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Orthodontics > Aetiology of Malocclusion > Flashcards

Aetiology of Malocclusion Flashcards

1
Q

What is the equilibrium theory?

A

Law of physics: Objects subjected to unequal forces will move to a different position in space

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2
Q

Is duration or magnitude of forces more important

A

Duration

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3
Q

What pressures affects the vertical and horizontal position of teeth?

A

Tongue, lips, cheeks at rest, as well as gingival and PDL fibres

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4
Q

Do masticatory forces and soft tissue pressures during swallowing have a major influence on teeth positions

A

No

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5
Q

What affects the dentition position

A
  1. Prolonged thumb sucking
  2. Forward resting tongue posture
  3. Macroglossia
  4. Incompetent lips
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6
Q

What affects the dentition vertically?

A

Periodontal ligament (eruption)
Opposing tooth
Tongue interposed between teeth

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7
Q

What affects the dentition transversely

A

Tongue vs cheek

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8
Q

How do muscles affect jaw growth?

A
  • Bone formation at points of muscle attachment -> enlargement of mandibular gonial angles in patients with hypertrophy of mandibular elevator muscles
  • Musculature is part of the soft tissue matrix, which growth carries the jaw down and forward
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9
Q

What is neuromuscular activity influenced by?

A

Genetics and environmentally-influenced behavioural and postural adaptations

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10
Q

Does greater use of jaws lead to increased jaw and dental arch dimensions?

A

Yes: differences in jaw size among racial groups reflect dietary differences and masticatory effort.
No: dental arch dimensions are established early so this influence must come early in life which is unlikely.

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11
Q

Does reduced biting force affect the amount of dental eruption and hence lower face height and overbite

A

Short face –> higher maximum biting forces than longer
Different biting forces is an EFFECT not a CAUSE of facial patterns

  • not a major factor in tooth eruption
  • not an etiologic factor for deep or open bite patients

Exception: Rare muscle dystrophy or weakness syndrome: downwards and backwards mandibular rotation + Excessive eruption of posterior teeth

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12
Q

What happens during thumb sucking

A
  1. Interference with incisor eruption –> AOB
  2. Mandibular is positiong downward to accomodate thumb –> excessive eruption of posterior teeth –> 1mm overeruption = 2mm AOB
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13
Q

Why is there constriction of maxillary arch during sucking habits

A
  1. Lowered tongue: reduced pressure on lingual surfaces of upper posterior teeth - posterior crossbite
  2. Increased cheek pressures: buccinators muscle contracts (greatest at corners of mouth) - tapered arch form
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14
Q

Does tongue thrust swallowing lead to AOB

A

NO - duration too short

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15
Q

When is tongue thrust swallow seen

A
  1. Transitional stage in normal maturation till age 6 (children change to solid food from soft bite) - no. of >6 children with tongue thrust 10x of AOB
  2. Individuals with displaced incisors - adaptation to achieve anterior oral seal (EFFECT not cause)
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16
Q

Does sustained forward resting tongue posture cause malocclusion

A

YES - affects vertical and horizontal position of teeth

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17
Q

Does mouth breathing cause malocclusion

A

unlikely a frequent etiological agent

Mouth breathing –> head extends (drops backwards) –> jaws move apart (elevation of maxilla and depression of mandible + tongue) –> man drops down

Results in:
1. Supraeruption of posterior teeth unless compensated by vertical growth of the ramus –> downwards and backwards rotation of ramus –> Increase in face height, AOB, increased OJ
2. Increased pressure from stretched cheeks –> constricts maxillary dental arch (+ elimination of tongue pressure) –> posterior crossbite

Classic adenoid facies: Narrow width dimensions, protruding teeth, lips separated at rest

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18
Q

How does soft tissue exacerbate or improve the malocclusion of Class II Div 1 patients?

A

Exacerbate:
1. Lower lip trap –> lower incisor retroclination and upper incisor proclination
2. Active lower lip + low lip line –> Retroclination of lower incisors
3. Forward resting tongue posture and lip incompetence or short upper lip –> Upper incisor proclination

Improve: Lip-to-lip seal by circumoral muscle activity –> reduce overjet severity

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19
Q

How do habits exacerbate malocclusion of Class II Div 1 patients

A

Non-nutritive sucking (>6hrs a day) –> proclination of upper incisors + retroclination of lower incisors

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20
Q

How do dental features exacerbate malocclusion of Class II Div 1 patients

A

Maxillary crowding –> labial displacement/proclination of upper incisors

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21
Q

How does soft tissue exacerbate the malocclusion of Class II Div 1 patients?

A
  1. High lower lip line (due to reduced LAFH) –> upper incisor retroclination
  2. Active muscular lips –> Bimax retroclination
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22
Q

How does increased inter-incisal angle cause crowding affect Class II div 2 malocclusions?

A

Lack of occlusal stop –> continued overeruption of incisors

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23
Q

How do dental features exacerbate malocclusion of Class II Div 1 patients

A
  1. Labial displacement/proclination of lower incisors
  2. Palatal displacement/retroclination of upper incisors
  3. Functional shift (Pseudo Class III) secondary to occlusal interferences
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24
Q

What skeletal features cause posterior crossbites?

A
  1. True transverse discrepancy (mismatch in the widths of the arches)
  2. Relative transverse discrepancy (positions)
    - Mandibular buccal crossbite - SK class III
    - Scissorsbite - SK Class II
  3. True skeletal asymmetry
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25
Q

What is the difference between hemimandibular elongation and hyperplasia

A

Elongation refers to only in the transverse plane (midline deviation) while hyperplasia refers to both the vertical (cant) and transverse plane

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26
Q

Does childhood fractures of the jaw affect mandibular growth

A

75% normal mandibular growth (not a big contributory factor)
Growth is affected if scarring restricts normal movements –> function is needed for growth
Facial asymmetry if it is unilateral or asymmetrically affected

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27
Q

What causes asymmetric mandibular deficiency

A

Rheumatoid arthritis/congenital absence of tissue eg. hemifacial microsomia

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28
Q

Does mouth breathing cause AOB or posterior crossbites?

A

not a major etiological factor

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29
Q

How does tooth size arch length discrepancies cause intra-arch orthodontic problems?

A

Causes crowding or spacing
Genetics:
- arch width
- arch length
- anomalies in dental development: size, shape, number of teeth

Environmental:
Premature loss of primary/permanent tooth

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30
Q

How does Hypodontia cause intra-arch orthodontic problems?

A
  • Retained primary teeth have poor prognosis :(
  • Spacing and drift of teeth
  • Lack of alveolar bone development
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31
Q

How does Macrodontia/Microdontia cause intra-arch orthodontic problems?

A

Macrodontia: crowding and displacement/impaction
Microdontia: Spacing and drift of teeth

Mismatch in size = disruption of normal occlusion

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32
Q

What is boltons’s discrepancy

A

MD width of upper teeth crowns should = lower teeth crowns

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33
Q

How does Supernumary teeth cause intra-arch orthodontic problems?

A
  • Impede eruption
  • Deflect eruption path –> displacement or rotation
  • Median diastema (mesiodens)
  • No effect :D
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34
Q

How does premature loss of deciduous teeth cause intra-arch orthodontic problems?

A
  1. Early loss of E:
    - Mesial drift and tipping of 6s (space loss esp maxilla - bone less dense hence tipping occurs easily)
    - Localised molar class II or III relationship
    - Impaction.displacement of successor
  2. Early loss of Cs
    - Distal drift and lingual collapse of incisors (space loss + midline deviations)
    - Impaction displacement of successor
  3. Early loss of 6s
    - KIV midline deviations
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35
Q

How does late lower incisor crowding occur?

A

Theories:
1. Late mandibular growth:
Forward –> lip pushes incisors lingually
Downwards or upwards rotation –> incisors move lingually
2. Lack of interproximal attrition in the modern diet
3. Presence of a third molar (active/passive role) –> weak association

36
Q

How does bimax proclination occur?

A
  1. Tooth size arch length discrepancy
  2. Lack of lip tonicity OR forward tongue resting posture

Ethnic origin: African American

37
Q

How does spacing occur?

A
  1. Generalised/localised microdontia
  2. Hypodontia (congenital absence or early removal)
  3. Pathologic tooth migration (eg. Perio)
  4. Median diastema
38
Q

How does a median diastema (max) occur + when does it persist?

A

Physiological (during transitional dentition)
- Early mixed dentition: frenal attachment attaches to the incisive papilla –> migrates labially to labial mucosa during normal development –> diastema closes as lateral incisors and canines erupt

Persists if:
1. Hypodontia/Macrodontia (usually laterals)
2, Thick frenal attachments
3. Frenal attachments remain at close proximity to incisive papilla
4. Supernumerary tooth
5. Digit sucking habit
6. Forward resting tongue posture

39
Q

How does displaced teeth occur?

A
  1. Abnormal position or orientation of tooth germ (eg. Palatally displaced canines)
  2. Space deficiency - affects teeth that erupt last in a segment (max canines and man 5s)
  3. Retained primary tooth
  4. Supernumerary teeth or cysts
  5. Habits
40
Q

What traits are hereditary

A

Both monogenic (1 gene) and polygenic (multiple genes) are hereditary

41
Q

What does polygenic mean

A

Many gene loci; each gene with a minimal effect and the effect of all genes being additive

Environmental factors sometimes play a larger role as one gene only has minimal effect

42
Q

What causes differences between monozygotic and dizygotic twins and what does the difference in these two categories suggest?

A

Monozygotic: environment
Dizygotic (50% of gene complement): genotype and environment

Difference suggest greater genetic effect

43
Q

What are the components involved in normal occlusion?

A
  1. The size of maxilla
  2. The size of mandible (ramus and body)
  3. Factors that affect relationship between the two skeletal bases eg. cranial base and environmental factors
  4. Arch form
  5. Size and morphology of teeth
  6. Number of teeth
  7. Soft tissue morphology and behaviour (both genetic and environmental)
44
Q

Are these heritable?
1. Craniofacial skeletal dimensions
2. Dentoalveolar (occlusal) traits:
2a. Arch width and arch length
2b. OJ, OB, molar r/s
3. Soft tissue morphology and behaviour

A
  1. Moderate to high (increased with age)
  2. Lower than 1, 2a>2b(decreased with age)
  3. Has a genetic component
45
Q

Are dental characteristics environmentally or dentally influenced?

A

Increasing environmental influence
Except specific malocclusion eg. Hypodontia, palatally displaced canines

46
Q

What are the etiology of malposition/malformation of jaws?

A
  1. Inherited patterns (majority)
  2. Defects in embryologic development (rare)
  3. Trauma (rare)
  4. Functional influences
47
Q

What are the racial tendencies for skeletal problems?

A

Class II: US and Northern European population
Class III: East Asian
AOB: African-Americans
Deep overbites: Caucasians

48
Q

Are Class II Div 1 malocclusions genetic?

A

Possibly polygenic inheritance: Mandibular retrognathia (with smaller man)

49
Q

Are Class II Div 2 malocclusions genetic?

A

Familial occurrence documented
Strong evi for genetics as main aetiological factor (100% moozygotic, 90% dizygotic)

Polygenic
Possibly autosomal dominant with incomplete penetrance and variable expressivity

50
Q

Is mandibular prognathism genetic?

A

Polygenic or multifactorial trait
Most famous example: “Hapsburg Jaw”
Autosomal dominant

Polygenic
- incidence in family (5x more)
- 6x higher in monozygotic vs dizygotic

51
Q

Are Class III malocclusions genetic?

A

Genetic and Environmental factors both play a role
Polygenic + Multifactorial!

Heredity:
- Heterogenous
- Monogenic influences in some families
- Multifactorial in others

Environmental:
- Nasal blockage
- Enlarged tonsils
- Hormonal disturbances
- Endocrine imbalances (Acromegaly –> increase growth hormone)
- Posture

52
Q

What is the polygenic multifactorial threshold model?

A

Polygenic model with a threshold requires a minimum number of genes to show.

Used to explain familial distribution and the prevalence within general population and siblings of affected persons

Possibly different modes of transmission in different families/populations

53
Q

Are vertical skeletal proportions genetic?

A

Greater heritability for TAFH, LAFH than UAFH (due to airway). PFH (due to dietary effects)

Altered function may play a role: increased nasal obstruction-> mouth breathing

54
Q

Is the craniofacial heritable?

A

Polygenic inheritance: Anterior cranial base
Mandibular body length
Lower face height

Multifactorial (genetics and environment):
Facial and Dental morphology

55
Q

Heredity in arch width and length vs other occlusal variables

A

Arch width and length > other occlusal variables

Intra-arch spacing and tooth position: 69-89%
Overbite 53%
Overjet: almost 0

56
Q

How does the pressure environment affect the tooth position genetically

A

Soft tissue morphology and behaviour which influences the dentoalveolar morphology has a genetic component

57
Q

What dental factors has genetic influence?

A

Tooth number
Tooth size
Tooth morphology
Tooth position
Tooth eruption

58
Q

What are the genes that influence the stability in dental patterning.

A

MSX1 and MXS2 gene

59
Q

Is tooth size solely genetic?

A

No
Polygenic multifactorial threshold model

60
Q

Is hypodontia isolated and hereditary?

A

Can be a syndrome eg. ectodermal dysplasia or isolated (more common)

Often familial (pop prevalence = 5%, familial prevalence = 50%)
High concordance rate in monozygous but discordance in dizygous

Polygenic model

61
Q

What are the genes that cause hypodontia

A

MXS1
PAX9
LTBP3
KROX-26 genes
Chromosomal location 10q11.2

62
Q

Is supernumary teeth heriditary

A

Genetic
Under the control of a number of different loci

Supported by twin studies and prevalence in family

63
Q

What other feature is associated with supernumary teeth

A

Increased MD width of maxillary incisors and canines

64
Q

Is ectopic maxillary canines hereditary?

A

Multifactorial - genetic and environmental

65
Q

Why is there particularly more disturbance in the normal development of maxillary canines?

A
  1. Long path of eruption (22mm from close to the floor of the orbit)
  2. Guidance theory of canine impaction - canine is guided by root of lateral hence missing, peg-shaped/small or short-rooted upper lateral incisors cause disruption to canine descent)
66
Q

Is ectopic maxillary canines usually buccally or palatally ectopic and is it associated with crowding?

A

15% buccal + associated with dental crowding
85% palatal + not associated with dental crowding

67
Q

Is palatally ectopic maxillary canines genetic?

A

Some genetic influence
(prevalence in fam > pop)

68
Q

What other symptoms are associated with palatally ectopic maxillary canines?

A

Hypodontia
Microdontia
Supernumerary teeth
Other ectopically positioned teeth
Spacing
Delayed dental development

69
Q

What are the proposed genes causing palatally ectopic maxillary canines

A

MXS1 and PAX9

70
Q

What is the local environmental effect causing ectopic maxillary canines

A

Missing or small maxillary lateral incisor on the same side

71
Q

Is maxillary canine - first premolar transposition hereditary?

A

Strong evidence yes
Familial occurrence
Bilateral occurrence
Female and different ethnic groups predominance

72
Q

What is incomplete vs complete transposition

A

Incomplete = only crown is transposed
Complete = root is also transposed

73
Q

Is submerged primary molars hereditary?

A

Significant genetic component
(prevalence in siblings 18%, prevalence in pop <10%)
(High concordance in monozygotic twins)

74
Q

Is primary failure of eruption (all teeth distal also affected) hereditary?

A

Clear genetic influence
Familial occurrence (1/4 of cases)

75
Q

What gene causes primary failure of eruption

A

Parathyroid hormone 1 receptor gene (PTHR1)

76
Q

Does mouth-breathing cause long-face

A

Numbers higher predominantly higher in long-face vs normal

Long-face NOT predominantly mouth breathers –> other aetiological causes

77
Q

What are environmental insults (Teratogens) in embryologic development and what does it cause?

A

Fetal alcohol syndrome: Midface deficiency
Aspirin, Cigarette smoke: Cleft lip and palate
Retinoic acid, thalidomide: Malformations similar to craniofacial microsomia and Treacher Collins Syndrome

78
Q

What are genetic disorders in embryologic development and what gene causes it?

A

Treacher Collins syndrome: TCOF1 gene
Craniosynostosis Syndromes: Fibroblast growth factor receptor genes
Crouzon’s Syndrome: Fibroblast growth factor receptor gene 2
Craniofacial microsomia
Cleft lip and palate

79
Q

What are some skeletal growth disturbances (Fetal moulding and birth injuries) and what do they cause

A
  1. Intrauterine moulding: Severe max deficiency, Severe man def and cleft palate (Pierre Robin seq)

Removal of growth restriction may lead to subsequent normal growth

  1. Birth trauma to mandible (rare)
80
Q

How does childhood fractures of the jaw affect the growth

A

Scarring around TMJ restricts condyle translation –> reduced function on that side –> reduced growth –> Facial asymmetry

Requires early intervention if deficient growth is observed

81
Q

How does muscle dysfunction affect the growth of the jaw

A

Loss of musculature due to damage to motor nerve –> no function –> no growth –> underdevelopment of the face

Excessive muscle contraction eg. torticollis –> restricts growth on affected side –> facial asymmetry

Decrease in tonic muscle activity eg. muscle dystrophy, cerebral palsy, muscle weakness syndromes –> mandible drops down –> increased anterior facial height + excessive eruption of posterior teeth + narrowing of max arch + AOB

82
Q

How does acromegaly affect the growth of the jaw

A

Anterior pituitary tumour that secretes excessive growth hormone –> excessive mandibular growth (Class III malocclusion in adult life)

83
Q

How does ankylosis of primary molars cause malocclusion?

A

Totally submerged = unlikely to exfoliate

  • Delays eruption of successor + dilaceration
  • Drifting of adjacent teeth into the space
  • Posterior open bite
84
Q

What are generalised causes of delayed tooth eruption

A
  1. Familial
  2. Hereditary gingival fibromatosis
  3. Down’s Syndrome
  4. Cleidocranial dysplasia
  5. Rickets
  6. Endocrine disorders
  7. Long-term chemoterapy
85
Q

What are local causes of delayed tooth eruption

A
  1. Mechanical obstruction (eg. retained deciduous tooth, supernumerary, cyst, mucosal barriers eg. scar tissue)
  2. Crowding
  3. Dilaceration (developmental, secondary to trauma)
  4. Abnormal position of crypt
  5. Ankylosis of deciduous tooth
  6. Primary failure of eruption
  7. Cleft lip and palate
  8. Radiotherapy
86
Q

What causes impaction/displacement of second premolars?

A

Ectopic eruption path of permanent first molars (too mesial) –> impacted against E –> root of E damaged –> mild (spontaneous disimpaction) OR severe –> early loss of E due to caries and/or root resorption –> space loss

Orthodontics (18 decks)

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