Jay Vuong
 |
WAS PROMPTED to write this article because it had occurred to me that many
practitioners, while approaching endodontic diagnosis from a practical,
hassle-free standpoint, do not have a complete understanding of pulpal
dynamics. An understanding of pulpal biology and how it translates
to clinical symptoms would help the dentist utilize appropriate treatment
regimens with the hope of maximizing the likelihood of a successful outcome.
We must agree that when it comes to root-canal
treatment, there is a great deal that we can do to ensure a successful
outcome. However, there are times when the most heroic or ideal procedural
effort does not ensure a predictable outcome or a symptom-free tooth on
which to build a restoration. Endodontic outcome, to me, then becomes
a question of probability or statistics. To increase the probability
of a successful clinical outcome, we must first start with an accurate
diagnosis—to begin, we must ask, “what state are the nerve and pulp
in?”
When patients come in with tooth pain, we
as dentists should not dismiss their discomfort. Statistically, patients
complaining of dental pain significant enough to mention to their dentist
tend to have endodontically related pain. As clinicians, we usually ask
a few questions or perform a few tests to see if root canal treatment is
appropriate to address the pain. Another way of looking at the situation
is that we are presented with an opportunity to match the pulpal condition
of a symptomatic tooth to a degenerative timeline that most teeth tend
to follow. The biological state of the pulpal tissues tends to give
correlating symptoms and radiographic clues.
As the pulp initially becomes damaged, it
becomes slightly inflamed at the site adjacent to the insult, exemplified
by gross decay with resulting inflammation to the underlying pulp horn.
This initial inflammation results in a heightened sensitivity to cold,
with a sensation of pain, often followed by a heightened sensitivity to
heat at a later time.
At first, the pain is initiated and sustained only
by the stimulus (this is reversible pulpitis). Later, as the pulpal swelling
spreads from the initial area of damage or irritation to the rest of the
pulpal tissue in the chamber, the pain initiated by the stimulus
becomes more prolonged (this is irreversible pulpitis). If enough
pulpal tissue becomes damaged, the pain may initiate or persist without
any stimulus at all. At the same time, the degenerative inflammation
of the pulp may reach down the entire length of the root or roots and begin
to cause the apical PDL to become inflamed (this is irreversible pulpitis
with periapical involvement). Now the patient may have not only a
throbbing toothache but also pressure sensitivity (to the pressure of chewing
or percussion). This stage marks a later point in the pulpal degenerative
timeline when the tooth is the “hottest” and usually the most difficult
to get numb. It is at this stage that most people would come in for
dental treatment if they hadn’t done so already. Radiographically,
we may not be able to see anything unusual periapically since x-rays only
show hard-tissue changes and not soft-tissue inflammation. The PDL
may look thickened once the lamina dura has resorbed slightly.
The Calm Before the Storm
IF THE PATIENT progresses past the period of pulpal inflammation mentioned
above without root-canal intervention, the tooth usually enters a calming
period. What this really means is that the nerves or pulp have completely
degenerated past the stage of total pulpal inflammation to became
necrotic. In this state, pain provoked or sustained by temperature
would have disappeared. Constant throbbing pain, or the continuous
dull radiating ache usually associated with pulpal swelling or degeneration,
also subsides. The tooth may still feel sensitive to pressure, since
the PDL may still be inflamed due to the presence of the adjacent irritating
necrotic debris of the pulp. Some teeth may become asymptomatic,
especially with the help of antibiotics and bite adjustment. However, the
tooth will not respond to temperature changes or electronic pulp testing.
This later stage of pulpal death can be view as
the calm before the storm. Because of the bacteria residing in the
necrotic pulp, the situation always has the potential to transition toward
an endodontic abscess. However, the transition can often take
months or even years, depending on a variety of factors. Although
many dentists try their best to medicate symptomatic teeth in the
hope of avoiding root-canal treatment before restoration, the truth is
that many of these teeth tend to feel better because they have slowly arrived
at this transitional stage of pulpal death.
The sedative dressing or temporary filling usually
acts as a nerve blocker (as eugenol does, for example) and is effective
as a topical pain medication. Unfortunately, the medication
does little to reverse the degenerative inflammatory process that has already
begun; pulpal recovery from acute inflammation usually is more dependent
on the degree of tissue damage sustained and whether the damage is in conjunction
with a bacterial presence. Radiographic evidence may appear within
normal limits. However, if teeth stay in this stage for a sustained
period of time, the bone around the root apex may resorb in the effort
to limit the antigenic irritation from the dead pulp. Periapical
radiolucency is then seen from a periapical film of the tooth.
Sometimes, if the cortical bone adjacent to the radiolucency is lost, a
fistula may develop from the area of inflammation or infection that can
be seen clinically as a stoma. Its formation is usually a pain-free event,
but the situation could become painful if the stoma became clogged or impacted.
When a tooth develops an endodontic abscess from
the transition period of pulpal death, pressure pain slowly becomes more
and more pronounced. The tooth may even become mobile. An infrequent
or continuous ache can also arise, not from the swelling of the pulp (which
is already dead) but from a swollen periodontal ligament or from a buildup
of pressure surrounding the periapical tissues of the tooth.
Edema, with a subsequent buildup of pus, usually creates pressure
that translates into pain. Swelling or tenderness is usually seen
intraorally adjacent to the root apexes. If the infection is not
allowed to drain (via a pulpal opening, fistula, or an incision),
extraoral swelling and lymph node involvement may develop as the abscess
spreads beyond the local confines of the periapical area and into the facial
planes. Radiographically, a noticeable radiolucency can usually be
seen beneath the abscessed tooth.
From this short discussion of pulpal deterioration,
you can see that the process is a continuous and dynamic one. As
dentists we are usually presented with a “snapshot” of the state of the
pulp in time. This basic understanding of the tooth’s pulp has given
me more assurance in my endodontic diagnosis. Although there are always
some exceptions, the symptoms that a patient presents with usually must
fall into the pulpal timeline discussed above if root-canal treatment is
to be helpful or meaningful. In the end, the root-canal treatment only
accomplishes the removal of the inflamed, degenerative, or dead pulpal
tissues from the tooth—and by doing so removes the source of pulpal
pain or limits the potential for future ligamental inflammation and periapical
bone destruction.
September-October 2002
|
Statistically,
patients complaining of dental pain significant enough to mention to their
dentist tend to have endodontically related pain.
|
