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Dr.Alyaa Asaad AL-Kafrawy
This research paper is about non carious lesions in teeth .
It includes the definition , the cause , the treatment and
the prevention techniques for them
MANAGING NONCARIOUS CERVICAL LESIONS
Noncarious cervical lesions (NCCLs) are defined as a loss
of hard dental tissue near the cementoenamel junction,
usually on the buccal surfaces of teeth, resulting in a
grooved or wedge-shaped area of missing tooth structure.
These lesions are increasing in prevalence, especially
among adolescentsand older adults.1 In particular,
lifestyle changes — includingthe increased consumption
of acidic drinks among younger patients and the number
of olderadults who take prescription medications, which
can cause hyposalivation and xerostomia — raise the risk
of NCCLs. Hyposalivation increases acidity in the oral
cavity, softening the tooth surface and facilitating tooth
loss (Figure 1).
FIGURE 1. Noncarious cervical lesions are present on
the buccal of upper and lower teeth.
A study reported that the prevalence of NCCLs in
teenagers and adultsranges from 11% to 62%, and the
number of lesions increases with age.2 Lesions most often
occur on the buccal of maxillary premolars, but are also
commonly found on other maxillary and mandibular
anterior and premolar teeth. The exact etiology of NCCLs
is unknown, but it is generally accepted that their cause is
multifactorial.1,3,4 The clinical endpointof NCCLs is the
wearing away of dentition. The mechanisms involved
includeacid erosion (the loss of tooth structureby acid
demineralization without the involvement of bacteria);
abrasion (friction resulting in loss of tooth structurefrom
dentifrices and toothbrushing); and abfraction (breaking
away of tooth structuredue to tensile stresses in the
cervical area).1,3,4
Acid erosion is the most important factor involved in the
development of NCCLs. Saliva normally keeps the oral
environment in the 7.0 pH range (neutral) due to its
ability to buffer acids. The source of acids can be intrinsic
— bulimia or gastroesophageal reflux disease (GERD),
for example — or extrinsic, such as acids from fruit
juices, sports and energy drinks, and wine, to name a few.
When oral acids bring the pH of the tooth surface below
4.5, demineralization of enamel and dentin can begin.5
EROSIVE CONCERNS
The action of strong acids causes the loss of calcium
(inorganic matter) from the tooth surface, followed by a
softening of the top layers of dentin and enamel. This
softened layer then becomes susceptibleto abrasive forces
in the oral cavity and is easily removed, potentially
causing wedge-shaped cervical lesions. The thin, softened
layer is between 0.2 µm and 3 µm thick and is repeatedly
removed by abrasive forces, leading to permanent loss of
tooth volume in the cervical area.6
The pH (less than 4.5), duration and the strength
(buffering capacity) of the acid challengeneed to be
considered. For example, cola (phosphoricacid) and
certain energy drinks (citric acid) have a similar pH, but
drinks containing citric acid are more erosive because
more buffering is required to return the pH above the
“critical” erosive point of pH 4.5.3Regular and diet sodas
and sports and energy drinks range from a pH of 2.5 to
3.4, respectively.7 Lemon, grapefruit and orange juices
also cause erosive damage to enamel. Gastric acids from
GERD are the most erosive, with a pH of 1.0 to 2.0.1 In
addition, patientswith gastric reflux often suffer from
hyposalivation.8
FIGURE 2. This patient has severe noncarious cervical
lesions.
Saliva plays an important role in oral health by cleansing
the oral cavity and diluting and buffering acids.
Individuals with xerostomia are much more susceptibleto
acid erosion. Patients are often advised to avoid brushing
for 30 minutes to 60 minutes immediately after an acid
exposure, presumably to allow softened surface enamel to
remineralize — but, in truth, more effective preventive
strategies (such as various fluoride-based therapies)
should be recommended. The reality is that softened
enamel is not remineralized by saliva over short time
periods, and will be worn away even in the absence of
tooth brushing by normal abrasive forces in the oral
cavity, such as chewing and tongue action.
Dental abrasion, anothercontributingfactor to NCCLs, is
defined as wearing away of dental hard tissues by
frictional forces.1 This can include wear caused by
toothbrushing, flossing, tongue action, abrasive foods, and
rubbing from opposing surfaces that are hard or rough,
such as unpolished porcelaincrowns.3 The effects of such
actions are usually more pronounced on dentin surfaces
than on enamel (Figure 2 and Figure 3).9
FIGURE 3. Toothbrush abrasion may be part of the
multifactorial etiology of noncarious cervical lesions.
It appears that toothbrushingalone — regardless of the
brush stiffness, filament size, aggressiveness or the
frequency of brushing — causes littleabrasive tooth
wear.1 Rather, it is the abrasiveness of the toothpaste
combined with brushing that is responsiblefor the loss of
tooth structure.10,11 Dentifrices that includewhitening
agents or productspromoted for their ability to control
tartar tend to be more abrasive than other types. That said,
all popularbrandsmarketed in the U.S. today comply
with abrasivity “safe limits” set by American Dental
Association and InternationalOrganization for
Standardization.12,13 Any toothpastewith a Relative
Dentin Abrasivity (RDA) value of 250 or below can be
used safely on a daily basis for a lifetime. Toothbrushes
with stiffer bristles, however, have been linked to gingival
recession.14
Abfraction is the microstructural loss of tooth structure
due to excessive occlusal forces transmitted to the
cervical area as flexural forces.1 These flexural forces,
usually caused by cyclic loading, may lead to the breaking
away of enamel rods in the cervical region of the tooth,
causing microfractures of cementum and dentin.4 Bruxism
may also contribute, although in the absence of acid there
is minimal erosive tooth wear.15
Anotherpossible modifying factor in abfraction formation
involves the mobility of teeth and the effects of occlusal
stresses in the formation of cervical lesions. A
relationship has been found between tooth cervical
lesions, tooth stability and periodontalsupport.15 Thus, as
tooth mobility increases, teeth are actually less susceptible
to excessive occlusal forces, as the teeth move under
occlusal loads, resulting in less concentrationof forces in
the cervical areas.16
While these interocclusal relationshipsmay be
contributingfactors in the formation of some NCCLs, it is
likely that clinical signs of abfraction in cervical areas are
not simply related to stress concentrations. Rather, they
may play a role, alongwith acid erosion and toothbrush
abrasion, in the multifactorial etiology of NCCLs.1,4
LESION MANAGEMENT
It’s important to note that NCCLs can occur at any time
and may worsen throughout a patient’slifetime. Without
intervention, they can result in tooth fracture,
hypersensitivity and cosmetic problems. Therefore, early
diagnosis is important in order to initiate behavioral
changes and avoid future invasive and expensive
restorative interventions.
Clinical management of NCCLs includes first identifying
the various etiologic factors present in a given patient. For
example, if a patient is an active bruxer, has wear facets
on the teeth, and presents with NCCLs, the clinician may
decide to prescribe an occlusal splint or night
guard.4 Occasionally, judicious occlusal adjustments of
interferences may be performed. Acid intake must also be
reduced.
Through the process of taking a comprehensive medical
history, clinicians should question patients regarding their
intake of acidic foods or beverages, includingfruits, wine,
and sports and energy drinks. It is important to monitor
the frequency, duration, sequencing, and the mode of
intake of these beverages. Sipping and swishing a drink,
for example, are much more erosive than gulping the
beverage, as the acidic beverage stays in contact with the
tooth surface for longer periods.17 Consuming dairy after
an acid challenge will help raise the pH and shorten the
duration of erosive insult.18 Medication use, especially
among older patients, should be reviewed, as drug-related
xerostomia can contributeto tooth surface loss.19 Finally,
patients should be asked about GERD, because there is a
correlation between this disorder and dental
erosion.20 These medical and behavioral factors have the
net, and possibly cumulative, effect of demineralizing the
tooth surface, which ultimately leads to the irreversible
loss of surface enamel via abrasive forces such as
toothbrushing, eating hard foods, and even cleaning with
toothpicks. If the risk factors cannot be eliminated
through behavioral changes or medical treatment, other
preventive actions should be taken.
KEY TAKEAWAYS
 Clinicians are seeing an increasing prevalence of
noncariouscervical lesions (NCCLs), especially
among adolescentsand older adults.1
 Lesions most often occur on the buccal of maxillary
premolars, but are also commonly found on other
maxillary and mandibularanterior and premolar teeth.
 While the exact etiology of NCCLs is unknown, it is
generally accepted their cause is multifactorial.1,3,4
 Early diagnosis is important in order to initiate
behavioral changes and preventive therapies that can
help patientsavoid invasive restorative interventions.
 Treatment should includeminimizing the intrinsic or
extrinsic acids that are the primary cause(s) of the
lesions.
 Brushing with a stannousfluoride toothpasteis a key
element in prevention management.
PREVENTION AND TREATMENT
Conservative preventive measures using fluoride
mouthrinses and topical fluoride should be professionally
managed.21 The use of fluoride varnish and bonding
agents can protect the teeth from acid attacks, but their
long-term effects may be limited.22 Stannousfluoride is
an important preventive tool to protect the tooth surface
from an acid challenge.23,24 It provides superior protection
for acid erosion versus sodium fluoride or
monofluorophosphateproducts. It has been shown that a
stabilized stannousfluoride toothpasteis effective in
preventing erosive tooth wear.25 The mode of action of
stannousfluoride is to form a thin layer of stannous-based
complexes on the surface of enamel, protectingthe
surface from acid attack.26,27 The patient also receives the
benefit of fluoride.26
Remineralization after an acid attack may be possible
with the use of topically applied pastes containingcasein
phosphopeptidesand amorphouscalcium
phosphate.28 These materials are supersaturatedwith
calcium and phosphateand can “recharge” and
remineralize demineralized tooth surfaces.
Treatment should includeminimizing the intrinsic or
extrinsic acids that are the primary cause(s) of lesions.
Treatment for cervical hypersensitivity due to NCCLs
may also be necessary. Using desensitizing dentifrices,
such as those containing potassium nitrateor stannous
fluoride, can be helpful.29 Other studies have shown that
the use of a self-etching adhesive, sealant or resin-bonded
flowable composite restoration may provide
comprehensive and rapid controlof
hypersensitivity.30 More advanced lesions can usually be
managed using resin-bonded composite restorations. In
rare instances, a crown or porcelain veneer may be
necessary.
Understandingthe etiology of NCCLs and making a
timely diagnosis will allow early and minimally invasive
interventions, such as the use stannousfluoride toothpaste
or fluoride varnish and sealants. Counselingfor
behavioral modifications — reducing the intake of acidic
foods and beverages, for example — is of utmost
importance. Emphasizing the need to take preventive
measures to help avoid enamel erosion in the first place
will help patientsmanage this common problem.
REFERENCES
1.Bartlett DW, Shah P. A critical review of non-carious
cervical (wear) lesions and the role of abfraction,
erosion and abrasion. J Dent Res. 2006;85:306–312.
2.Huysmans MC, Chew H, EllwoodRP. Clinical studies
of dental erosion and erosive wear. Caries Res.
2011;45(Suppl 1):60–68.
3.BarbourME, Rees GD. The role of erosion, abrasion
and attrition in tooth wear. J Clin Dent. 2006;17:88–93.
4.Grippo JO, Simring M, Coleman TA. Abfraction,
abrasion, biocorrosion,and the enigma of noncarious
cervical lesions: a 20-year perspective. J Esthet Restor
Dent. 2012;24:10–23.
5.Lussi A, SchlueterN, RakhmatullinaE, Ganss C.
Dental erosion — an overview with emphasis on
chemical and histopathological aspects. Caries Res.
2011;45(Suppl 1):2–12.
6.Addy M, Shellis RP. Interaction between attrition,
abrasion and erosion in tooth wear. Monogr Oral Sci.
2006;20:17–31.
7.von FraunhoferJA, Rogers MM. Effects of sports
drinks and otherbeverages on dental enamel. Gen
Dent. 2005;53:28–31.
8.Campisi G, Lo Russo L, Di Liberto C, Di Nicola F,
Butera D, Vigneri S, Comilato D, Lo Muzio L, Di Fedi
O. Saliva variations in gastroesophageal reflux
disease. J Dent. 2008;36:268–271.
9.Lussi A, Schaffner M. Progression of and risk factors
for dental erosion and wedge-shaped defects over a 6-
year period. Caries Res. 2000;34:182–187.
10. Moore C, Addy M. Wear of dentinein vitro by
toothpasteabrasives and detergents aloneand
combined. J Clin Periodontol. 2005;12:1242–1246.
11. Harpenau L, Noble W, Kao R. Diagnosis and
management of dental wear. J Calif Dent Assoc.
2011;39:225–231.
12. ISO Dentistry — Dentifrices — Requirements, test
methods and marking. 11609:1995(e).Available at:
http://www.iso.org/iso/iso_catalogue/catalogue_tc/cata
logue_detail.htm? csnumber=38010. Accessed January
18, 2016.
13. American Dental Association AcceptanceProgram
Guidelines: Fluoride-ContainingDentifrices (2005).
Available at:
http://www.ada.org/~/media/ADA/Science%20and%20
Research/Files/guide_fluoride_dentifrice.ashx.
Accessed January 18, 2016.
14. Niemi ML, SandholmL, Ainamo J. Frequencyof
gingival lesions after standardized brushing as related
to stiffness of toothbrush and abrasiveness of
dentifrice. J Clin Periodontol. 1984;11:254–261.
15. Brandini DA, Pedrini D, Panzarini SR, BeneteIM,
Trevisan CL. Clinical evaluation of the association of
non-cariouscervical lesions, parafunctionalhabits and
TMD diagnosis. Quintessence Int. 2012;43:255–262.
16. Kuroe T, Itoh H, Caputo AA, Nakahara H. Potential
for load-inducedcervical stress concentrationas a
function of periodontalsupport.J Esthet Dent.
1999;11:215–222.
17. Grobler S, Jenkins G, Kotze D. The effects of the
composition and method of drinking of soft drinks on
plaquepH. Br Dent J. 1985;158:293–296.
18. Lussi A, Jaeggi, T, Zero D. The role of diet in the
etiology of dental erosion. Caries Res. 2004;38:34–44.
19. Wiener RC, Wu B, Crout R, Wiener M, Plassmann
B, Kao E, McNeil D. Hyposalivation and xerostomia in
dentateolderpatients. J Am Dent Assoc. 2010;141:279–
284.
20. Farahmand F, Sabbaghian M, Ghodousi S,
Seddighoraee N, Abbasi M. Gastroesophageal reflux
disease and tooth erosion: a cross-sectional
observational study. Gut Liver. 2013;7:278–281.
21. Lussi A, Hellwig E. Risk assessment and causal
preventive measures. Monogr Oral Sci. 2014;25:220–
229.
22. Austin RS, Stenhagen KS, Hove LH, et al. A
qualitative and quantitative investigation into the effect
of fluoride formulations on enamel erosion and erosion
abrasion in vitro. J Dent. 2011;39:648–655.
23. Lussi A, Carvalho TS. The future of fluorides and
otherprotective agents in erosion prevention. Car Res.
2015;49(Suppl 1):18–29.
24. Carvalho TS, Colon P, Ganss C, Huysmans MC,
Lussi A, SchlueteN, Schmalz G, Shellis RP, Tveit AB,
Wiegard A. Consensus report of the European
Federation of Conservative Dentistry: erosive tooth
wear-diagnosis and management. Clin Oral Investig.
2015;39:277–283.
25. Bellamy PG, Harris R, Date RF, et al. In situ clinical
evaluation of a stabilized, stannousfluoride
dentifrice. Int Dent J. 2014;64:43–50.
26. Faller RV, Eversole SL. Protective effects of SnF2-
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27. Algarni AA, Lippert F, Hara AT. Efficacy of
stannousfluoride and their combination in dentin
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28. CochraneNJ, Cai F, Huq NL, Burrow MF, Reynolds
EC. New approachesto enhancedremineralization of
enamel. J Dent Res. 2010;89:1187–1197.
29. West NX, Seong J, Davies M. Management of
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30. Veitz-Keenan A, Barna JA, StroberB, et al.
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506.
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Non carious lesions Operetive research project

  • 2. This research paper is about non carious lesions in teeth . It includes the definition , the cause , the treatment and the prevention techniques for them
  • 3. MANAGING NONCARIOUS CERVICAL LESIONS Noncarious cervical lesions (NCCLs) are defined as a loss of hard dental tissue near the cementoenamel junction, usually on the buccal surfaces of teeth, resulting in a grooved or wedge-shaped area of missing tooth structure. These lesions are increasing in prevalence, especially among adolescentsand older adults.1 In particular, lifestyle changes — includingthe increased consumption of acidic drinks among younger patients and the number of olderadults who take prescription medications, which can cause hyposalivation and xerostomia — raise the risk of NCCLs. Hyposalivation increases acidity in the oral cavity, softening the tooth surface and facilitating tooth loss (Figure 1). FIGURE 1. Noncarious cervical lesions are present on the buccal of upper and lower teeth. A study reported that the prevalence of NCCLs in teenagers and adultsranges from 11% to 62%, and the number of lesions increases with age.2 Lesions most often occur on the buccal of maxillary premolars, but are also commonly found on other maxillary and mandibular anterior and premolar teeth. The exact etiology of NCCLs
  • 4. is unknown, but it is generally accepted that their cause is multifactorial.1,3,4 The clinical endpointof NCCLs is the wearing away of dentition. The mechanisms involved includeacid erosion (the loss of tooth structureby acid demineralization without the involvement of bacteria); abrasion (friction resulting in loss of tooth structurefrom dentifrices and toothbrushing); and abfraction (breaking away of tooth structuredue to tensile stresses in the cervical area).1,3,4 Acid erosion is the most important factor involved in the development of NCCLs. Saliva normally keeps the oral environment in the 7.0 pH range (neutral) due to its ability to buffer acids. The source of acids can be intrinsic — bulimia or gastroesophageal reflux disease (GERD), for example — or extrinsic, such as acids from fruit juices, sports and energy drinks, and wine, to name a few. When oral acids bring the pH of the tooth surface below 4.5, demineralization of enamel and dentin can begin.5 EROSIVE CONCERNS The action of strong acids causes the loss of calcium (inorganic matter) from the tooth surface, followed by a softening of the top layers of dentin and enamel. This softened layer then becomes susceptibleto abrasive forces in the oral cavity and is easily removed, potentially causing wedge-shaped cervical lesions. The thin, softened layer is between 0.2 µm and 3 µm thick and is repeatedly
  • 5. removed by abrasive forces, leading to permanent loss of tooth volume in the cervical area.6 The pH (less than 4.5), duration and the strength (buffering capacity) of the acid challengeneed to be considered. For example, cola (phosphoricacid) and certain energy drinks (citric acid) have a similar pH, but drinks containing citric acid are more erosive because more buffering is required to return the pH above the “critical” erosive point of pH 4.5.3Regular and diet sodas and sports and energy drinks range from a pH of 2.5 to 3.4, respectively.7 Lemon, grapefruit and orange juices also cause erosive damage to enamel. Gastric acids from GERD are the most erosive, with a pH of 1.0 to 2.0.1 In addition, patientswith gastric reflux often suffer from hyposalivation.8 FIGURE 2. This patient has severe noncarious cervical lesions. Saliva plays an important role in oral health by cleansing the oral cavity and diluting and buffering acids. Individuals with xerostomia are much more susceptibleto acid erosion. Patients are often advised to avoid brushing
  • 6. for 30 minutes to 60 minutes immediately after an acid exposure, presumably to allow softened surface enamel to remineralize — but, in truth, more effective preventive strategies (such as various fluoride-based therapies) should be recommended. The reality is that softened enamel is not remineralized by saliva over short time periods, and will be worn away even in the absence of tooth brushing by normal abrasive forces in the oral cavity, such as chewing and tongue action. Dental abrasion, anothercontributingfactor to NCCLs, is defined as wearing away of dental hard tissues by frictional forces.1 This can include wear caused by toothbrushing, flossing, tongue action, abrasive foods, and rubbing from opposing surfaces that are hard or rough, such as unpolished porcelaincrowns.3 The effects of such actions are usually more pronounced on dentin surfaces than on enamel (Figure 2 and Figure 3).9 FIGURE 3. Toothbrush abrasion may be part of the multifactorial etiology of noncarious cervical lesions.
  • 7. It appears that toothbrushingalone — regardless of the brush stiffness, filament size, aggressiveness or the frequency of brushing — causes littleabrasive tooth wear.1 Rather, it is the abrasiveness of the toothpaste combined with brushing that is responsiblefor the loss of tooth structure.10,11 Dentifrices that includewhitening agents or productspromoted for their ability to control tartar tend to be more abrasive than other types. That said, all popularbrandsmarketed in the U.S. today comply with abrasivity “safe limits” set by American Dental Association and InternationalOrganization for Standardization.12,13 Any toothpastewith a Relative Dentin Abrasivity (RDA) value of 250 or below can be used safely on a daily basis for a lifetime. Toothbrushes with stiffer bristles, however, have been linked to gingival recession.14 Abfraction is the microstructural loss of tooth structure due to excessive occlusal forces transmitted to the cervical area as flexural forces.1 These flexural forces, usually caused by cyclic loading, may lead to the breaking away of enamel rods in the cervical region of the tooth, causing microfractures of cementum and dentin.4 Bruxism may also contribute, although in the absence of acid there is minimal erosive tooth wear.15 Anotherpossible modifying factor in abfraction formation involves the mobility of teeth and the effects of occlusal stresses in the formation of cervical lesions. A relationship has been found between tooth cervical
  • 8. lesions, tooth stability and periodontalsupport.15 Thus, as tooth mobility increases, teeth are actually less susceptible to excessive occlusal forces, as the teeth move under occlusal loads, resulting in less concentrationof forces in the cervical areas.16 While these interocclusal relationshipsmay be contributingfactors in the formation of some NCCLs, it is likely that clinical signs of abfraction in cervical areas are not simply related to stress concentrations. Rather, they may play a role, alongwith acid erosion and toothbrush abrasion, in the multifactorial etiology of NCCLs.1,4 LESION MANAGEMENT It’s important to note that NCCLs can occur at any time and may worsen throughout a patient’slifetime. Without intervention, they can result in tooth fracture, hypersensitivity and cosmetic problems. Therefore, early diagnosis is important in order to initiate behavioral changes and avoid future invasive and expensive restorative interventions. Clinical management of NCCLs includes first identifying the various etiologic factors present in a given patient. For example, if a patient is an active bruxer, has wear facets on the teeth, and presents with NCCLs, the clinician may decide to prescribe an occlusal splint or night guard.4 Occasionally, judicious occlusal adjustments of
  • 9. interferences may be performed. Acid intake must also be reduced. Through the process of taking a comprehensive medical history, clinicians should question patients regarding their intake of acidic foods or beverages, includingfruits, wine, and sports and energy drinks. It is important to monitor the frequency, duration, sequencing, and the mode of intake of these beverages. Sipping and swishing a drink, for example, are much more erosive than gulping the beverage, as the acidic beverage stays in contact with the tooth surface for longer periods.17 Consuming dairy after an acid challenge will help raise the pH and shorten the duration of erosive insult.18 Medication use, especially among older patients, should be reviewed, as drug-related xerostomia can contributeto tooth surface loss.19 Finally, patients should be asked about GERD, because there is a correlation between this disorder and dental erosion.20 These medical and behavioral factors have the net, and possibly cumulative, effect of demineralizing the tooth surface, which ultimately leads to the irreversible loss of surface enamel via abrasive forces such as toothbrushing, eating hard foods, and even cleaning with toothpicks. If the risk factors cannot be eliminated through behavioral changes or medical treatment, other preventive actions should be taken.
  • 10. KEY TAKEAWAYS  Clinicians are seeing an increasing prevalence of noncariouscervical lesions (NCCLs), especially among adolescentsand older adults.1  Lesions most often occur on the buccal of maxillary premolars, but are also commonly found on other maxillary and mandibularanterior and premolar teeth.  While the exact etiology of NCCLs is unknown, it is generally accepted their cause is multifactorial.1,3,4  Early diagnosis is important in order to initiate behavioral changes and preventive therapies that can help patientsavoid invasive restorative interventions.  Treatment should includeminimizing the intrinsic or extrinsic acids that are the primary cause(s) of the lesions.  Brushing with a stannousfluoride toothpasteis a key element in prevention management. PREVENTION AND TREATMENT Conservative preventive measures using fluoride mouthrinses and topical fluoride should be professionally managed.21 The use of fluoride varnish and bonding agents can protect the teeth from acid attacks, but their long-term effects may be limited.22 Stannousfluoride is
  • 11. an important preventive tool to protect the tooth surface from an acid challenge.23,24 It provides superior protection for acid erosion versus sodium fluoride or monofluorophosphateproducts. It has been shown that a stabilized stannousfluoride toothpasteis effective in preventing erosive tooth wear.25 The mode of action of stannousfluoride is to form a thin layer of stannous-based complexes on the surface of enamel, protectingthe surface from acid attack.26,27 The patient also receives the benefit of fluoride.26 Remineralization after an acid attack may be possible with the use of topically applied pastes containingcasein phosphopeptidesand amorphouscalcium phosphate.28 These materials are supersaturatedwith calcium and phosphateand can “recharge” and remineralize demineralized tooth surfaces. Treatment should includeminimizing the intrinsic or extrinsic acids that are the primary cause(s) of lesions. Treatment for cervical hypersensitivity due to NCCLs may also be necessary. Using desensitizing dentifrices, such as those containing potassium nitrateor stannous fluoride, can be helpful.29 Other studies have shown that the use of a self-etching adhesive, sealant or resin-bonded flowable composite restoration may provide comprehensive and rapid controlof hypersensitivity.30 More advanced lesions can usually be managed using resin-bonded composite restorations. In
  • 12. rare instances, a crown or porcelain veneer may be necessary. Understandingthe etiology of NCCLs and making a timely diagnosis will allow early and minimally invasive interventions, such as the use stannousfluoride toothpaste or fluoride varnish and sealants. Counselingfor behavioral modifications — reducing the intake of acidic foods and beverages, for example — is of utmost importance. Emphasizing the need to take preventive measures to help avoid enamel erosion in the first place will help patientsmanage this common problem. REFERENCES 1.Bartlett DW, Shah P. A critical review of non-carious cervical (wear) lesions and the role of abfraction, erosion and abrasion. J Dent Res. 2006;85:306–312. 2.Huysmans MC, Chew H, EllwoodRP. Clinical studies of dental erosion and erosive wear. Caries Res. 2011;45(Suppl 1):60–68. 3.BarbourME, Rees GD. The role of erosion, abrasion and attrition in tooth wear. J Clin Dent. 2006;17:88–93. 4.Grippo JO, Simring M, Coleman TA. Abfraction, abrasion, biocorrosion,and the enigma of noncarious cervical lesions: a 20-year perspective. J Esthet Restor Dent. 2012;24:10–23. 5.Lussi A, SchlueterN, RakhmatullinaE, Ganss C. Dental erosion — an overview with emphasis on
  • 13. chemical and histopathological aspects. Caries Res. 2011;45(Suppl 1):2–12. 6.Addy M, Shellis RP. Interaction between attrition, abrasion and erosion in tooth wear. Monogr Oral Sci. 2006;20:17–31. 7.von FraunhoferJA, Rogers MM. Effects of sports drinks and otherbeverages on dental enamel. Gen Dent. 2005;53:28–31. 8.Campisi G, Lo Russo L, Di Liberto C, Di Nicola F, Butera D, Vigneri S, Comilato D, Lo Muzio L, Di Fedi O. Saliva variations in gastroesophageal reflux disease. J Dent. 2008;36:268–271. 9.Lussi A, Schaffner M. Progression of and risk factors for dental erosion and wedge-shaped defects over a 6- year period. Caries Res. 2000;34:182–187. 10. Moore C, Addy M. Wear of dentinein vitro by toothpasteabrasives and detergents aloneand combined. J Clin Periodontol. 2005;12:1242–1246. 11. Harpenau L, Noble W, Kao R. Diagnosis and management of dental wear. J Calif Dent Assoc. 2011;39:225–231. 12. ISO Dentistry — Dentifrices — Requirements, test methods and marking. 11609:1995(e).Available at: http://www.iso.org/iso/iso_catalogue/catalogue_tc/cata logue_detail.htm? csnumber=38010. Accessed January 18, 2016. 13. American Dental Association AcceptanceProgram Guidelines: Fluoride-ContainingDentifrices (2005).
  • 14. Available at: http://www.ada.org/~/media/ADA/Science%20and%20 Research/Files/guide_fluoride_dentifrice.ashx. Accessed January 18, 2016. 14. Niemi ML, SandholmL, Ainamo J. Frequencyof gingival lesions after standardized brushing as related to stiffness of toothbrush and abrasiveness of dentifrice. J Clin Periodontol. 1984;11:254–261. 15. Brandini DA, Pedrini D, Panzarini SR, BeneteIM, Trevisan CL. Clinical evaluation of the association of non-cariouscervical lesions, parafunctionalhabits and TMD diagnosis. Quintessence Int. 2012;43:255–262. 16. Kuroe T, Itoh H, Caputo AA, Nakahara H. Potential for load-inducedcervical stress concentrationas a function of periodontalsupport.J Esthet Dent. 1999;11:215–222. 17. Grobler S, Jenkins G, Kotze D. The effects of the composition and method of drinking of soft drinks on plaquepH. Br Dent J. 1985;158:293–296. 18. Lussi A, Jaeggi, T, Zero D. The role of diet in the etiology of dental erosion. Caries Res. 2004;38:34–44. 19. Wiener RC, Wu B, Crout R, Wiener M, Plassmann B, Kao E, McNeil D. Hyposalivation and xerostomia in dentateolderpatients. J Am Dent Assoc. 2010;141:279– 284. 20. Farahmand F, Sabbaghian M, Ghodousi S, Seddighoraee N, Abbasi M. Gastroesophageal reflux
  • 15. disease and tooth erosion: a cross-sectional observational study. Gut Liver. 2013;7:278–281. 21. Lussi A, Hellwig E. Risk assessment and causal preventive measures. Monogr Oral Sci. 2014;25:220– 229. 22. Austin RS, Stenhagen KS, Hove LH, et al. A qualitative and quantitative investigation into the effect of fluoride formulations on enamel erosion and erosion abrasion in vitro. J Dent. 2011;39:648–655. 23. Lussi A, Carvalho TS. The future of fluorides and otherprotective agents in erosion prevention. Car Res. 2015;49(Suppl 1):18–29. 24. Carvalho TS, Colon P, Ganss C, Huysmans MC, Lussi A, SchlueteN, Schmalz G, Shellis RP, Tveit AB, Wiegard A. Consensus report of the European Federation of Conservative Dentistry: erosive tooth wear-diagnosis and management. Clin Oral Investig. 2015;39:277–283. 25. Bellamy PG, Harris R, Date RF, et al. In situ clinical evaluation of a stabilized, stannousfluoride dentifrice. Int Dent J. 2014;64:43–50. 26. Faller RV, Eversole SL. Protective effects of SnF2- Part III. Mechanism of barrier layer attachment. Int Dent J. 2014;64(Suppl 1):16–21. 27. Algarni AA, Lippert F, Hara AT. Efficacy of stannousfluoride and their combination in dentin erosion prevention in vitro. Braz Oral Res. 2015;29:1– 5.
  • 16. 28. CochraneNJ, Cai F, Huq NL, Burrow MF, Reynolds EC. New approachesto enhancedremineralization of enamel. J Dent Res. 2010;89:1187–1197. 29. West NX, Seong J, Davies M. Management of dentinehypersensitivity: efficacy of professionally and self-administered agents. J Clin Periodontol. 2015;42(Suppl):S256–S302. 30. Veitz-Keenan A, Barna JA, StroberB, et al. Treatments for hypersensitive noncariouscervical lesions: a PractitionersEngaged in Applied Research and Learning (PEARL) Network randomized clinical effectiveness study. J Am Dent Assoc. 2013;144:495– 506. SHARE THIS: