Download Dr. Ward Noble Professor, Dugoni School of Dentistry University of

Solutions for Today’s Increasing
Dental Wear
Dr. Ward Noble !
Professor, Dugoni School of Dentistry!
University of Pacific!
San Francisco, CA
[email protected]
QUESTION:!
How many have patients who look like these?
EROSIVE TOOTH WEAR
….is tooth structure loss involving acid
erosion and frictional forces from attrition and
abrasion.!
Tooth surface loss (TSL) involves two distinct
processes:
*
Acid erosion- dissolution!
- softening!
* Wear- frictional loss due to attrition,
abrasion and abfraction=add’l TSL
ACID EROSION
The chemical dissolution of dental
hard tissues without bacterial
involvement
WEAR
Loss of tooth structure from
abrasion and attrition. Involves
frictional forces but also softening
from acids.
Thus, EROSIVE TOOTH WEAR
ETW is usually multifactorial
Little wear occurs without first softening teeth with
an acid challenge
Note the dynamics!
of severe ETW.!
Etiology?
Is there a loss of
vertical dimension
(VDO)?
Cause of tooth wear?
attrition?
abrasion?
erosion?
Erosive Tooth Wear
ETW is often not noted until there is pain and/
or there is an esthetic problem.
DHx: Braces removed in 2007,!
had dental cleanings, finally
sought care in 2015.!
MHx: Bulimia, 2007-2015.
Projectile vomiting increases the rate of tooth surface loss .
2007
2015
Age 13
DE changes are subtle,
with little pain and
minimal functional or
esthetic impact,
but….age 18 to 85???
Age 18
Lussi & Jaeggi,”Dental Erosion”,2011
CARIES vs. EROSION
Caries:!
*Involves bacteria!
*Can be reversible !
*Subsurface lesions!
*pH => 4.5!
!
Erosion:!
*No bacteria-intrinsic/
extrinsic acids!
*Surface lesions/irreversibile!
*Subject to abrasion/wear
Why don’t we have any caries?
DENTAL EROSION
PREVALENCE is increasing among children and adolescents:!
*in 2-5 year-olds: 31% showed some wear!
*in 5-9 year-olds: 100% had erosion (48% DE)!
*in 11-13 year-olds: 100% had erosion!
*overall: 30.4% (Meta-analysis)
↓ caries/↑ erosion
Al-Malik,2002!
Jaeggi and Lussi, 2004!
Chadwick, 2005!
Salas et al. J Dent 2015:43:42-50
Erosive tooth wear
often increases
with age.
Vered,Lussi,et al. Clin Oral Investig,2014;18;1985-90
Demographic shifts will lead to increased
awareness and treatment of erosive tooth
wear. !
Our patients will outlive their teeth!!
DEMOGRAPHIC CHANGES
More people are living longer, keeping their teeth!
and are more affluent, active and esthetically sensitive!
Edentulism-2014
1974: 45.6% edentulous!
1994: 28.6%!
2008: 22.9%!
2015: 17% (est.)!
(over age 65)!
JDentRes 2014
Therefore, we will be seeing more patients with
wear…they are literally ‘outliving’ their teeth!
A major risk factor in older patients is hypo salivation!
related to use of multiple medications
Over age 65=6 Rx medications daily!
I feel a lot better now that I stopped taking all the pills you
gave me!
Scully C, Oral Diseases 2003;9:165-176
SALIVA IS THE MOST IMPORTANT
BIOLOGIC RISK FACTOR IN ETW.
*
*
*
*
*
Oral clearance - acids, bacteria, CHO
Dilution
Buffering of acids
Supersatuation of calcium and phosphorus
Provides mucins and proteins to help build healthy biofilm or pellicle
* Saliva: a factor in risk assessment for
caries and acid erosion
FACT: Nothing happens on the tooth until it happens in the saliva!!
EXTRINSIC ACID EROSION
http://www.businessinsider.com/us-calorie-consumption-surged-in-the-80s-2013-9,!
accessed 3/4/16 (USDA-Credit Suisse Research)
>40 gallons/year
(2014)
http://mobile.businessinsider.com/american-soda-consumption-a-hugeoutlier-2013-9; Accessed 3/4/2016 (Credit Suisse Research)
UCLA Center for Health Policy Research, 2013
Acid attacks from soft drinks, sports and energy
drinks, fruits, juices, wine, chlorine in pools, etc.
Sports drinks = 10X worse than coke
Energy drinks = 13 times worse that coke
Intrinsic Acids
*Acids originating in the stomach (HCl)
*Can be related to gastroesophogeal
reflux disease (GERD), bulimia,
anorexia and alcoholism.
Severity of acid attack depends on:
* pH of acid
* Buffering capacity of acid
* Is drink ‘swished’ or sipped, vs. gulped
* Contact time - fruit that is ‘mulled’
* Viscosity and temperature of liquid
* Saliva -dilution, clearance (dehydration)
* Thickness of pellicle
Ask your patients “HOW” they consume their acidic drinks!
“The Perfect Storm”
A patient who is a bruxer, has sleep
apnea, GERD and medication-induced
hypo-salivation!!
Patient Profile:
* Age 55+
* Obese
* Neck size 17+”
* Drinks and smokes
* High stress
ENAMEL vs. DENTIN
ENAMEL: INORGANIC=85%!
ORGANIC=2%!
WATER=11%
DENTIN: INORGANIC=47%!
ORGANIC=33%!
WATER=21%
Each tissue reacts differently to an acid challenge.
Ganss C, et al. MonoOralSci 2014;25:99-107
Ganss C, et al. Eur J Oral Sci 2009;117:225-260
WHAT IS THE EROSIVE PROCESS??
After acid attack, calcified material is
removed, leaving soft organic matrix
which is easily abraded away with
brushing, bruxing, etc.
After an acid attack (demineralization) eroded area
is a softened layer=susceptible to abrasion, etc.
Huysmans, CarRes 2011;45(suppl 1):60-68
Erosive effects are different in enamel and dentin
Demineralized organic matrix (DOM)
Scully C, Oral Diseases 2003;9:165-176
ENAMEL vs. DENTIN
EROSIVE EFFECTS ON ENAMEL:!
MORE DEMIN AND BULK LOSS (HIGHER
MINERAL CONTENT)
EROSIVE EFFECTS ON DENTIN:!
LESS BULK LOSS(LESS MINERAL) BUT SOFTER
ORGANIC MATRIX
Is this patient right- !
or left-handed?
Tooth Wear
Is a function of:
* Attrition
Bruxism
* Abrasion
* Abfraction
* Acid Erosion
Is always multifactorial.
Interaction between attrition (abrasion) and
erosion = Erosive Tooth Wear
Dr. Michael Nelson
NON-CARIOUS CERVICAL LESIONS
(NCCL’S)
Multifactorial Etiology
ACID EROSION
NCCL’s
ABRASION
ABFRACTION
PROBLEMS WITH NCCLs
Teeth are weakened
PROBLEMS WITH NCCLs
Teeth can become sensitive
PROBLEMS WITH NCCLs
Can result in esthetic issues
MULTIFACTORIAL ETIOLOGY
1. Tooth flexure
Abfraction?
In the absence of dietary acids there is little or no
erosive tooth wear
MULTIFACTORIAL ETIOLOGY
1. Tooth flexure
2. Toothbrush abrasion
MULTIFACTORIAL ETIOLOGY
1. Tooth flexure
2. Toothbrush abrasion
3. Acid erosion
Bottom line: Multifactorial etiology!
“BRUXISM” is not !
a diagnosis
This should be called!
“EROSIVE TOOTH WEAR”
Think in terms of “EROSIVE TOOTH
WEAR” and not just bruxism:
This will open a whole new area for
improving a patient’s overall HEALTH,
because signs and symptoms of wear are
often related to things other than teeth.
Prevalence of Sleep Bruxism
* 14-18% of children and adolescents
* 8% of 25-65 year olds
* 3% of adults over 65
Thus....SB decreases with age.
Tooth ‘wear’ in a 70 y.o. patient probably is not from
‘bruxing’.
Laberge L, et al, Pediatrics. 2000;106:67-74
Obhayon MM and Guilleminault C,
Chest. 2001;119;53-61
Diagnosis (of Bruxism?)
WEAR is not a good indicator.
There is a poor relationship between occlusion bruxism and
tooth wear.
Tooth wear is mostly related to an ‘acid attack’ !!
Kato T et al, J
Orofac Pain.
2003;17:191-213
Occlusion may be important
with the “Effects” of bruxism
Improvements in occlusion may help
control the impact of bruxing (tooth
fractures, mobility, hypersensitivity) and
improve chewing function, but NOT help
sleep bruxism.
Management of occlusion is still very important!!
Lavigne GJ et al, J Oral Rehab. 2008;35:476-494
TREATMENT
Detailed Diagnosis and Etiology
Modify Behaviors
Preventive Strategies
Early Intervention
Conservative Restorative Care
Occlusal Appliances
Rehabilitation, if Needed
TREATMENT
Detailed Diagnosis and Etiology
Modify Behavior
Prevention
Fluoride Treatment-toothpastes
Stannous fluoride provides a protective layer to
resist acid attacks
Brush before a meal, not after!!
Tooth surface following acid challenge
Stannous Flouride
Sodium
SodiumFlouride
Flouride
Control
Ravishankar, Gen Dent
2013;61:56-59
Use during day, prior to acid attack
Use at night, assuming no GERD
Brush BEFORE meals!
and wait at least 1 hour!
AFTER eating before!
brushing!
MANAGEMENT STRATEGIES
*
*
*
*
*
Behavioral modification
Preventive therapies-limit acid challenge
Don’t ‘watch and wait’
Use sealant
Restore-MID
RESTORATIVE MANAGEMENT
??
Don’t “watch and wait!”
Cavalho,JOI:2014
TREATMENT
Restore using conservative, ‘no-prep’
minimally invasive restorations
Note that where
composite is
present there is
no erosion.
Babour, MonogrOralSci 2014
MINIMALLY INVASIVE DENTISTRY!
FOR TREATMENT OF THE!
SEVERELY WORN DENTITION
Consider how the concept of ‘supragingival dentistry’
could simplify your practice….
*
*
*
*
*
*
No cord packing or soft tissue problems!
Less time spent prepping!
Higher impression success - with or without
digital!
Less tooth removal and less sensitivity!
Relies on bonded restorations, thus less
retention!
Overall, less invasive and more conservative
‘Minimally invasive’ and ‘supragingival dentisty’ have
been made possible by improvements in adhesive
technics.
but…
…longterm success if mainly related to ability to bond
to enamel = superior adhesive seal than to dentin.
“ENAMEL IS KING!!”
There is little indication for the use of PFMs. This is
the era of all-ceramic restorations and less need for
retention and resistance form.
Christensen, JADA, 2014
MUST EMBRACE NEW PHILOSOPHIES
TRY TO KEEP MARGINS SUPRAGINGIVALLY AND RETAIN AS
MUCH ENAMEL AS POSSIBLE.
Minimally Invasive Restorations
For ceramics: need 1.2-1.5 clearance!
For composites can go down to 0.6 clearance!
Must use rounded line angles and shoulders at margins
Minimally Invasive Restorations
What is the minimal thickness of ‘no prep’ posterior
composite veneers?
Could be down to 0.6mm, vs. porcelain
Composites with minimal changes after 36 months
Ramseyer, et al. J Adhesive Dent 2015
Had less fractures with composite
than with porcelain.
Success with composites:
*
*
*
*
*
*
*
*
Enamel Is “king”.!
Do SELECTIVE ETCH - use phosphoric acid (ER)!
on enamel ONLY.!
There is no need to use adhesive (Opto-Bond Solo).!
Do not use bur to roughen dentin (bur creates !
‘smear layer’, which weakens dentin bond.!
Use self-etch (SE) on dentin and enamel.!
Be sure to scrub SE and air-thin (do NOT air dry).
Air Abrasion improves all bond strengths.
Dentin bonds
weaken after 12-24
months!!
Demineralization of enamel and dentin
To help control MMP activity in dentin, scrub
with CHX AFTER etch (or primer) but
BEFORE adhesive application.
2.0% chlorhexidine gluconate
Activa is a Resin-modified glass ionomer (RMGI):!
Bioactive-releases/recharges w/calcium,
phosphate and fluoride.!
May use Primer, but not adhesive.!
“Prevention is more
preferable than treatment.”
[email protected]
30 years old
Dx: Gastroparesis, GERD, vomiting
Meds: Prilosec, Nexium
FMX
FMX
No Treatment?
Composites?
Crowns?
Should take a minimally
invasive approach to
treatment
There is no true loss of vertical dimension, but
it was necessary to open the VDO 2.0 mm for
“RESTORATIVE CONVENIENCE”.
‘Smile design’ is essential!
Casts of diagnostic wax ups
“Suck-downs” of diagnostic wax ups
Splint is placed over original!
cast…note space that will be
filled with composite
Completed ‘no prep’
composite provisionals at
new VDO
At this point minimally invasive
preps can be cut directly through
the composite, minimizing the
amount of tooth structure loss
and maximizing residual enamel
for bonding.
Upper anterior preps are started,
using posterior composites to
stabilize occlusion at new VDO.
Crowns are cemented.
E.Max Crowns
#6-11
Posterior quadrants can be sequentially prepared and new
provisionals are cemented.
Note that all
margins are
supragingival =
easier impression
and cementation
110
For cementation of E.Max crowns use same
bonding sequence as used for veneers.
Final restorations in place.
A night guard was
provided.