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Ortho > Test 1 > Flashcards

Test 1 Flashcards

1
Q

Who is the Father of Orthodontics?

A

Dr. Edward Angle.

First classification of malocclusion.

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2
Q

What is “normal occlusion” according to Angle?

A

MB cusp of upper molar in MB groove of lower molar. Good dental arch form and good tooth alignment.

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3
Q

What is a problem of Angle’s classification?

A

Not sufficiently detailed as it only looked at the first molar.

Assumes MX molar is in constant position to cranium.

Important characteristics are absent: Transverse, vertical, skeletal discrepancies, protrusion/retrusion, doesn’t consider other teeth.

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4
Q

What are some advantages of Angle’s Classification?

A

First def. of normal. Orderly classification of malocclusion. Short cut. Orderly decrease in data base.

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5
Q

What did Martin Dewey do?

A

Propose subdivisions of Class 1.

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6
Q

Simon Classification

A

Attempted to relate Casts and Teeth to Cranium.

Frankfort horizontal plane, Orbital plane (anteroposterior) Sagittal plane (median palatal raphe) plane, transverse.

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7
Q

Cephalometric radiography

A

Accurate assesment skeletal relation of jaws. Dental and Dental/skeletal relation. Growth studies.

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8
Q

Ackerman-Proffit Classification System

A

5 categories of discrepancy.

Skeletal dental and soft tissue in all 3 planes of space.

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9
Q

Neutocclusion

A

Class 1

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10
Q

Distocclusion

A

Class 2

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11
Q

Mesiocclusion

A

Class 3

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12
Q

What is the range of each classification category?

A

6 mm.

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13
Q

Incidence of normal

A

30%

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14
Q

Incidence of Class 1

A

50-55%

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15
Q

Incidence of Class 2

A

15-20%

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16
Q

Incidence of Class 3

A

1%

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17
Q

What factors have a high heritability?

A

Craniofacial dimensions, jaw size and possibly jaw position.

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18
Q

What factors have a low heritability?

A

Arch size and arrangement.

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19
Q

What are some environmental factors?

A

Mouth breathing, tongue (resting position vs thrust), soft diet, sleep position.

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20
Q

What is the etiology of crowding

A

Genetics + environment

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21
Q

What is the etiology of Class 1 non-skeletal problems such as crossbites and tooth malalignment

A

Environmental

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22
Q

What is the etiology of a skeletal Class 2 malocclusion

A

Genetic. MN AP deficiency common.

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23
Q

What is the etiology of a skeletal Class 3 malocclusion?

A

Genetic. 50% MX deficient. 50% MN excess. Usually a combination.

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24
Q

What is the etiology of an openbite?

A

Environment for thumb sucking and breathing. Genetic for vertical growth.

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25
Q

Where is the cuspid located in normal occlusion? In Class 1?

A

MX cuspid between MN canine and 1st bicuspid. In class 1 it’s position is variable.

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26
Q

Bimaxillary protrusion

A

Both jaws protrude

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27
Q

Overbite

A

Vertical overlap

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28
Q

Overjet

A

Horizontal overlap

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29
Q

What plane causes posterior crossbites?

A

Transverse. Can be skeletal, dental or combination.

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30
Q

Unilateral vs bilateral posterior cross bite

A

Unilateral-can be bilateral with a functional shift of the mandible to one side to gain maximum interdigitation. Bilateral is the more severe discrepancy. Both can occur in any classification of malocclusion.

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31
Q

Functional Unilateral Crossbites

A

Asymmetric growth. Big reason for early treatment, because it can be eliminated with expansion therapy.

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32
Q

How is functional chewing different with crossbite.

A

Cycle has an abnormal path, they chew more slowly. Correction of crossbite increased speed of chewing, but not the path.

Bite force is less.

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33
Q

Molar relationship in Class 2 Div 1.

A

MB cusp of MX 1st molar occludes in the embrasure between MN first molar and 2nd bicuspid.

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34
Q

Canine and anterior relationship in Class 2 Div 1

A

Upper cuspid occludes on or anterior to MN canine. There is an extra overjet that results from the molar relationship. Centrals are normal to labially inclined.

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35
Q

How do muscle functions affect a Class 2 Div 1 malocclusion?

A

Abnormalities are common. Can increase deformity, such as lower lip habit. Tongue may be low and thrust forward for lip seal.

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36
Q

TMD problems in Class 2 Div 1

A

Increased incidence. No canine guidance.

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37
Q

What are the most common skeletal patterns with Class 2 Div 1?

A

Mandibular AP deficiency. Retrognathia. Mandibular retrustion. (Most common)

Maxillary AP excess. Maxillary protrusion.

Vertical Relations. Excess or deficiency. Affects molar relationship and lower face height.

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38
Q

Which grows more AP in adolescence? MN or MX?

A

MN.

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39
Q

Does Class 2 correct due to jaw growth?

A

NO. Jaws change, teeth don’t.

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40
Q

Do Class 2s grow differently than Class 1?

A

Girls: MX grows more horizontally and procline. MN grows more horizontally.
Boys: Increased MX forward growth. MX and MN teeth procline more.

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41
Q

Overjet

A

Horizontal excess.

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42
Q

Anterior deep bite

A

Anterior vertical excess

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43
Q

Anterior Open Bite

A

Anterior vertical deficiency

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44
Q

Class 2 Div 2 Distinguishing features.

A

Class 2 molars. Upright MX incisors, in labioversion. Cuspid in Class 2 relation. Usually a deep bite.

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45
Q

Class 2 Div 2 muscle functions

A

Abnormal placement of lip pressure. Normally higher on incisal than cervical.

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46
Q

Class 2 Div 2 skeletal pattern

A

Highly variable. Mandibular retrusion. Flat mandibular plane angle. “

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47
Q

Class 2 Div 2 Facial appearance

A

Strong chin, straight or convex profile.

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48
Q

Class 3 Distinguishing characteristics

A

Molar: MB cusp of MX molar occludes in embrasure between MN 1st and 2nd molar.
Cuspid: MX cuspid occludes between MN 1st and 2nd bicuspid.
Usually an anterior crossbite

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49
Q

Class 3 muscle function

A

Perioral may be abnormal due to anterior crossbite. Tongue position may be low causing a well rounded lower arch and narrow MX arch.

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50
Q

Dental only malocclusion class 3

A

MX retrustion or MN protrusion. (the teeth, not the bones)

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51
Q

Skeletal pattern Class 3

A

50% MX retrustion, AP deficient. 50% MN protrustion, AP excess.

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52
Q

Class 3 Subdiv right/left

A

Class 3 only on one side.

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53
Q

Pseudo Class 3

A

Anterior cross bite.

Functional shift of mandible anterior.

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54
Q

Mastication efficiency effected by a Class 3.

A

34% decrease in efficiency.

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55
Q

Branchial Arches

A

Arise in the 4th week. Bordered medially by the pharynx.

Each arch contains an artery, cartilage and nerve. Clefts or grooves separate the arches.

Endoderm forms the pouch Ectoderm forms the cleft.

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56
Q

What cartilage is a scaffold for the mandible and what arch does it come from?

A

Meckel’s. 1st branchial arch.

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57
Q

What nerves come from what arch?

A

5, 7, 9, 10.

1st: Trigeminal (mandibular)
2nd: Facial
3rd: Glossopharyngeal
4th: Vagus

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58
Q

What are the derivatives of the 2nd branchial arch?

A

Auricle and external auditory canal and cervical sinus. Facial nerve.

Skeletal: Stapes, styloid process, body and lesser horn or hyoid bone, stylohyoid ligament.

Hyoid stapedia artery.

MUSCLES OF FACIAL EXPRESSION.

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59
Q

What are the derivatives of the 1st branchial arch?

A

Median nasal process, lateral nasal process, maxillary process, and mandibular process.
MUSCLES OF MASTICATION.
Malleus, incus, sphenomandibular lig. Meckel cart.
Maxillary artery.

60
Q

3rd Branchial arch derivatives

A

Epithelium around the ear body and greater horn of the hyoid bone. Nerv 9.

Internal carotid artery.
Stylopharyngeous.

61
Q

4th-6th branchial arches

A

Epithelium around the ear. Vagus nerve. Laryngeal cartilages with some spinal accessory nerve innervation.

Right subclavian artery. Aorta.
Pharyngyal and laryngeal muscles.

62
Q

Pouch derivatives

A

1: Middle ear and auditory tube
2. supra tonsillar fossa
3. Thymus and parathyroid
4. Thymus, parathyroid and ultimobranch body.

63
Q

What are the 5 stages of development?

A

1: Germ layer formation and initial organization.
2: Neural tube formation and intitial oropharynx.
3: Origin, migration, and interation cell population.
4: Formation of organ systems-pharyngeal arches
5: Final differentiation into skeleton, muscles and nerves.

64
Q

When does fetal alcohol syndrome occur?

A

During the first stage of germ layer formation and initial organization. 17 days post fertilization.

Underdeveloped midface, mental retardation, physical defects.

65
Q

When does Anencephaly occur?

A

2nd stage: Neural tube formation.

Cranial vault and cerebral hemispheres rae mizzing or in small masses.

66
Q

When doe hemifacial microsoma occur?

A

3rd stage: origin, migration, interaction of cell populations.

67
Q

What drugs interfere with migration of neural crest cells?

A

Thalidomide, accutane, isotretinoin.

68
Q

When does Mandibulofacial Dystostosis occur?

A

Treacher-collins syndrome. 3rd stage: origin, migration and interaction of cell populations. Excess cell death in trig gang. Secondary effects on neural crest cells.

1st branchial arch deformity. 
-hypoplasia in MN and zygoma
Antimongoloid slant
Deformed ears and external auditory canals.
Eartags
Macrostomia
High or cleft palate.
69
Q

When does clefting of lip occur?

A

During the 4th stage or formation of organ systems. It is the failure to fuse median and lateral nasal process.

28-38 days in.

70
Q

What are the incidences of cleft lip and palate?

A

Jap: 1:500
Cauc: 1:800
AA: 1:2500
Palate only: 1:2500

71
Q

When does clefting of palate occur?

A

4th stage, formation of organ systems. 42-55 days. 60% occur with cleft lip.

72
Q

When does macrostomia occur?

A

4th stage. Unusually large mouth.

73
Q

When does a facial cleft occur?

A

4th stage. goes up to the eye.

74
Q

When does synostosis syndromes occur?

A

5th stage, final differentiation of tissues.

Early closure of cranial and facial sutures. Distortion and lack of growth.

75
Q

When does Crouzon’s syndrom occur?

A

5th stage: final differentiation.

Underdevelopment of midface with bugling of eyes. Prenatal fusion of superior and posterior sutures of maxilla along wall orbit.

Usually leads to class 3.

76
Q

When does growth velocity peak?

A

18-22 weeks following fertilization.

77
Q

When do girl’s height growth velocity peak? Boys?

A

Girls: 11-13
Boys: 13-16

78
Q

What are some factors that effect physical development?

A

Pattern of growth, premature birth/low birth weight. Chronic illness. Early trauma.

79
Q

What is the Pierre-Robin Sequence?

A

Retrognathia, glossoptosis (retraction of the tongue), airway obstruction.

80
Q

Describe the infantile swallow

A

Active contracture of lips, tongue contacts lower lip. Little activity in posterior tongue or pharyngeal muscles. Disappears after 1 year.

81
Q

Describe the adult swallow

A

Lips relaxed, tongue tip against the alveolar process behind the central incisors. Posterir teeth together. Get it by age 8. Anterior open bite delays development.

82
Q

Juvenile Chewing vs. Adult Chewing

A

Juvenile has increased elevator muscle activity, complexity of tongue movements. Lateral moves laterally upon opening then back to midline.

Adult: Mandible moves straight down on opening and moves laterally to bring teeth into contact with food.

Transition to adult at age 12. Cuspids?

83
Q

Posterior Cross bites effecting oral function

A

Fewer teeth contact, decreased bite force, abnormal chewing pattern, asymmetric MN growth, functional lateral shift.

84
Q

What is the trend of development?

A

Gradient from anterior to posterior. Lips mature first, then progresses to posterior of mouth.

85
Q

Normal sequence of eruption of primary teeth?

A

MN centrals. MX and MN incisors. MX and MN 1st molars. MX and MN canines. MN then MX 2nd molars.

86
Q

What are the primate spaces?

A

MX: Lateral and canine
MN: canine and first molar.

87
Q

What age is desiduous dentition complete?

A

3 years.

88
Q

What is pre-emergent eruption?

A

Labial drift of the follicle.

89
Q

What are the 2 required processes of eruption?

A

Resorption of the bone and primary teeth.
Eruption mechanism which moves the tooth into the resorbed area.

They are separate mechanisms but must occur together.

90
Q

What is the rate-limiting and controlling factor in eruption?

A

Resorption.

91
Q

What are factors that affect the resorption?

A

Occurs even when permanent tooth is absent. Accelerated by inflammation, occlusal trauma or orthodontics. Slowed down by splinting or absence of permanent tooth.

92
Q

Eruption mechanism

A

Localized in PDL. Root lengthening is not a factor. A defect is primary failure of eruption.

93
Q

Why do teeth fail to erupt?

A

Usually due to mechanical obstroction. Ankylosed decidous teeth, inadequate space, syndrome such as cleidocranial dysplasia, etc.

94
Q

Cleidocranial dysplasia

A

Lack of permanent tooth eruption. Supernumerary teeth, bone resistant to resorption. gingival fibrosis

95
Q

Gingival fibrosis and eruption.

A

Can be a part of a syndrome or the result of a premature loss of primary teeth and hyper keratinization of the overlying gingival tissue

96
Q

Primary Failure of Eruption

A

May affect 1 or more posterior quadrants. Molars and sometimes bicuspids, not incisors.
Defect in eruption mechanism. Path is cleared by resorption, but teeth still don’t erupt.
TEETH CANNOT BE MOVED BY ORTHO FORCES.
All teeth distal are involved.
Treatment: remove affected teeth.

97
Q

Post-emergent eruption spurt

A

Very rapid eruption

98
Q

Juvenile occlusal equilibrium

A

Greatly slowed after teeth reach occlusion. Eruption at night, intrusion with eating. Parallels jaw growth. Forces on tooth.

99
Q

Adult Occlusal equilibrium

A

Very slow rate. Face height constant or increases.

100
Q

What are the Rules of Thumb?

A

Teeth erupt when approximately 3/4 of the root is developed.
Eruption time is usually 1.5 years/quarter stage.
If deciduous tooth is lost before 1/3 of the root his formed, decreases eruption rate. After 1/2 root is formed, increases eruption rate.

101
Q

Timeline of eruption

A

5 years from crypt to emergence
At alveolar crest when 2/3 of root is developed.
12-20 months from alveolar crest to occlusion.

102
Q

Gender and tooth eruption

A

Girls erupt their teeth 3-4 months earlier than boys.

103
Q

What are some influencing factors on tooth eruption?

A

Sex, skeletal development, disease, nutrition, genetics, periapical lesions, caries. Premature exfoliation. Premature birth. Eruptive forces.

104
Q

MX vs MN early loss of primary teeth?

A

Eruption sequence hastened in MX, no effect in MN.

105
Q

Premature birth and eruption?

A

PMB-earlier eruption of incisors and first molars.

106
Q

What are influencing factors on eruptive forces?

A
  1. Crypt position (anterior incisor movement)
  2. Presence or absence of adjacent teeth.
  3. Presence or absence of deciduous tooth.
  4. Rate of bone/tooth resorption.
  5. Adequate eruption mechanism.
  6. Mesial drift
  7. Oral musculature.
  8. Anterior component of force of occlusion.
107
Q

What are normal changes in eruption?

A
  1. Incisor Crowding (due to available incisor space)
  2. Maxillary midline diastema.
  3. Upper incisor alignment.
  4. Arch dimension changes. Arch width increases. Intercanine width. Arch length changes. Leeway space.
108
Q

What are options for managing an open bite?

A

Erupt the anterior teeth or intrude the posterior teeth.

109
Q

If you don’t know the cause of malocclusion, how does that affect your management?

A

May be difficult to predict the outcome of treatment, to achieve the desired outcome and to retain the achieved outcome.

110
Q

For an individual patient with malocclusion, how likeley is it that you will be able to identify the specific etiologic factor that caused the malocclusion?

A

Low. Only 5% of the US population has malocclusion with have a specific known cause.
60% of the US population has a malocclusion that is the result of a complex and poorly understood combination of hereditary and environmental influences.
35% have normal occlusion.

111
Q

How does our knowledge or lack of knowledge regarding etiology influence management?

A

If we know the cause:

  1. Address the causal factor.
  2. Manage the effect
  3. Delay treatment until after the causal agent is no longer active (ex. genetically excessive MN growth)
112
Q

If we don’t know the cause of a malocclusion how do we manage uncertainty?

A

Communicate. Inform. Clarify expectations. Discuss options. Costs/risks vs. benefits. Underpromise, overdeliver.

If the benefits are low and risks are high, you need to recognize that and counsel them that no treatment is a real option.

113
Q

What are the 3 main ways to manage uncertainty?

A

Communicate, inform and involve.
Leave good options open initially, monitor and reassess through treatment.
Do no harm, avoid ineffective or harmful treatments.

114
Q

What are the 2 major cateogires of causal agents?

A

Genetic and environment.

115
Q

Describe the thumbsucking malocclusion.

A

Anterior openbite. Flared and spaced MX incisors. Lingually positioned MN incisors. Narrow open arch. Possible crossbite.

116
Q

How does thumbsucking work to cause a malocclusion?

A

Amount of pressure is not a big deal, it is the amount of time. 6 hours. Openbite is caused by interference with anterior eruption and excessive posterior eruption. The narrow MX arch decreases the tongue pressure.

117
Q

How is thumbsucking best managed?

A

The objective is internal motivation. The kid needs to want to do it. Most changes resolve spontaneously if the habit is discontinued before the eruption of permanent incisors at about 6 yo. Don’t waste too much energy before then. Peer pressure helps. At incisor eruption, start addressing it. Often helps if you treat them as an “adult” and have them take charge of their own care. Reminders, and rewards. A cemented reminder is often successful. Don’t start ortho treatment until the habit has stopped.

118
Q

Does a tongue thrust cause an open bite?

A

No. Could be a result of facilitating swallowing or a stage of maturational development. But the duration is too short. You need that 6 hours.

119
Q

How does tongue posture create malocclusion

A

Openbite wherever the tongue is postured interocclusally or pushing on teeth producing large arches with generalized spacing. Pressure on teeth for more than 6 hours per day.

120
Q

How do you manage tongue posture?

A

Remove tongue from between the teeth either with surgical reduction (low predictable benefit with high cost) or with a tongue crib (problematic for long term stability). Reposition the teeth to widen arches to get around tongue (buccal lingually) or close space without encroaching on the tongue (poor stability). Often hard cases to manage. No treatment or limited objectives: get the teeth straight, but leave the openbite or some spaces.

121
Q

What type of malocclusion can a condylar fracture cause?

A

Asymmetric growth and mandibular asymmetry with asymmetric posterior occlusion. There is scarring in the area that restricts normal growth movements and the soft tissues cannot pull MN forward along with the rest of the growing face. 75% have normal growth.

122
Q

How is a condylar fracture best managed?

A

LEAVE IT ALONE. But you want early mobilization of the joint. You don’t want to reposition surgically because it usually just causes more scarring.

123
Q

If asymmetry occurs in a condylar fracture, how do you manage?

A

Growth modification if growing. If there is no translation of the condyle, it is unlikely to respond normally. It is appropriate to remove restriction surgically before growth modification.

124
Q

Does early loss of primary teeth cause malocclusion?

A

Yes, posterior crowding and a poor molar relationship. Permanent molars move mesially when a space opens. Forces from the active contraction of transseptal fibers in the gingiva plus or minus the pressures from the lips and cheeks.

125
Q

How do you manage the early loss of primary teeth?

A

Block the permanent molar from mesial eruption through space maintenance. Regain space if needed if drift has occurred and hold tit.

126
Q

Early loss of primary first molar or canine. Describe malocclusion.

A

Crowding and asymmetry if loss is on one side only from distal drift of anterior teeth.

127
Q

Does mouth breathing cause malocclusion?

A

Yes. Openbite, increased overjet, narrowing of maxilla. Posturing of the mouth could change the equilibrium pressures on the jaws and teeth. Posterior teeth could supererupt, the MN rotates down and back, opening the bite anteriorly and increasing overjet. Increased pressure from the stretched cheeks cause narrow MX arch.

Nasal airway obstruction or habit.

128
Q

How is mouthbreathing managed?

A

If nasal airway is obstructed, send to ENT for surgery. The effect on the future facial growth pattern is unpredictable. Important to do no harm

Habits can be difficult to address effectively.

Communicate! Uncertainty regarding cause and unpredictability of outcome.

Address the effect. Malocclusion. Intrude posterior teeth. Delay definitive treatment until after growth is complete. Orthognathic surgery.

129
Q

What are possible etiologic factors if the class 2 is skeletal?

A

Genetics, mouth breathing, fetal molding/birth injuries, muscle dysfunction.

130
Q

How do you manage a skeletal class 2?

A

Decrease uncertainty. Manage uncertainty. Avoid irreversible procedures. Do no harm.

131
Q

What are possible etiologic factors of an open bite?

A

Genetics, digit habit, tongue posture, mouth breathing, muscle weakness, idiopathic condylar resorption.

132
Q

How do we manage an open bite?

A

Decrease uncertainty. This is through thorough medical history, observing, data, etc. Manage uncertainty. Address most likely cause or effect.

133
Q

Growth vs. Development

A

Growth: Anatomic phenomenon. Increasing in physical size or number of cells.
Development: physiological and behavioral phenomenon. Increase in complexity or specialization.

134
Q

Reflects Proportionality

A

Change in proportional relationships over time.

135
Q

Cephalocaudal Gradient of Growth

A

The further from the top of the head, the more the structure grows. MX vs MN.

136
Q

Differential Jaw Growth

A

MX grows at a similar rate as the head. MN grows more similarly to the rest of the body.

137
Q

Give 2 examples of growth centers.

A

Epiphysis of long bone and synchondrosis of cranial base. Area where growth is controlled.

138
Q

What causes the cranial vault to expand?

A

Brain grows and sutures of the cranial vault allows for expansion and increased growth at periosteal suture growth SITES. Notice it is not a growth CENTER. The brain is causing the growth.

139
Q

What forms of bone growth does the Maxilla have?

A

Lateral is INTRAMEMBRANOUS.

Nasal Septum is CHONDROCRANIUM.

140
Q

What type of growth does the mandible have?

A

Translational. Up and back. Not of endochondrial origin. Condyle is a growth site.

141
Q

What are the cranial base synchondroses?

A

GROWTH CENTERS
Spheno-ethmoid
Inter-sphenoid
Spheno-occipital

142
Q

What are the mechanisms of MN morphological change?

A 
Cortical drift (addition and subtraction) concerning shape. Resorption and appostion. 
Translocation (displaced from one position to another)
143
Q

What are the 3 theories of growth control?

A

Bone/periosteum, cartilage, soft tissue/epigenetics.

144
Q

Functional Matrix theory

A

Moss in 1960 said that the genetic control is in the soft tissue.

145
Q

What is the Cartilage theory?

A

Cartilage is the determinant, and location of genetic control. Worked for longbones, SO synchondroses, Nasal septum, but not condylar. It appears that they can and do act as independently growing centers.

146
Q

Craniofacial Neurotrophism

A

Neural control of craniofacial skeletal morphogenesis and growth by the transmission of certain signaling proteins.

Ortho (2 decks)

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