CLINICAL EBOOK SERIES

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DEVELOPMENTS IN
DENTAL PAIN
MANAGEMENT
MAY 2021

2 C E C R E D I T S

TEMPOROMANDIBULAR DISORDERS

Frontline Temporomandibular
Joint/Orofacial Pain Therapy for Every Dental Practice
Lisa Germain, DDS, MScD; and Louis Malcmacher, DDS, MAGD

C L I N I C A L U P D A T E

OPTIONS IN PAIN MANAGEMENT

Innovations in Local Anesthesia

are Easing the Pain of Dentistry
Paul A. Moore, DMD, PhD, MPH

SUPPORTED BY AN UNRESTRICTED GRANT FROM DIRECTADENTALGROUP • Published by AEGIS Publications, LLC © 2021
 The Importance of
Pain Mitigation
of Continuing Education in Dentistry

A
MAY 2021 | www.compendiumlive.com

PUBLISHER
Matthew T. Ingram
n overriding factor in patients’ evaluation of Continuing Education in Dentistry
SPECIAL PROJECTS DIRECTOR
of treatment is often dental pain manage- C. Justin Romano
ment. However, navigating their individual SPECIAL PROJECTS COORDINATOR
responses to pain is a complex process. As part June Portnoy
of Continuing Education in Dentistry
of the Compendium clinical eBook series, we MANAGING EDITOR
Bill Noone
are pleased to offer another edition on dental pain manage-
CREATIVE
ment to keep practitioners up to date on developments that Claire Novo
will improve the patient experience. EBOOK DESIGN
Jennifer Barlow

“Frontline Temporomandibular Joint/Orofacial Pain Therapy

Copyright © 2021 by AEGIS Publications, LLC. All
for Every Dental Practice” is the continuing education resource rights reserved under United States, International and

– a critical topic as patients with chronic orofacial pain will
often turn to their dentists first. As the authors explain, TMD
is often painful and disabling, but responsive to conservative
therapy. Reducing pain and restoring range of motion can sig-
nificantly change quality of life.
In the accompanying clinical update, Paul A. Moore, DMD,
Pan-American Copyright Conventions. No part of this
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Printed in the U.S.A.

PhD, MPH, shares his insights on “Innovations in Local

Anesthesia are Easing the Pain of Dentistry.” The author ex-
plores the latest highly advanced technologies and their imple-
mentation into everyday dental practice. As some of these inno-
vations can be expensive and time consuming, it is imperative
that practitioners have the information to weigh the potential
advantages and costs.

Compendium’s educational content is focused on bringing

proven solutions to the practice, including those that im-
prove patient experience and practice management. Visit us Chairman & Founder
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tinuing support.
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Jeffrey E. Gordon

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 CONTINUING EDUCATION TEMPOROMANDIBULAR DISORDERS

Frontline Temporomandibular
Joint/Orofacial Pain Therapy for
Every Dental Practice
Lisa Germain, DDS, MScD; and Louis Malcmacher, DDS, MAGD

ABSTRACT: Temporomandibular disorders (TMD) are a group of conditions affecting the

temporomandibular joint and/or muscles of mastication. TMD may present along with
many comorbid pain syndromes such as myofascial pain, headache, and neck and back stiff-
ness with limited range of motion, as well as fibromyalgia and chronic fatigue syndrome. The
diagnosis and management of TMD is complex and, many times, multidisciplinary. However,
dentists can provide their patients with frontline temporomandibular/orofacial pain thera-
py with didactic and hands-on training that provides a better understanding and a conserva-
tive approach for treatment of TMDs.
LEARNING OBJECTIVES

• Explain how orofacial pain • Describe the functioning of • Identify various treatments,
occurs and the types of pain the temporomandibular joint including frontline
that a patient may have and muscles temporomandibular/orofacial

T
pain therapy

he control of pain, its diagnosis, and
treatment of its causes is an impor-
tant obligation for dental profes-
sionals. Yet many patients who
report that they have chronic orofa-
cial pain can be easily dismissed, misdiagnosed,
and/or treated incorrectly as the etiology for
their symptoms remains shrouded in mystery.
This leaves the patient frustrated, disappointed,
and, worst of all, still in chronic pain.
Orofacial Pain
By definition, orofacial pain is associated with
the hard and soft tissues of the head, face, and
neck. When any of these tissues receive nox-
ious stimulation, impulses are sent through
the trigeminal nerve to the brain.1 Brain cir-
cuits primarily responsible for processing
complex behavior interpret these signals
as “an unpleasant sensory and emotional
DISCLOSURE: Dr. Germain had no disclosures to report.
Dr. Malcmacher is President of the American Academy of Facial Esthetics and a consultant for STATDDS™.
experience associated with actual or poten-
tial tissue damage, or described in terms of
such damage.”2
The density of the anatomic structures in
this region of the body makes diagnosis a com-
plex process. It is quite common for patients
to describe the site where they are feeling
pain and be totally unaware that the source
is elsewhere.3 The referred-pain phenomenon
is caused by the convergence of multiple sen-
sory nerves that carry input to the trigeminal
spinal nuclei from cutaneous and deep head
and neck tissues.1,3
Toothache pain is among the most common
forms of orofacial pain.4 Once toothache pain
is ruled out, however, TMDs and headaches
rise to the top of the list. Many times, these
can all occur together in a comorbid situation.
In addition, fibromyalgia, chronic fatigue syn-
drome, or any other condition that presents

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 CONTINUING EDUCATION
Because one of the essential keys of
prob­lem solving in this arena is the history
of the illness, the patient interview needs to be
per­formed by the treating dentist.
with chronic pain will further complicate the
clinician’s ability to determine the causality.5
Diagnosis in these cases is difficult but is best
achieved like “peeling an onion”—eliminating
the symptoms one layer at a time.
The Temporomandibular Joint
The temporomandibular joint (TMJ) is a com-
plex joint that provides both rotational and glid-
ing movements of the mandible. Structurally,
it is composed of the mandibular condyle de-
signed to fit into the glenoid fossa of the tem-
poral bone. An articular disc made of dense fi-
brocartilage separates the bones from making
direct contact with each other. Blood vessels
and nerves are not present in the anterior por-
tion of the disc. However, the posterior portion
of the disc has rich innervation and is quite vas-
cular. The joint is lubricated by synovial fluid.1
The muscles of mastication are responsible
for the movement of the TMJ. They are one
of the major muscle groups in the head, with
the other being the muscles of facial expres-
sion. The four muscles of mastication are the
masseter, temporalis, medial pterygoid, and
lateral pterygoid.3
Temporomandibular Disorders
Temporomandibular disorders (TMD) are a
group of musculoskeletal and neuromuscu-
lar disorders that predominantly involve the
functional joint, muscles, and disc of the TMJ.
TMD should be considered in every differen-
tial diagnosis of facial pain because it is the
most common cause of nondental pain.
4 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
TEMPOROMANDIBULAR DISORDERS
Proper diagnosis requires a detailed history
of onset, duration, what makes it better, and
what makes it feel worse. Along with persis-
tent jaw pain, patients will commonly report
earache, headache, and diffuse facial pain. In
addition, they may complain of radiating pain
or stiffness in the face, jaw, or neck, limited
movement or locking of the jaw, painful click-
ing, popping or grating in the jaw joint when
opening or closing the mouth, and possibly
changes in the way that their teeth fit together.
These symptoms can be worse when patients
awaken in the morning or can gradually wors-
en throughout the day.
Threshold, localization, pain sensitivity, and
description of pain vary greatly from patient to
patient due to both genetic and environmental
factors. This fact, coupled with the complexity
of the pain mechanism itself, highlights the
importance of proper diagnosis and treatment
of each patient’s case.6
Because one of the essential keys of prob-
lem solving in this arena is the history of the
illness, the patient interview needs to be per-
formed by the treating dentist. This gives the
patient a chance to tell his or her story and will
undoubtedly reveal many factors that influ-
ence the manifestation of the condition. This
is also a way to casually observe the patient’s
lip and jaw habits, facial expressions, and pos-
ture, and can reveal much about the patient’s
emotional status, such as frustration with the
pain. By validating these concerns, the dentist
will build rapport and trust.
Historically, malocclusion has been
 CONTINUING EDUCATION TEMPOROMANDIBULAR DISORDERS

considered a primary cause of TMD. However, Myofascial Pain Syndrome

recent studies have shown that poor occlusion
accounts for a low incidence of cases.7-9
TMDs have many classification systems. In
simple terms, the pain is either arthrogenous
or myogenous. Arthrogenous (joint and disc)
TMDs are most commonly caused by disc dis-
placement or occur secondary to degenerative
disc diseases, anklyosis, dislocation, infection, or
neoplasia. The underlying cause for myogenous
TMDs is muscular hyperactivity and dysfunction
secondary to bruxism, hypermobility, or external
stressors. Myogenous TMD can cause ischemia
in the facial skeletal muscles. Irreversible mus-
cle cell damage can begin after approximately 3
hours of ischemia and are paralleled by progres-
sive microvascular damage in the facial skeletal
muscles. This, in turn, can add to the facial pain
and the degenerative pathophysiology cycle.
Patients with myogenous TMD will report more
comorbid disorders and more severe pain than
patients with arthrogenous TMD.10 Hence, front-
line TMJ therapy focuses on the treatment of
the hyperactivity in the muscles of mastication.
According to the National Institute of Dental
and Craniofacial Research, the most common
form of TMD is myofascial pain syndrome
(MPS).11 This chronic inflammatory disorder
affects both muscle and fascia. Repetitive mo-
tions, injury to muscle fibers, and excessive
strain on ligaments and tendons are the prima-
ry causes. Patients also frequently report de-
pression or fatigue and may exhibit behavioral
changes. What differentiates TMD-related
MPS from other muscle pain syndromes is the
presence of trigger points that have the abil-
ity to refer the pain to other areas of the head
and neck.
Trigger points (Figure 1 through Figure 4)
are the result of excessive muscle contraction
and dysfunction of the motor endplate. This
type of muscle spasm in a muscle is different
from the entire muscle being tight. Because of
the localized overcontraction, the blood flow
to the immediate area stops. This, in turn, re-
sults in a restriction of the blood supply (isch-
emia). The accumulation of metabolic waste

Fig 1. Fig 2.

Fig 1. Masseter attachment trigger points near the upper musculotendinous junction of superficial layer
and central trigger points of superficial layer with referred pain patterns to lower jaw, teeth, and gingival
area. Fig 2. Masseter attachment trigger points of the lower superficial layer with referred pain patterns
to lower jaw and above eyebrow.

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 CONTINUING EDUCATION
products and toxins sensitizes the trigger
point, causing it to send pain signals and fur-
ther increase contraction. Thus, the physiol-
ogy of a trigger point involves a vicious cycle
of a metabolic crisis.
Clinically, trigger points can be identified
by examining signs, reproducing symptoms,
and performing manual palpation. Firm pal-
pation of the muscle belly usually results in
the location of one or more sore, nodular areas
within a tight band of muscle fibers. A twitch
response is often elicited when pressure is ap-
plied followed by the spread of referred pain.12
Masseter Muscle
The masseter is the major muscle of masti-
cation and derives its name from the Greek
word meaning “to chew.” The mandible is the
only bone of the skull that is actually move-
able, while the maxilla remains fixed; thus,
the masseter is constantly in use. Located on
each side of the face in the parotid region at
the back of the jaw, these muscles are easily
visible or palpable when the patient clenches
the jaw, as they contract strongly just in front
of the lower portion of the ears.
Fig 3.
Fig 3. Masseter trigger points of the upper posterior deep layer below TMJ with referred pain patterns to
ear area. Fig 4. Tempororalis trigger points (TrP) and referred pain.
6 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
TEMPOROMANDIBULAR DISORDERS
The average human can bite with a force
of 150 pounds, and bites of more than 250
pounds are within the norm. The masseter
achieves these seemingly impossible forces
because it has the mechanical advantage of
a lever arm that is much shorter than other
muscles. Because it is highly active, the mas-
seter is likely to tense when a person is emo-
tionally distressed, concentrating, or angry.
When the tension endures for extended peri-
ods, the development of MPS trigger points
is common.
In general, masseter trigger points cause
pain in the eye, face, jaw, and teeth. An un-
explained earache can be a result of masseter
trigger points, and research by Simons et al12
reports trigger points of the masseter can even
cause an itch deep in the ear. Trigger points
in the deep layer of the masseter may also be
a cause of tinnitus (ringing noise in the ear
with no cause). Figure 1 through Figure 3 illus-
trate trigger points in masseter muscle and the
common referral patterns (shown in red).12
It is important to note that the facial nerve
is a motor nerve that innervates the muscles
of facial expression. Care should be taken to
Fig 4.
 CONTINUING EDUCATION
know the facial nerve anatomy when treating
trigger points in the deep masseter near the
zygomatic arch.
Temporalis Muscle
The temporalis is a large, thin fan-shaped
muscle located in the side of the skull above
and in front of the ear. Although the masseter
is the more powerful muscle, the temporalis
is a large and important chewing muscle. It
starts at the temporal bone of the skull but
passes all the way down beneath the zygomat-
ic arch (cheek bone), attaching to the man-
dible, enabling it to assist the masseter in clos-
ing the jaw but also to retract the mandible.
Before treating this area, the clinician should
bear in mind that the temporal branch of the
facial nerve mentioned above runs through
the anterior temporalis.
By placing your fingers just above your
ear while clenching and unclenching your
jaw, you will be able to feel the temporalis
at work. If you clench your jaw very tightly,
you will feel a powerful contraction in the
temporalis. Figure 4 illustrates how signifi-
cantly temporalis trigger points can refer to
the upper teeth as well as the head, cheek,
eye, and ear areas. Often, if this is mistaken
for odontogenic pain, root canals might be
performed. However, in these cases, a pa-
tient’s pain persists because of the incorrect
diagnosis and treatment.
Treating With Botulinum
Neurotoxin Type A
In the spirit of “do no harm,” noninvasive and
reversible modalities should be used as front-
line treatment.13 Many palliative treatments
can be used alone or in combination with each
other to manage TMD pain. These include
(but are not limited to) splint therapy, mas-
sage, physical therapy, biofeedback, acupunc-
ture, chiropractic therapy, spray and stretch
with ethyl chloride, antidepressants, narcotics,
and nonsteroidal anti-inflammatory drugs.14
7 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
TEMPOROMANDIBULAR DISORDERS
However, the use of botulinum neurotoxin
type A (BoNT-A) could also be considered.
In addition to its well-publicized cosmetic
uses, BoNT-A (Botox, Dysport, Xeomin) has
been approved by the US Food and Drug
Administration (FDA) for painful conditions
potentially related to TMD, such as cervical
dystonia and migraine.15,16
BoNT-A is an injectable pharmaceutical
agent derived from the bacterium clostridi-
um botulinum. Given in small doses, this pu-
rified protein can be used to selectively relax
the strength of skeletal muscles by interfering
with the release of acetylcholine at the neu-
romuscular junction. Hence, the muscle will
not be able to contract with the same intensity
because the amount of available neurotrans-
mitter has been reduced. As stated above, the
constant, sometimes dysfunctional, contrac-
tion of the muscles of mastication can be the
primary cause of the trigger point in MPS-
related TMD. When BoNT-A is placed in sev-
eral spots in the belly of the muscles, it will
reduce the hyperactivity in the muscle and, in
turn, reduce the patient’s pain.17
Treatment with BoNT-A for TMD takes a
week or so to work and will last 3 to 4 months.
The treatment will then wear off without any
negative consequences. Normal functions
such as speaking, swallowing, and biting are
left unaffected, while there will be a reduc-
tion in pain and discomfort. Unlike systemic
medications that affect the patient’s entire
body, this treatment can focus on the source
of the problem. Both active and latent trigger
points respond well to these injections, and
the patient will periodically report immediate
pain relief from the injection itself because it
has a “dry needling” effect. While TMD has
no cure, patients who receive regular treat-
ment with BoNT-A find that the effects of the
treatment become longer lasting as time goes
by. This therapy has been used successfully
on many patients who have not responded to
other treatments.18
 CONTINUING EDUCATION
Practitioners considering using BoNT-A
for frontline TMJ therapy and orofacial pain
would benefit from taking a course with one-
on-one mentored live-patient training. Such a
course should include the anatomy, physiology,
pharmacology, adverse reactions, and poten-
tial complications involved with these treat-
ments. The cost of commercially available
BoNT-A to a practitioner is approximately
$600 for a 100-unit vial. Before using BoNT-A,
it is also imperative that practitioners take re-
sponsibility for following the regulations set
by the board of dentistry and laws of the state
where they practice.19
Bruxism and Dental Sleep Medicine
Oral parafunction is the habitual use of any
part of the mouth, tongue, and jaw that is un-
related to eating, drinking, and speaking. The
most common parafunctional habit is bruxism,
also known as clenching and grinding. These
destructive forces have been linked with TMD
for several reasons. The amount of pressure
placed on teeth during functional habits is 20
psi to 80 psi (0.14 MPa to 0.55 MPa), but the
Fig 5.
Fig 5 and Fig 6. Preoperative (Fig 5) and postoperative (Fig 6) photographs of a patient treated with
BoNT-A for hypertrophy of the masseter muscles. Notice the slenderizing of the face.
8 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
TEMPOROMANDIBULAR DISORDERS
pressure can range from 300 psi to 3000 psi
(2.07 MPa to 20.7 MPa) while bruxing. This,
in turn, places significantly more stress on
the muscles of mastication; and, as they are
overworked, MPS and the formation of trigger
points ensue.
Masseter Hypertrophy
When examining a patient for TMD-related
MPS caused by bruxism, a clinician may
often find trigger points in the masseter
muscles. Patients frequently present with
such severe hypertrophy of the masseter
muscles that the bulge in the muscle causes
facial distortion. Masseter hypertrophy can
be treated with BoNT-A injections using the
same protocol used to treat TMD pain in
the masseter. The injections will decrease
the intensity of the contractions, and as the
muscle begins to relax, the patient will not
be able to clench with the same force. In ad-
dition to pain reduction, the end result is
a desirable slenderizing of the face as the
masseter loses its hypertrophic appearance
(Figure 5 and Figure 6).19
Fig 6.
 CONTINUING EDUCATION
Obstructive Sleep Apnea
Obstructive sleep apnea (OSA) occurs when
repeated episodes of complete or partial
blockage of the upper airway happen during
sleep. During an OSA episode, the diaphragm
and chest muscles work harder to open the
obstructed airway and pull air into the lungs.
A patient with OSA is likely to have TMD and
nocturnal bruxism.20-22
The American Academy of Dental Sleep
Medicine classifies sleep bruxism as a sleep-
related movement disorder.23 A home brux-
ism and sleep study monitor is a cost-effective
way for a dentist to obtain data on the patient’s
sleep apnea and diagnose bruxism. The in-
formation that can be collected from this test
includes oxygen levels, masseter muscle activ-
ity for bruxism, pulse, airflow, snoring, chest
movement, and body position during sleep.
Once the data obtained from a bruxism/
sleep study confirms that the apnea-hypopnea
index (AHI) may indicate the presence of OSA,
the dental practitioner should contact the pa-
tient’s physician, who can make the definitive
medical diagnosis of OSA. The practitioner
can then intervene. For patients with mild
or moderate OSA, dental appliances or oral
mandibular advancement devices that prevent
the tongue from blocking the throat and/or
advance the lower jaw forward can be made.
These devices help keep the airway open dur-
ing sleep. In many cases, the patient will no
longer have nocturnal bruxism once treated.24
Headaches
The association between sleep, brux-
ism, TMD, and headaches has long been
recognized.25 Headaches afflict a large por-
tion of the population and, with varying se-
verity, can result in discomfort, disruption of
daily activity, lost days at work, and, occasion-
ally, debilitating pain. Although about 30%
of headache sufferers are periodically func-
tionally impaired, many do not seek medical
care.26,27 Typically, patients report various
9 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
TEMPOROMANDIBULAR DISORDERS
headache symptoms in conjunction with a
dental examination.
Tension-Type Headaches
and Migraine
The tension-type headache (TTH) is the most
common primary head pain, and most of the
population will experience this at least once
in their lifetimes.28 Findings from the dental
examination will generally reveal that pain
generating from the masticatory musculature
can be episodic and chronic and may be in-
distinguishable clinically and therapeutically
from migraine. It is likely that some TTHs and,
correspondingly, some TMDs represent a vari-
ant form of migraine or have a migraine-like
component.29,30 In fact, there is a somewhat
overlapping diagnosis of headache attributed
to TMD in accordance with the diagnostic/
TMD criteria and the International Headache
Society criteria.31,32
The relationship between a TMD and
headache is well recognized in the litera-
ture. Patients receiving a diagnosis of either
migraine or TTHs, which may be caused by
myalgia of the temporalis muscle, will have
signs and symptoms consistent with TMD.
Strengthening this relationship between TMD
and headache is the fact that patients who
have undergone treatment for TMD report
a decrease in symptoms of headache. Recent
evidence suggests that patients who have a di-
agnosis of vascular or migraine headache have
a higher prevalence of TMD as a contributing
cause of their pain than the general popula-
tion. In addition to the trigeminal nerve, the
facial nerve and muscles of facial expression
are intricately involved with the headache/
TMD continuum.33-35
On October 15, 2010, the FDA approved
BoNT-A injections to prevent headaches in
adults with chronic migraine. The treatment
protocol involves selective relaxation of hy-
perfunctional muscle of mastication and fa-
cial muscles with BoNT-A. The idea is to
 CONTINUING EDUCATION
In addition to controlling TMD, serious den­tal
problems such as destruction of the teeth or
restorations, tooth mobility, and periodontal disease,
all caused or exacerbated by bruxism, can be avoided.
administer the smallest, effective dose neces-
sary to relieve the pain; the dosage is based on
each patient’s response to the therapy. Again,
dentists who are considering administering
BoNT-A injections are urged to take an ap-
propriate hands-on training course and follow
the rules of the state where they practice.
The mechanism with which BoNT-A re-
lieves migraine pain is not clearly understood.
It is thought that because it controls uncon-
scious jaw movement, it lessens the load on
the muscles and, thus, alleviates grinding-
related headaches.36 However, the release of
neuropeptides, particularly calcitonin gene-
related peptide (CGRP), is considered an
integral component in the pathophysiology
of migraine.37 In addition to its effect on the
autonomic nervous system, it has been shown
that BoNT-A can directly decrease the amount
of CGRP released from trigeminal neurons.
This finding suggests BoNT-A may also reduce
headache pain because it has a direct effect on
the central nervous system.37
Cervicogenic Headaches
Neck pain and cervical muscle tenderness are
common symptoms of primary headache dis-
orders. A diagnosis of cervicogenic headaches
(CGHs) is made when head pain arises from
bony structures or soft tissues of the neck.
This can be a perplexing pain disorder that is
refractory to treatment if it is not recognized.
The condition’s pathophysiology is likely re-
ferred from one or more muscular, neurogenic,
osseous, articular, or vascular structures in the
10 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
TEMPOROMANDIBULAR DISORDERS
neck. It is often a sequela of head or neck inju-
ry but may also occur in the absence of trauma.
The clinical features of CGH may mimic those
commonly associated with primary headache
disorders such as TTH or migraine, and, as a
result, distinguishing among these headache
types can be difficult.38
The diagnosis of CGH can often be made af-
ter a careful history and physical examination
is performed. The criteria may include one
or more of the following symptoms: moder-
ate or severe pain reported in the occipital,
frontal, temporal, orbital, neck, and back re-
gions; intermittent or chronic pain generally
deep and non-throbbing; head pain triggered
by neck movements; or restricted range of
motion in the neck. Patients with CGH will
usually present with a forward head posture.
Muscular trigger points are usually found in
the suboccipital, cervical, and shoulder mus-
culature. These trigger points can also refer
pain to the head when manually or physically
stimulated.38,39
Studies indicate 44.1% of patients with
CGH have MPS-related TMD. In addition, it
has been shown that patients with CGH who
receive TMD therapy had increased range
of motion in the neck. On palpation, trigger
points are usually found in the suboccipital,
cervical, and shoulder musculature. When
manipulated, these areas often refer pain
to the head, even though the neck muscu-
lature is the source of the pain.39 Like other
MPS-related pain, this area responds well to
BoNT-A injections.
 CONTINUING EDUCATION
Conclusion
TMD is a collection of clinical entities that are
often painful and disabling. Yet, they are self-
limiting and usually respond to conservative
therapy such as injection with BoNT-A. Basic
principles of management to reduce pain and
restore range of motion will reduce disabil-
ity and often contribute to reducing primary
headache disorder if it coexists.
In addition to controlling TMD, serious den-
tal problems such as destruction of the teeth or
restorations, tooth mobility, and periodontal
disease, all caused or exacerbated by bruxism,
can be avoided. Other benefits of TMD treat-
ment include elimination of nocturnal brux-
ism, reduction in jaw tension, and decreased
chronic neck and shoulder pain. Dentists who
suspect a TMJ or bruxism condition should
have the patient tested with a home bruxism/
sleep monitor test before performing any
treatment to obtain a baseline reading of the
patient’s bruxism episodes and AHI.
Patients with chronic orofacial pain will of-
ten seek the help of their dentists when symp-
toms arise. Didactic and hands-on education
is recommended to become proficient in the
treatment of TMD and orofacial pain in every-
day dental practice.
ABOUT THE AUTHORS
Lisa Germain, DDS, MScD
Faculty, American Academy of Facial Esthetics, Private
Practice, New Orleans, Louisiana
Louis Malcmacher, DDS, MAGD
President, American Academy of Facial Esthetics, Private
Practice, Bay Village, Ohio
Queries to the author regarding this course may be submitted
to authorqueries@aegiscomm.com.
REFERENCES
1. Balasubramaniam R, Klasser GD. Orofacial pain
syndromes: evaluation and management. Med Clin
North Am. 2014;1998(6):1385-1405.
2. Mersky H, Bogduk N. Classification of Chronic
Pain. 2nd ed. Seattle, WA: IASP Press; 1994:59-71.
3. Okeson JP. Bell’s Orofacial Pains. 6th ed. Chicago,
IL: Quintessence Publishing Co, Inc.; 2005:162-167.
11 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
TEMPOROMANDIBULAR DISORDERS
4. Lipton J, Ahip J, Larach-Robonson D. Estimated
prevalence and distribution of orofacial pain in the
United States. J Am Dent Assoc. 1991; 124(10):115-121.
5. Aaron LA, Burke MM, Buchwald D. Overlapping
conditions among patients with chronic fatigue
syndrome, and temporomandibular disorder.
. 2000;160(2):221-227.
6. Okeson JP. Management of Temporomandibu-
lar Disorders and Occlusion. 5th ed. St Louis, MO:
Mosby; 2003:10-79.
7. Turp J, Schindler H. The dental occlusion as
a suspected cause for TMD’s: Epidemiologi-
cal and etiological considerations. J Oral Rehabil.
2012;39(7):502-512.
8. Luther F. TMD and occlusion. TMD and occlusion
part II. Damned if we don’t? Functional occlusal
problems: TMD epidemiology in a wider context. Br
Dent J. 2007;202(1):E3.
9. Turp JC, Kowalski CJ, Stohler CS. Temporoman-
dibular disorders—pain outside the head and face
is rarely acknowledged in the chief complaint. J
Prosthet Dent. 1997;78(6):592-595.
10. Klasser GD, Bassiur J: Differences in reported
medical conditions between myogenous and
arthrogenous TMD patients and its relevance
to the general practitioner. Quintessence Int.
2014;45(2):157-167.
11. Schiffman E, Ohrbach R, Truelove E, et al; for the
International RDC/TMD Consortium Network, Inter-
national association for Dental Research; Orofacial
Pain Special Interest Group, International Associa-
tion for the Study of Pain. Diagnostic Criteria for
Temporomandibular Disorders (DC/TMD) for Clinical
and Research Applications: recommendations of the
International RDC/TMD Consortium Network and
Orofacial Pain Special Interest Group. J Oral Facial
Pain Headache. 2014;28(1)2014:6-27.
12. Simons DG, Travell JG, Simons LS, Cummings BD.
Myofascial Pain and Dysfunction: The Trigger Point
Manuel, Vol 1 - The Upper Half of the Body. Balti-
more, MD: Williams & Wilkins; 1999:11-178.
13. Syrop S. Initial management of temporomandib-
ular disorders. Dent Today. 2002;21(8):52-57.
14. Stohler CS, Zarb GA. On the management of
temporomandibular disorders: a plea for a low-tech,
high-prudence therapeutic approach. J Orofac Pain.
1999;13(4):255-261.
15. Greene CS, Laskin DM. Long term evaluation for
myofascial pain dysfunction syndrome: a compara-
tive analysis. J Am Dent Assoc. 1983:107 (2):235-238.
16. Management of temporomandibular disorders.
National Institutes of Health Technology Assessment
Statement. 1966;127(11):1595-1606.
17. Ludlow CL, Hallett M, Rhew K, et al. Therapeu-
tic use of type F botulinum toxin. N Engl J Med.
1992;326:349-350.
18. Malcmacher L. Botox therapy for every dental
 CONTINUING EDUCATION
practice. Dent Today. 2009;28(8):101-103.
19. Malcmacher L. Botulinum toxin for frontline TMJ
syndrome and dental therapeutic treatment. Dental
Economics. 2013:93-99.
20. Manfredini D, Lobbezoo F. Relationship be-
tween bruxism and temporomandibular disorders:
a systematic review of literature from 1998 to 2008.
Oral Surg Oral Med Oral Pathol Oral Radiol Endod.
2010;109 (6):e26-e50.
21. Glaros AG. Incidence of diurnal and nocturnal
bruxism. J Prosthet Dent. 1981;45(5):545-549.
22. Goulet JP, Lund JP, Montplaisir J, et al. Daily
clenching, nocturnal bruxism, and stress and their
association with TMD symptoms. J Orofac Pain.
1993;7:89.
23. American Academy of Sleep Medicine. The
International Classification of Sleep Disorders, 3rd
ed. Darien, IL: The American Academy of Sleep
Medicine, 2014.
24. Simmons JH, Prehjn R. Airway protection:
The missing link between nocturnal bruxism and
obstructive sleep apnea. Sleep. 2009;32(abstract
suppl):A218.
25. Sharav Y, Benoliel R, eds. Orofacial Pain and
Headache. 2nd ed. Hanover Park, IL: Quintessence
Pub; 2015:123-165.
26. Rasmussen BK. Migraine and tension-type
headache in a general population: precipitating fac-
tors, female hormone, sleep pattern and relation to
lifestyle. Pain. 1993;53(1):65-72.
27. Saper JR, ed. Clinician’s Manual on Headache.
Philadelphia, PA: Science Press; 1995:1-86.
28. Schiffman E, Halet D, Baker C, Lindgren B.
Diagnostic criteria for screening headache pa-
tients for temporomandibular disorders. Headache
1995;35(3):121-135.
29. Schellhas KP, Wilkes CH, Baker CC. Facial pain,
headache, and temporomandibular joint inflamma-
tion. Headache 1989;29(4):228-231.
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TEMPOROMANDIBULAR DISORDERS
30. Haley D, Schiffman E, Baker C, Belgrade M. The
comparison of patients suffering from temporoman-
dibular disorders and a general headache popula-
tion. Headache 1993;33(4):210-213.
31. Schokker RP, Hansson TL, Ansik BJ. Differences
in headache patients regarding response to treat-
ment of the masticatory system. J Craniomandib
Disord. 1990;4(4):228-232.
32. Gerwin RD, Dommerholt J, Shah JP. An ex-
pansion of Simons’ integrated hypothesis of trig-
ger point formation. Curr Pain Headache Rep.
2004;8(6):468-475.
33. Schiffman E, Ohrbach R, Truelove E, et
al. Diagnostic Criteria for Temporomandibular
Disorders(DC/TMD) for clinical and research ap-
plications: recommendation of the International
RDC/TMD Consortium Network and Orofacial Pain
Special Interest Group. J Oral Facial Pain Headache
2014;28(1):6-27.
34. Headache Classification Committee of the Inter-
national Headache Society. The International Clas-
sification of Headache Disorders, 3rd edition (beta
version). Cephalalgia. 2013:33(9):629-808.
35. Bolay H, Reuter U, Dunn AK, et al. Intrinsic brain
activity triggers trigeminal meningeal afferents in a
migraine model. Nat Med. 2002;8(2):136-142.
36. Aoki KR. Evidence for antinociceptive activity of
botulinum toxin type A in pain management. Head-
ache. 2005;43(suppl 1):9-15.
37. Edvinsson L. Calcitonin gene-related peptide
(CGRP) and the pathophysiology of headache: ther-
apeutic implications. CNS Drugs. 2001;15(10):745-
753.
38. Haldeman S, Dagenais S. Cervicogenic head-
aches: a critical review. Spine J. 2001;1(1):31-46.
39. von Piekartz H, Lüdtke K. Effect of treatment
of temporomandibular disorders (TMD) in patients
with cervicogenic headache: a single-blind, random-
ized controlled study. Cranio. 2011;29(1):43-56.
 CONTINUING EDUCATION 1 QUIZ 2 Hours CE Credit

Frontline Temporomandibular Joint/

Orofacial Pain Therapy for Every Dental Practice
Lisa Germain, DDS, MScD; and Louis Malcmacher, DDS, MAGD

TAKE THIS FREE CE QUIZ BY CLICKING HERE: COMPENDIUMLIVE.COM/GO/DEVPAINMANAGE

ENTER PROMO CODE: DEVPAIN

1. Blood vessels and nerves are not present in 6. Clinically, trigger points can be identified by:
which portion of the disc?  A. examining signs
A. posterior B. reproducing symptoms
B. anterior C. performing manual palpation
C. inferior D. All of the above
D. superior
7. When a clinician examines a patient for TMD
2. The Temporomandibular joint is lubricated related MPS caused by bruxism, it is common
by: to find trigger points in which muscles:
A. laqueous humour. A. masseter.
B. synovial fluid. B. temporalis.
C. cerebrospinal fluid. C. medial pterygoid.
D. interstitial fluid. D. lateral pterygoid.

3. TMD should be considered in every differential 8. About what percentage of headache

diagnosis of facial pain because: sufferers are periodically functionally
A. it is the most common cause of dental pain. impaired?
B. it is the most common cause of nondental A. 10%
pain. B. 30%
C. t he facial nerve innovates both teeth and C. 50%
the TMJ. D. 70%
D. the abducens nerve innovates both teeth
and the TMJ. 9. The mechanism with which the BoNT-A
relieves migraine pain is:
4. One of the essential keys of problem solving A. based on local interactions with the
OF TMD is: autonaumic nervous system.
A. an in depth occlusal analysis. B. b ased on local interactions with the somatic
B. r eview of a full mouth set of dental nervous system.
radiographs. C. a mechanism that interferes with calcium
C. the history of the illness. channel blocking of the myelin sheath.
D. charting of tooth mobility. D. not clearly understood.

5. TMDs pain is: 10. A diagnosis of cervicogenic headaches
A. spontaneous only. (CGHs) is made when head pain arises from:
B. intermittent only. A. bony structures or soft tissues of the neck.
C. psychosomatic only. B. the area of the hyoid bone.
D. either arthrogenous or myogenous. C. a severely retrognathic mandibular position.
D. a severely prognathic mandibular position.

Course is valid from 6/1/20 to 6/30/23. Participants must at-
tain a score of 70% on each quiz to receive credit. Participants
receiving a failing grade on any exam will be notified and per-
mitted to take one re-examination. Participants will receive an
annual report documenting their accumulated credits, and are
urged to contact their own state registry boards for special CE
requirements.
AEGIS Publications, LLC, is an ADA CERP Recognized
Provider. ADA CERP is a service of the American Dental
Association to assist dental professionals in identifying
quality providers of continuing dental education. ADA
CERP does not approve or endorse individual courses or
instructors, nor does it imply acceptance of credit hours
by boards of dentistry. Concerns or complaints about a CE
provider may be directed to the provider or to ADA CERP at
www.ada.org/cerp.
AEGIS Publications, LLC, is designated as
an Approved PACE Program Provider by the
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provider are accepted by the AGD for Fellow-
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extends from 1/1/17 to 12/31/22.
Provider ID# 209722.

13 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com

 CLINICAL UPDATE OPTIONS IN PAIN MANAGEMENT

Innovations in Local Anesthesia are

Easing the Pain of Dentistry

T
Paul A. Moore, DMD, PhD, MPH

he development of safe and effective local anesthesia ABOUT THE AUTHOR

has been one of the most significant contributions Paul A. Moore, DMD, PhD, MPH
Professor, Pharmacology and Dental
toward creating the advanced restorative and sophis- Anesthesiology, Department of Dental
ticated surgical procedures used in dentistry today. Public Health, University of Pittsburgh
The amide local anesthetic agents and basic delivery School of Dental Medicine, Pittsburgh,
Pennsylvania
systems (eg, cartridges, needles, syringes) that are currently available
to dental practitioners offer an array of options to effectively manage
the pain associated with dental treatments.
It took nearly a century from the time cocaine and its local
anesthetic properties were identified and isolated in 1860, to
its topical application for ophthalmologic surgery, to the in-
troduction of needles and syringes that could permit nerve
block and infiltration anesthesia, to the synthesis of procaine
and other ester anesthetics, until the discovery of lidocaine,
the first amide local anesthetic introduced into dental prac-
tice. The glass cartridge system, containing formulations of
the highly effective amide anesthetics lidocaine, mepivacaine,
prilocaine, articaine, and bupivacaine, has become one of the
most sophisticated single-dose sterilized packaging systems
ever developed.
Today, the solution of 2% lidocaine with 1:100,000 epineph-
rine remains the most versatile and popular local anesthetic
formulation used in the United States.1 It is ostensibly the "gold
standard" to which all other local anesthetics are compared.
The 2% lidocaine 1:50,000 epinephrine formulation provides
the therapeutic benefit of enhanced hemostatic properties,
which is particularly useful for oral and periodontal surgery.
Articaine, introduced in the United States in 2000, has gained
popularity among dentists because of its superior onset, du-
ration, potency, and tissue diffusion properties. Mandibular
infiltrations have been found to aid in establishing profound
anesthesia when inferior alveolar block anesthesia is incom-
plete.2 Bupivacaine, the only long-acting local anesthetic used
in dentistry, has found an important niche in the management
of postoperative pain. The 6 to 8 hours of potential anesthesia
and analgesia seen following bupivacaine injection can mini-
mize postoperative pain after oral surgical procedures such as
third-molar extractions and thereby possibly limit the need for
prescription opioid analgesics. Mepivacaine and prilocaine are

14 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com

 CLINICAL UPDATE
the only local anesthetics in dentistry formu-
lated without a vasoconstrictor and have found
a role in treating cardiovascularly impaired
patients and other medically compromised pa-
tients who may not tolerate a local anesthetic
containing a vasoconstrictor.
The amide agents currently available in
dentistry are extremely safe and fulfill most
of the characteristics of an ideal local anes-
thetic (Table 1). These local anesthetic agents
can be administered with minimal tissue ir-
ritation and with little likelihood of inducing
severe allergic reactions. The available agents
and formulations provide rapid onset and can
be tailored to surgical procedures of various
durations. The agents offer anesthesia that is
completely reversible, and systemic toxicity
is rarely reported. Case reports of children
experiencing local anesthetic toxicity have
been scarce in the past 25 years because of
education toward more conservative dosage
calculations, improved emergency care, and
greater awareness of the potential for local an-
esthetic toxicity among dental practitioners.
Unfortunately, the ideal local anesthetic agent,
one that would induce regional "analgesia"
by selectively inhibiting only pain pathways
without interrupting transmission of other
sensory and motor nerve functions, has yet to
be discovered.3
New and Clever Strategies
Using these safe and effective amide local
anesthetics, various innovations have been
advanced in dentistry that provide valuable
TABLE 1
Characteristics of an Ideal Local Anesthetic
➊ Administration of the anesthetic should be non-irritating.
➋ Allergic reactions to the local anesthetic must be rare.
➌ Rapid onset and adequate duration of anesthesia
is essential.
➍ Anesthesia must be completely reversible.
➎ With proper dosing, minimal systemic toxicity is essential.
➏ Anesthesia would be best if selective to nociception
(pain).
15 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
OPTIONS IN PAIN MANAGEMENT
options for managing the needs of unique
patient populations and fulfilling specific
procedural requirements. With the devel-
opment of specialized high-pressure syring-
es, single-tooth anesthesia can be delivered
using periodontal ligament (PDL) injection
techniques. Such techniques provide a valu-
able alternative when block anesthesia is in-
adequate. Similarly, intraosseous injections
have become increasingly popular because
of improved armamentarium.4 Advances
in computer technology have also been ap-
plied to dental anesthesia to control the rate
of administration, thereby limiting injec-
tion discomfort.
Additional innovative strategies to advance
the field of dental anesthesia have been in-
troduced in the past decade. A small startup
company recognized the desire to reverse the
numbing sensation in soft tissue following rou-
tine local anesthesia in certain patient popula-
tions. The pharmacologic strategy for reversal
of local anesthesia is based on the use of an
alpha adrenergic antagonist, phentolamine,
that opposes the vasoconstrictive effects of
epinephrine. By administering phentolamine,
the vasoconstrictive properties of epineph-
rine can be reversed and the duration of soft-
tissue anesthesia significantly decreased. In
essence, the formulation of 2% lidocaine with
1:100,000 epinephrine, where the duration
of lip and tongue anesthesia may last 3 to 4
hours, more closely resembles 2% lidocaine
plain (with a soft-tissue duration in the 45- to
60-minute range) following the phentolamine
injection. This product has been shown to ac-
celerate the return of soft-tissue sensation and
function, the loss of which is associated with
mandibular and maxillary dental anesthesia,
by about 50%.5 The product has a niche among
adult patients who find prolonged anesthesia
annoying and dysfunctional. Local anesthe-
sia reversal may prevent children and special-
need patients from chewing and mutilating
their lips following dental procedures.
 CLINICAL UPDATE
A needleless anesthetic for maxillary
anesthesia that has been developed and
marketed employs technology that uses
an intranasal spray delivery system of 0.2
mL per dosing unit. The anesthesia blocks
the anterior and middle superior alveolar
nerves. The anesthetic solution contains
tetracaine (30 mg/mL) and is combined
with the vasoconstrictor oxymetazoline (0.5
mg/mL) to improve the duration of anesthe-
sia. With repeated intranasal sprays, pulpal
anesthesia of maxillary premolars, canines,
and incisors can be achieved without the
use of a needle injection.6 This approach
has found a place in treating patients who
are needle phobic and may be advantageous
with younger children.
Several companies are developing local
delivery preparations that may extend the
duration of local anesthesia beyond a few
hours to potentially a few days. If postop-
erative pain can be safely and effectively
blocked for an extended period, the need
for opioid analgesics may be diminished.
Although several strategies are being devel-
oped, the product currently on the market
uses the long-acting local anesthetic bupi-
vacaine encapsulated in a formulation of
liposomes. The proposed mechanism for
the prolonged anesthetic is a delayed, sus-
tained breakdown of the liposomes in tissue
resulting in prolonged release of anesthetic
at the injection site.6 Studies are underway
to demonstrate the utility of this potentially
opioid-sparing strategy.
In medicine, it has been known for decades
that combining the two topical local anesthet-
ics lidocaine and prilocaine creates a eutectic
mixture (EMLA) that increases the efficacy
of topical anesthesia. A product for use in
dentistry has been developed that provides
an alternative to dental injections to estab-
lish the soft-tissue anesthesia required for
periodontal procedures such as deep scal-
ing and root planing.7 The product used in
16 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
OPTIONS IN PAIN MANAGEMENT
dentistry is formulated with an additive that
has reverse thermoplastic properties. The
formulation, packaged in a glass cartridge,
is a liquid at room temperature but converts
to a gel at body temperature after applica-
tion into a periodontal pocket. The efficacy of
this product appears to be enhanced because
the gel remains in the pocket for an extended
period of time.
Dental local anesthetic cartridges contain
solutions that are formulated at an acidic pH
(2.5 to 6.5) to maintain the stability of lo-
cal anesthetics in an aqueous solution. The
higher acidity may cause a stinging sensation
when infiltration anesthesia is administered.
Various systems that buffer the solution with
a small amount of sodium bicarbonate have
been developed for dental practice. Many pa-
tients report less discomfort upon injection,
and the time needed to establish profound
anesthesia may be decreased.8
Meeting the Challenge
Each of these advances is aimed at better
achieving the goals of an ideal local anesthetic
for dentistry. Some newer treatment strate-
gies to improve patient comfort come from
procedures that are less invasive and require
little to no anesthesia. For example, the rou-
tine use of sealants and the introduction of
silver diamine fluoride can help temporarily
arrest dental caries and reduce the need for
invasive painful operative procedures.
Translating these highly advanced tech-
nologies into everyday dental practice can be
challenging. Some of these innovations can be
expensive and their potential advantages may
not warrant the costs. Others may necessitate
additional chairtime and, therefore, may be
difficult to integrate into routine practice.
Additionally, the advantages of these new and
innovative local anesthetic strategies may be
thwarted by a lack of patient acceptance for
nasal spray administration or prolonged fa-
cial numbness.
 CLINICAL UPDATE
Dentistry has come a long way from when
cocaine was discovered and the therapeutic
value of local anesthesia was first realized.
The safety and effectiveness of dental local
anesthesia has now been established. Dental
practitioners continue to pursue anesthetic
innovations that meet the needs of their prac-
tices and provide better pain control and sat-
isfaction to their patients.
REFERENCES
1. Moore PA, Nahouraii HS, Zovko J, Wisniewski SR.
Dental therapeutic practice patterns in the U.S. I:
Anesthesia and sedation. Gen Dent. 2006;54
(2):92-98.
2. Robertson D, Nusstein J, Reader A, et al. The
anesthetic efficacy of articaine in buccal infiltration
of mandibular posterior teeth. J Am Dent Assoc.
2007;138(8):1104-1112.
3. Moore PA, Hersh EV. Local anesthetics: phar-
17 COMPENDIUM EBOOK SERIES May 2021 | Volume 42 Number 4 www.compendiumlive.com
OPTIONS IN PAIN MANAGEMENT
macology and toxicology. Dent Clin North Am.
2010;54(4):587-599.
4. Moore PA, Cuddy MA, Cooke MR, Sokolowski CJ.
Periodontal ligament and intraosseous anesthetic
injection techniques: alternatives to mandibular
nerve blocks. J Am Dent Assoc. 2011;142(suppl
3):13S-18S.
5. Hersh EV, Moore PA, Pappas AS, et al. Reversal of
soft tissue local anesthesia with phentolamine me-
sylate in adolescents and adults. J Am Dent Assoc.
2008;139(8):1080-1093.
6. Hersh EV, Saraghi M, Moore PA. Two recent
advances in local anesthesia: intranasal tetracaine/
oxymetazoline and liposomal bupivacaine. Curr Oral
Health Rep. 2017;4(3):189-196.
7. Magnusson I, Geurs NC, Harris PA, et al. Intrapock-
et anesthesia for scaling and root planing in pain-
sensitive patients. J Periodontol. 2003;74(5):597-602.
8. Fitton AR, Ragbir M, Ma M. The use of pH ad-
justed lignocaine in controlling operative pain in the
day surgery unit: a prospective randomized trial. Br
J Plast Surg. 1996;49(6):404-408.
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