Bruxism Flashcards
(65 cards)
1
Q
Define bruxism
A
Involuntary mandible excursive movements/ clenching that cause intermittent inter-occlusal friction over the unconsciously selected teeth
2
Q
Define attrition
A
tooth to tooth - physiological wear
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
4
Q
Define abrasion
A
foreign object in mouth like brush
5
Q
Define erosion
A
from acids
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
7
Q
What are the 2 main groups of etiological factors for bruxism?
A
- peripheral
- central/physiopathological
8
Q
What is the peripheral etiology of bruxism (2)
A
- occlusion
- anatomy
9
Q
What is the cental/physiopathological etiology of bruxism (4)
A
- dream alterations
- dopaminergic system alterations
- medicines
- genetic
10
Q
Whats ramffords theory?
A
Occlusion is the first resposible for onset of bruxism. Prematurities and balanced side occlusal contacts
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
12
Q
Who made theories about bruxism?
A
- rammford
- Bailey &rugh, and Kardachi
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
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
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
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
17
Q
What are the genetic factors for bruxism? (3)
A
- little evidence
- 23% of monozygotic twins
- family pattern 20-35%
18
Q
Stress and personality for bruxism?
A
- smaller than previously assumed
- unclear as it is different in different people
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
20
Q
How are bruxist patients different? (4)
A
- histological tooth characteristics
- ability to discriminate change
- muscle problem
- reduced ability to respond to changes
21
Q
How are bruxists classified? (2)`
A
- moment
- activity
22
Q
How are bruxists classified by moment? (3)
A
- day
- night
- mixed
23
Q
How are bruxists classified by activity? (3)
A
- clenching
- grinding
- bracing
24
Q
Describe centric/clenching vs bracing/eccentric? (4)
A
- more difficult diagnosis
- more difficult to control
- > acute lesions
- > muscular problems
25
bruxism symptomatology? (2)
- muscular and articular
| - dental
26
Bruxism symptomatology: muscular and articular? (4)
- specially in centric bruxism
- pain and tenderness in elevator muscles
- functional limitation
- can affect the muscles of the neck
27
Bruxism symptomatology: muscular and articular treatment? (2)
- mouth opener
| - muscle relaxant prior to a long session
28
bruxism symptomatology: dental?
- occlusally and inscially
- centric: inverted cusps and abfraction lesions
- eccentric: smooth and polished surfaces, wear out of functional areas. attrition
29
What does dental wear depend on? (6)
- thickness and hardness of enamel
- pH
- age
- presence of more abrasive materials (porcelain)
- number of teeth present
- malocclusions (overbites)
30
Bruxism protrusive pattterns?
*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
Bruxism lateral or horizontal pattterns? (3)
- canine guide flattening
- group function apperance
- affectation of lateral sectors
32
bruxisms: dental wear anteriorly? (3)
- disappearance of incisal mamelons
- enamle and dentin at same level
- DD with erosion
33
bruxisms: dental wear posteriorly? (3)
- loss of occlusal anatomy
- concave occlusal faces = inverted cusps (clenching)
- cup of volcano lesions are typical of erosion
34
Bruxism symptomatology: detnal? (6)
- 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
What are the degrees of bruxism? (4)
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
Bruxism enamel tooth lesion?
• 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
Enamel wear: occlusal attrition?
eccentric bruxism or grinding
38
Enamel wear: cervical abfraction?
centric bruxism or clenching
39
What is attrition influenced by? (4)
* Diet
* Number of teeth
* Restoration materials in the mouth
* Which teeth are worn first??? Depends on the type occlusion an wear pattern
40
Dentin function? (3)
* 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
Dentin permeability? (3)
* 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
Describe peripheral dentin? (4)
* 20.000 tubules /mm2
* 0,8 micr. diameter
* 4% of the dentin surface area
* Highly interconnected system
43
Describe inner dentin? (4)
- 65.000 tubules mm2
- 2,5 to 3 micr. diameter
- 12% dentin surface area
- Less interconnections
44
Dentin physiology? (2)
- dentin tubules: constant mineralizations
| - intertubular dentin wall thickens progressively and occludes the tubular light
45
Dentin physiopathology/pathophysiology?
• With certain stimuli the proportion of tubular sclerosis can be
accelerated.
• Formation of reparative or tertiary dentin.
46
How is the dentin in bruxist patients? (4)
* Dentin surface mineralization
* Formation of sclerotic dentin
* Formation of tertiary or reparative dentin
* Pulp inflammation
47
What is sclerotic dentin? (3)
• 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
What is tertiary/reparative dentin? (5)
• 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
Dentin and attrition? (3)
➢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
Adhesion on attrition lesions? (4)
• 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
How to improve dentin adhesion on attrition?
• 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
What is pulp composed of? (3)
* Stem Cells
* Fundamental substance (water, proteins, carbohydrates…)
* Collagen fibers.
53
What are the supporting vital structures of pulp? (3)
- nerve
- vascular
- cellular
54
Pulp physiopathology
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
Aged teeth: reduced repair potential ?
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
intial changes that can use preventative treatment in bruxists?
- flattened canine guide
- cervical abfractions
- cusp fracture
- muscular problems
57
preventative treatment for bruxists?
- make patient aware of problem + fix them + mouthguard
58
Where is abfraction seen usually?
- almost always buccal surfaces of upper and lower premolars
- canines
- buccal surface of molars
59
How do we restore abfraction lesions?
- roughen surface
- enamel bevel
- composite: flow or microfilled
- occlusion adjustment always
60
What would be considered palliative treatment in bruxism?
- general wear
- non supported enamel
- hypersensitivity areas
*treat the sensitivity & restore with composite resin
61
Bruxism bad prognosis ?
* Insufficient support tissue
* Insufficient adhesion strength
* Pulp response: unpredictable
* Unfavorable occlusal loads in intensity and/or direction
62
Posterior restorative objectives? (3)
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
Anterior restorative objectives? (7)
• 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
Which mandibular position do we resotre bruxists to? (2)
• Non functional alterations: MI: lying down and
sitting.
• If functional alterations: 1st treat the alteration and later the restorative treatments in CR
65
How to avoid contacts on the margins of the restoration?
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.
