IR Jan obrien

11/2/04

5:31 pm

Page 1

CLINICAL

Pre-emptive analgesia and other

concepts in dental pain management
John OBrien explains
how you can help your
patients to avoid pain
associated with dental
procedures
As dentists we are inextricably
linked with pain, both in the
publics perception of us and
through the nature of the work
we carry out. The public
perception will, in time, change,
as dentistry changes and as we
continue to develop in the role
of prevention. In addition, the
larger proportion of our patients
are gradually moving away from
the idea of dentistry being a
necessary evil resorted to only
when in pain to the idea of
seeing a dentist on a regular
basis and expecting a more
advanced restorative role.
However, the inescapable fact
is that our profession involves
surgery to varying degrees and
surgery involves a certain
amount of tissue damage,
which, even in the hands of the
most experienced surgeon, leads
to variable levels of postoperative pain.
We are all familiar with the
fact that we can do relatively
atraumatic surgery for one
patient who goes on to
experience severe post-operative
pain and yet with the next
patient we perform a
particularly difficult procedure
and that patient reports minimal
pain. The degree of pain is
largely subjective on the
John OBrien BDS (NUI),
Cert OFP, is a graduate of
University College Cork. He
recently completed his postgraduate studies in orofacial
pain at UCLA in Los Angeles.
He has practices confined to
orofacial pain management in
Dublin and Galway.
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patients part and we do not have

any way of measuring the pain
experienced or, for that matter,
comparing pain levels
experienced by one person with
that experienced by another.
We do know that the
emotional state of a patient at the
time of a pain-inducing
experience can influence their
perception of pain. The interplay
of mood and pain is a very
complex subject, and is nowhere
as simple as is sometimes
assumed by exasperated
practitioners who may think that
pain, in the absence of signs of
injury, is imaginary or true
psychogenic in origin, as may
likewise be assumed for patients
presenting with seemingly
bizarre symptoms that do not fit
the accepted norms of acute
pain. Patients occasionally report
a history of having a low or high
pain threshold; this may or may
not have any basis in fact and
cannot be relied upon when
planning post-op pain relief.
It is likely that in the none too
distant future we will be able to
assess patients for their
susceptibility to pain and equally
be able to assess patients as to
which pain medication will be
best suited to them. When pain

occurs, we will be able to use a

medication that targets only the
specific receptors involved in that
particular individuals pain. This
will make medicating more
effective, as well as preventing
the side effects now experienced,
particularly with the opioid
group of medications. Until then
we are left with the situation
where we use the same
medication for all individuals,
accepting that different
medications work better on
different individuals. Correctly
used, this is a system that can
continue to serve us well in the
vast majority of acute pain
situations. However, we need to
remember that even with the
improvements seen in pain
medications in recent years, the
overall levels of acute pain
management still leave a lot to be
desired. This is a situation that,
with minimal effort on our part,
could easily be improved.
Unfortunately, too often we
instruct our patients to call if
they have pain or instruct them
to use a certain medication if
they are experiencing pain. In
many cases patients will wait
until the pain is well established
before taking any action. In
reality, pain medications should

be instituted immediately
following a surgical procedure. It
is difficult to differentiate
between procedures that warrant
routine use of analgesic
medication and those that do
not. Experience tells us that
most patients do not experience
significant pain following simple
extraction except in the case of a
so-called dry socket. However,
any form of surgery has a risk of
post-operative pain sufficient to
warrant the routine use of
analgesic medications.
It is important that we have
some knowledge of the
mechanism of pain production
seen after surgery or traumatic
injury to the oral tissues. This
trauma leads to the release of
what are termed algogesic
substances in the damaged
tissues. These substances include
bradykinin, histamine, substance
P, serotonin and, perhaps most
importantly from a pain control
point of view, prostaglandin, this
being the principle target of
many of our simple analgesics.
The release of these substances
at the site of injury leads to
activation of peripheral nerve
endings with transmission of a
pain impulse, which is
transmitted to the brain for
interpretation as pain. The net
result of the trauma is swelling
in the surrounding area and a
tenderness to light pressure,
which is not normally seen in
non-damaged tissue. This
process at the site of the injury is
referred to as peripheral
sensitisation and indicates that
the nerve endings are more
easily activated into transmission
of pain impulses or a lowering of
the required stimulus threshold
in this area.
Adequate local anaesthesia is
the first step in pain control.
Although the local anaesthetic
does not have any role to play in
preventing or reducing the
peripheral sensitisation, it does
effectively block the transmission
Irish Dentist January 2004

IR Jan obrien

11/2/04

5:31 pm

of the pain impulse from the

area back to the brain, via the
spinal cord, or in the case of the
trigeminal system for dental
pain, via the trigeminal sensory
nucleus in the brainstem area.
We are aware that the
ongoing pain signals from the
damaged area leads to a
phenomenon in the trigeminal
nucleus/ spinal cord, which we
term wind-up. Wind-up
essentially means that repeated
stimulation of the second order
or relay neurons in the
trigeminal nucleus leads to the
development of an amplified
response to incoming pain
signals from the pain site. If this
situation is allowed to continue,
we find that the pain levels are
increased to a point that is more
difficult to manage with simple
medications. The first key,
therefore, in post-surgical pain
management is to prevent windup developing. In the case of
surgery in other areas of the
body, for example the abdominal
cavity, this may involve the use
of epidurally administered local
anaesthetic in addition to a
general anaesthetic. The rationale
for the supplementary use of
local anaesthetic is that a general
anaesthetic provides none of the
pain impulse blocking properties
that local anaesthetic provides
and merely works by preventing
the brain from processing the
incoming pain signals. In
dentistry we are fortunate that
most of our procedures are
carried out with local
anaesthetic. It should be noted
that when choosing a local
anaesthetic for a surgical-type
procedure that is likely to
produce post-operative pain, it is
better to use a longer, as
opposed to short, acting variety.
The trend nowadays is to avoid
unnecessary post-procedural
numbness for patient comfort
and this is reasonable in routine
dental work. As we know that it
takes approximately two hours
for wind-up to develop, we
would ideally like to prevent
pain transmission for this time if
possible and then supplement
our anaesthesia with an analgesic
type medication.
Given the inflammatory
nature of post-operative pain, a
medication belonging to the
non-steroidal anti-inflammatory
Irish Dentist January 2004

Page 2

(NSAID) group is ideal. Aspirin

was the first available of this type
of medication and although a
very effective pain medication, it
has largely fallen out of common
usage in these situations due to
its pronounced gastric side effects
and tendency to interfere with
haemostasis. We now tend to use
medications such as Ibuprofen,
albeit caution must be exercised
as the same side effects are noted
with all the NSAID group. (Note:
Paracetamol has very little antiinflammatory effect and is
therefore not ideal in postsurgical pain management.)
NSAIDs work by inhibiting the
cylcooxygenase (cox) enzymes.
There are known to be at least
two types of cox enzyme. Cox-1
enzyme has an important role to
play in platelet aggregation and
the production of gastroprotective mucins, with the cox2 enzyme only being produced
in tissue injury-type situations,
where it is responsible for the
production of prostaglandins.
Prostaglandins have a major role
in pain, in the periphery (site of
injury) and we now know that
they are found after
injury/surgery in the central
nervous system, specifically the
spinal cord and its counterpart
for dental pain, the trigeminal
nucleus in the brain-stem. It was
always believed that NSAIDs
worked in the periphery, but
recent research points to a strong
role in the central nervous
system as well. Administering an
NSAID such as Ibuprofen has
effects in both these areas and
probably in others of which we
are currently uncertain. By
reducing prostaglandin
production, it prevents the
development of wind-up. If we
combine an NSAID with our
local anaesthetic, we get initial
benefit from the latter and, given
that the NSAID takes up to one
hour for full effect, we get a
contiguous effect if we give the
NSAID immediately after the
surgical procedure. With this
regimen, hopefully our
combination is making the
development of wind-up or
amplified pain response less
likely, however continued use of
the NSAID is essential to cover
the period whilst initial healing
takes place. This is thought to
extend from four to five days

after the surgical procedure.

There has been some
suggestion that this ideal of pain
prevention can be taken to a
further extent by pre-medicating
with analgesic medications
before a procedure, the feeling
being that by doing so we may
provide enhanced pain
management. This practice is
commonly referred to as preemptive analgesia and to date
there are no studies showing any
increased benefit with this
regimen and it would appear
that adequate peri-operative and
post-operative pain control are
the methods of choice. Until
there is more conclusive
evidence in this regard there
does not seem to be any
advantage in this modality.
The principal side effects of
the NSAID medications of gastric
bleeding and delayed
haemostasis can be partly
negated with the use of the
recently developed cox-2 type
medications. These medications,
to varying degrees, target the
cox-2 as opposed to the
benevolent cox-1 enzyme. There
are different cox-2 active
medications available in Ireland,
some such as nimesulide are less
cox-2 selective than the cox-2
specific, rofecoxib and
valdecoxib, which are
recommended for acute pain
management. A single dose of
rofecoxib 50mg daily (marketed
in Ireland as Ceoxx) is the
analgesic equivalent of
Ibuprofen, 400mg four times
daily, a highly regarded
medication in dental postsurgical management. The twice
daily dosing of nimesulide
(Aulin) and once daily dosing of
rofecoxib and valdecoxib
(Bextra) has very definite
advantages in terms of patient
compliance. However, care must
still be taken in the use of cox-2
specific medications in those
with a history of gastro-intestinal
bleeding and they are, as for all
NSAIDs, contra-indicated in
patients with active GI ulceration
and may exacerbate asthma in
susceptible individuals. In these
individuals a non-NSAID
medication should be used, with
a likely choice being a
paracetamol/opioid combination.
In conclusion, we need to
break away from the attitude

where patients are informed that

they should call the surgery if
they experience post-operative
pain and a prescription will be
arranged for them. Similarly,
advising patients to take
medications if they cannot cope
with the pain is not entirely
satisfactory. If we can
satisfactorily prevent wind-up
with the use of local anaesthetic
supported with analgesic use
from an early stage we will
render the development of more
intractable pain states less likely.
I do not think patients will be
critical of us for prescribing
medications when they report an
absence of post-operative pain. It
is also important to remember
that poorly managed acute pain
is a known factor in the
development of unremitting
chronic forms of pain, with as
many as 10% of chronic pain
patients blaming a surgical
procedure for their subsequent
problems. The fact that the
figures are probably considerably
lower following dental
procedures does not excuse the
use of analgesics. This lower
figure in dentistry is probably
related to the high proportion of
dental procedures carried out
under the protection of local
anaesthetic; we can improve
these figures!

References
Besson JM (1999) The neurobiology of
pain. Lancet, 8 May
Dickinson AH (1995) Central acute
pain mechanisms. Annals of Medicine
27: 223-227
Julius D, Basbum AI (2001) Molecular
mechanisms of nociception. Nature.
423: 13 September
Koltzenburg M (2000) Neural mechanisms of cutaneous nocicptive pain.
The clinical journal of pain 16(3): Sup
Merrill RL (2000) Neurophysiology of
orofacial pain. Oral and Maxillofacial
Surgery Clinics of North America, May
Orofacial Pain: From basic science to
clinical management. Edited by: James
P Lund
Payne R (2000) Limitations of NSAIDs
for pain management: Toxicity or
lack of efficacy The Journal of Pain
1(3): Sup 1
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