Heredity
- Neuromuscular system
- Bone
- Teeth
- Soft parts (other than nerve and muscle)
Developmental defects of unknown origin
Trauma
- Prenatal trauma and birth injuries
- Postnatal trauma
Physical agents
- Prenatal
- Postnatal
Habits (thumb and finger sucking, tongue sucking, lip biting etc.)
Disease
- Systemic diseases
- Endocrine disorders
- Local diseases
Malnutrition

Salzmann's Pre and Post-natal Etiologic Factors of Malocclusion

Genetic
Congenital
Developmental
Environmental
Functional

Graber's Classification of Etiologic Factors

easiest method of classifying etiology of malocclusion

General Factors

those factors that operates on the dentition from without

Heredity
Congenital
Environment
- Prenatal
- Postnatal
Predisposing metabolic climate and disease
- Endocrine imbalance
- Metabolic disturbance
- Infectious disease
Dietary problems
Abnormal pressure habits and functional aberrations
- Abnormal suckling
- Thumb and finger sucking
- Tongue thrust and tongue sucking
- Lip and nail biting
- Abnormal swallowing habits
- Speech defects
- Respiratory abnormalities
  - Tonsils and adenoids
- Psychogenic tics and bruxism
- Posture
Trauma and accidents

Local Factors

those factors that are immediately associated with the dentition

Anomalies
- Supernumerary
- Missing Teeth
Anomalies of tooth size
Anomalies of tooth shape
Abnormal labial frenum
Premature loss
Prolonged retention
Delayed eruption of permanent teeth
Abnormal eruptive path
Ankylosis
Dental caries
Improper dental restoration

General Factors Explained

1. Heredity

Certain racial and familial characteristics tend to recur.
May inherit tooth size from one parent and jaw size from the other parent.
Two recessive traits may combine to become a dominant characteristic, or a dominant trait may be offset by the other parent's trait and disappear.
Hereditary Racial influence
- Dental characteristics show racial influence.
- Philippines: Malocclusion is almost nonexistent.
- Mixture with other racial strains caused jaw size discrepancies and occlusal disharmonies.
Hereditary facial type
- Three general types:
  - Brachycephalic - broad round heads
  - Dolicocephalic - long narrow heads
  - Mesocephalic - shape in between the first two
Hereditary Influence on the Growth and Developmental Pattern
- Morphogenetic pattern has a strong hereditary component.
- Example: A child is slow in losing deciduous teeth and erupting permanent teeth, similar to their mother and siblings.

Heredity and Specific Dentofacial Morphologic Characteristics

Heredity has a role in the accomplishment of specific dentofacial attributes.
Affected by heredity:
- Tooth size
- Arch length and width
- Height of the palatal vault
- Crowding or spacing
- Overbite and overjet
- Position and configuration of muscles
- Tongue size and shape
- Character of the oral mucosa

2. Congenital Defects

A. Cleft Lip and Palate

1/3 to 1/4 of all cases have a familial history of this deformity.
Lateral incisors may be missing, atypical in shape, or "twinned."
In the area of the cleft, teeth are frequently jumbled.
In a unilateral cleft, the teeth on one side of the cleft are usually in lingual crossbite with the opposing lower teeth.
Cleft Lip
- A tightly repaired lip can force the premaxilla structure lingually.
Cleft Palate
- Correction of lingual crossbite should include not only the teeth but also correction of the whole medially displaced basal bone structure.

B. Cerebral Palsy (CP)

A paralysis or lack of muscular coordination attributed to intracranial lesion.
Tissues are quite normal, but because of lack of motor control, the patient does not know how to use them properly.
Problems with swallowing, difficulty eating, difficulty speaking, exaggerated reflexes (spasticity), stiff muscles, rigidity, lack of coordination, slow movements.
Intellectual disabilities, psychiatric conditions, seizures, difficulty with vision and hearing, variations in muscle tone, urinary incontinence, abnormal touch or pain perceptions, difficulty walking, scissors-like gait.
Abnormal mastication, deglutition, respiration, and speech are necessary for the maintenance of normal occlusion.

C. Torticollis

"Wry neck" - abnormal muscle forces.

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Foreshortening of sternocleidomastoid muscle can cause changes to bony morphology of cranium and face.
If this problem is not treated early, malocclusion will be uncorrectable.
Preoperative torticollis: facial asymmetry.
Postoperative torticollis: improved mandibular posture.

D. Cleidocranial Dysostosis

Unilateral or bilateral, partial or complete absence of clavicle in conjunction with delayed cranial suture closure, maxillary retrusion, and possible mandibular protrusion.
Retarded eruption of permanent teeth.
Retained deciduous teeth.
Supernumerary teeth.

E. Congenital Syphilis

A pregnant mother who has syphilis can spread the disease through the placenta to the unborn infant.
Abnormally shaped teeth and malposed teeth.
Hutchinson teeth.

3. Environment

A. Prenatal Influence

Abnormal fetal posture and maternal fibroids can cause facial asymmetries with temporary deformity.
German measles and drug-induced deformities (thalidomide) cause gross congenital deformities, including malocclusion.

B. Postnatal Influence

Delivery induced deformation of the upper jaw.
Obstetricians frequently insert forefinger and middle finger into baby's mouth to ease passage through birth canal, which can result in deformation.
Extensive scar tissue from burn may produce malocclusion.
Accidents like falls produce condylar fracture followed by facial asymmetry.
Mandibular fractures.
Wearing a plaster neck cast for four months due to fractured cervical vertebra has caused maxillary incisors labially and mandibular incisors to fit deep into palatal mucosa.

4. Predisposing Metabolic Climate and Disease

Diseases with paralytic effect are capable of producing malocclusion.
- Muscular dystrophy: a hereditary condition marked by progressive weakening and wasting of the muscles.
- Cerebral palsy.
- Poliomyelitis.
Poliomyelitis or polio is a highly infectious disease caused by the poliovirus.
- The virus is transmitted through contaminated food and water and multiplies in the intestine, from where it can invade the nervous system.
- Can cause muscle weakness resulting in an inability to move.
Acute febrile diseases may slow down growth and development.
- May cause disturbance in tooth eruption and shedding that predispose to malocclusion.
- Measles, mumps, chicken pox, dengue, malaria.
Thyroid problems
- Hypothyroidism: abnormal resorption and delayed eruption pattern, retained deciduous teeth, and malposed teeth.
- Teeth are normal in size but are crowded in jaws that are smaller than normal.

5. Dietary Problems

Malnutrition: Vitamin A deficiency, beri beri, rickets, and scurvy can produce severe malocclusions.
- Main problem: upsetting dental developmental timetable.
- Premature loss.
- Prolonged retention.
- Abnormal eruptive paths.
Rickets: Vitamin D deficiency; enamel and dentin defects; hypoplastic (often discolored) enamel, large pulp chambers, short roots.
Scurvy: Vitamin C deficiency, swollen gingivae; gingival friability; periodontal destruction.

6. Abnormal Pressure Habits

A. Abnormal Suckling/Swallowing

Forward mandibular posture.
Tip of the tongue contacts the vermilion border of the upper lip (Class III).
Oral seal is effected by the tongue and upper lip.
Malocclusion is made worse by compensatory malfunction of musculature.
Excessive buccal pressure leads to lingually inclined incisors.

B.1 Finger Sucking Habit (birth to 4 years of age)

Mostly caused by mother not spending enough time nursing her infant.
Babies turn to finger and thumb sucking habits as a replacement for the needed sensation from breastfeeding.
Breastfed babies have fewer abnormal perioral muscle habits.
Breastfeeding
- Feelings of euphoria.
- Sense of security.
- Feeling of warmth and being wanted.
- Child feels warmth of the breast from the lips extending well away from the mouth.
- Mandible moves up and down rhythmically and forward and backward by flat condylar path as buccinator mechanism alternately contracts and relaxes.
- Reduces bruxism and clenching due to sensory satisfaction during feeding act.
Conventional nipple
- Warmth of breast and mother's body is lacking.
- Physiology of suckling is not duplicated.
- Contacts only the vermilion border of lips.
- Mouth is propped open and lip seal is difficult.
- Abnormal muscle pressure as compensatory response to excessive opening required.
- Presence of air intake with milk.
- Suckling becomes sucking: with enlarged hole at the end of nipple, child does not have to do much.
Nuk Sauger nipple
- Physiologically designed nursing nipple which closely stimulates natural activity of nursing action.
- The entire perioral area can contact the warm nipple base, which adapts to contours of the lips.
- Greatly reduces the need and desire of infant for supplemental thumb sucking exercise.
- Broad adaptive rubber base that can mold to lip contours.
Edwall physiologic pacifier
- Primary exerciser: Designed to stimulate a normal nursing motion and euphoric climate.
- Secondary exerciser: Larger, for children after the 1st year of life; palatal contact stimulates dental arch width growth.
Breaking the child's finger sucking habit during the time that it is normal to expect (1 to 1½ years) is the same as ignoring the basic physiology of infancy.
Attempts to break the habit give the children an "attention-getting mechanism."
No parent should call attention to the habit, regardless of provocation."
Damage to occlusion is confined largely to the anterior segment for the first 3 years of life.
- Reduce overbite.
- Increase overjet.
- Incisor spacing in the maxillary arch.
- Slight crowding and lingual positioning of lower anterior teeth.
Damage is usually temporary, provided the child starts with a normal occlusion with no hereditary malocclusion pattern.

B.2 Finger Sucking Habits (after age four)

Ineffectual badgering attempts of the family to break the habit ensures continuation beyond the time it would have been dropped autonomously by the child.
Permanent deformation of malocclusion is when a child continues the habit beyond 3½ years of age.
Sequence of Events:
- Increase in overjet
- Lower lip cushions to lingual of upper anterior - Upper anterior move farther forward
- Incomplete anterior lip seal during swallowing - Abnormal mentalis function - Flattening of lower anteriors
- Full-fledged MALOCCLUSION
- Compensatory tongue thrust during swallow
- Compensatory muscle activity - Enhancement of malocclusion.
Determinants of malocclusion
- Duration of habit
- Frequency during day and night
- Intensity

C. Tongue Thrust and Tongue Sucking

Activities frequently associated with the finger habit.
A retention of the infantile suckling mechanism.
With continuation of finger habit, mature swallow pattern does not develop on time.
The tongue does not drop back as it should and continues to thrust forward.
Upper lip: functionless, hypotonic, retracted, or short. Condition referred to as "incompetent resting lip posture."
The tongue thrusts forward to aid the lower lip in closing off during the swallowing act.
Lower lip + tongue exert upward and forward force against premaxillary segment enhancing malocclusion.
Increase overjet and overbite.
Posterior teeth supraerupt and eliminate interocclusal clearance.
VDR (Vertical dimension at rest) and VDO (Vertical dimension of occlusion) become the same with posterior teeth in contact at all times.
Side effect of bruxism.
Narrowing of maxillary arch as the tongue drops lower in the mouth.

D. Lip and Nail Biting

Biting on the lower lip or merely sucking it gives a child the same sensory satisfaction obtained from finger sucking.
Dropping the finger habit for the new, more convenient but unfortunately more powerful lip habit.

E. Abnormal Swallowing Habits

Improper deglutition.

F. Speech Defects

G. Respiratory Abnormalities

Mouth breathing.

Local Factors Explained

1. Anomalies

A. Supernumerary Teeth

Should be left alone if they are completely out of line of occlusion.
Of major concern to the dentist is the frequency of deflection or non-eruption of permanent teeth.
Mesiodens: occurs near the midline, palatal to maxillary incisors; usually conical in shape; may erupt toward the floor of the nose.

B. Missing Teeth

More frequent than supernumerary teeth.
Order of frequency of absence:
1. Third molars
2. Maxillary lateral incisors
3. Mandibular second premolars
4. Mandibular incisors
5. Maxillary second premolars
Missing teeth are usually bilateral, more frequent in permanent teeth.
Roots of deciduous teeth may not resorb and they should be maintained unless it is creating irregularities in the dental arch because of its larger mesiodistal dimension.

2. Anomalies of Tooth Size

The size of teeth is largely determined by heredity.
Malocclusion has a greater tendency in large teeth than in smaller teeth.

3. Anomalies of Tooth Shape

Peg lateral: most frequent departure from normal; excessive spacing often occurs in the maxillary anterior segment.
Maxillary central incisors: may be deformed owing to congenital cleft; occasionally cingulum is pronounced with heavy marginal ridges forcing the teeth out labially.
Mandibular second premolars: may have an extra lingual cusp, increasing its mesiodistal dimension.

4. Abnormal Labial Frenum

Can cause midline diastema.
At birth, the frenum is attached to the alveolar ridge with fibers running into the lingual interdental papilla.
As teeth erupt and alveolar bone is deposited, frenum attachment migrates superiorly (10-12 years old) OR fibers persist between central incisors and intermaxillary suture.
a. Blanche Test
- A diagnostic adjunct that helps to determine the role of frenum.
- Lift the upper lip and pull outward and look for blanching of the soft tissues lingual to and between two central incisors.
- The presence of blanch indicates high frenal attachment as a cause of midline diastema.
b. Periapical radiograph
- The presence of notching in the interdental bone is a diagnostic of a thick and fleshy frenum.
Frequently during orthodontic treatment, interposed fibers will atrophy, making frenectomy unnecessary.
Hereditary component is a major factor in persistent diastemas.

5. Premature Loss of Deciduous Teeth

Premature loss of deciduous second molar will very likely lead to mesial drift of first permanent molar and blocking of erupting second premolars.
When a premolar erupts, it is deflected buccally or lingually into a position of malocclusion.
The maxillary molar often rotates with the mesiobuccal cusp moving lingually.

6. Prolonged Retention

If the roots of the deciduous teeth are not resorbed properly, uniformly, or on schedule, the permanent successors may be either withheld from eruption or they may be deflected into malposition.
Fragments of deciduous roots retained in the alveolar process should be removed as they may deflect the permanent tooth in its eruptive path.
Clues to the pattern of shedding and eruption of permanent teeth:
- Eruption time of deciduous teeth
- Loss of deciduous incisor and replacement by permanent
- Hereditary pattern
- Endocrine history
Hypothyroidism: delayed developmental pattern and prolonged retention of deciduous teeth is common.

7. Delayed Eruption of Permanent Teeth

Possible causes:
- Endocrine disorder
- Congenital absence of permanent teeth
- Presence of supernumerary or deciduous root
- Mucosal barrier
- Bony crypts
Mucosal barrier
- Heavy mucosa that deteriorates before the advancing tooth.
- If eruptive force is not vigorous, the mucosa can effectively stop the erupting tooth for a period of time.
- Preventive dentistry: excise the mucosa when a tooth appears ready to "pop" but does not.
- Checking the state of eruption of the same tooth in other segments will help the dentist decide whether to "excise" the mucosa or not.
Bony crypt
- Bone which forms in the line of eruption of the permanent tooth.
- Like the mucosal barrier, it effectively bars the eruption of permanent teeth.
- Preventive dentistry: curette the bony barrier.
- Radiographic examination and checking of timetable in other segments should be made before making a decision to curette.

8. Abnormal Eruptive Path

Secondary manifestation of primary disturbance.
Hereditary pattern of severe crowding.
Presence of supernumerary teeth.
Retained deciduous teeth.
Physical barrier.
Mechanical interference by orthodontic treatment.
Idiopathic.

9. Ankylosis

Due to an injury, as a result of which part of the periodontal ligament is perforated and a bony "bridge" forms, joining the lamina dura and cementum.
"Submerging tooth" - other teeth are erupting, but the ankylosed tooth is not.

10. Dental Caries

Carious lesion should be repaired to maintain the integrity of dental arches.
Unrepaired proximal carious lesions can cause loss of arch length.

11. Improper Dental Restoration

Overextended proximal restorations can alter arch length and create malocclusion.
Too tight contact causes: elongation of either the tooth being restored or adjacent teeth; creates functional prematurities; severely strains canine-lateral contact; breaks the continuity of the arch.
The need for anatomic restoration is not limited to mesiodistal dimension.
- Restoration with poor occlusal anatomic contact: encourages tooth shift and can permit elongation of opposing teeth.
Poorly placed thick restoration on occlusal surface can move a tooth into a crossbite relationship.

Note