Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Resto 3 > Bruxism > Flashcards

Bruxism Flashcards

1
Q

Define bruxism

A

Involuntary mandible excursive movements/ clenching that cause intermittent inter-occlusal friction over the unconsciously selected teeth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define attrition

A

tooth to tooth - physiological wear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define abfraction

A
  • abrasive cervical lesion induced by occlusal stress
  • flexural forces.
  • enamel fractures and exposes dentin
  • hypersensitivity
  • no time for sclerotic dentin creation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define abrasion

A

foreign object in mouth like brush

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define erosion

A

from acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Bruxism epidemiology? (4)

A
  • 6-8% mid age population
  • 1/3 world population
  • same prevalence men and women
  • higher prevalence in asians > euro-americans, and hispanic > than africans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 2 main groups of etiological factors for bruxism?

A
  • peripheral

- central/physiopathological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the peripheral etiology of bruxism (2)

A
  • occlusion

- anatomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the cental/physiopathological etiology of bruxism (4)

A
  • dream alterations
  • dopaminergic system alterations
  • medicines
  • genetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Whats ramffords theory?

A

Occlusion is the first resposible for onset of bruxism. Prematurities and balanced side occlusal contacts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Whats kardachi and bail&rughs theorys?

A
  • Interference removal doesnt eliminate bruxism

- occlusal scheme is relevant in force distribution during episodes but no proof of it being the etiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Who made theories about bruxism?

A
  • rammford

- Bailey &rugh, and Kardachi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Anatomical factors for bruxism?

A
  • more assymetry in condyle height
  • more bicigomatic and cranium width
  • more square maxilar arch
  • no evidence showing factors related to anatomy of the orofacial region
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Physiopathological factors MORE involved in etiology of bruxism?

A
  • sleep alterations
  • brain chemistry alterations
  • some medication and illegal drugs
  • tobacco / alcohol
  • genetics
  • traumas & diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What sleep alterations affect bruxism?

A
  • bruxism is parasomnia - same group of disorders such as sleepwalking, night fear*
  • arousal response
  • micro wake ups
  • sudden movements
  • increase in heart rate
  • respiratory changes
  • increased muscular activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which meds affect the dopaminergic system? (4)

A
  • SSRIs
  • amphetamine abuse
  • Nicotine stimulates 2x more = bruxism 5x more
  • alcohol same effect as nicotine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the genetic factors for bruxism? (3)

A
  • little evidence
  • 23% of monozygotic twins
  • family pattern 20-35%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Stress and personality for bruxism?

A
  • smaller than previously assumed

- unclear as it is different in different people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Why are we always concerned about bruxists? (5)

A
  • present dental injuries - attrition and abfraction
  • more difficult restorations
  • always feel soemthing and everything breaks
  • get tired and harder to work
  • harder to accept the truth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How are bruxist patients different? (4)

A
  • histological tooth characteristics
  • ability to discriminate change
  • muscle problem
  • reduced ability to respond to changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How are bruxists classified? (2)`

A
  • moment

- activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How are bruxists classified by moment? (3)

A
  • day
  • night
  • mixed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How are bruxists classified by activity? (3)

A
  • clenching
  • grinding
  • bracing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe centric/clenching vs bracing/eccentric? (4)

A
  • more difficult diagnosis
  • more difficult to control
  • > acute lesions
  • > muscular problems
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

bruxism symptomatology? (2)

A
  • muscular and articular

- dental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Bruxism symptomatology: muscular and articular? (4)

A
  • specially in centric bruxism
  • pain and tenderness in elevator muscles
  • functional limitation
  • can affect the muscles of the neck
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Bruxism symptomatology: muscular and articular treatment? (2)

A
  • mouth opener

- muscle relaxant prior to a long session

28
Q

bruxism symptomatology: dental?

A
  • occlusally and inscially
  • centric: inverted cusps and abfraction lesions
  • eccentric: smooth and polished surfaces, wear out of functional areas. attrition
29
Q

What does dental wear depend on? (6)

A
  • thickness and hardness of enamel
  • pH
  • age
  • presence of more abrasive materials (porcelain)
  • number of teeth present
  • malocclusions (overbites)
30
Q

Bruxism protrusive pattterns?

A

vertical
- shortening of crown and incisors
(aesthetic)
- there wont be posterior teeth affection (no descreased in VD)
- dentoalveolar compnsatory eruption of the anterior sector

31
Q

Bruxism lateral or horizontal pattterns? (3)

A
  • canine guide flattening
  • group function apperance
  • affectation of lateral sectors
32
Q

bruxisms: dental wear anteriorly? (3)

A
  • disappearance of incisal mamelons
  • enamle and dentin at same level
  • DD with erosion
33
Q

bruxisms: dental wear posteriorly? (3)

A
  • loss of occlusal anatomy
  • concave occlusal faces = inverted cusps (clenching)
  • cup of volcano lesions are typical of erosion
34
Q

Bruxism symptomatology: detnal? (6)

A
  • Occlusal trauma: periodontitis and dental mobility
  • Dental hypersensitivity. Pulp exposure. 2ndry dentin and
    sclerotic dentin . Brown areas. Pulp chamber reduction.
  • Pulpitis and pulp necrosis
  • Vertical dental fissures and fractures
  • Bone involvement:
    A. Centric: bone resorption
    B. Excentric. Condensing osteitis and exostoses. Hypercementosis
35
Q

What are the degrees of bruxism? (4)

A

1 Enamel wear
2 enamel and dentin wear
3 crown length reduced by 1/3 OR lingual/buccal advanced wear
4 more than 1/3 crown length reduced or pulp injury

36
Q

Bruxism enamel tooth lesion?

A

• Enamel has a Knoop hardness of 343, dentin 68
• Physiological wear by attrition or frictional contact against the
enamel or restorative materials = 29 Micron/year

37
Q

Enamel wear: occlusal attrition?

A

eccentric bruxism or grinding

38
Q

Enamel wear: cervical abfraction?

A

centric bruxism or clenching

39
Q

What is attrition influenced by? (4)

A
  • Diet
  • Number of teeth
  • Restoration materials in the mouth
  • Which teeth are worn first??? Depends on the type occlusion an wear pattern
40
Q

Dentin function? (3)

A
  • Provides elastic base for enamel.
  • Protective cover for the pulp.
  • Vital tissue without vascular supply or innervation. It responds to thermal, chemical or tactile stimuli.
41
Q

Dentin permeability? (3)

A
  • Dentin permeability is directly related to its protective function.
  • When the outer layer of enamel or cement is lost, the exposed tubules become conducts between pulp and external oral environment.
42
Q

Describe peripheral dentin? (4)

A
  • 20.000 tubules /mm2
  • 0,8 micr. diameter
  • 4% of the dentin surface area
  • Highly interconnected system
43
Q

Describe inner dentin? (4)

A
  • 65.000 tubules mm2
  • 2,5 to 3 micr. diameter
  • 12% dentin surface area
  • Less interconnections
44
Q

Dentin physiology? (2)

A
  • dentin tubules: constant mineralizations

- intertubular dentin wall thickens progressively and occludes the tubular light

45
Q

Dentin physiopathology/pathophysiology?

A

• With certain stimuli the proportion of tubular sclerosis can be
accelerated.

• Formation of reparative or tertiary dentin.

46
Q

How is the dentin in bruxist patients? (4)

A
  • Dentin surface mineralization
  • Formation of sclerotic dentin
  • Formation of tertiary or reparative dentin
  • Pulp inflammation
47
Q

What is sclerotic dentin? (3)

A

• Hypermineralized dentin:
Chronic superficial attacks of slow mechanism.
Defensive barrier.
Vitreous appearance or transparent.
• Total occlusion of the tubule by peritubular dentin creation and intratubular calcification
• Harder and more radiopaque dentin than primary
dentin

48
Q

What is tertiary/reparative dentin? (5)

A

• Produced by atypical odontoblasts.
• In severe attrition, it is formed in the roof of the pulp
chamber.
• Irregular structure, with less number of tubules than primary or secondary dentin.
• Less mineralized than sclerotic dentin, but more than normal dentin.
• Defined line or interface.

49
Q

Dentin and attrition? (3)

A

➢Dentin sclerosis due to the obstruction of dentinal tubules and precipitation of rhombohedrons crystals. Vitreous appearance.
Low permeability. Not sensitive to external stimuli.
➢Areas of complete hypermineralization without tubules
exposure.
➢Sclerotic mineralized formations.

50
Q

Adhesion on attrition lesions? (4)

A

• We don’t have much enamel.
• Surface tubular sclerosis.
• Deep dentin, larger diameter tubules, sclerosed, less
intertubular dentin surface.
• Areas of very severe wear = Tertiary or reparative dentin.

51
Q

How to improve dentin adhesion on attrition?

A

• Include normal peripheral dentin.
• Increase x2 time of etching over the sclerotic dentin. More
resin tags and thicker hybrid layer.
• Removal of all the superficial layers.
• Self etching adhesives

52
Q

What is pulp composed of? (3)

A
  • Stem Cells
  • Fundamental substance (water, proteins, carbohydrates…)
  • Collagen fibers.
53
Q

What are the supporting vital structures of pulp? (3)

A
  • nerve
  • vascular
  • cellular
54
Q

Pulp physiopathology

A

Evolves from a young connective tissue (lax), rich in cells and
poor in fibers to an aged connective tissue (dense) poor in cells
and rich in fibers, with a greater internal mineralization of
diffuse type and less reactivity.
• These changes are noticeable in response to a certain external
stimuli (attrition)

55
Q

Aged teeth: reduced repair potential ?

A
  1. Reduced blood supply.
  2. Smaller pulp chamber.
  3. Lower interrelation between cells and collagen fibers.
  4. Loss and degeneration of myelinated and un-myelinated nerves.
  5. Loss of the water from the fundamental substance.
  6. Increased intra-pulp mineralization.
56
Q

intial changes that can use preventative treatment in bruxists?

A
  • flattened canine guide
  • cervical abfractions
  • cusp fracture
  • muscular problems
57
Q

preventative treatment for bruxists?

A
  • make patient aware of problem + fix them + mouthguard
58
Q

Where is abfraction seen usually?

A
  • almost always buccal surfaces of upper and lower premolars
  • canines
  • buccal surface of molars
59
Q

How do we restore abfraction lesions?

A
  • roughen surface
  • enamel bevel
  • composite: flow or microfilled
  • occlusion adjustment always
60
Q

What would be considered palliative treatment in bruxism?

A
  • general wear
  • non supported enamel
  • hypersensitivity areas

*treat the sensitivity & restore with composite resin

61
Q

Bruxism bad prognosis ?

A
  • Insufficient support tissue
  • Insufficient adhesion strength
  • Pulp response: unpredictable
  • Unfavorable occlusal loads in intensity and/or direction
62
Q

Posterior restorative objectives? (3)

A

1 The restoration must ensure stability both in the adjacent and antagonist teeth.
2 Uniform and at the same time occlusion in closure + in
harmony with anterior contacts.
3 The new occlusion must guide the forces against the long
axis of the teeth. Occlusal table.

63
Q

Anterior restorative objectives? (7)

A

• Should provide an anterior guide during the eccentric movements.
• Anterior contacts always lower than posterior in maximal intercuspal position.Bad
behavior with over-occlusal load.
• Be careful in palatal restorations on upper incisors and lower incisal edge.
• Analyze the degree of over-occlusal load before and after the restoration. Fremitus.
• Evaluate anterior guide in one or more teeth.
• Analyze the protrusive and lateral movements.
• Readjust the occlusion in “ready to eat” position.

64
Q

Which mandibular position do we resotre bruxists to? (2)

A

• Non functional alterations: MI: lying down and
sitting.
• If functional alterations: 1st treat the alteration and later the restorative treatments in CR

65
Q

How to avoid contacts on the margins of the restoration?

A
  1. Previous analysis by checking contacts before the cavity.
    2 Flattening the antagonist cusp to move the contact within the
    restoration or outwards on the tooth if there is enough tooth
    surface.
    3 Evaluate active cusp coverage if we can’t avoid the contact.

Resto 3 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions