Etiology of Orthodontic Problems

Malocclusion and dentofacial abnormalities are caused not by

some pathologic process but by moderate distortions of normal
development

Deformity – tissue that initially formed normally and then failes to

continue normal development

Malformation – tissues that did not form normally from the

beginning

Specific Causes of Malocclusion

Disturbances in Embryologic Development

- most defects in embryos are of genetic origin but the effects from the
environment also are important
- Teratogens – chemical and other agents producing embryologic
defects if given at critical time; typically cause specific defects if
present at low levels but if given in higher doses do have lethal effects

- During weeks 3 to 8 after fertilization – from dislike shape to distinctly

human form  characterized by formation of the neural plate
(developing central nervous system), elevation of its lateral margins
to form the neural tube, then its closure (4th week)  accompanied
by ventral and lateral folding (differential growth)  formation of foregut
- lengthening and bending of the heart tube  heart development
- Appearance of primitive oral cavity (stomodeum) and formation of the tissues contributing to the jaws
(maxillary prominence and first arch), nose, ears
 - Fetal alcohol syndrome FAS
– phenotype arises in the
third week of development
and is due to deficiencies of
midline tissue of the
developing brain (neural
plate) and is typically
caused by exposure to very
high maternal ethanol

levels; delay in development

matches the skeletal delay
- many craniofacial defects
are related to neural crest
cell abnormalities, including
cell death and migration
errors. Neural crest cell
migration away from the
cranial neural folds occurs
in the latter part of the third and early part of fourth week

- Neural crest cells make up practically all of the mesenchyme (loose connective tissue) of the face and
differentiate into much of its skeletal and connective tissue, including the bones of the jaw and the
teeth
- Treacher Collins syndrome – reduced levels of mesenchymal tissue, especially in the lateral aspects of
the face; due to mutation in the TCOF1 gene
- Craniofacial microsomia (hemifacial microsomia) – deficient development in
lateral facial areas, external ear deformed, ramus of the mandible and
associated soft tissues (muscle, fascia) are deficient or missing  first
pharyngeal (mandibular arch)
- Neural crest cells migrate through the lower (pharyngeal) arches and play
major role in formation of the heart and great vessels
- Typical lip clefts – unilateral, bilateral, complete or incomplete
- Lip – closure is normally completed by the 7th week
- Secondary palate – union early in fetal period of development (weeks 9 and 10)
 - Causes of cleft lip and palate – exposure to some teratogens, maternal smoking
- Craniosynostosis syndromes involve developmental
abnormalities that become evident in the fetal period 
abnormally early closure of the sutures  ideal time for
surgery is between 6 and 9 months of age
- Crouzon’s syndrome  most frequently in the group of
synostosis syndromes affecting the face  mutation in
fibroblast growth factor receptor 2 on chromosome 10 
underdevelopment of the midface and eyes (bulge from
their sockets)  prenatal fusion of the superior and
posterior sutures of the maxilla along the wall of the orbit;
sometime extends posteriorly into the cranium producing
distortions of the cranial vault  surgery to release the
sutures + distraction osteogenesis to advance the orbits often is necessary

Growth Disturbances in the Fetal and Perinatal Period

Fetal molding and birth injuries

- Intrauterine molding or trauma to the mandible during the birth process (use of forceps)

INTRAUTERINE MOLDING

- Pressure against the developing face prenatally may lead to distortion of rapidly growing areas
- Rare occasions  arm pressed across the face in utero  severe maxillary deficiency at birth
- Head flexed tightly against the chest preventing the mandible from growing forward normally 
because of decreased volume of amniotic fluid
- Pierre Robin sequence  cleft palate, extreme mandibular deficiency at birth, reduced volume of the
oral cavity  early mandibular advancement via distraction osteogenesis
- Stickler syndrome  defect in cartilage formation  limited growth potential

BIRTH TRAUMA TO MANDIBLE

- Use of forceps might damage either or both of TMJ  heavy pressure could cause internal
hemorrhage, loss of tissue, subsequent underdevelopment of the mandible

Progressive Deformities in Childhood

Childhood Fractures of the Jaws

- Frequent falls and impacts of childhood – condylar neck of the mandible is particularly vulnerable 
condylar process tends to regenerate well after early fractures
- Unilateral condylar fracture is much more frequent than bilateral fractures  usually regenerates
without repercussions but it problems arises it is asymmetric growth deficiency with the injured side
(or in bilateral fractures the more severely injured side) lagging behind  if there is enough scarring
around TMJ to restrict translation of the condyle, the subsequent growth will be restricted 
conservative management at the time of injury and early mobilization of the jaw to minimize any
restriction movement
- Old condylar fracture is most likely cause of asymmetric mandibular deficiency in child but rheumatoid
arthritis or congenital absence of tissue can be problem in TMJ
 Muscle Dysfunction
- Facial muscles can affect jaw growth in two ways – formation of bone at the point of muscle
attachments depends on the activity of the muscle and muscles are important part of the total soft
tissue matrix whose growth normally carries jaws downward and forward
- Excessive muscle contraction can restrict growth in much the same way as scarring after injury 
torticollis – twisting of the head because of excessive tonic contraction of the neck muscles on one side
(at first sternocleidomastoid)
- Major decrease in tonic muscle activity  mandible drops downward  increased anterior face
height, distortion of facial proportions and mandibular form, excessive eruption of the posterior teeth,
narrowing of maxillary arch and anterior open bite

Disturbances Arising in Adolescence or Early Adult Life

- Condylar hyperplasia – now hemimandibular hypertrophy  proliferation of the condylar cartilage
and body of mandible  unilateral excessive growth – may stop spontaneously
- Acromegaly – caused by anterior pituitary tumor that secrets excessive amounts of growth hormone,
excessive growth of mandible may occur creating skeletal class III malocclusion in adult life  growth
stops when tumor is removed or irradiated – skeletal deformity persists and orthognathic surgery
-

Disturbances of Dental Development

- Contributors to isolated class I malocclusion

Congenitally Missing Teeth

- Tooth agenesis – congenitally missing teeth  phenotype in more than 150 syndromes  results from
disturbance during the initial stages of formation of tooth (initiation and proliferation)
- Anodontia – congenital total absence of teeth
- Oligodontia – congenital absence of many teeth
- Hypodontia – congenital absence of only few teeth; polygenic multifactorial model of etiology 
absent tooth will be the most distal tooth of any given type
- Primary tooth buds give rise to the permanent teeth  if not primary teeth then there will be no
permanent successor but it is possible that the primary teeth is present but permanent teeth is absent
- Ectodermal dysplasia  sparse hair and absence of sweat glands and anodontia or oligodontia

Malformed and Supernumerary Teeth

- Abnormalities in tooth size and shape  disturbances during the morphodifferentiation of
development (might be some carryover from the histodifferentiation stage)
- Most common – variation in size  maxillary lateral incisors, mandibular/maxillary second premolars
 - Supernumerary teeth – disturbances during initiation and proliferation stages
- Mesiodens  supernumerary in the maxillary midline
- Cleidocranial dysplasia  missing clavicles, many supernumerary and unerupted teeth and failure of
succedaneous teeth to erupt

Traumatic displacement of teeth

- Trauma to primary tooth displaces permanent tooth bud  trauma occurs while the crown of
permanent tooth is forming – enamel formation will be disturbed and there will be defect in the crown
OR trauma occurs after the crown is complete  root formation may stop, leaving permanently
shortened root or may be distortion of root form (dilaceration)

Genetic Influences
- Certain types of malocclusion run in families
- Hapsburg jaw – prognathic mandible is best known example
- Inherited disproportion between size of teeth and size of jaws (spacing/crowding) and between size
and/or shape of the upper and lower jaw
- Long-face pattern of facial deformity seems to be inherited
- Open bite is largely due to external influences – sucking habits or tongue posture

Environmental Influences
- Form-function relationship during the lifetime of individual may be significant in the development of
malocclusion and dentofacial malformations
- Altered function would be a major cause of malocclusion

Equilibrium Considerations
- Dentition is normally in equilibrium
- Teeth normally experience forces from masticatory effort, swallowing
and speaking but do not move
- During mastication, the fluid in the PDL space acts as shock absorber so
that the soft tissues in the PDL are not compressed, although bending of
alveolar bone occurs
- Light forces of long duration (6 hours or so per day) is important in
determining whether there is enough of an imbalance of forces to lead
to tooth movement
- Light sustained pressures from lips, cheeks and tongue at rest are
important determinants of tooth position

Masticatory Function
- Pressures generated be chewing activity affect dentofacial development  greater use of the jaws
with higher and/or more prolonged biting force could increase dimensions of the jaws and dental
arches OR less use of jaws might lead to underdeveloped dental arches and crowded and irregular
teeth could affect how much teeth erupt – affecting lower face height and overbite and open bite
relationships
 Function and Dental Arch Size
- Size and shape of muscular processes of the jaws reflect muscle size and activity
- Enlargement of the mandibular gonial angles – hypertrophy of the mandibular elevator muscles
- Coronoid process occur in children when temporalis muscle function is altered after injuries
- Vertical jaw relationships clearly are affected by muscular activity
- Dental arch dimensions are established early

Biting Force and Eruption

- Excessive overbite or anterior open bite usually have posterior teeth that are infra- or supra-erupted
- Short-face have higher and long-face lower maximum biting forces than those with normal vertical
dimensions
- Force exerted by the masticatory muscles is not a major environmental factor in controlling tooth
eruption

Sucking and Other Habits

- Engage in non-nutritive sucking of thumb or pacifier – sucking habits during the primary dentition
years have little if any long-term effect but if habits persists beyond the time that permanent teeth
begin to erupt  malocclusion characterized by flared and spaced maxillary incisors, lingually
positioned lower incisors, anterior open bite and narrow upper arch is likely result  combination of
direct pressure on the teeth and alteration in the pattern of resting cheek and lip pressures
- Thumb or finger placed between anterior teeth, mandible must be
positioned downward to accommodate it, and impedes incisor eruption
 separation of the jaws alters vertical equilibrium on the posterior
teeth  more eruption of posterior teeth than might have occurs
- 1 mm of elongation posteriorly open the bite about 2 mm anteriorly 
can develop anterior open bite
- Arch form is affected by alteration in the balance between cheek and
tongue pressures
- Child who sucks vigorously is more likely to have narrow upper arch than the one who just placed the
thumb between the teeth

Tongue Thrusting
- Tongue thrust swallowing – placement of the tongue tip forward between
incisors during swallowing  presence of large overjet and anterior open bite
- Mature or adult swallow pattern appears in some normal children as early as
age 3 but is not present in the majority until about age 6
- Tongue thrust swallowing in older patients  infantile swallow
- Delay in the normal swallow transition can be expected when a child has a
sucking habit

Respiratory Pattern
- Respiratory needs are primary determinant of the posture of the jaws and tongue
- Breathing through the mouth could change the posture of the head, jaw and tongue  alter
equilibrium of pressures --? Affect both jaw growth and tooth position  lower the mandible and
tongue and extend (tip back) the head
- 3 effects on growth would be expected
1) anterior face height would increase and posterior teeth would super-erupt
 2) mandible would rotate down and back, opening the bite anteriorly and increasing overjet
3) increased pressure from the stretched cheeks might cause a narrower maxillary dental arch
- Chronic respiratory obstruction can be produced by prolonged inflammation of the nasal mucosa
associated with allergies or chronic infection
- The pharyngeal tonsils or adenoids normally are large in children and partial obstruction from this
source may contribute to mouth breathing in children
- Some lip separation at rest (lip incompetence) is normal in children, many children who appear to be
mouth breathers may not be
- Sleep apnea – mandibular deficiency can contribute to its development but also obesity, age, gender
and jaw relationships

Etiology in Contemporary Perspective

- Jaw function is related to the development of malocclusion and inheritance of malocclusion