Management of Non-carious

lesions
❖ Management of Non-Carious Lesions
❖ Introduction:
Loss of tooth tissue occurs in a number of ways, dental caries and trauma being the
more obvious ones but tooth wear in its own right is now assuming greater
importance. Tooth wear can occur by abrasion, attrition and erosion, abfraction.
Other hard tooth tissue defects are fracture, localized non hereditary enamel
hypoplasia, hypocalcification and discoloration
❖ Tooth wear (Non carious lesions)
These are lesions not associated with the presence of microorganisms that cause
defects in tooth structures.
• Tooth wear is a general term describing the loss of dental hard tissues from the
surfaces of the teeth caused by factors other than dental caries, trauma, and
developmental disorders. It is also termed as Non-Carious Tooth Surface Loss
(NCTSL)
• Severely worn dentitions present one of the greatest challenges in dentistry. Yet the
treatment planning process for severe wear can be simplified if the rules for
programmed treatment planning are precisely adhered to in correct sequence.
➢ In analyzing tooth wear, we should make a distinction between physiologic
wear and pathological wear.
➢ Physiologic Wear:
All occlusions wear to some degree causing what is called physiological wear which is
considered an age-related normal process.
➢ Clinical picture:
• It results in progressive but very slow loss of convexity on the cusps, accompanied
by flattening of cusp tips on the posterior teeth.
• Some wear facets may be found, but they should be minimal in length and depth,
also loss of mamelons on the anterior teeth occurs.
• physiologic wear results in both shortening the vertical length of the teeth and
narrowing the horizontal width of the teeth.
➢ Pathological Wear:
• Tooth wear may be regarded as pathological if the rate of wear is greater than
expected or atypical for the patient’s age.
Signs & symptoms:
• Pain or discomfort
• Functional problems
• Deterioration of esthetic appearance
➢ Pathological wear term can be applied if there is substantial loss of tooth structure,
with dentin exposure and significant loss (≥1/3) of the clinical crown.
➢ The distinction between pathological and physiological Tooth Wear can be
difficult to determine. Therefore, it is of paramount importance that a sequential
diagnostic procedure is followed and always keep in mind that rate and degree of
wear can determine if the process is physiological or pathological.
➢ Classification & Etiology:
• Tooth wear is classified into:
1. Attrition.
2. Abrasion
3. Abfraction.
4. Erosion.

➢ Identification of the etiology is essential for the successful management of the

pathology.

1. Attrition:

Attrition is defined as the mechanical wear of tooth structure due to tooth to tooth
contact without any foreign substance intervention.
It may be described as physiological wearing off, however others consider that
attrition is a pathological kind of wear.
➢ The pathological causal factors for attrition are:
• parafunctional habits, bruxism (stressful tooth grinding), clenching.
• Natural teeth opposing porcelain of high hardness
• lack of posterior support
• TMJ disorders.

❖ Clinical appearance of attrition:

1-Occlusal surface attrition (Occlusal wear):

a) Flattening of the inclined planes.
b) Facet formation.
c) peripheral, ragged, sharp enamel edges
d) Enamel worn off and dentin exposure.
e) flattening of incisal edges (with mamelons loss) and cusp tips with well
f) Loss of vertical dimensions of teeth. {fig.1}

2-Proximal surface attrition (proximal surface facets):

It includes the proximal surface wear at the contact area because of the
physiologic tooth movement (mesial drifting) causing:
• Flattening of proximal surface
• widening or increase in dimension of proximal contact areas, which is more
susceptible to decay.
• Mesiodistal dimension of the teeth is decreased, leading to drifting, with the
possibility of overall reduction in the dental arch.
Fig.1.Attrition associated with loss of vertical dimensions

2. Abrasion: {Fig.2.}
- Is the non-carious, a mechanical surface loss of tooth structure resulting from
direct frictional forces between the teeth and an external object, or from
frictional forces between contacting teeth in the presence of an abrasive
medium.
- Toothbrush abrasion is the most common example, where improper brushing
techniques causes localized cervical lesions on the labial surface of teeth.
- It most commonly affects the premolars and canines, usually along the
cervical margins.
- Presents in a V-shaped caused by excessive lateral pressure whilst tooth-
brushing.
- The surface is shiny rather than carious, and sometimes the ridge is deep
enough to see the pulp chamber within the tooth itself.
- Toothbrush abrasion lesions are characterized by being linear in outline,
following the path of brush bristles. The surface is extremely smooth and
polished.
- In case of tooth brushing abuse, both patient and material related factors
influences its spread.
Patient factor Material factor
• Brushing technique. • Type of bristle material.
• Frequency of brushing. • Stiffness & end-rounding of
• Time of brushing. bristles.
• Force applied during • Flexibility of tooth brush.
brushing. • Abrasiveness, PH and the
amount of dentifrices.

- Pipe-smoking depression abrasion occurring at the latero-anterior portion of

the arch coinciding with the location of the pipe-stem. {Fig.3.}
- Strong use of toothpicks, inter-dental brushes, especially when they are
inserted along with toothpaste between adjacent teeth can cause proximal
abrasion.
- Certain occupational habits such as cutting sewing thread or holding nails
with incisor teeth can create specific localized form of abrasion.

Fig.2. abrasion due to tooth brushing

Fig.3.pipe smoking abrasion

3. Abfraction
• It describes a wedge‑shaped defect at or near to cemento-enamel junction of a
tooth. Lesions due to abfraction are also termed as ‘cervical stress lesions’.
• The theory of abfraction sustains that tooth flexure and bending in the cervical
area is caused due to occlusal compressive forces and tensile stresses, resulting
in microfractures of the hydroxyapatite crystals of the enamel and dentin with
further fatigue and deformation of the tooth structure & disruption of the
chemical bonds enamel rods.
• Abfraction lesions are said to be facilitated by the thin structure of the enamel
and the low packing density of the Hunter–Schreger band (HSB) at the cervical

area.
➢ Clinical picture:
• WEDGE OR V-SHAPED lesions with clearly defined internal & external
angles. Also, they may be C-SHAPED with rounded floors or mixed-shaped
with flat cervical & semicircular occlusal walls.

4. Erosion:
- It is the chemical loss of dental hard tissues by non‑bacteriogenic acid
following the drop in pH of the oral cavity below critical pH, i.e. 5−5.5.
- Grippo and Simring have decried the use of this term. They suggest that
erosion refers to loss of material from action of fluids against a structure, as in
beach erosion from water, but no such mechanism exists in the mouth. So, it is
inappropriate terminology or a misnomer, and the term erosion should be
discarded from dental literature.
- The term BIOCORROSION is more appropriate as it includes all forms of
chemical, biochemical, and electrochemical degradation.
Tooth erosion is termed extrinsic, intrinsic or idiopathic, according to (case history
taking); the acids producing tooth destruction may be exogenous, endogenous or unknown
origin.
I) Extrinsic Erosion: is the result of exogenous acids (Extrinsic factors).

a- Environmental factors: (Occupational)

• Airborne acidic contaminates of the working environment, as → acid fumes by workers

in factories.
→ Battery factory workers (exposed to sulfuric acid).
→ Research laboratory workers who exposed to laboratory acids.
→ Acidic water of swimming pools.
b- Dietary factors:
• The most frequently consumed erosive acids are fruit acids and phosphoric acid
contained in fresh fruits, fruit juices and soft drinks.
. E.g.→ Citrus fruit juices and other acidic fruit juices.
→Acidic carbonated beverages.
→ Wines.
c- Medications:
Low pH medicaments and oral hygiene products come in contact with the teeth
may cause dental erosion.
→  Use of vitamin C (ascorbic acid).
→ Chewable tablets of acetylsalicylic acid (aspirin).
→ Iron tonic products with low pH of 1.5.
d- Behavioral factors:
• ingestion of acidic fruit juices on a daily basis.
• Unusual eating, drinking and swallowing habits, which increase the direct contact time
of acidic food with the teeth.
• The consumption of acidic food at bedtime.

d- Healthier lifestyle:
Many individuals today are assuming healthier lifestyle involving regular exercise and
what is considered healthy diets with more fruits and vegetables.
e- Professional tooth cleaning:
• Dental patients who get their teeth polished as part of their regular check up.
• This leads to loss of several microns of enamel each time which increase susceptibility to
erosion due to removal of the outerfluoride-rich surface layer.
• The use of tooth bleaching agents to whiten teeth.
II) Intrinsic Erosion:
➢ Intrinsic erosion results from the gastric content entering the oral cavity as the
stomach acid has a pH of approximately 2, which is highly erosive to the
dentition. The effect can be particularly damaging to the dentition, especially
the palatal surfaces, when continual episodes are involved.
This can be from a variety of voluntary or involuntary habits and diseases:
➢ Involuntary regurgitation of gastric acids may be a result of
gastrointestinal disturbances, such as during pregnancy, gastro-oesophageal
reflux disease (GERD), vomiting, hiatus hernia, as a side-effect of some
medications or through alcoholism.
➢ Voluntary regurgitation is increasing due to increasing incidence of eating
disorders, such as anorexia nervosa. Also, bulimia, a psychological disorder
that is characterized by self-induced vomiting is another cause for voluntary
regurgitation.
III) Idiopathic Erosion: is the result of acids of unknown origin, i.e. erosion -
like pathology where neither tests nor anamnesis is capable of providing an
etiologic explanation.
➢ Clinical picture:
• In general, erosive lesions present clinically when in enamel only as
rounded and smooth lesions with loss of surface contour. This can lead to
dished out lesions, broad concavities, cupping or cratering with abraded
enamel edges peripheral to the cups or craters or dished out lesions.
• Teeth may appear translucent, due to thinning of the enamel anteriorly, or
darker due to the exposed dentine.
• Teeth may appear glazed (tooth surface being worn away).
• Anterior teeth may chip or fracture.
• Teeth may appear to become shorter.

• In extrinsic erosion, for example from dietary intake, tooth wear is often
observed on the buccal cervical surfaces of the maxillary teeth with
upper premolars are the most affected and the occlusal surfaces of the
mandibular posterior dentition, erosive wear tends to create broader
dished-out shallow lesions in comparison to the sharply defined margins
associated with abrasion.

• In intrinsic erosion, TW tends to present on the palatal surfaces of the

maxillary anteriors and posterior lingual & occlusal surfaces equally on
both arches. The lingual surfaces of lower anterior teeth are often not
affected due to the protective nature of the tongue covering them from
exposure to the acid attack.

• Restorations stand proud from the teeth. Amalgam restorations will be

raised above or higher than the eroded surface which is called amalgam
island.

Erosion of palatal surface.

Erosion affects labial surface Amalgam Island

of upper anterior teeth.

❖ Management of Non-Carious Lesions

Treatment of tooth substance loss (attrition, abrasion and erosion,

abfraction) may be required for a variety of reasons:
• Poor esthetics of the worn teeth &  sensitivity or pain.
• Severe tooth loss → non-vital tooth → infection.
•  Masticatory function → difficulty in eating.
• TMJ disorders.
• Problems in phonation (anterior teeth).
• To protect the tooth from further loss by restorations.
So, Dentists’ role is to early recognize patients at risk and propose a preventive
protocol. This is achieved by taking a thorough patient’s history.

• Tooth wear management is defined as the complete scope of care including

diagnosis, risk assessment, prevention (primary, secondary and tertiary) and
monitoring.
Schematic flow chart of Tooth wear management: to restore or not?

Tooth wear

Physiological Pathological

• No Treatment Etiological factors identification, elimination

• Regular recall appointments Risk evaluation
Wear grading

Prevention, monitoring, counselling

Patients with sensitivity, pulp exposure -Absence of symptoms, dynamic wear

▪ Need to improve function, mastication - patient not interested in treatment
▪ esthetics

Active management No treatment

Regular control
Therefore, regardless of the severity of the condition, prevention is the first step
following risk evaluation. Effective counselling and monitoring provide valuable
info on:
1. The nature and rate of any ongoing wear
2. Patient compliance
3. Effect of preventive measures and the need to refine them

Prevention of tooth wear

Primary level of prevention: (Population based)
General advices given to the patients.
The WATCH strategy is a preventive approach encouraging a lifestyle that is both
healthy and dentally healthy, irrespective of whether patients present with significant
tooth wear or not.

Key discussion points for water:

• Patients should be encouraged to drink more water
• Two to four litres per day or eight or more standard glasses is a suitable quantity for
adults
• The more water a patient consumes on a daily basis, the less the patient resorts to other
drinks that would otherwise further contribute to the overall dietary intake of sugars and
acids
• At times of dehydration, saliva protection is reduced, the mouth dries and the sensation
of thirst is created.

Key discussion points for acids and alcohol:

• Consumption of acidic beverages contributes significantly to the dental erosion
component and tooth wear in many individuals
• Patients should be encouraged to restrict consumption of acidic drinks to meals times.
Water is ideal in-between meals
• Alcohol, being dehydrating, reduces salivary flow protection of the teeth. Wines and
spirits with mixers are frequently highly acidic. Chronic alcoholism is associated with
numerous long-term effects on the upper gastrointestinal tract and its associated glands,
the liver and pancreas, and relevant to tooth wear promote gastro-esophageal reflux

Key discussion points for taste

• Taste stimulates saliva flow
• Fresh fruit and vegetables are excellent salivary stimulants
• Citric acid in oranges, grapefruit, pineapple and lemons is the best natural salivary
stimulant known .
• Prolonged sucking of citrus fruit is detrimental to tooth structure due to extended
contact time.
• The consumption of fruit should not be discouraged on the basis of their acidity, as
fresh fruit are still preferable to modified foods and beverages and are good sources of
vitamin C.

Key discussion points for calcium, caffeine and chewing gum

• Dietary calcium in milk, cheese and yogurt is to be encouraged
• Yogurts are acidic, but their high calcium content prevents them from being agents of
significant dental erosion
• Coffee and tea can have a dehydrating effect
• Patients should be advised to drink an extra glass of water for each cup of coffee or tea
they consume
• Chewing sugar-free gum promotes saliva flow
• Short duration chewing of gum for 5 min after meals is beneficial

Key discussion points for health

• A healthy lifestyle and diet with regular exercise is ideal

Secondary level of prevention (individual based):

Customizing the prevention protocol according to risk factor. Advice should be carefully
chosen according to the diagnosis, etiologies and risk level.

Type 2ry level of prevention

Attrition • occlusal splints.
• Psychological, behavior therapy
• Reduce smoking, coffee, alcohol consumption
• Advise patient to brush 1 hour post acid attack
Abrasion • Psychological therapy
• Protection against abrasive dust via respiratory masks
• Avoid high abrasive tooth paste
Secondary level of erosion prevention by professional and individual
prophylactic measures:
Irrespective of the etiology of erosion, the following elements of prevention must be
considered when designing a prophylactic strategy:
• Measures to diminish frequency and severity of acid challenge.
• Measures to enhance the defense mechanisms of the body, i.e. Salivary flow and pellicle
formation.
• Measure/to enhance acid resistance, remineralization and rehardening of the tooth
surface.
• Measures to provide chemical protection.
• Measures to weaken abrasive influences.
• Measures to provide mechanical protection.

1- Diminishing frequency and severity of acid challenge:

• The optimal preventive measure is to remove the source of acid or prevent it from
reaching the teeth.
• If erosion is of dietary origin:
→ Decrease the frequency of consumption of acid food
→ Such food must be restricted to main meals.
→ Acid drinks should be drunk quickly or should be consumed
through a straw.
→ Effervescent vitamin tablets should be substituted by capsules to be swallowed
entirely.
• Patients suffering from chronic regurgitation should be referred to a physician.
2. Measures to enhance salivary flow:
Saliva is known to have many properties that can serve a protective function against
dental erosion:
• Dilution and clearance of erosive agents from the mouth.
• The neutralization and buffering of dietary acids.
• Maintaining of supersaturated state due to the presence of calcium and phosphate in
saliva.
• Providing calcium and phosphate and possibly fluoride necessary for remineralization.
• Saliva also contains buffers to resist changes in pH (bicarbonate
content).
N.B. Bicarbonate content of stimulated saliva is higher than that of resting saliva.
So, Measures that stimulate salivary flow rate, e.g. sugar-free chewing gum
consequently are anti-erosive and support remineralization.

3. Enhancing acid resistance, remineralization and rehardening:

• Calcium and phosphate and fluoride must be present in remineralizing solutions.

• The re-hardening of enamel surfaces is not the result of re-growth of etched and partly
dissolved apatite crystals but it is due to precipitation of calcium phosphates which are
poorly soluble in acid, such as brushite (CaHPO4) or dicalcium phosphate (Ca PO4 12)
into the porous enamel matrix.
• Thus, the term repair may be more appropriate than the term "remineralization".
• The most important factors in the repair of softened enamel are the saliva and
fluoride.
4. Measures to provide chemical protection:
Acid neutralization by buffering components of the diet:
→ Patients advised to hold some milk in the mouth for a short time after fruit
consumption or vomiting.
→ Milk and cheese have been shown to re-harden pre-softened enamel.
→ Improve salivary alkalinization by neutralizing agents in chewing gum
formulations.
→ Sucking of sugar free anti-acid tablets.
→ The use of bicarbonate containing toothpastes.
5. Measures to minimize abrasive influences:
• Very low abrasive toothpaste should be recommended for patients suffering from
erosion.
• Using glycerin as a suspension medium in the dentifrices reduced abrasion about
88%.
• Because freshly etched enamel is easily abraded, patients with erosion are advised
not to brush immediately following consumption of acid food, reflux or
regurgitation.

6.Providing mechanical protection:

• It has been known that the application of a sealant onto etched intact enamel leads to
a marked increase of acid resistance. It is recommended etching and sealing of early
erosive lesions in order to stop further progression by chemical dissolution and
mechanical wear.
• Fluoride lacquer (polyurethane based containing difluoro-silane) can be expected to
provide a double protective action than NaF varnish based on natural resin, namely
decrease enamel surface softening during acid exposure and mechanical protection
against wear, so it is therefore recommended as a professional prophylactic measure
for initial erosive lesions. Larger lesions warrant the use of restorative treatment.
• Desensitization:
Application of copal varnishes, potassium oxalate or other desensitization products
provide only some temporary pain relief.
• Desensitizing dentifrices:
> Many anti-sensitivity dentifrices form a protective layer (precipitated minerals)
on dentin that blocks exposed tubules.
> Application of (strontium chloride hexahydrate) in a dentifrice form.
> However, these desensitizing dentifrices often take 1 to 3 months for required
results to be realized.
• Fluorides:
- Fluoride treatments with or without ionophoresis, provide some pain relief.
- Ionophoresis treatments using small electronic currents to introduce sodium
fluoride and/or corticosteroids into the tubules usually require multiple
applications.
Tertiary level of prevention
Restorative therapy for NCCls
Restorative treatment may be necessary if:
a) The structural integrity of the tooth is threatened.
b) The tooth (dentin) is hypersensitive.
c) The defect is esthetically unacceptable to the patients.
d) Pulpal exposure is likely.

Abrasion:
Treatment modalities:
1. remove the cause of abrasion before ttt & restoration.
2. Knowing the causative factor first and try to prevent the patient from practicing the
causative habits. (Correct or replace the iatrogenic dental work if it is present).
3. desensitize the exposed dentin before restorative treatment is started, as if the
sensitive teeth are restored immediately, they will remain sensitive to thermal
changes forever.
Desensitization can be done by:
→ Topical application of 10% stannous fluoride.
→ Ionophoresis using an electrolyte containing fluoride ions can also be used.
4. Restorative treatment:
A. If the lesions are multiple, shallow (less than 0.5 mm in dentin), wide and involve
enamel or cementum only → no need to restore. Only, edges at the defect should be
eradicated to → smooth, non-demarcating pattern relative to adjacent tooth
surface which is very important for esthetic and plaque control.
The tooth surface should be treated with fluoride solution to improve its caries
resistance.
B. If the lesions are wedge V shaped and exceeds 0.5 mm into dentin
it should be restored.
i. If the abrasive lesions at a non-occluding tooth surface → no need for cavity
preparation and the restoration can be done in one of the direct tooth-colored
materials.
ii. If the abrasive lesions are deep and at an occluding tooth surface → metallic
restoration should be used.

RESTORATIVE THERAPY FOR EROSIVE LESIONS

Lesions limited to enamel:
Enamel erosion, with no dentin exposed, the teeth are not hypersensitive. For esthetic
complains, a composite resin or porcelain veneer should be considered as the
treatment of choice as it seals the enamel and recontours the tooth.
Lesions into dentin:
At a certain stage, dentin becomes exposed. A structural change of the tooth substrate
occurs as dentin is a dynamic tissue, a clear characterization of sensitive dentin (open
tubules) and non-sensitive or sclerotic dentin (closed tubules) .

➢ Sensitive dentin:
Many of these hypersensitive dentin lesions are symptomatic and can range from
minor sensation to extended painful episodes for the patient.
Dentin hypersensitivity is a common reason for patient complaints and treatment
need. Fluid movements in the dentinal tubules (the hydrodynamic theory) are usually
caused by stimuli, such as cold air and water and mechanical probing, which rushes
painful hypersensitive dentin. Microorganisms in dentinal tubules can also cause
irritation and pain.
➢ Non-sensitive dentin or sclerotic dentin:
Reactive sclerosis occurs in response to slowly progressive or mild irritations like
abrasion and chemical erosion. Dentinal tubules may become partially or completely
obturated by the growth of peritubular dentin or by the precipitation of mineral salts
within the tubular orifices. Calcification of the dentin tubules has been reported on
teeth exhibiting occlusal attrition and advancing cervical lesions. The hydroxyapatite
crystals occlude the dentinal tubules, thereby sealing the dentin and reducing
sensitivity.

The most common materials used to restore NCCLs are:

• Resin composites,
• Glass ionomer cements (GI),
• Resin-modified glass ionomers (RMGI)

• Conventional Glass ionomer vs Resin modified glass ionomer:

They are especially effective for treating non-carious cervical lesions and in
older patients who often experience reduced salivary flow, which makes them
more susceptible to caries. Releasing fluoride ions from these cements into the
underlying dentin will prevent tooth decay, Resin-modified glass ionomer
cements have the highest chance of survival for restoring NCCLs over the
conventional glass ionomer.
• Glass ionomer vs Composite resin:
• Despite their excellent clinical performance in terms of retention, glass- ionomers
commonly present with lower esthetic features (higher surface roughness, lower
color stability, and lower wear resistance) and inferior mechanical properties when
compared to resin-based restorative materials.
• Composite resin with low elastic modulus is also recommended in these lesions.
• So, micro filled composite is the material of choice in the cervical area.
• In the occlusal area, (hybrid composite is more indicated because of their wear
resistance.
• Doubling the etching time have been investigated for conditioning sclerotic dentin.
• Type of adhesive:
▪ 2 steps etch and rinse or 2 steps self-etch showed the most favorable and durable
clinical bonding performance than one – step adhesives.
• Composite or Porcelain Veneers:

• Especially if the labial surfaces are involved, one can choose for the direct or indirect
composite veneer or even porcelain veneers.
• The advantages of porcelain veneers are their esthetics and durability. In
addition, if the incisal margins are eroded, porcelain veneers are able to cover the
lost tooth structure.

• Crown and bridge work:

An extensive defect that needs repairing of the vertical dimension often requires
extensive crown and bridgework.

• Occlusal adjustments and night guard fabrication

• Occlusal adjustment and night-guard fabrication are recommended if the abfraction
factor coincides.
• Treatment of lesions will be ineffective in the. long term, unless the etiological
factors are eliminated.

Dental erosion affecting the palatal aspects of the maxillary teeth

Abrasion of the upper and lower incisors produced from contact with a pipe stem

Sever attrition

Intrinsic erosion