Bruxism Flashcards
Define bruxism
Involuntary mandible excursive movements/ clenching that cause intermittent inter-occlusal friction over the unconsciously selected teeth
Define attrition
tooth to tooth - physiological wear
Define abfraction
- abrasive cervical lesion induced by occlusal stress
- flexural forces.
- enamel fractures and exposes dentin
- hypersensitivity
- no time for sclerotic dentin creation
Define abrasion
foreign object in mouth like brush
Define erosion
from acids
Bruxism epidemiology? (4)
- 6-8% mid age population
- 1/3 world population
- same prevalence men and women
- higher prevalence in asians > euro-americans, and hispanic > than africans
What are the 2 main groups of etiological factors for bruxism?
- peripheral
- central/physiopathological
What is the peripheral etiology of bruxism (2)
- occlusion
- anatomy
What is the cental/physiopathological etiology of bruxism (4)
- dream alterations
- dopaminergic system alterations
- medicines
- genetic
Whats ramffords theory?
Occlusion is the first resposible for onset of bruxism. Prematurities and balanced side occlusal contacts
Whats kardachi and bail&rughs theorys?
- Interference removal doesnt eliminate bruxism
- occlusal scheme is relevant in force distribution during episodes but no proof of it being the etiology
Who made theories about bruxism?
- rammford
- Bailey &rugh, and Kardachi
Anatomical factors for bruxism?
- 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
Physiopathological factors MORE involved in etiology of bruxism?
- sleep alterations
- brain chemistry alterations
- some medication and illegal drugs
- tobacco / alcohol
- genetics
- traumas & diseases
What sleep alterations affect bruxism?
- 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
Which meds affect the dopaminergic system? (4)
- SSRIs
- amphetamine abuse
- Nicotine stimulates 2x more = bruxism 5x more
- alcohol same effect as nicotine
What are the genetic factors for bruxism? (3)
- little evidence
- 23% of monozygotic twins
- family pattern 20-35%
Stress and personality for bruxism?
- smaller than previously assumed
- unclear as it is different in different people
Why are we always concerned about bruxists? (5)
- 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 are bruxist patients different? (4)
- histological tooth characteristics
- ability to discriminate change
- muscle problem
- reduced ability to respond to changes
How are bruxists classified? (2)`
- moment
- activity
How are bruxists classified by moment? (3)
- day
- night
- mixed
How are bruxists classified by activity? (3)
- clenching
- grinding
- bracing
Describe centric/clenching vs bracing/eccentric? (4)
- more difficult diagnosis
- more difficult to control
- > acute lesions
- > muscular problems
bruxism symptomatology? (2)
- muscular and articular
- dental
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
Bruxism symptomatology: muscular and articular treatment? (2)
- mouth opener
- muscle relaxant prior to a long session
bruxism symptomatology: dental?
- occlusally and inscially
- centric: inverted cusps and abfraction lesions
- eccentric: smooth and polished surfaces, wear out of functional areas. attrition
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)
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
Bruxism lateral or horizontal pattterns? (3)
- canine guide flattening
- group function apperance
- affectation of lateral sectors
bruxisms: dental wear anteriorly? (3)
- disappearance of incisal mamelons
- enamle and dentin at same level
- DD with erosion
bruxisms: dental wear posteriorly? (3)
- loss of occlusal anatomy
- concave occlusal faces = inverted cusps (clenching)
- cup of volcano lesions are typical of erosion
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
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
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
Enamel wear: occlusal attrition?
eccentric bruxism or grinding
Enamel wear: cervical abfraction?
centric bruxism or clenching
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
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.
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.
Describe peripheral dentin? (4)
- 20.000 tubules /mm2
- 0,8 micr. diameter
- 4% of the dentin surface area
- Highly interconnected system
Describe inner dentin? (4)
- 65.000 tubules mm2
- 2,5 to 3 micr. diameter
- 12% dentin surface area
- Less interconnections
Dentin physiology? (2)
- dentin tubules: constant mineralizations
- intertubular dentin wall thickens progressively and occludes the tubular light
Dentin physiopathology/pathophysiology?
• With certain stimuli the proportion of tubular sclerosis can be
accelerated.
• Formation of reparative or tertiary dentin.
How is the dentin in bruxist patients? (4)
- Dentin surface mineralization
- Formation of sclerotic dentin
- Formation of tertiary or reparative dentin
- Pulp inflammation
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
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.
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.
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.
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
What is pulp composed of? (3)
- Stem Cells
- Fundamental substance (water, proteins, carbohydrates…)
- Collagen fibers.
What are the supporting vital structures of pulp? (3)
- nerve
- vascular
- cellular
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)
Aged teeth: reduced repair potential ?
- Reduced blood supply.
- Smaller pulp chamber.
- Lower interrelation between cells and collagen fibers.
- Loss and degeneration of myelinated and un-myelinated nerves.
- Loss of the water from the fundamental substance.
- Increased intra-pulp mineralization.
intial changes that can use preventative treatment in bruxists?
- flattened canine guide
- cervical abfractions
- cusp fracture
- muscular problems
preventative treatment for bruxists?
- make patient aware of problem + fix them + mouthguard
Where is abfraction seen usually?
- almost always buccal surfaces of upper and lower premolars
- canines
- buccal surface of molars
How do we restore abfraction lesions?
- roughen surface
- enamel bevel
- composite: flow or microfilled
- occlusion adjustment always
What would be considered palliative treatment in bruxism?
- general wear
- non supported enamel
- hypersensitivity areas
*treat the sensitivity & restore with composite resin
Bruxism bad prognosis ?
- Insufficient support tissue
- Insufficient adhesion strength
- Pulp response: unpredictable
- Unfavorable occlusal loads in intensity and/or direction
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.
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.
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
How to avoid contacts on the margins of the restoration?
- 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.
