Essentials of Orthodontics textbook Flashcards
Ideal occlusion
Dentition where the teeth are in the optimum anatomical position, both in the mandibular and maxillary arches (intramaxillary) and between the arches when the teeth are in occlusion (intermaxillary).
Malocclusion
Dental anomalies and occlusal traits that represent a deviation from the ideal occlusion.
Rationale of orthodontic treatment
Malocclusion can cause issues related to dental health and/or related to oral health related quality of life issues arising from appearance, function and/or psychosocial impact of teeth.
Need for treatment depends on impact of the malocclusion and whether treatment is likely to provide a demonstrable benefit to the patient.
Need for orthodontic treatment
The IOTN is used.
In the UK, the unmet orthodontic treatment need for children within deprived households is higher than average at 40% for 12 year olds and 32% for 15 year olds.
Potential benefits to dental health
There is no evidence to support benefit in cases of caries, periodontal disease, TMD.
Evidence to support in cases of:
1. Crowding where one or more of the teeth are pushed buccally or lingually out of the alveolar bone trough, resulting in reduced periodontal support and localised gingival recession.
2. Class III malocclusion where lower incisors in crossbite are pushed labially
3. traumatic overbites, which occur when teeth bite onto gingiva, can lead to gingival inflammation and loss of periodontal support over time.
Localised periodontal problems
Gingival biotype is thin
Crowding causes teeth to be pushed out of bony trough, resulting in recession.
Traumatic overbites
Anterior crossbites
Increased overjet
U/E Impacted teeth
Crossbites associated with mandibular displacement
Dental Trauma
Risk is x2 in individuals with overjet >3mm
Overjet greater contributory risk factor in girls than in boys
Tooth impaction
when normal tooth eruption is impeded by another tooth, bone, soft tissues or other pathology.
Supernumerary teeth can cause impaction.
Ectopic teeth are those that have formed and subsequently moved into the wrong position.
U/E teeth can cause local pathology – resorption of adjacent roots/cystic change.
Ortho tx of impacted teeth may be indicated to reduce the risk of pathology.
Caries
Research has failed to show a correlation between malocclusion and caries.
Cases of special learning needs.
Plaque induced periodontitis
Weak association between malocclusion and plaque induced periodontitis.
TMD
Group of related disorders with multifactorial aetiology including psychological, hormonal, genetic, traumatic and occlusal factors.
Debate as to whether orthodontic treatment causes TMD or whether orthodontic therapy aids TMD.
In cases of TMD, a comprehensive assessment should be conducted prior to orthodontic treatment commencing.
Psychosocial wellbeing
peer victimisation in the adolescent orthodontic patients is 12%
Risks factors for root resorption
shortened roots with evidence of previous resorption
pipette shaped or blunted roots
teeth prev traumatised
patient habits
iatrogenic
Root resorption
On average 1mm of root lost for 2 years of FA tx
Demineralisation
early, white, reversible lesions in the development of caries
Prev 2-96%
Lesions may regress post tx
Enamel damage
as a result of trauma/wear from orthodontic appliances.
Band seaters, band removers, bracket removal can cause fracture of enamel.
During removal of adhesives – fast bur can cause damage.
Pulpal injury
excessive apical root movement
reduction of blood supply to pulp
E/O damage
Contact dermatitis in 1% cases due to nickel
Failure to achieve treatment outcomes
Operator factors
- errors of diagnosis
- errors of tx planning
- anchorage loss
- technique errors
- poor communication
Patient factors
- poor oral hygiene/diet
- failure to wear appliance/brackets
- repeated appliance breakages
- FTA
- unexpected unfavourable growth
Aetiology of malocclusion
Missing central incisor - supernumerary tooth - inherited
U/E upper central incisor - dilaceration (trauma) - environmental
Functional occlusion
Occlusion free of interferences to smooth gliding movements of mandible with no pathology.
Quantitive assessment of malocclusion
Each feature of malocclusion is given a score and the summed total is then recorded –PAR Index
Worst feature of malocclusion is recorded IOTN
Angle’s Classification
- Neutroocclusion
MB of upper first molar occludes with MB cusp of lower first molar. - Distocclusion
MB cusp of upper first molar occludes distal to the Class I post normal relationship - Mesiocclusion
prenormal relationship
MB cusp of lower first molar occludes mesial to the Class I relationship
British Standards Incisor Classification
- Lower incisor edges occlude with or lie immediately below cingulum plateau of upper central incisors
- Lower incisor edges occlude posterior to cingulum plateau of upper incisors.
Div I - upper incisors proclined and inc overjet
Div II - upper incisors retroclined. overjet is minimal
- lower incisors sit anterior to cingulum plateau of upper incisors. overjet reduced.
MOCDO
Missing teeth
Overjet
Crossbite
Displacement
Overbite
PAR Score
Developed to measure the success of ortho tx.
Difference between PAR scores at the start and upon completion of treatment can be calculated, and from this a percentage change in PAR score, which is a reflection of the success of tx.
ICON
Index of complexity, outcome and need
IOTN + PAR
Average calcification times primary teeth (months)
central incisors - 12-16
lateral incisors - 13-16
canines - 15-18
first molars - 14-17
second molars - 16-23
Average eruption dates of primary teeth (months)
central incisors - 6/7
lateral incisors - 7/8
canines - 18/20
first molars - 12/15
second molars - 24/36
Commencement of calcification mandibular permanent teeth (months)
Central incisors - 3-4
Lateral incisors - 3-4
Canines - 4-5
First premolars - 21-24
Second premolars - 27-30
First molars - around birth
Second molars - 30-36
Third molars - 96-120
Commencement of calcification maxillary permanent teeth (months)
Central incisors - 3-4
Lateral incisors - 10-12
Canines - 4-5
First premolars - 18-21
Second premolars - 24-27
First molars - Around birth
Second premolars - 30-36
Third molars - 84-108
Eruption of mandibular permanent teeth (years)
Central incisors - 6-7
Lateral incisors - 7-8
Canines - 9-10
First premolars - 10-12
Second premolars - 11-12
First molars - 5-6
Second molars - 12-13
Third molars - 17-25
Eruption of maxillary permanent teeth (years)
Central incisors - 7-8
Lateral incisors - 8-9
Canines - 11-12
First premolars - 10-11
Second premolars - 10-12
First molars - 5-6
Second molars - 12-13
Third molars - 17-25
Development of dental arch
The difference in widths –> leeway space (in general 1-1.5mm in mandible and 2-2.5mm in maxilla)
Arch width is measured across the arch between the lingual cusps of the second deciduous molars or second premolars.
Between the ages 3-18yrs 2-3mm increase occurs.
Abnormalities of exfoliation and eruption
Screening
- 10yrs maxillary canines palpable in 70% of cases
- 11yrs maxillary canines palpable in 95% of cases
Eruption cyst
- accumulation of fluid/blood in the follicular space overlying the crown of an erupting tooth
- usually rupture spontaneously
Failed eruption
- Disruption in normal sequence of eruption
- Asymmetry in eruption pattern between contralateral teeth. If a tooth on one side of the arch has erupted and 6 months later there is still no sign – radiographs
Mixed dentition problems
Early loss of teeth
deciduous canine/first molar - centreline shift. consider contralateral extn.
deciduous second molar - permanent first molar will drift forwards
Balancing v Compensating extn
Balancing - the extn of contralateral tooth. Centreline problems.
Compensating - removal of equivalent opposing tooth. maintain occlusal relationship between arches.
Infra-occlusion
Tooth fails to achieve or maintain occlusal relationship with adjacent or opposing teeth.
1-9% children
Impacted first permanent molars
impaction of first permanent molar against second deciduous molars occurs in approx 2-6% cases and is indicative of crowding.
mild cases can be managed with by tightening a brass separating wire around the contact point between two teeth over a period of about 2 months.
severe cases can be dealt with using an appliance.
Dilaceration
Distortion or bend in the root of a tooth. Affects upper central/lateral incisor typically.
There appears to be 2 distinct aetiologies:
1. developmental. usually affects isolated central incisor. F>M. Crown of the affected tooth is turned upward and labially.
- Trauma. Intrusion of a deciduous incisor leads to displacement of underlying developing permanent tooth germ. Characteristically, that causes the developing permanent tooth crown to be deflected palatally, and the enamel and dentine forming at the time of the injury are disturbed, giving rise to hypoplasia.
management:
crown is exposed surgically and traction is applied to align the tooth, provided that the root apex will be sited within cancellous bone at the completion of crown alignment.
Supernumerary teeth
Additional to the normal series.
2% in permanent dentition.
1% of primary dentition.
Morphology
1. Supplemental. resembles a tooth.
2. Conical. conical supernumerary most often occurs between upper central incisors. Most commonly associated with displacement of the adjacent teeth, can also cause failure of eruption or not affect the other teeth.
3. Tuberculate: type is described as being barrel shaped, but usually any supernumerary which does not fall into the conical or supplemental categories. associated with failure of eruption.
4. Odontome: variant is rare. Both a compound (conglomeration of small tooth like structures) and complex (amorphous mass of enamel and dentine)
Failure of eruption
common reason for non-present maxillary central incisor
Displacement
associated with displacement or rotation of an erupted permanent tooth. management involves removal of supernumerary tooth then FA.
Crowding
Supplemental type. Remove most displaced tooth.
No effect
incidental finding
First permanent molars
1st molars are rarely the first tooth of choice for extn as their position within the arch means that little space is provided anteriorly for the relief of crowding or correct of incisor relationship.
Rules
- if dentition is uncrowded extn of 1st permanent molars should be avoided
- maxilla there is a greater tendency for mesial drift and so the timing of extn of upper 1st molar is less critical
In the lower arch, a good spontaneous result is more likely if:
- lower 2nd molar has developed
- the angle between the long axis of the crypt of the lower second molar and the first permanent molar is between 15 and 30
- a crypt of the second molar overlaps with the root of the first molar
Median diastema
98% of 6yr olds
49% of 11yr olds
7% 12-18yr olds
Factors:
- Physiological
- Familial
- Small teeth in large jaws
- Missing teeth
- Midline supernumerary
- Proclination of upper labial segment
In cases where the MD is >3mm, it may be necessary to consider appliance tx to approximate the central incisors to provide space for the laterals and canines to erupt.
What to refer and when
Deciduous dentition
CLP
Craniofacial abnormalities
Mixed dentition
Severe CIII skeletal problems
Delayed eruption of permanent incisors
Presence of supplemental incisors
Impaction of 1st perm molars
First perm molars of poor prognosis
Ectopic canines
Hypodontia
Marked mandibular displacement
patients with medical problems
pathology
Mechanisms of bone formation and growth
Intramembranous osiffication - formation of bone in a membrane
Endochrondral ossification - bony replacement of a cartilagenous model
Maxillary complex
complex structure including maxilla, palatal, zygomatic, ethmoid, vomer and nasal bones.
Separate bones join with each other and the anterior cranial base at sutures.
until the age of 7, growth of the maxillary complex occurs in downwards and forwards displacement and by drift and remodelling.
As the growth of the brain and calvarium slows, so does the maxillary growth. Forward displacement of the maxillary complex allows space for the maxilla to grow backwards, lengthening the dental arch posteriorly in the area of the tuberosities, allowing room for the permanent molars to erupt.
Ortho interventions to advance the maxilla, eg., protraction head gear in Class III cases, are reported to be more successful before the age of 10 when the sutures around the maxilla are more amenable to displacement.
Interventions to expand the maxilla by RME are reported to be more successful before the age of 16.
Periodontal ligament
PDL consists of cells surrounded by type 1 collagen and oxytalan fibres and a ground substance consisting of proteoglycans and glycoproteins.
fibroblasts are responsible for producing and degrading the PDL fibres
Cementoblasts are responsible for cementum
osteoblasts are responsible for bone production and coordination of bone deposition and resorption
osteoclasts are responsible for bone resorption
cells rests of Malassez are responsible for dealing with dead cells and debris
Cells involved in bone homeostasis
Osteoblasts - production of bone. recruit and activate osteoclasts. balance been bone resorption and deposition, controlled by osteoblast. become surrounded by mineralised bone and become osteocytes.
Osteocytes - continue to communicate with each other via cytoplasmic extensions in canaliculi in the bone. responsible to detecting mechanical load on bone.
Osteoclasts - large multinucleate cells responsible for resorption of bone. Found on the bone surface undergoing active resorption in pits called Howship’s Lacunae.
Cellular events in response to mechanical loading
application of mechanical load affects PDL by causing fluid movement in PDL space and by stretching and compressing the collagen fibres and ECM. this leads to deformation of alveolar bone. this distortion in the pdl and alveolar bone are detected by cells which are connected to ECM by proteins known as integrins in their cell walls.
4 basic stages of tooth movement:
1. matrix strain and fluid flow in the pdl and alveolar bone
2. cell strain, secondary to matrix strain and fluid flow
3. cell activation and differentiation
4. remodelling of the pdl and alveolar bone
BMPs
group of growth factors known to induce formation of bone and cartilage
bone morphogenetic proteins
CTSK
Enzyme in the bone remodelling and resorption
expressed in osteoclasts
cathepsin K
CSF-1(M-CSF)
Colony stimulating facotr (macrophage CSF)
polypeptide growth factor found in bone matrix and produced by osteoblasts. acts directly on osteoclast precursor cells to control proliferation and differentiation into osteoclasts
Il-1
interleukin 1
potent stimulator of bone resorption and inhibitor of bone deposition
MMPs
matrix metalloproteinases
range of enzymes produced to break down unmineralised ECM
OPG
produced by osteoblasts in response to RANKL, decrease the activity of osteoclasts to regulate bone resorption
Prostaglandin E-2
Mediator of bone resorption. produced in sites of inflammation. produced by cells in response to mechanical loading. inc production of intracellular messengers.
receptor activator of nuclear factors
produced by osteoblasts.
stimulatory factor for differentiation, fusion, activation and survival of osteoclasts.
tissue inhibitors of metalloproteinases (TIMPs)
Produced by various cell types to bind to MMPs to inhibit or reduce their activity
chain of cellular events when pdl is subjected to COMPRESSIVE load
- mechanical loading causes strain in ECM of PDL and in alveolar bone causing fluid flow
- strain in ECM is sensed by PDL cells due to their connection to ecm via integrins. osteocytes in the bone also sense the mechanical force by fluid flow through the canaliculi.
- osteocytes respond to mechanical deformation by producing BMPs and other cytokines which activate osteoblasts. fibroblasts produce MMPs. Osteoblasts respond by producing PGE-2 and leukotrienes.
- osteoblast production of PGE-2 and leukotrienes leads to an elevation of intracell messengers. cause osteoblasts to produce IL-1 and CSF-1 and increase in receptor activator of nuclear factor.
- IL-1 is produced by osteoblasts and macrophages also increases the production of RANKL by osteoblast.
- RANK L and CSF 1 cause increased attraction and proliferation of blood monocytes which fuse to form osteoclasts. RANKL also stimulates the osteoclasts to become more active.
- osteoblasts bunch up to expose the underlying osteoid and produce MMPs to degrade the osteoid and to give osteoclasts the access to the underlying mineralised bone. osteoblasts also produce OPN which causes osteoclasts to attach to the exposed bone surface
- osteoclasts resorb the bone by excreting hydrogen ions into the matrix, softening the hydroxyapatite crystals, then use proteases such as Cathepsin K to break down the ECM
- Osteoblasts also produce inhibitors of some enzymes and cytokines (TIMPs and OPG to ensure that bone resorption is carefully controlled)
Chain of cellular events when pdl is subject to TENSION
- in areas of tension, osteoblasts are flattened and the osteoid remains unexposed
- cells in the pdl increase the amount of a specific secondary messenger (ERK in response to tension)
- ERK signalling induces the expression of RUNX-2 which in turn causes an increase in osteoblast number, possibly by inducing differentiation of fibroblasts into osteoblasts.
- osteoblasts clump into groups, secreting collagen and other proteins composing the organic matrix, then produce hydroxyapatite, which mineralises the matrix resulting in new bone
optimal force levels of different tooth movements (grams)
tipping –50-75
bodily movement –100-150
root uprighting –75-125
extrusion –50-100
intrusion –15-25
cellular events during root resorption
external apical root resorption is a complex inflammatory process that occurs in virtually all patients undergoing treatment.
apical portion of root is removed by odontoclast
Facial growth
facial development begins a 4wks (5 swellings - frontonasal, 2 maxillary, 2 mandibular around the stomodeum (primitive mouth))
maxilla and mandible derive from the first pharyngeal arch into which cranial neural crest cells have migrated
bone formation occurs by either intramembranous or endochondral ossification
bone growth occurs by remodelling and displacement
calvarium ossifies intramembranously, closely following the growth of the brain. growth is complete at 7yrs.
cranial base ossifies endochondrally. growth at the spheno-occipital synchondrosis occurs in 2 directions until the mid teens.
maxilla and mandible ossify intramembranously and undergo complex patterns of remodelling. displaced forwards and downwards in relation to cranial base. growth occurs posteriorly at the tuberosities (maxilla) and ramus (mandible) to accommodate the permanent dentition.
the mandible experiences rotational growth and most individuals having an upward and forward direction of rotation.
facial growth continues at low level in the adult. growth continues for longer in boys in the AP and V dimensions.
