E. Matthew Skulsky, DDS
One of the first theories of pain
that was postulated is the specificity theory whereby it is thought that
peripheral pain receptors in body tissue project to a centralized pain center
in the brain via A-delta and C fibers. In addition, receptors in the lateral
spinothalamic tract of the spinal cord carry the nerve signals throughout the
central nervous system (CNS) to a pain center in the thalamus1.
The pattern theory was first
proposed by Weddell2 and Sinclair3 and is based upon the
premise that all nerve endings are alike, except those providing innervation to
hair cells, and pain is produced by intense stimulation of nonspecific
receptors. Their theory is contradictory to the aforementioned Specificity
Theory and has been shown to be false with later studies.
Theory of Pain
The gate control theory of pain
sought to explain why thoughts and emotions can influence the intensity of pain
perception. First proposed by Melzack and Wall in 1965, they assert that a
stimulus evokes nerve impulses which relay signals to the cells of the
substantia gelatinosa (SG) in the dorsal horn of the spinal cord, the
dorsal-column fibers that project to the brain, and the first central
transmission cells in the dorsal horn. Further, they state the SG functions as
the gate which modulates the afferent patterns before influencing the
transmission cells. The afferent signals in the dorsal column system act as a
central activator of brain processes and the transmission cells activate neural
mechanisms responsible for pain and perception of stimuli. In other words, the
individual's perception of pain is a function of his/her emotional state and
past experiences and not solely dependent upon the type or intensity of the
When no input comes in to the SG,
there is no subsequent transmission to the brain. Normal somatosensory input
happens when a majority of large fibers are stimulated as opposed to small
(pain receptor) fibers. The small-fiber stimulation is inhibited by the gate
providing negative feedback. When small fibers are preferentially stimulated,
there is no inhibitory feedback from the large fibers and the signal is
transmitted to the brain and perceived as a painful stimulus4.
The neuron is the most basic
cellular unit of the central and peripheral nervous systems. Afferent nerves
conduct sensory impulses to the CNS while efferent, or motor, neurons conduct
impulses from the CNS to the periphery. The sensation of pain is initiated at
the skin, tissue, or mucosal level where the dendritic zone (free nerve
endings) starts the impulse which travels along an axon until it reaches the
brain for interpretation. The axon is covered by a nerve membrane known as the
axolemma which contains a gelatinous substance, axoplasm, that encases the
axon. Surrounding the membrane or axolemma, there may or may not be a myelin
sheath which can help speed up the transmission of nerve impulses along the
In a resting nerve, electrical
resistance keeps sodium, potassium, and chloride ions from flowing into the
axoplasm. Upon stimulation, the electrical
potential is slightly decreased (known as slow polarization). This changes the
conductivity and the membrane now allows sodium and potassium ions to pass into
the axoplasm. The transfer of ions across the membrane provides the energy
source allowing the impulse to propagate along the axon until reaching the CNS.
If there is enough polarization to reach the threshold potential, a rapid
depolarization of the membrane occurs. The electrical potential is then
reversed which results in an external negatively charged environment and an
internal positively charged environment. After the depolarization is complete,
the membrane gradually returns to the normal resting potential5.
of local anesthetics and vasoconstrictors
Local anesthetics block the
conductivity of neurons by inhibiting the influx of sodium ions through ion
channels in the nerve membrane. Receptors within the sodium channels house the
binding sites for most local anesthetic compounds. The affinity of the
compounds is significantly greater during either the activated or inactivated
states, as opposed to minimal receptor affinity in the resting state. This
property leads to the conclusion that the neural fibers having more rapid
firing rates are most susceptible to local anesthetic action. Clinically, this
explains why the trigeminal nerve branches V1, V2and
V3 which contain only small, rapid-firing sensory fibers respond
well to anesthesia. The diameter of a nerve fibercorrelates to its
firing rate thus the reason that pain fibers are more sensitive than pressure
or proprioceptive fibers and this explains why a patient may still feel
pressure during a routine dental extraction in the absence of any pain
The structure of all local
anesthetics have three common components, namely the lipophilic aromatic ring,
and intermediate ester or amide linkage, and a tertiary amine. The rate of
onset of an anesthetic is related to the proportion of molecules that exist in
a lipid-soluble (rapid onset) versus a water-soluble (slower onset) state. In
order to be stabilized for transport and administration, the molecule is
formulated as a hydrochloride salt rendering it in a water-soluble state that
must be converted at the site of injection. In an acidic environment, such as
in inflamed tissue or a localized infection, this transformation is less likely
to occur making it more challenging to achieve anesthesia at these sites7.
The intermediate linkage is what
classifies the anesthetic as an amide-type or ester-type and is noteworthy in
patients with allergies to local anesthetics. Typically, patients allergic to
amide-type local anesthetics can be administered ester-type anesthetics with no
complications. It also helps to determine the pattern of elimination during
metabolism. The tertiary amine is what aids in binding and metabolism of the
anesthetic molecule. If this amine exists in a tertiary form, with 3 chemical
bonds, it is lipid-soluble and if it exists in a quaternary form, with 4
chemical bonds it will be water-soluble6.
action of specific anesthetics
In regards to the aforementioned
intermediate linkages, amides are metabolized in the liver whereas esters, such
as benzocaine, are hydrolyzed in the bloodstream by plasma esterases5,6.
Most commonly used anesthetics such as lidocaine, mepivicaine, bupivicaine are
amides, as esters have been mostly eliminated due to an incidence of allergy
reports5. Articaine is the one exception as it has an amide
intermediate linkage but also contains an ester side chain causing it to be
metabolized in a manner consistent with ester-type anesthetics6. Each anesthetic binds at a different site
along the nerve membrane5.
The time to achieve anesthesia is
directly related the anesthetics lipid solubility. Other contributing factors
the time for onset include the vasodilatory properties inherent in anesthetics
(faster onset) as well as sequestration is adjacent adipose tissues or myelin
sheaths (slower onset). Concentration of the anesthetics is also significant as
the commercially-available articaine in 4% concentration has a faster onset
than the equally lipid-soluble bupivicaine which comes in a 2% preparation.
Onset of anesthetic action is
first and foremost determined by the proportion of molecules that exist in a
lipid-soluble state versus a water-soluble state. The more molecules in the
tertiary structure at physiologic pH (7.4), the faster the onset with be. This
proportion is expressed and can be calculated using the Henderson-Hasselbalch equation: log (cationic form/uncharged
form) = pKa – pH
Moreover, an anesthetic with a
neutral pKa of 7.4 injected into healthy tissue at pH 7.4, there would exist an
equal proportion of charged and uncharged molecules. However, only the half
these molecules would be able to enter the membrane and contribute to
anesthesia in the patient. All anesthetic compounds have an actual pKa greater
than 7.4. In sites with significant inflammation or infection, the body's pH is
lowered beyond 7.4 and this an anesthetic with a lower pKa such as mepivicaine
(pKa = 7.6) is a better choice than bupivicaine, which has a pKa of 8.16.
The duration of action of local
anesthetics is variable based upon their affinity to bind to protein. In the
bloodstream, anesthetics can reversibly bind to plasma proteins. The greater
this protein affinity is, the longer the time it will sustain neural blockade
and result in anesthesia. This explains why bupivicaine, a long-acting local
anesthetic, binds 95% of proteins whereas mepivicaine, a short-acting
anesthetic, only has a 55% protein binding affinity6. (Figure 2.)
also be affected by the time an anesthetic remains in close proximity to the
nerve fibers. In order to increase this time, and slow the absorption to the
bloodstream, vasoconstrictors or vasopressors are added to many formulations of
anesthetics. Most common is epinephrine is 1:50,000 (for best hemostasis),
1:100,000 or 1:200,000 concentrations. Levonordefrin is also a commonly used
vasoconstrictor. These additives allows the anesthetic molecules to remain at
the site of injection for a longer time, thus more anesthetic crosses the
neural membrane and reduces pain transmission, as opposed to being transported
through the bloodstream, metabolized, and excreted5,7. The use of
vasoconstrictors should be carefully balanced against the risks in patients
with hypertension, cardiovascular disease, or hyperthyroidism. No more than 2
carpules of lidocaine with 1:100,000 epinephrine should be used on
Local anesthetics have been
linked to approximately 50% of all deaths in dental offices. The proper dosage
of anesthetic is the lowest dose that will produce adequate anesthesia.
Toxicity can be caused by a simple overdose or miscalculation, administration
to an allergic or sensitive individual, intravascular injection, or by improper
drug combinations. High levels of any local anesthetic in the bloodstream can
affect the cardiovascular system, the nervous system, and local tissues. Thus,
aspiration before injection should be a critical step in the practitioner's
technique. Negative aspiration does not guarantee that the bevel of the needle
is not in a vessel at the time of injection.
Symptoms of toxicity include a
patient that is overly sleepy, or lethargic, after administration of the local
anesthetic. Other signs and symptoms
include slurred speech, excitement, shivering, muscular twitching, and tremor
of facial muscles or extremities. Some patients also feel warm, flushed skin,
lightheadedness, dizziness, diminished sight, tinnitus, or disorientation. If a
patient takes a CNS depressant, the combination with local anesthesia will
reduce the toxic level for the patient and the dosage given should be monitored
even more closely and potentially reduced.
For lidocaine, the toxic limit,
according to Malamed Handbook of Local Anesthesia8 is 2 mg/lb with a
maximum dosage of 300 mg. In a 2% lidocaine carpule, there is 20 mg of
xylocaine per mL of the drug solution. A typical carpule is 1.8 mL in volume,
so 20 mg/mL x 1.8 mL = 36 mg per carpule. Thus, for a 180 lb. patient, he/she
could be safely administered up to 8 carpules to stay under the maximum
recommended dose of 300 mg. In pediatric patients, a 50 lb. child may only be given up to 2.7 carpules to
safely stay under the toxic limits8.
Symptoms of epinephrine overdose
include fear, anxiety, restlessness, headache, tenseness, perspiration,
dizziness, tremor of limbs, heart palpitations, and weakness. The patient will
experience an elevated blood pressure and heart rate. Some mild forms of these
symptoms can be experienced by patients even following low dosages of
To prepare the armamentarium for
patient injection, the syringe should be removed from the sterilization pouch,
the needle should be firmly attached to the screw end. Then, the practitioner
should retract the piston fully, and insert the cartridge, making sure to
engage the harpoon. The colored cap on the needle should be removed just before
the time of injection. To recap the needle after the injection, the scoop
technique is the preferred method; needles should never be recapped by hand5.
Syringes for local anesthesia
administration come in five basic types with the most widely used being the
metal aspirating syringe. Others include breech-loading, metal (self-aspirating
or non-aspirating), pressure injectors, jet injectors, and plastic syringes.
Pressure injectors are used mainly for intraligamentary injections to the
periodontal ligament (PDL). Caution must be used as these can make it possible
to bruise the tissue by rapid administration of anesthetic solution (20 seconds
for 0.2 mL of solution is the recommended rate). Plastic syringes are lighter
and are considered more esthetically pleasing to nervous patients5.
Needles are available in a wide
variety of lengths and diameters. Long, 25-gauge needles should be used for
inferior alveolar nerve blocks, Gow-Gates and Akinosi mandibular blocks. Short,
25 or 27-gauge needs are recommended for use with other injections. Smaller
needles tend to deflect more as they are inserted into tissue, and with the use
of topical anesthetics, do not result in any less pain or trauma to the
patient. After 3 or 4 injections on the same patient, the needle should be
changed as it can become dull causing the patient to feel the insertion5.
In the United States, most
anesthetic cartridges, or carpules, contain 1.8 mL of anesthetic solution. A
latex or rubber stopper treated with silicone keeps the liquid contained in the
syringe and allows for easy propulsion of the solution through the needle. The
opposite end usually contains an aluminum cap with a semipermeable membrane.
Inside the cartridge is the local anesthetic, sodium chloride, distilled water,
and potentially a vasoconstrictor drug with preservative5. Each type
of local anesthetic has its own color-coded ring that encircles the cartridge
and is standardized across manufacturers.
Additional armamentarium commonly used for
local anesthetic administration include topical anesthetics which are strongly
recommended to be applied to the anticipated injection site in advance. These come
in a variety of forms including ointments, gels, pastes, and sprays. Further,
applicator sticks for the topical anesthetic are often necessary along with
cotton 2x2 gauze and a hemostat.
OF LOCAL ANESTHETIC ADMINISTRATION
On every patient in the dental
clinic, including those who will be receiving local anesthetics, a complete and
thorough medical history is required. The medical history should be reviewed
for updates with the patient at each visit; if there have been any changes to
their medical history, these should be noted in the chart with the date. After discussing with the patient and based
on clinical expertise, the dentist must determine whether to proceed with
treatment, reschedule the patient for another day, or postpone treatment until
the patient's physician is consulted to provide a medical clearance. Before
treatment is commenced, and local anesthetic is injected, the patient's vital
signs (blood pressure, heart rate, respiration rate) should be taken and noted
in the chart5. If severe anxiety is present, it is not safe to
administer local anesthesia and the patient should either be rescheduled when
he/she is more relaxed or be treated under sedation in the future if the
anxiety cannot otherwise be managed successfully.
Society of Anesthesiologist's Physical Status Classification System
The most widely accepted
assessment of peri-operative risk was adopted by the American Society of
Anesthesiologists. This can be used as an aid to dental professionals in
determining how to proceed with medically-compromised patients. There are
currently six classifications to determine the fitness of the patient before
ASA Class I
– Healthy individual, no medical conditions
ASA Class II
– Mild systemic disease
III – Severe systemic disease
ASA Class IV
– Severe systemic disease that is a constant threat to life
ASA Class V
– A moribound individual who is not expected to survive without the operation9
ASA Class VI
– A declared brain-dead individual whose organs are being removed for donor
Generally, ASA classes I and II
are safe to proceed in an outpatient dental clinic. Class III patients may
require a medical consult before commencing treatment and Class IV patients
should likely be treated in a surgical center or hospital setting that is
equipped to deal with any potential complications. ASA Class V and VI patients
are not candidates for dental procedures and would be handled by hospital
emergency rooms or intensive care units.
Firstly, in order to provide the
most atraumatic injection, both patient and practitioner should be as relaxed
as possible. The tissue should be penetrated up to the end of the bevel.
Monitor the patient for any signs of discomfort and slowly deposit a drop or
two of anesthetic solution. Then advance the needle slowly to the target depth,
deposition solution slowly along the way. If bone is contacted, deposit a few
drops there as well, pause for a few seconds due to the significant innervation
and vascularization that exists in this area. Aspirate the syringe: if
aspiration is negative (no blood in the cartridge), deposit a few more drops,
aspirate again and deposit more anesthetic. If aspiration produces blood in the
cartridge, withdraw the needle slightly and repeat the process. After injection
is complete, slowly withdraw the needle and recap it using a proper technique5,8.
The extent of the effectiveness of a local
anesthetic depends upon where the anesthetic is deposited relative to the
nerve(s) innervating the tooth. Local infiltration techniques deposit
anesthetic near superficial nerve endings and anesthesia is limited to that
targeted area like a papilla or frenum. Field block anesthesia deposits
solution near terminal nerve branches and provides pain reduction for a wider
area of treatment such as injecting near the apex of a tooth, effectively
numbing the tooth and the surrounding tissue. Nerve block anesthesia deposit anesthetic
near the main nerve trunk providing for the broadest area of profound
anesthesia as is seen in the IAN block which can numb the tongue, teeth, and
soft tissue on the ipsilateral side of injection5,7,8.
of Maxillary Anesthesia
Also known as maxillary
infiltration, this is the most popular injection to achieve pulpal anesthesia
of the maxillary anterior teeth. It is ideal for numbing a single tooth or
perhaps 2-3 teeth to be treated. A 25 or 27 gauge short needle is to be used,
which is inserted at the height of the mucobuccal fold near the apex of the
tooth. The bevel of the needle should be pointed towards the bone and
approximately 1/3 of a cartridge deposited after negative aspiration.
Superior Alveolar (PSA) Nerve Block
The PSA nerve block is used for
obtaining anesthesia in the maxillary molars. Again a short 25 or 27 gauge
needle is to be used, inserted at the height of the mucobuccal fold by the
maxillary second molar. The needle's path of insertion is up, back, and inward
towards the PSA nerve. For this block, approximately ¾ to a full cartridge of
anesthetic may be required. Keep in mind that sometimes, the mesiobuccal root
of the maxillary first molar will not be innervated by the PSA and a
supplemental injection site may be needed if working on this tooth.
Superior Alveolar (MSA) Nerve Block
The MSA nerve is only present in
about 20% of the population and should only be used in cases where the
infraorbital and PSA injections do not provide adequate anesthesia to posterior
teeth. The technique is the same as the PSA only the site is at the mucobuccal
fold of the maxillary second premolar.
Infraorbital nerve blocks will
anesthetize the area from the maxillary central incisor to the premolar area.
It is the preferred technique over multiple supraperiosteal injections as one
can use less anesthetic and cause less trauma to the patient with fewer
injection sites. The practitioner must locate the infraorbital foramen near the
lower border of the orbit. Then, with a short 25 gauge needle inserted in the
mucobuccal fold over the first premolar, ½ to 2/3 cartridge of anesthetic is
deposited after negative aspiration. After withdrawing the needle, it is
important to apply finger pressure to the patient's fact over the foramen area
to help the anesthetic penetrate into the foramen.
Palatine Nerve Block
The greater palatine nerve
innervates the palatal gingiva and mucosa distal to the canine on the side of
the injection. Using a short 27 gauge needle, with the bevel towards the
palate, palpate for the depression of the foramen is felt, typically just
medial to the second molar and about ¾ of an inch below the free gingival
margin of the first and second molars. Dry the site, apply topical for 2
minutes and apply pressure with the cotton applicator. Inject along the way
until reaching the palatal bone, while still providing pressure with the swab,
only a few drops of anesthetic is needed due to the tautness of the tissue.
The nasopalatine nerve innervates
the hard palate, gingiva, and mucosa for anterior tissue lingual to the first
premolar. The site of injection is just posterior to the incisive papilla. The
technique should be identical to the greater palatine block, just with a
different site of administration5.
of Mandibular Anesthesia
Alveolar Nerve (IAN) Block
A long 25 gauge needle should be
used for this block to numb the mandibular teeth on the side of the injection
along with the buccal mucosa and bone of the teeth anterior to the mandibular
first molar. The site of injection is at the medial border of the ramus at the
pterygomandibular raphe. This should be about 1.5 cm above the mandibular
occlusal plane with the bevel pointed towards the bone. The barrel of the
needle should be parallel with the occlusal plane of the molars and be centered
over the mandibular premolars on the opposite side. Advance the needle slowly,
depositing a few drops along the way until the ramus is contacted. Withdraw
slightly, aspirate, and deposit ¾ to a full syringe of anesthetic If bone is
not contacted, the needle is likely too far posterior and the injection should
be attempted again with the barrel over the contralateral first molar5,8.
The buccal nerve is not
anesthetized with the IAN block. It innervates the tissue and periosteum buccal
to the molars. A long 25 gauge needle should be used following the IAN block if
working in the relevant area. The needle is to be inserted in the mucous
membrane distobuccal to the last molar with the bevel facing the ramus. Tissue
should be pulled taut, the needle should penetrate 2-4 mm into tissue,
contracting bone. Aspirate the syringe, and if negative, slowly deposit 1/8 of
There are numerous other
injection techniques which are used for limited applications. For example a
periodontal ligament (PDL) injection can be used as a supplement for an
extraction or periodontal surgery to provide more depth of anesthesia to a
tooth without adversely numbing other teeth, the tongue, or lips. Intraosseous
injections may allow access into the pulp chamber of an affected tooth.
Intraseptal injections can be given into the papilla to control hemostasis and
provide additional soft tissue or osseous anesthesia5.
in Dental Specialties
In endodontics, if a tooth is
considered “hot” and cannot be fully numbed by means of one of the
aforementioned techniques, sometimes the treating doctor will slowly inject
some anesthetic directly into the pulp chamber of the tooth. Proceed with
caution as this technique can be mildly unpleasant for the patient and should
be used as a last resort. After a few drops are deposited into the pulp
chamber, the nerve should be anesthetized and root canal therapy should be able
to be completed. Intraosseous injections, as well as PDL injections may be
useful in providing endodontic therapy to a patient in need5.
The most common complication
associated with local anesthesia is pain on injection. This can be caused by
injecting too rapidly, injecting too much solution, or having a rough or
nervous dental practitioner5,8.
Parasthesia is the feeling of
unwanted, prolonged numbness and can be caused by the needle damaging the nerve
or passing through it10. Most parasthesias resolve on their own
within several months. However, the patient should be closely monitored for resolution
and appropriate referral to a neurologist or oral surgeon may be warranted8.
After the dental appointment, the
patient may experience a hematoma if the needle nicks one or more blood vessels
during the injection. These occur most often after a PSA block or IAN block.
Advise the patient of possible soreness, but the hematoma should resolve on its
own within 7-14 days and typically does not require additional treatment5,10.
Trismus, or difficulty in opening
the mouth, is caused by trauma to muscles of blood vessels in the infratemporal
fossa. Sometimes, depositing too much anesthetic solution in this area can
bring about symptoms of trismus. Heat therapy and exercise of the jaw muscles
are the recommended treatment and if symptoms do not resolve in 2-3 days,
antibiotics or referral to a specialist may be necessary5,8,10.
(Facial nerve paralysis)
If the local anesthetic is
injected into the parotid gland, containing branches of the facial nerve, the
patient's face will droop and he/she will not be able to close their eye. This
usually occurs as a complication of a failed IAN block, and is thus
self-limiting, meaning symptoms will dissipate as the anesthetic is metabolized5,8.
Systemic complications in response to local
anesthetic administration are rare, but when they occur, can be severe, even
life-threatening. These would include toxicity as described earlier in this
review, along with seizures, coma, or death. These can manifest in healthy
patients or in medically-compromised patients. Timeliness of response is key in
order to minimize the long-term effects of any complications. In patients with
known or unknown sensitivities to local anesthetics or the preservatives used,
anaphylactic shock is also a possible outcome. By obtaining an adequate medical
history, sticking to the dosage guidelines, and being astutely aware of all
changes in a patient's appearance/vitals, a practitioner can hopefully
intervene before a systemic complication becomes life-threatening; prevention
(Treanscutaneous electrical nerve stimulation)
Proper electronic dental
anesthesia can eliminate the need for topical and injectable local anesthetics
during a procedure. The patient can control the level of the electrical
impulses which relates to the level of anesthesia needed. There are many
theories as to the underlying mechanism, but none have been proven definitive
yet5. This alternative form of anesthesia has yet to catch on in the
mainstream dental marketplace.
The DentiPatch is an adhesive
patch containing 46.1 mg of lidocaine. Resembling a Band-Aid, it provides mild
topical anesthesia for a quick procedure or prior to injection of a local
anesthetic5. As with the TENS device, this has also failed to
transform the marketplace.
The WaterLase laser created by
Biolase, while not an alternative form of local anesthesia eliminates the need
for anesthetic when performing a restorative or simple surgical procedure.
Again, the mechanism is not fully understood, but a filling, including
inlays/onlays may be prepared and caries removed from a tooth by use of the
laser. This is marketed towards dentists who want to be on the cutting-edge of
technology as well as patients whom are fearful and experience anxiety in
response to the injections of local anesthetics12.
- Head, H. Studies
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- Weddell, G. Annu.
Rev. Psychol.1955; 6: 119.
D.C. Brain 1955; 78: 584.
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& Wall, P.D. Science 1965; 150: 3699.
A.S. Local Anesthetic Review. The Academy of Dental Learning & OSHA
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& Reed, K.L. Local Anesthetics: Review of Pharmacological Considerations. Anesth.
Prog. 2012; 59: 90-102.
- Berde, C.B.,
Strichartz,G.R. Local Anesthetics. In:
Millers, R.D., Eriksson, L.I., Fleisher, LA. Et al, eds. Miller's
Anesthesia. 7th ed. Philadelphia, PA: Elsevier, Churchill
S.F. Handbook of Local Anesthesia. Maryland Heights, MO: Mosby; 2004.
Classification of Physical Status. Anesthesiology. 1963; 24: 111.
- Schatz, M.
Adverse reactions to local anesthetics. Immunol Allergy Clin North Am. 1992;
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et. al. ASRA Practice Advisory on Local Anesthetic Systemic Toxicity. Regional
Anesthesia and Pain Medicine. 2010; 35(2): 152-161.
Lasers. http://www.biolase.com//products/iplus. Accessed June 12, 2014.