Dental Light Curing

Dental Light-Curing—Assessing
the Blue-Light Hazard

Dayane Oliveira, DDS, MS, PhD, Mateus Garcia Rocha, DDS, MS, PhD*
KEYWORDS
Light curing units Photopolymerization Blue-light hazard Eyewear protection
Occupational exposure
KEY POINTS
Dental light-curing units emit high-power visible light that can cure resin materials in
seconds; however, the use of high-power visible light can cause critical health
issues.
Dental personnel should be trained to use light-curing units (LCUs), and they should wear
protective eye filters when operating or manipulating LCUs.
If the use of LCUs is causing you persistent afterimages or blurred vision, you have been
exposed to an excessive amount of light, and you should improve your LCU safety
measures.
The misuse of high-power LCUs can cause soft tissues burns and pulpal inflammation;
however, the use of the correct radiant exposure and tooth cooling techniques (ie, in-
crease of airflow to the tooth while curing by using an air syringe) can reduce any potential
risks of using these LCUs.
INTRODUCTION
Light-curing units (LCUs) are essential for photopolymerization in modern dentistry.

The basic idea is to instantly transform a liquid or viscous monomer into a solid mate-
rial on light exposure inside the patient’s mouth.1 Because a photopolymerization re-
action involves a photoinitiator system, a polymerizable medium (monomers), and an
LCU, a strong correlation exists between them.2
The literature on how to properly light-cure dental materials is vast.3 However,
such devices may pose severe risks to dental personnel and patients. Therefore,
the objective of the present article is to review the characteristics of the blue light
emitted by LCUs, the physiology of the human eye and dental tissues to visible light,
and how to efficiently use LCUs to mitigate risks and conduct proper light curing in
dentistry.
Center for Dental Biomaterials, Department of Restorative and Dental Sciences, University of
Florida - College of Dentistry, 1395 Center Drive D9-6, Gainesville, FL, USA
* Corresponding author.
E-mail address: mrocha@dental.ufl.edu
Dent Clin N Am - (2022) -–-

https://doi.org/10.1016/j.cden.2022.05.004 dental.theclinics.com
0011-8532/22/ª 2022 Elsevier Inc. All rights reserved.
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Foundation Hospital and Research Centre from ClinicalKey.in by Elsevier on September 18, 2022. For
personal use only. No other uses without permission. Copyright ©2022. Elsevier Inc. All rights reserved.
2 Oliveira & Rocha
LIGHT CURING IN DENTISTRY
Light curing in dentistry was first attempted clinically in the early 1970s using ultravi-
olet light (UV, about 365 nm).4 However, this photopolymerization system did not suc-
ceed due to the harmful effects of the UV energy being exposed to human eyes
(corneal burns and cataract formation), poor depth of penetration into materials,
and many issues with the properties of the UV-cured dental materials.4 In 1976,
advances in visible light polymerization allowed the development of resin materials
containing camphorquinone (CQ) and reducing agents (ie, tertiary amines) photopoly-
merized by blue light.2,5 The advantages of using visible light revolutionized dentistry
and resin-based materials are considered long-lasting treatments for restorative
dentistry.5 Because long visible wavelengths penetrate deeper into materials, the
depth of cure of these materials was increased. Thus, besides improving the proper-
ties of light-cured resin materials, it also allowed a reduced chair time. The incremental
technique increased from a single millimeter to now 2 to 5 mm 4,5 Although visible light
curing has reduced potential hazards for developing cataracts and macular degener-
ation compared with UV light curing, it still can cause direct retinal burning and retinal
photochemical damage. The potential for visible light curing in dentistry to cause
or contribute to macular degeneration in dental personnel over their working lifespan
remains unknown.6–8
For many years, Quartz-Tungsten Halogen (QTH) LCUs were very popular. QTHs
emit the entire visible spectral range from an incandescent light bulb, and a prism fil-
ters violet and blue light.4 However, in 2009, the European Union and other countries
began a phase-out of inefficient incandescent bulbs to widen efforts to deal with
climate change.9 In modern dentistry, light-emitting diodes (LEDs) are the most pop-
ular LCUs, as they have several advantages compared with QTH, such as portability,
power efficiency, and more consistent light output.3,4
The first and second generations of dental LEDs, also called monowave or single
peak, emit a narrow band within the blue light range (420–495 nm) with a peak around
460 nm (Fig. 1A).4,10 Later, with other photoinitiator systems with absorption in
different regions of the light spectrum, LED LCUs with light emission in both the violet
Fig. 1. Curing lights. (A) Single peak; (B) multipeak; (C) Quadwave; (D) laser.

Dental Light-Curing 3
(380–420 nm) and blue range were released into the market. These LCUs, also known
as multiwave, polywavea, or multipeak LCUs, are devices made up of a combination of
2 or more LED chips emitting over different wavelengths (Fig. 1B).3,4,10 The multipeak
LEDs emit light from 380 to 540 nm, comprising the violet and blue range. More
recently, a new generation of curing lights emitting red and near-infrared (NIR) was
released on the market (Fig. 1C). The so-called Quadwaveb technology claims to in-
crease the degree of conversion and reduce polymerization shrinkage. However, at
the present moment, there is no scientific evidence that red and NIR lights have ben-
efits on modern composites containing CQ or other alternative violet or blue light–
absorbing photoinitiators.
Dental laser diodes were released into the market claiming to light-cure dental mate-
rials in 1s (Fig. 1D). Lasers (plural for the acronym Light Amplification by Stimulated
Emission of Radiation) are distinguished from other light sources by their coherence.
Laser beams have a minor divergence to concentrate their power at a great distance.
Also, the narrow emission spectrum from the lasers is designed to excite the photoini-
tiators used within the red blood cells at their maximum absorption efficiency. Although
some materials can efficiently photopolymerize in this curing condition, these lasers can
be considered medical devices with a high potential to cause injuries if misused. Ac-
cording to the United States Food and Drug Administration (FDA) 501(k) premarket noti-
fication regulations, dental curing lasers are class II medical devices with a moderate
risk of injuries. However, lasers with more than 500 mW of power are classified as
high-powered Class 4 visible-beam lasers. A Class 4 laser operator should be trained
by a Laser Safety Officer (LSO) with the duties and responsibilities defined in the
ANSI Z136 standard published by the American National Standard Institute (ANSI).
The critical problem with visible light curing is that the wavelength needed to initiate
the photoinitiator systems overlap within the frequencies known to cause photochem-
ical and photothermal injuries to ocular, gingival, and pulp tissues.11–13 Furthermore,
contemporary light-curable materials require radiant exposure of 10 to 40 J/cm2 to
polymerize dental materials adequately.3,14 To deliver this amount of energy in a short
exposure time, the use of high-powered LCUs with a high capacity of light emission is
required.3,7,13 LCUs are considered high-powered when emitting 1000 mW/cm2 or
higher. Nowadays most LCUs on the market are considered high-powered. Despite
the clinical advantage of light-activating materials in seconds, high-irradiance visible
light can cause critical health issues.7,8
THE BLUE-LIGHT HAZARD
Exposure to blue light is very significant in modern life. Most of the population is
exposed to artificial light over the entire day. Because light has a cumulative effect
and its power is affected by several characteristics, such as wavelength, intensity,
and duration of the exposure, it is crucial to consider the power and the spectral
output of the dental LCUs to minimize the risks associated with excessive blue-light
exposure.
Potential Ocular Hazards

In humans, photoreception occurs in the retina by 3 photoreceptors: cones, rods, and
the intrinsically photosensitive retinal ganglion cells.6 Fig. 2A shows the human eye
a
Polywave is a trademark of Ivoclar Vivadent.
b
Quadwave is a trademark of Vista Apex.

4 Oliveira & Rocha
Fig. 2. (A) Cross-section view of the human eye anatomy. The eye is a fluid-filled sphere en-
closed by 3 layers of tissue. The first layer is a tough white fibrous tissue (Sclera) that con-
nects with a specialized transparent tissue (Cornea) that permits light to enter the eye.
The second layer of tissue includes 3 distinct but continuous structures: the Iris, the Ciliary
Body, and the Choroid. It contains 2 sets of muscles with opposing actions, which allow
the size of the Pupil to be adjusted under neural control. Only the innermost layer of the
eye, the Retina, contains neurons that are sensitive to light and can transmit visual signals
to the Optical Nerve. The Macula is a part of the Retina responsible for the central vision
(sharp, clear, fine detail, straight-ahead vision). The Macula has a very high concentration
of photoreceptor cells. (B) The interaction of electromagnetic radiation to human eye tis-
sues. The optical hazards are associated with the frequency and penetration of the different
electromagnetic radiations. Ozone is a gas present in the upper layers of the atmosphere
and serves as an exogenous protection layer against harmful ultraviolet (UV) radiation.
UV can cause photochemical injury to the cornea (photokeratitis) and lens (cataract) of
the eye (180–400 nm). Thermal injury to the retina of the eye is like to happen from 400
to 1400 nm; blue-light photochemical can injure the retina of the eye (principally 400–
550 nm); near-infrared thermal hazards to the lens (approximately 800–3000 nm); thermal
injury (burns) of the cornea of the eye (approximately 1400 nm to 1 mm); thermal or photo-
chemical injury to the skin from high irradiances.
anatomy. Different investigations have shown that exposure to light of specific wave-
lengths or intensity may induce severe damage to the eye.15,16 This type of damage is
called light-induced damage. The eyes are at risk of injury from acute and long-term
exposure to solar and artificial optical radiation (Fig. 2B). The severe dangers that
UV radiation presents to both eyes and skin are well established. Increasing evidence
has alerted scientists and clinicians to the damage that long-term exposure to visible
light may cause to retinal photoreceptors.
Light can cause damage via 3 mechanisms: photomechanical, photothermal, and
photochemical.6 Photomechanical damage is due to a rapid increase in the amount
of energy captured by the retinal pigment epithelium (RPE), which may cause irre-
versible damage to the RPE and lead to photoreceptor damage. This type of retinal
damage depends on the amount of energy absorbed and not on the spectral
composition of the light. Photothermal damage occurs when the retina and the
RPE are exposed to brief (<10 s) but intense light that significantly increases the
temperature of these tissues. These injuries can happen to patients and dental
personnel who do not wear appropriate personal protective equipment (PPE).17
They are primarily caused via accidental direct exposure to high-power light irradi-
ation from imprudent use of LCUs by an untrained operator. These accidents can
be very severe with lasers, as they can sustain the high power over longer dis-
tances due to the coherence of the light beam. When using a dental LCU, the major
concern is that cumulative irradiation of the eye may cause permanent damage to
the macula and the RPE over the long term.

A more common type of retinal damage is photochemical damage, which occurs

when the eyes are exposed to high-intensity light in the visible range (390–600 nm).6
Several lines of evidence suggest that visual photopigments (eg, rhodopsin and
cone opsins) are involved in this type of damage. Early studies also provided evidence
that the action spectrum for light-induced photoreceptor damage is similar to the ab-
sorption spectrum of rhodopsin. Still, later studies indicated that blue light (400–
440 nm) might be more damaging; this has been termed the “blue-light hazard."18
Fig. 3 shows the blue-light hazard function defined as the capability of light to produce
photochemical retinal damage as a function of wavelength. Current studies suggest
that there are 2 distinct types of photochemical damage. The first type is associated
with short but intense exposure to light affecting the RPE. The second type is associ-
ated with more prolonged but less intense light exposure, affecting the outer segment
of the photoreceptors. Short (up to 12 hours) exposure to blue light may induce dam-
age in the RPE (in primates),19 and a clear relationship has been found between the
extent of the damage and the oxygen concentration.20 Because antioxidative physio-
logic processes (ie, lipofuscin mediation) can reduce the harm associated with oxida-
tive processes, it is recommended that the radiance, weighted by the blue-light hazard
function, received by the eye should not exceed an average of 10 mW/(cm2 sr) over a
total viewing time of up to 167 minutes in a day.
Because the peak absorption for CQ is about 455 to 481 nm, dental LCUs are opti-
mized to perform in the wavelength range where the blue-light retinal injury also oc-
curs. A previous study13 demonstrated that under clinically relevant conditions, at a
viewing distance of 40 cm, the daily maximum permissible cumulative exposure
time to blue light from the LCU is 7 seconds (5 mW/cm2) and approximately 11 minutes
(630–690 seconds) (0.053 mW/cm2) for direct and indirect, reflected light, respec-
tively. When wearing loupes, there is an increase in the radiant flux (mW) entering
Fig. 3. Spectrum of the blue-light hazard function representing the relative spectral sensi-
tivity of the human eye to the visible light. It is based on the relative spectral effectiveness
of optical radiation to induce retinal photochemical injury. The blue-light retinal injury oc-
curs primarily from exposure in the wavelength range between 380 and 550 nm, with the
sensitivity of the retina peaking at approximately 440 nm.

6 Oliveira & Rocha
the eye. Although the radiant flux received by the eye is greater when loupes are used,
the image is magnified and therefore distributed over a broader area of the retina,
causing the calculated maximum cumulative daily exposure time to increase to be-
tween 16 and 28 minutes. Even so, this maximum daily exposure may be easily
exceeded by dentists who place more than 10 restorations a day or by orthodontists
or their assistants when bonding brackets onto teeth. Also, the beneficial effect of eye
movements to reduce the time-averaged retinal irradiance for a small source may be
reduced because loupes induce a greater fixation of looking at one spot on a tooth.
The second type of light-induced photochemical damage occurs with more pro-
longed (12–48 hours) but less intense light exposure.6 Several publications suggest
that long-term chronic exposure to blue light may accelerate retinal aging and age-
related macular degeneration.15 This type of damage was initially observed in albino
rats and other species. The cones seem to be more vulnerable compared with the
rods. Although neural retina in humans and rodents have differences in organization
and sensitivity to light, the RPE is highly analogous. It has the same functions and
ages in the same way in most species. Therefore, phototoxicity data from animal
models concerning RPE should be more closely related to human phototoxicity. It is
important to note that the methods used to calculate those values were the same
for primates and rodents. Recent studies have shown that radiant exposure of
0.5 J/cm2 already causes cell death, and if the blue-light hazard weighting is consid-
ered, this global dose corresponds to 0.06 J/cm2; this means that cell death with a
dose of blue light about 180-fold smaller than the exposure limit values is being
detected in animal studies. This evidence suggests that the phototoxicity data ob-
tained in primates and used to establish the current regulations related to the photo-
biological safety of light sources must also be reevaluated.
Intrinsically photosensitive retinal ganglion cells control body temperature, hormon-
al levels, sleep duration and quality, cognitive performance, and other physiologic var-
iables.6 However, excessive exposure to blue light can also disrupt the circadian
cycles causing fatigue, stress, mood disorders, and other physiologic and psycholog-
ical issues. Chronic light exposure at the wrong time, at night during shift work, for
example, may contribute to shifts of the circadian clock phase, dependent on dura-
tion, wavelength, and intensity of light.
Still, the evidence of the detrimental effect of blue light on the retina should be taken
with caution. Most of the damaging effects of blue light are demonstrated in animals or
isolated cell cultures directly exposed to blue light. In humans, direct evidence of
acute light–induced retina damage from accidental high-intensity artificial or sunlight
exposure is obvious. However, there is an increased need for observational studies
into whether long-term exposure to blue light from LCUs in dental settings causes
damage to the retina. Further studies on the ocular hazards of using loupes and the
overall cumulative effects of other high-output light sources in the dental office are
required.
Potential Hazards to Pulp and Gingival Tissues

Adverse effects of elevated temperatures on dentin and pulpal structures are signifi-
cant. According to the most-cited study in the field, as temperature increased (higher
than normal oral temperature) from 5.5 to 11 C, at 1 mm into dentin, the possibility of
pulp necrosis increased from 15% to 60%.21 However, it is well known that this all de-
pends on the duration and exact nature of the thermal challenge. A follow-up study
indicated that an 11.2 C increase would still be considered safe and not damage
pulpal tissues.22 Some in vivo and in vitro measurements have also demonstrated
slower temperature changes within the pulp due to dynamic temperature regulation

by the surrounding soft tissue and constant blood flow. The temperatures developed
at 1 mm into dentin could have been less in a more clinically simulative environment.
These controversial results are attributable to the fact that it is impossible to track
the temperature changes in specific localized pulp areas or to precisely determine
how much irradiation to these areas is caused by the exposure (Fig. 4). Overall, the
heat seems not to be the major injury factor, at least in the short term. However, it
is certain to play a role in postoperative inflammation or necrosis in the long term,
especially when combined with other factors such as caries and high-speed bur
injuries.
On the other hand, the blue light also directly irradiates surrounding soft tissues,
especially in cervical restorations, crown cementations, or bleaching procedures.
This direct irradiation causes a significant reduction in the proliferative activity of the
fibroblasts and increases intracellular reactive oxygen species (ROS) levels and mito-
chondrial disorders regardless of temperature increase.23
Mitochondria contain flavin proteins that underlie photoinduced hydrogen peroxide
production (Fig. 5). All molecules have an excitation wavelength, and ROS are always
produced when oxygen is present. In this case, flavins have an excitation wavelength
within the blue-light region. Blue light also can release nitric oxide from intracellular
stores in mitochondria and contribute to energy depletion and cell death.24 Gingival
recession can be induced by the inhibition of fibroblasts proliferation and the degra-
dation of collagen synthesis due to ROS.
Fig. 4. Class IV light-activation scenario with direct light irradiation spreading intensity ac-
cording to the origin of exposure. The power estimation was done by image pixel intensity
calibration based on previous studies.13

8 Oliveira & Rocha
Fig. 5. Photo-induced hydrogen peroxide production in the mitochondria.
Moreover, when these curing lights generate heat, they have the potential to cause
damage to the soft tissue. For that reason, the use of high-power LEDs or lasers im-
poses even more risk of burns. Heat can cause burns because direct heat exposure to
cells causes protein denaturation, cell membrane leakage, activation of cytokines, and
cessation of blood flow leading to cell death.25 Depending on the amount of heat, the
damage can be immediate or long term.
Thermal injuries occur when energy is transferred from the heat source to the human
tissue, causing an increase in the local temperature. When the temperature increases
greater than a certain threshold, known to start at 44 C, irreversible cell injury occurs
within 6 hours. When the temperature increases beyond 51 C, the injuries are
immediate.26,27
CLINICAL CONSIDERATIONS TO MITIGATE THE RISKS OF USING DENTAL LIGHT-

CURING UNITS
For a health care provider, safety is essential, and as with any other powerful medical
device, such as radiography, computed tomography, and MRI, with the proper pre-
cautions and training, the benefits of powerful LCUs can outweigh the risks. Despite
scientific evidence for visible light risks primarily based on animal studies, sufficient
evidence indicates that appropriate precautions should be used by dental personnel
when using LCUs.13,28–31 The American Dental Association Council on Dental Mate-
rials, Instruments, and Equipment recommend using protective eyewear when using
all LCUs.32
Eyewear Protection
Dental personnel should protect their eyes from the LCU to prevent ocular damage.
The protective light filters should not completely block longer wavelengths, allowing
the visualization of the treatment field while curing adequately. The dentist is respon-
sible for providing appropriate PPE to the patient to prevent potential injuries or side
effects caused by medical and dental devices.
The FDA considers curing lights to be Class II medical devices (capable of posing a
moderate risk to the patient, user, or both) that must meet approval standards before
they can be sold in the United States. Although there are standards for protective
eyewear, PPEs purchased aftermarket are Class 1 medical devices (low risk to the pa-
tient, user, or both) exempt and not required to submit proof of efficacy and safety

before being sold in the United States. LCUs emit light in different wavelength ranges.
There is a lack of aftermarket regulation of light protective filters. Not all protective fil-
ters are efficient at blocking the shorter wavelengths or longer wavelengths; but even
in the worst-case scenario, the filters still have been shown to block more than 97% of
the light from the LCU.33 However, some shields might not filter all the light spectrum
appropriately or can be damaged after multiple exposures. Dental professionals need
to ensure that the protective glasses’ wavelength range as declared by the manufac-
turer is adequate for the intended function (Fig. 6).
Importantly, lasers used for dental light-curing are considered high-powered
(>500 mW) Class 4 lasers. A Class 4 laser can cause a significant eye injury if the
direct or reflected beam enters the eye. It can burn skin, gingival tissues, and mate-
rials, particularly dark and lightweight materials (ie, Rubber Dam). They should be
used with extreme caution, and to prevent eye exposure, the operator should always
be aware of the beam location. The dentist, the patient, and anyone else in the room
should always wear the appropriate laser-certified protective goggles. The laser
should not be activated until it is in the patient’s mouth over the area to be cured.
Also, some PPEs might filter the wavelength, but after consecutive exposures, ther-
mal damage to the plastic shield is expected, as these PPEs do not have resistance
to the heat generated by the filtering of high energy. For example, after 3 direct ex-
posures with a Class 4 dental light-curing laser, a regular orange goggle can have its
shield’s integrity compromised (Fig. 7). Although this article is intended for the
reader’s educational, instructional, and informational purposes, it is not a substitute
for a knowledgeable and trained LSO with the duties and responsibilities defined in
the ANSI Z136.
Dental personnel have different options for PPEs. Based on previous studies, each
one of the PPEs has advantages and disadvantages according to its protective effi-
cacy and convenience (Fig. 8).7 In general, untrained dental personnel believe that
the "look away" method is the most convenient and efficient method to avoid blue-
light exposure. However, this method is not indicated because the user can no longer
monitor the location of the light tip when they look away, and it may result in soft tissue
burns, inadequate light curing, and deficient restorations.
Fig. 6. Eye protection for single peak, multipeak, Quadwave, and laser LCUs. * Indicates
Thermal Damage to the google was found after the first exposure and it compromised
the shield integrity.

10 Oliveira & Rocha
Fig. 7. Dental laser LCU can cause damage to the orange goggles that are not laser certified.
The sign of laser radiation hazard for Class IV lasers needs to be visible to patients and
dental personnel when using lasers.
Prevention of Pulpal and Gingival Tissue Injuries

Gingival tissue injuries are most likely to happen near the cervical area of the tooth (ie,
cervical restorations, crown cementation, bleaching blockers around the gum line, and
so forth). In these clinical scenarios, preventing such injuries is performed by carefully
positioning the LCU toward the tooth and avoiding exposure to the gingiva. It is known
that the curing light should always be positioned parallel to the surface to be light-
cured.3 The axial contour of all facial and buccal surfaces of the teeth are not straight
but rather slightly convex. Thus, aiming the curing light appropriately will allow correct
exposure to the material being light-cured and reduce the amount of exposure to the
surrounding soft tissues (Fig. 9).
Fig. 8. Advantages and disadvantages of different eyewear personal protective equipments.

Fig. 9. Left side shows the correct LCU positioning to prevent soft tissue injuries. The tip
needs to be in close contact with the restoration, and it should avoid overlap the soft tissues.
Right side shows the tip inclined toward the gingival tissue.
Interestingly, rubber dam isolation cannot protect gingiva when high radiant expo-
sure values are delivered. The presence of a rubber dam does not entirely block the
light and instead increases the probability of gingival burns because of the rubber
dam’s heat absorption.34
For that reason, it is also thoughtful to prevent the overheating induced by the light-
curing process. The most efficient way to overcome this problem is to directly blow air
from an air syringe on the tooth that is being light-cured.35 The air will cool down the
tooth and avoid temperature increase. Of course, while light curing, the dentist needs
both hands to hold the curing light and stabilize it on the tooth surface being light-
cured. Thus, training dental assistants to hold safety orange blockers and blow air
on the tooth being cured can be very handy to maintain safety and efficiency.
The cooling down method using the air syringe does not only protect the gingiva
from burn injuries but prevents possible overheating of the pulp tissue while light-
curing deep restorations. Although the heat seems not to be the major factor of injury
in the short term, it can cause postoperative inflammation and induce necrosis of the
pulp in the long term and should not be disregarded.36
SUMMARY
LCUs are extensively used in dentistry to polymerize dental materials. These mate-
rials require high-powered blue light (from 420 to 495 nm) to be efficiently cured in a
short curing time. However, cumulative exposure to intense blue light is associated
with severe ocular pathologies such as retinal damage and potentially macular
degeneration. Also, LCUs pose risks of injuries to the patients’ skin, gingival, and
pulpal tissues. Nevertheless, the use of high-powered LCUs by trained dental
personnel with appropriate safety measures can mitigate the risks and provide
patients efficient, high-quality dental care offered by materials with adequate
photopolymerization.
CLINICS CARE POINTS
LCUs used should be approved medical devices, and the eye protection must meet
photobiological safety standards.
It is recommended to use the PPEs provided by the manufacturer of the LCU. However, if a
third-party manufactures the orange shields or glasses, ensure that they protect against
the wavelengths emitted by the LCU in use.
If using lasers, make sure to train your dental personnel. Use the laser in a safe, close
environment; display the laser radiation sign and be cautious of the use of high-power LCUs.

12 Oliveira & Rocha
To avoid accidents, wear appropriate PPE when manipulating, cleaning, or using a dental
LCU.
Do not leave the LCU in the high-power mode and remove the batteries, if possible, for
cleaning and disinfection.
Never direct the tip of the LCUs directly onto skin and gingival tissues.
Avoid pulpal inflammation by blowing air on the tooth while light-curing the restorations in
close proximity to the dental pulp.
DISCLOSURE
The authors have no commercial or financial conflicts of interest with this article.
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Dental Light Curing

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Dental Light-Curing—Assessing

the Blue-Light Hazard

Light-curing units (LCUs) are essential for photopolymerization in modern dentistry.

Dent Clin N Am - (2022) -–-

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LIGHT CURING IN DENTISTRY

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THE BLUE-LIGHT HAZARD

Potential Ocular Hazards

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A more common type of retinal damage is photochemical damage, which occurs

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Potential Hazards to Pulp and Gingival Tissues

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Fig. 5. Photo-induced hydrogen peroxide production in the mitochondria.

CLINICAL CONSIDERATIONS TO MITIGATE THE RISKS OF USING DENTAL LIGHT-

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Prevention of Pulpal and Gingival Tissue Injuries

Fig. 8. Advantages and disadvantages of different eyewear personal protective equipments.

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CLINICS CARE POINTS

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1. Fouassier JP, Lalevée J. Photoinitiators for polymer synthesis: scope, reactivity,

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