed supernumerary teeth. These teeth have abnormal morphology and do not resemble normal teeth.Extra teeth that resemble normal teeth are called supplemental They result from disturbances during the initiation and proliferation stages of dental development.no definitive time when supernumerary teeth may develop. may form prior to birth or as late as 10- 12 years of age. usually develop from a 3rd tooth bud arising from the dental lamina near the permanent tooth bud teeth.
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LOCAL FACTORS
Supernumerary teeth can cause:
1. Non-eruption of adjacent teeth
2. Delay the eruption of adjacent teeth
3. Deflect the erupting teeth into abnormal locations
4. Crowding in the dental arches.
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LOCAL FACTORS
ANOMALIES OF TOOTH SIZE:
There should be harmony between the tooth size and the arch length, and also between the maxillary and mandibular tooth size, in order to have normal occlusion.
An increase in size of teeth results in crowding while, smaller sized teeth predispose to spacing. Anomalies of size of teeth can be of 2 types: 1.Microdontia 2. Macrodontia
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LOCAL FACTORS
ANOMALIES OF TOOTH SHAPE: Anomalies of tooth size and shape are often interrelated. Abnormally shaped teeth predispose to malocclusion. Anomalies of tooth shape include:1. The presence of peg shaped maxillary lateral incisors is often accompanied
by spacing and migration of teeth.2. Abnormally large cingulum on maxillary incisors- Prevent establishment of normal overbite and Overjet. The involved tooth is usually in labio-version due to the forces of occlusion.3. Additional lingual cusp of mandibular 2nd premolars-Increase the mesio-distal dimension of tooth
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LOCAL FACTORS
4. Fusion- Fused teeth arise through the union of 2 normally separated tooth germs. 5. Gemination- Results from attempt at division of single tooth germ
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LOCAL FACTORS
6. Congenital syphilis – It is often associated with hypoplasia of maxillary and mandibular anteriors. Characteristics of congenital syphilis are “Hutchinson’s incisors” and “mulberry molars”.
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LOCAL FACTORS
7. Dilaceration – Dilacerated tooth often fails to erupt to proper level and can thus interfere with normal occlusion. They may also complicate extraction of teeth and may interfere with tooth movement and alignment.
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LOCAL FACTORS
8. Dens evaginatus –
A developmental condition that appears
clinically as an accessory cusp or a globule of
enamel on the occlusal surface between the
buccal and lingual cusps mainly of premolars.
It may result in incomplete eruption,
displacement of teeth and may interfere with
normal occlusion.
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LOCAL FACTORS
ABNORMAL LABIAL FRENUM: shows spacing between the maxillary central incisors due to presence of the fibrous tissue ,labial frenum.
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LOCAL FACTORS
PREMATURE LOSS OF DECIDUOUS TEETH:Specifically, it refers to the stage of development of the permanent tooth that will succeed the
lost primary tooth. Premature loss can occur due to: 1. Caries 2. Trauma 3. Endocrinal disturbances like hyperthyroidism 4. Metabolic disturbances like hypophosphotasiaWhen a primary tooth is lost before the permanent successor has started to erupt, bone may
reform atop the permanent tooth, delaying its eruption. When its eruption is delayed, more time is available for other teeth to drift into space that would have been occupied by the permanent tooth.
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LOCAL FACTORS
PROLONGED RETENTION OF DECIDUOUS TEETHCan occur because of :-
1. Absence of underlying permanent teeth2. Endocrinal disturbances such as hypothyroidism and hypopituitarism3. Ankylosed deciduous teeth that fail to resorb4. Malposition of erupting permanent teeth
Prolonged retention of deciduous anteriors usually results in lingual or palatal eruption of their permanent successor
Prolonged retention of buccal teeth results in eruption of the permanent teeth either buccally or lingually or may remain impacted within the jaws.
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LOCAL FACTORSDELAYED ERUPTION OF PERMANENT TEETH Probable causes for delayed eruption of permanent teeth :-
1. Early loss of a primary tooth might cause formation of a bony crypt over the succedaneous tooth.
2. Presence of supernumerary tooth can block the eruption of permanent tooth.3. Presence of a heavy mucosal barrier can prevent the permanent tooth from
emerging into the oral cavity.4. Presence of odontomas or other cysts and tumors might prevent the permanent
tooth from erupting.5. Presence of deciduous root fragments that have not resorbed may block the
erupting permanent tooth.6. Presence of ankylosed deciduous teeth may cause delay in eruption of permanent
teeth.7. Congenital absence of permanent teeth
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LOCAL FACTORSABNORMAL ERUPTIVE PATH: This is usually a secondary manifestation of a primary disturbance. Some causes of abnormal eruptive pathway are:1. In cases of arch length deficiency, deflection of the erupting tooth may be merely an
adaptive response to the condition present.2. Presence of supernumerary teeth, retained deciduous teeth, root fragments, bony
barrier or mucosal barrier may result in abnormal eruptive pathway.3. Traumatic displacement of tooth buds–
A deciduous tooth may be driven into the alveolar process, and though it may erupt later, it may displace the developing successor in an abnormal direction.4. 1st and 2nd permanent molars are occasionally impacted; 3rd are frequently impacted by
an abnormal path of eruption.5. Coronal cysts can also cause abnormal eruptive paths.
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GRABER’S CLASSIFICATIONET
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LOCAL FACTORSANKYLOSIS: Ankylosis is encountered relatively frequently during the 6 –12 year age period. It may result due to an injury of some sort as a result of which a part of the periodontal membrane is perforated and a bony “bridge” forms joining the lamina dura and cementum. The “bridge” need not be large to stop the normal eruptive force of a tooth. The most commonly affected tooth is mandibular 2nd deciduous molar. Accidents or trauma, infections, certain congenital disorders like cleidocranial dysostosis predispose to ankylosis of teeth.
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GRABER’S CLASSIFICATIONET
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LOCAL FACTORS
DENTAL CARIES: Caries can lead to premature loss of deciduous or permanent teeth thereby causing migration of contiguous teeth, abnormal axial inclination and supra-eruption of opposing teeth. Proximal caries that has not been restored can cause migration of adjacent teeth into the space leading to a reduction in arch length. A substantial reduction in arch length can be expected if several adjacent teeth involved by proximal caries are left un-restored.
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GRABER’S CLASSIFICATIONET
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LOCAL FACTORSIMPROPER DENTAL RESTORATIONS:Malocclusion can be caused due to improper dental restorations.Undercontoured proximal restorations result in loss of arch length due to drifting of adjacent teeth to occupy the space.Overcontoured proximal restorations might bulge into the space to be occupied by a succedaneous tooth and result in a reduction in this space. Overhang or poor proximal contacts may predispose to periodontal breakdown around these teeth.Premature contacts on an overcontoured occlusal restoration can cause a functional shift of the mandible during jaw closure, whereas, under- contoured occlusal restorations can lead to the supra-eruption of the opposing teeth.
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CONCLUSIONET
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No longer can conscientious orthodontists look at a child’s mouth, observe a space deficiency and then attribute it to the premature loss of teeth or prolonged retention of teeth. In the past, local “causes” were stressed but today we know the importance of general factors in etiology of malocclusion along with the local causes. Knowledge·of the contribution of genetic and environmental causes of malocclusion obligates clinicians to differentiate between patients whose malocclusions are primarily of genetic origin from patients whose malocclusions are primarily of environmental origin.
Abnormal morphologic structures in the face and dentition that have a high degree of heritability require different treatment approaches from those structures that are influenced primarily by environmental factors.
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CONCLUSIONET
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For most patients the differentiation between genetic and local environmental factors is of great importance when choosing the appropriate treatment and retention plans.
Retention of a treated malocclusion is a challenge because the genetic and environmental etiologic factors responsible for the malocclusion may continue to draw the treated teeth back into malocclusion.(AJO 81,82,83,84,85)
Stability of treated malocclusions appears to be similar in growing and adult patients.(AJO 94)
Addressing known etiologic factors during treatment can produce more stable occlusions after treatment.
Prevention of genetic causes for malocclusion is not possible at this time. In contrast, the prevention of environmental causes holds much promise.
63ETIO
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