Periodontal disease is the bleeding (inflammation) that occurs in the
gums (gingiva) when the dental plaque is allowed to accumulate and to
persist on the tooth surfaces. The bacteria in the plaque produce many
chemicals which can diffuse into the gums and cause the tissue to swell
and bleed. In some ways the reaction of the gums to the plaque resembles
the way the skin of the finger responds to a sliver. What is happening is
that the bacteria in the plaque produce enzymes, lipopolysaccharides, and
waste products such as hydrogen sulfide, butyric acid, etc., that elicit
an inflammatory response in the adjacent periodontal tissue. This
inflammation can result in the loss of attachment fibers that hold the
tooth in place in the jawbone. If unchecked, this process can eventually
result in the loosening of the tooth followed by tooth loss.
There are two ways of viewing periodontal disease, namely that it is a
dirty mouth problem and that the individual needs to keep his teeth clean,
usually with professional help for the remainder of his/her life. This can
be compared with another treatment approach which is aimed towards the
reduction and/or elimination of certain specific germs in the plaque and
employs the usage of chemical antimicrobial agents. Both of these
approaches are summarized below and in the figures.
The Nonspecific Plaque Hypothesis
The nonspecific plaque hypothesis makes the assumption that periodontal
disease is mainly a dirty mouth condition due to the accumulation of
plaque on the tooth surfaces. From this assumption the goal of any
treatment is to keep the amount of plaque below a certain threshold in
order to maintain periodontal health. This can be done by meticulous oral
hygiene, and when this isn't practiced by the individual, gingival
inflammation (gingivitis) can occur which might, with time, extend to the
periodontal ligament which holds the teeth to the underlying jaw bone. If
the plaque accumulations are no longer within reach of the toothbrush in
pockets about the teeth, then the inflammatory process can often proceed
without notice. A pocket is just what is sounds like, a pocket or space
forms between the tooth and the gums that becomes a secure place for the
germs to multiply forming what the dentist calls subgingival plaque. See
illustration below. This plaque may harden and is then called calculus or
tartar.
In the illustration above, the gingival margin (gum line seen at the
right of the figure) serves to differentiate two types of plaque: the
supragingival plaque seen at the top and the subgingival plaque
seen at the bottom of the pocket. Note that the kinds of bacteria (germs)
in the two types of plaque are different, with worm-like spirochetes and
gram negative rods (G-R) dominating the subgingival plaque. It is these
spirochetes and gram negative rods that contribute to periodontal disease,
as they release toxins into the gingival (gum) tissue, with a few even
penetrating into the tissue, where they are destroyed by host inflammatory
cells. Host inflammatory cells are represented in the figure as T cells (T
with circle, T-lymphocytes), B cells (B with circle, B-lymphocytes), M
cells (M with circle, monocytes/ macrophages) and polymorphonuclear cells
(circles with the curved black C-like structure inside).
The inflammatory cells cause the gums to redden, swell and bleed, in a
process known as inflammation. This inflammatory condition can
usually be detected by the dentist or dental hygienist. Clinical studies
have shown that the bacteria that cause these inflammatory reactions can
be kept at low levels by cleaning or debriding the roots of the teeth by a
dental procedure known as scaling and root planing (debridement). This
procedure has to be repeated several times during the year in a patient
with periodontal pockets. If the pockets are 6 mm or deeper, then
debridement is difficult to achieve, and the clinician usually uses a
surgical procedure to gain access to the inaccessible plaque and calculus
deposits. Certain teeth that are extensively involved are often extracted,
as clinical experience indicates that they will not respond to the
cleaning procedures. This approach reportedly is successful in about 80 to
85% of patients with advanced forms of periodontal disease, who receive
treatment. When the debridement approach fails, as in the so-called
refractory patient, these individuals are often given systemic
antibiotics.
This treatment approach is nonspecific in nature as it is directed to
physically reducing the numbers of all types of germs that are in the
plaque. Because it is labor intensive and open-ended, it can become
expensive. This is particularly true when periodontal surgery is
recommended, as then
the cost
of treatment can be several thousand dollars. The debridement
procedures are recommended to be given 2 to 5 times a year for a lifetime.
This nonspecific treatment approach involves three modules of
treatment: scaling and root planing the teeth to remove the
bacteria on the root surfaces (debridement), access surgery to
debride the root surfaces hidden within the gingival pockets, and the
prescription of systemic antimicrobials, usually tetracyclines, if the
patient is non-responsive to the first two approaches (see figure below).
Since the overgrowth of all bacteria (germs) is thought to be the
cause of gum inflammation (a dirty mouth), there is no need to determine
which bacteria are involved (no need to diagnose an infection).
The Specific Plaque Hypothesis
In recent years, considerable evidence has been provided by the
research community that most advanced forms of periodontal disease are
associated with the overgrowth in the subgingival plaque of a finite
number of germs (the Specific Plaque Hypothesis). The germs which
overgrow are usually anaerobic gram negative bacterial species, with hard
to pronounce names, such as Porphyromonas gingivalis, Bacteroides
forsythus and Treponema denticola.. This suggests that
antimicrobials that are specific for these germs might be of value in the
treatment of advanced forms of periodontal disease.
The modules of treatment of a specific periodontal plaque infection
would be identical to those used for the nonspecific plaque
treatments, except that there would be a need to diagnose an infection,
and the sequence of using the modules would be different (see illustration
above). This change in sequence is extremely important, because the
systemic antimicrobial (antibiotic) would be given in combination with the
debridement procedures, and not held in reserve to treat patients who do
not respond to the surgical procedures. In fact, when treating according
to the specific plaque hypothesis, it is the surgical module that is held
in reserve, only to be used about those teeth which do not respond
completely to the antimicrobial approach. In the specific plaque treatment
paradigm, antimicrobials are used to prevent or reduce access surgery,
whereas in the nonspecific plaque treatment paradigm, access surgery is
used to prevent or reduce the use of systemic antibiotics.
We have conducted four double-blind studies in which we treated
patients with tooth cleanings and short term usage (one to two-weeks) of
metronidazole or doxycycline to see if this treatment would result in
restoration of periodontal health. In three of these studies we used as
our treatment outcome (does it work?) the reduction in the need for
periodontal surgery and in tooth extraction. In all four studies the
antimicrobial treatment resulted in significantly better results than was
obtained in our control groups who received the traditional scaling and
root planing procedures. These results suggest that most forms of
periodontal disease respond to antimicrobial treatments as if they were
indeed specific bacterial infections.
But antimicrobial agents are not magic bullets that can be routinely
used to treat a chronic infection such as periodontal disease. There is
much to be learned about how to use these agents appropriately. In order
to make an appropriate choice of an antimicrobial agent, it is necessary
to make a bacterial diagnosis of which germs have actually overgrown in
the subgingival plaque.
(See section on Chairside Diagnostic for Periodontal Disease
