Orthodontics

1. Clinical examination
1. Facial patterns: Frontal view
 Mesoprosopcic: average
 Leptoprosopic: Long face, i.e. dolichofacial, generally these patient have VME- vertical maxillary
excess also may present with an open bite (skeletal) with a divergent facial profile.
 Euryprosopic: these are the short face type (brachyfacial) and may present with a deep open bite,
and have a convergent facial profile
Once this assessment has been made check the symmetry of the face with lips at rest/lips together/and
smiling. Also check the cant of the occlusal plane (that is put a pop-stick on the mouth of the patient and
check where it tilts.

2. Facial patterns: Profile view

 Straight: orthognathic- class I
 Convex: retrognathic class II, with a posterior divergent note that the mandible is usually
retrognathic but the maxilla can be prognathic.
 Concave: Prognathic- class III with an anterior divergent profile, note that often the mandible is
prognathic but the maxilla may also be retrognathic
Note that the facial pattern generally reflects the dental pattern but not always.
Then also check the
Naso-labial angle: This depends on the nose and lip morphology and asks the question what will the naso-
labial angle become with growth and or treatment.

3. Lip variation: Note that with lip growth, they trail behind the growth of the jaw and because lip height is
relatively short in the mixed dentition lip separation is often maximal at this stage and decreases during
adolescents. This is because the soft tissues will move downwards relative to the dentition.
Generally length of the lip ranges from 18-22 mm, which is about normal. Also consider the lip position is
relation to the teeth: that is at rest and with the patient smiling, is there incisor display/gingival display/lip
trap/ are the lips even competent (i.e. competent, potentially competent, and incompetent) also check the
lip tome- relaxed and in function
 Management of lip related problems:
o Correct the overjet: that includes both eliminating the Para-functional habit and uses the
appropriate appliances
o Correct the face height: of the problem is of skeletal origin and there is a long face with
incompetent lip than may need to consider orthopedics or orthognathic surgery.
o Promote nasal respiration: lip exercises to emphasize seal; also can refer to ENT surgery to
turbinate’s, nasal septum, adenoids, and polyps. Also consider if that patient has chronic
rhinitis or asthma
o Lip lengthening: freeing the mentalis attachment.

4. Tongue variation: An infant will swallow with a tongue thrust at birth and before teeth erupt. A mature
swallow without a tongue thrust s normal when the teeth do erupt, that is the teeth are usually in contact
during this form of swallow (creates the seal). If this is reversed then we will often see that most anterior
open bites are accompanied with a forward tongue position and function, therefore suspect mouth
breathing. The most important thing to consider here, is whither a tongue thrust causes a dental open bite
or is it an adaption to the open bite. There are a few theories to suggest the driving force of soft tissue
adaptation:
 Function determines form, (Rogers 1918)
 Tongue thrust is dominant (Straub 1969)
 Most tongue is adaptive (Ballard 1962)
 Form determines function (Subtelney 1973)
Unless there is severe skeletal deformity or neuromuscular disorder, the tongue seems important in
molding the dental arches but its role as a primary cause of malocclusion has been controversial. The idea
behind soft tissue pressures is that, although the pressure applied are light in there favor is the duration at
which these light forces are applied, studies have shown that the duration threshold seems to be about 4-6
hour, and since these light pressures form lips/cheek and tongue are maintained most of the time, it would
be reasonable to expect that these pressures may affect tooth position.
 Management of tongue-related problems: main one is patient awareness of tongue position,
o Myo-functional modification: speech therapy and desensitized techniques
o Barriers- various fixed or removable appliances
o Change the form: dental arch shape and occlusion by orthodontic, orthopedic or surgical
means, or partial glossectomy. Note that true macro-glossia is rare but tongue dysfunction
does occur.
Case study: patient with anterior open bite was given awarness exercises and after the anteror open bite
was fixed there was a posterioro open bite, due to the buccal tongue posture. Porper education and
monitoring is very important.

5. Cheek variation:
Adaptive to mouth breathing and has been related to narrow maxillary arch form (cross-bites) and
associated with low tongue position i.e. anterior open bite.
 Management of cheek-related problems:
o Investigate mouth breathing
o Apply expansion as needed: removable or fixed appliances/slow (SME) or rapid (RME) rate,
and possibly consider surgically assisted for adults.

6. Adenoid/tonsils
Adenoid faces- is an adaptive vertical facial growth changes- mainly a cause of mouth breathing which leads
to increased lower face height and lower and forward tongue posture. The respiratory demands lead to
head extension, tissue stretching and face lengthening.
 Management of adenoid and tonsil problems: surgery however surgeons are quite conservative
these days.

Equilibrium theory
Force duration is more important than magnitude-resting pressure is the
key, posture influences resting pressure and respiration affects posture.

Treatment timing:
 Early treatment: deciduous and mixed dentition- this is called phase I treatment.
o Prevention: maintaining the normal development and preventing problems which could
“hypothetically occur”
o Interception: development is not taking place as it should ad treatment is needed to eliminate
or reduce the problem. Note that orthodontic or orthopedics procedures may be used with
the aim to facilitate later treatment should still be needed.
 Adolescent’s treatment: early secondary dentition this is around puberty – also known as Phase II
treatment:
o Also here there is prevention/interception and correction, note some orthopedics possible
but mainly relies on orthodontic, the management of skeletal imbalance my require
camouflage or surgical approaches.
 Adult: essentially the non-growing phase;
o Only correction here, treatment options are often compromised by the patients’ history .
2. Asymmetry
Perfect symmetry is unnatural; there are not really any solid patterns that are seen between sex and age
(possibly more mandible in males or more mid-face in females). Some skeletal problems may be
progressive, and soft tissue integument may mask or accentuate skeletal form, also dento-alveolar
compensation can complicate diagnosis. If function is asymmetrical then TMJ adaptation may occur and
molar relation is often asymmetric- (drifting, functional mandibular shift). Occlusal variability as increase in
recent evolutionary terms and tooth size instability is also common.
Types:
 Cranio-facial: Tessier clefts classification form 1-13
 Upper third: plagiocephaly, fibrous dysplasia, orbital dystopias
 Mid third: Cleft lip and palate, fibrous dysplasia, lymphangiomata, plexiform neurofibroma, hemi-
facial atrophy (Romberg’s syndrome), hemi-facial hypoplasia (Treacher-Collins syndrome), Hemi-
facial hypertrophy, secondary (e.g. adapted to mandibular growth anomaly)
 Lower third enlargement: unilateral condylar hyperplasia, mandibular hemi-hypertrophy, hemi-
facial and hemi-body hypertrophy, tumors and dysplasias, asymmetric masseteric hypertrophy.
 Lower third deficiency: Congenital unilateral mandibular hypoplasia, acquired unilateral mandibular
hypoplasia, and TMJ ankylosis.
The examination
Assess in 3 planes:
View Examination
Draw a vertical, inter-pupillary line, facial
midline, and check the: nose tips and
bridge, chin position, and smile (midline
shifts-don’t get confused if there are
missing teeth) and symmetry. Note make
sure that the eyes are level in the natural
head position.
- Check the occlusal cant, note that how to
level depends on the overbite, curve of
Spee, age and the incisor to lip line and
face type.
Functional shifts, when the patient is in
function, check for interferences and
slides particularly where cross bites and
sub-divisions are detected.

Ensure that the chin is at rest and patient

is biting in centric occlusion. Check the:
forehead, orbits, malars, (cheek bone)
nose, mouth, ear and chin, also very
important to check the mouth on opening
to check maxillary rotation, and at rest
during mandibular opening and closure.
Midlines to be checkreference point?
Dental asymmetry:
Make sure that all the teeth are present, and assess tooth sizes carefully, look for localized
displacements (and apply lischer’s criteria) consider the effects of tooth size disharmony (apply Boltons
analysis) and look carefully at arch shape, what would be the occlusal consequences.
Just quickly on etiology, the above factors can be affects be genetic and congenital conditions, pathologies,
occlusion (e.g. tooth loss, habits, interferences), dental (agenesis, size/shape variations) and trauma always
consider the cause and any other contributing factors.
Note that diagnosis is critical, and the etiology can be complex, carefully examine the face (in all three
planes) and preferably in the natural head position, both at rest and in function. Work form centric relation
and check for slides. Note that management may ne difficult but really depends on the diagnosis. Any
moderate skeletal asymmetry may respond well to orthodontic camouflage or otherwise consider surgery.
However functional and dental asymmetry usually respond favorably.

3. Impression and study models

Requirement: over-extended and deep in the labial and buccal sulcus, this reveals the alveolar contours and
the apical base, should be thick, rounded peripheral roll this helps with trimming the study models. Also
accurate reproduction of the surface detail, minimal air
bubbles, and complete recording of all teeth.
The preparation:
Once the tray is loaded make sure that the lips are out of
the way before seating the tray, generally seat the tray from
the posterior to the anterior. Also need to get the bite
record, which is usually taken when the teeth are in inter-
cuspal position.

The purpose:
 Recording pre-treatment, progress and end of
treatment condition this is a medico-legal record,
 Diagnostic aid, to assess the tooth size analysis, arch form
analysis, space analysis and occlusal analysis.
 Treatment planning and case presentation
 Research: n growth and development, treatment efficacy
and post treatment changes.
4. Aetiology
There are a number of factors that all interact together to create the occlusion. They incl.: hereditary factors,
congenital factors, environmental factors, growth and development and adaptions to function. Malocclusion
is an end consequence of interactions between some or all these factors, and occlusion change throughout
life as different factors are imposed, the precise cause of all aspects of malocclusion is mostly unknown.
Bascially can be split up into two categories:
1. General factors;
a. Heredity
o Genetic imbalance, major mutants (autosomal dominant, autosomal recessive sex linked) and
polygenic. This is where the twin studies become very important to consider.
o The big question to ask is malocclusion is it OFTEN caused by genetic factors? Malocclusion can be
inherited in two major ways: the first is inherited disproportion of the tooth size and size of the
jaw, and the other is disproportional size or shape between the upper and the lower jaw, which
would cause improper occlusal relationships.
o The most influential individual Prof. Stockard who cross breed dogs, and showed that dramatic
malocclusion did occur but more so form jaw size discrepancies as opposed to tooth size, jaw
imbalances. However the problem was the dogs in the experiment, had achondroplasia (deficient
mid face growth)
o The classic way to determine the extent to which these characteristic are inherited is to examine
identical twins. A list was created called heritability factors
b. Congenital:
o CLP cerebral palsy, etc. note that many of these have genetic basis.
c. Environmental: pre-natal, and post-natal
o This can include habits that the mother had during pregnancy and also any events that affect the
occlusion throughout life, e.g. burns, trauma, tumors,
d. Metabolism and disease: endocrine imbalance, metabolic disturbance, infectious
o These mainly affect the tooth formation and eruption.
e. Dietary problems
o If nutrition is compromised sufficiently overall growth and development may be affected (often
delayed) and homoeorrhesis may occur if there is restoration of nutrition before growth ceases,
malocclusion tends not to respond to this catch up growth.
f. Abnormal pressure habits and functional aberrations
o This incl. abnormal suckling, finger and thumb sucking, tongue thrust, lip and nail biting, abnormal
swallowing, speech defects, tonsils and adenoids, bruxism and abnormal respiration. Note that
intensity and duration are most important. Note that the image below shows that neonate forward
tongue posture and the variations in adult tongue position (d: shows the retained infantile
posture). The second image shows normal adenoids and B: shows forward tongue position due to
enlarged tonsil and adenoid.
g.

g. Posture:
o Unproven and interestingly head posture relative to the cervical spine seems to relate to certain
malocclusion types.
h. Trauma and accidents
 o The investigation has demonstrated that in a large sample of 164 twins environmental factors have
an unquestionable influence on developing malocclusions and that genetic features ay play less
important role than previously thought.

2. Local factors:
a. Tooth number: agenesis, supernumeraries
o Agenesis: anodontia where all teeth are missing, oligodontia: many teeth missing >6 i.e. ectodermal
dysplasia, hypodontia: 1 or several teeth missing incidence is about 6% (excl. third molars)
female: male  3:2 and generally associated with numerous syndromes, e.g. Down syndrome CLP,
and has strong family links, mostly affects secondary teeth.
o Supernumeraries: incidence 1%, (80%) occur in the anterior maxilla, female: male 1:2, most
common cause of upper incisor failure to erupt, and causes 10% of upper midline diastemas, and
associated with numerous syndromes. E.g. mesioden
o Can manifest itself as
1. Germination: arises form the splitting of a tooth germ
2. Fusion: arises from the union of two tooth germs, involves dentine but usually
separate pulp chambers, note that separation is more definite than germination,
counting gives 1 (or more) less than expected unless fused with a
supernumerary.
3. Concrescence: similar to fusion but only involves cementum.
o The Butler’s Field theory: within each field there is one tooth that is presumed to be the stable
b. Tooth size: this can be a manifestation of dentinogenesis imperfecta, etc.
c. Tooth shape
o Apart form aesthetics this affects the occlusion and space condition in the arches, aberrations
during the histo- and morpho-diffrentiation stages. They manifest as: accessory cusps,
germination, fusion, concrescence, dilacerations, peg-shaped laterals, talon cusps, dens-invaginata,
taurodontism, macrodontia and mircodontia.
d. Pre-mature tooth loss
o Usually results in loss of arch space, most space lost in the first 6 weeks then slows by 6 months,
secondary teeth may erupt, faster if the primary is lost within 6 months of expected exfoliation and
the roots are one half to two thirds formed. Un-erupted teeth migrate to the space with less
tipping, while erupted teeth then to tip into the space created: maxillary molars-mesio-palatal,
mandibular molars: mesial tip with little rotation, premolars: mesial or distal tip. Note that teeth
tend to also erupt as they tip.
o When a unit within the dental arch is lost the arch tends to contract and the space to close. At one
time this space closure was attributed, entirely to mesial drift of posterior teeth, which in tern was
confidently ascribed to forces form occlusion. Although a mesially directed force can accompany
occlusion, it probably is not a major factor in closure of spaces in a dental arch. The contemporary
view is that mesial drift is a phenomenon of the permanent molars only. The major reason these
teeth move mesially when a space open up is their mesial inclination, so they erupt mesially as well
as occlusally. So basically a molar is likely to drift mesially more rapidly in the absence of occlusal
contacts than if they are present.
o Mesial drift of the permanent first molar after a primary second molar is lost pre-maturely can
significantly contribute to crowding in the posterior part of the dental arch. In particular in the
past this has been a significant reason as to why premolars misalign.
o Also when a priary canine is lost premeaturly there is a tendency for the space to close, occurs
primarily by distal drift of the incisors and NOT the mesial drift of the posterior teeth. The
reasonfor distal drift is: 1. Force form active contraction of transceptal fibers in the gingiva and 2.
Pressure from the lips and the cheek.
o This is the major cause of crowding class I
e. Prolonged tooth retention: also known as Ankylosis
o If eruption is delayed of the permanent teeth this will generally lead to malocclusion, only when
the teeth drift into improper places, also if a tooth is delayed in eruption suspect Ankylosis.
Ankylosis of the primary tooth although may delay the eruption of the permanent tooth generally
has no lasing effects.
 f. Delayed eruption: can be due to either impaction, Ankylosis, agenesis, ectopic eruption, the distance
of tooth germ from normal, tooth malformation, obstruction, trauma/infection of tooth germ,
displacement by neoplasm, systemic disorder, inadequate arch space, and heredity etc.
g. Abnormal eruption path: ectopic eruption
o Occasionally, malposition of permanent tooth bud can lead to eruption in the wrong direction; it is
most likely to occur in the maxillary first molars. If the eruption path of the maxillary carries it too
far mesial at the early stage, the permanent molar is unable to erupt and the of the second primary
molar may be damaged. Also the mesial position of the permanent molar means that the arch will
be crowded unless the child receives treatment.
o Ectopic eruption of other teeth is rare, but can result in transposition of teeth or bizarre eruption
positions. Mandibular second pre-molars, sometimes erupt distally and can end up in the ramus,
also a poor eruption of other teeth especially maxillary canines usually is due to the eruption path
being altered by a lack of space.
h. Diastemas formation
o Mircodontia, macrognathia, supernumeries e.g. mesioden, peg laterals +/- agenesis, incisor
proclination (thumb sucking, lip trap, tongue trap) and the ugly duckling stage, expansive lesions
i.e. cysts
i. Abnormal labial frenum
o Can have an abnormally large labial frenum, which may cause diastemas formation or can have no
frenum at all.
j. Mucosal barriers: thick fibrous gingiva which ay obstructs the eruption path of a permanent tooth.
k. Ankylosis: presents as an infra-occluded tooth, when the tooth cementum has fused to the
surrounding bone.
l. Dental caries and inadequate restorations

5. Cephalometrics
Defined as the measurement of the head. The history Pacini and Carrera 1992 produced the first lateral
head film but not standardized, and Broadbent in 1931 in the USA independently developed the
cephalometer and standardized the radiograph image.
The equipment:
o Cephalostat: steadies and positions the head, central X-ray beam passes through the ear rods, locates
the mid-sagittal plane (MSP) of the head at the standardized distance from the X-ray source and film
o Collimated X-ray source: 5 feet from MSP is often used but can differ,
o Aluminum or plastic wedge: attenuates the beam to enhance soft tissue imaging
o Film cassette: film and rare earth intensifying screens are being replaced by CCD and phosphor plate
digital technology
The measurements:
o Kilovoltage determines penetrance (beam energy): this relates to contrast and grey scale range and
the usual range is 65 to 90 kV (ADH is about 77 kV)
o Milliamperage (mA) determines the image brightness
o Dose is proportional to mA and time: increase mA and decrease time to limit movement distortion
the ADH usually 12 mA and 0.4 to 0.64 seconds
o Filmless
digital
technology:
enables
image
manipulation
and
enhancement
and reduced
kV decreases
dosage
Limitations:
1. Enlargement distortion:
o The side nearest the film is least enlarged the enlargement value given is for the MSP i.e. the
average of left and right sides.
o Also the beam also diverges concentrically i.e. least enlargement is in the center at the ear rods
and the greatest is at the periphery head width is important i.e. broad heads have greatest left to
right difference in enlargement
o Asymmetry can be difficult to assess due to apparent size difference which may just be
enlargement or head rotation projection errors and identification errors

2. Only a 2-D representation (3-D cone beam CT is coming!): we see multiple, superimposed cross-
sectional images of complex shapes therefore, the anatomy is distorted
3.