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THE TRADITIONAL APPROACH TO
TREATING PERIODONTAL DISEASE
Dentists have "grown up" with the understanding that periodontal disease is
caused by certain pathogenic bacteria. Simply stated, the traditional view is that these
bacteria adhere to the teeth in the form of plaque and, if not removed, the bacteria and
their by-products can lead to gingival inflammation (gingivitis), which if left untreated
will lead to eventual destruction of the periodontal attachment and supporting structure
including bone (destructive periodontitis).
This view of the bacterial etiology of periodontal disease was the foundation of a
methodology for treating the disease using specific therapeutic regiments and then
monitoring the response to treatment using certain clinical assessment tools. In essence,
following the course of disease after therapy relies on such well-established parameters
as bleeding on probing, attachment loss, evidence of further bone loss, suppuration and
related clinical findings. Treatment very often has two major objectives: elimination of
bacteria and pockets. Indeed, for many dentist, the existence of a pocket is interpreted
as a sign of active periodontal disease and is used to justify more aggressive treatment.
Does this traditional viewpoint of the etiology, treatment and monitoring of periodontal
disease accurately reflect current research findings? In light of growing legal concerns
over failure to document and appropriately treat active periodontal disease, are today's
dentists armed with the correct tools for accurately assessing patients? Indeed, could it
be possible that overtreatment of some patients may prove to be as problematic a legal
issue as undertreatment?
An examination of the current understanding of the etiology of periodontal disease
sheds light on the previous questions, and the answers give cause for serious reflection
regarding the need to supplement our current methodologies for assessing the presence and
severity of the disease, planning treatment and monitoring patients.
A CURRENT VIEW OF THE
ETIOLOGY OF PERIODONTAL DISEASE
When examining the etiology of periodontal disease, it is helpful to remember that
gingivitis is non-destructive inflammation of the gingival tissues. If this inflammation
does not progress to a destructive disease that results in loss of attachment or bone, we
do not have, by definition, "active" periodontal disease or periodontitis. We
simply have an inflammatory reaction similar to the reaction that occurs when a wound
heals. It is important for dentists to be able to distinguish between non-destructive
gingivitis and destructive periodontal disease when planning treatment and monitoring a
patient's periodontal status. Conversely, if active or destructive disease is underway,
delaying therapy may lead to unnecessary attachment or bone loss.
Studies by a number of researchers indicate that the destructive periodontal disease
process is the result of an infection-induced host immune response. While a variety of
pathogenic bacteria have been identified that play an important role in the disease
process, the mere presence or even concentration of these bacteria does not necessarily
mean that destructive or active disease exists or will in the future. All dentists and
hygienists have seen patients who defy the traditional view of the etiology of periodontal
disease. There are patients who have excessive amounts of plaque and calculus, yet over
time exhibit nothing more than gingival inflammation, or gingivitis. Other patients
practice meticulous oral hygiene and have very little plaque, yet they suffer attachment
or bone loss on one or more site.
The reason for this disparity is the patient's own immune response to bacterial
challenge. As with many diseases, like the common cold, host resistance plays an important
role in periodontal disease. While pathogenic bacteria are indeed linked to periodontal
disease, as many types of microbes are linked to the common cold, active disease occurs
only when host defenses are incapable of handling this microbial challenge. Basically, if
a person's immune system can effectively deal with a mouthful of pathogenic bacteria,
there will be no destructive periodontal disease.
THE HOST IMMUNE RESPONSE
When a pathogenic bacterial challenge occurs in the oral cavity, endotoxins released in
the gingival sulcus by these bacteria activate the host's immune system to deal with the
challenge. This host response involves leukocyte cells whose job it is to protect the
tissues from pathogens. Leukocytes rush to the site to destroy the bacteria and, in the
defensive process, they generate a variety of host cell components, including matrix
metalloproteinases or neutral protease enzymes. If these enzymes, primarily collagenase,
are activated in concentrations greater than that needed to destroy the bacteria, they con
actually break down the connective tissue of the host's own periodontal attachment and,
eventually, the bone. Therefore, the presence of these neutral protease enzymes in
sufficient concentrations in the gingival sulcus is a recognized indicator of active
periodontal disease and place that site at high risk for further attachment loss.
It is ironic that in periodontal disease, as in such conditions as rheumatoid arthritis
and corneal ulceration, it is the host's own immune response that actually produces tissue
destruction. The pathogenic bacteria act as the catalyst to initiate this host response.
It is important to recognize that local inflammatory and immune mechanisms can vary form
site to site within the patient's mouth. Thus, one site may experience high levels of
destructive enzymes and active disease while another site has normal levels of enzymes and
no active disease. This helps explain the site-specific and episodic nature of periodontal
disease observed clinically. Non-destructive gingival inflammation, or gingivitis,
represents nothing more than a normal inflammatory response of the host to infection. In
most cases, this inflammation will not progress to the destructive phase because the host
is able to control the bacterial challenge. Because bleeding sites indicate a departure
from health, the inflammation should be treated with the appropriate level of therapy, but
the patient should not be overtreated on the assumption that simple inflammation
represents active periodontal disease or will automatically progress to the destructive
stage.
The traditional view that gingivitis is a precursor to destructive periodontal disease
is not true for many patients. In fact, based on recent surveys, as well as longitudinal
clinical research, we now know that a relatively small percentage of cases of gingivitis
advance to periodontitis. We also know that the presence of a periodontal pocket does not
necessarily mean that this site will experience further breakdown.
This leads to a discussion of effective management of periodontal disease. If the
etiology of periodontal disease has a strong host component, and every individual (and
periodontal sites within individuals) differs in terms of host resistance to infection,
perhaps our traditional methods for identifying ongoing periodontal disease are
incomplete. Current knowledge indeed indicates that additional tools are needed to
correctly evaluate patients at risk and render the appropriate level of treatment.
LIMITS OF CURRENT CLINICAL MEASURES TO
IDENTIFY ONGOING DESTRUCTIVE DISEASE
Signs of inflammation, including bleeding on probing and the existence of pockets are
used routinely to indicate the presence of periodontal disease. In fact, many dentists and
hygienists believe that the presence of a pocket means that active disease is present and
the pocket should be eliminated. This view requires a reassessment, in many cases, and the
traditional modalities used to detect ongoing periodontal disease must be supplemented by
current knowledge and techniques.
Traditional techniques for determining the presence and severity of periodontal disease
are essentially retrospective in nature. Probing for pocket depth reveals loss of
attachment and bone after the loss has occurred. Radiographs reveal bone loss that has
already taken place. Bleeding on probing indicates inflammation, but we know that
relatively few sites showing such inflammation progress into a destructive phase of
disease. Suppuration, an indication of inflammatory response, does not mean that tissue
destruction will necessarily follow. The nature of the host's immune response is a major
determinant of the outcome of bacterial challenge and, in order to properly evaluate a
patient's periodontal status, his/her individual immune response must be monitored along
with conventional methods of evaluation.
It is easy to envision how certain patients who show no current visible clinical signs
of inflammation are labeled "healthy", yet we know that a small percentage of
these patients (e.g., immune compromised) will experience site-specific or even widespread
periodontal breakdown in the future. These patients are often undertreated, or treatment
is delayed, based on traditional clinical criteria. In contrast, many patients with
"pockets" may very well have achieved a stable situation whereby their immune
system has effectively neutralized the bacterial challenge and no further breakdown will
occur. Unfortunately, many of these patients are labeled "unhealthy" due to the
existence of pockets, and they are often overtreated. A more accurate assessment of the
therapeutic endpoint is needed. From a legal liability standpoint, the time may well come
when overtreatment of periodontal disease will be as serious a concern for dentists as
undertreatment or failure to treat.
This is not to say that traditional clinical indices are useless. They are part of a
needed system to evaluate and monitor patients' periodontal status. However, they do not
constitute a complete system. One missing ingredient in an optimum system for monitoring
periodontal disease has been a method for evaluating host immune response and
differentiating active disease from mere inflammation. If a current perspective of active
disease can be added to the retrospective tools now representing the standard of care, a
more complete system for evaluating patients and specific sites will be possible, and
individualized treatment planning can be more accurately tailored to each patient's needs.
THE NEED FOR A NEW APPROACH
As clinicians, we are reasonably secure today in knowing when to initially treat. We
are less certain, however, in knowing when we have reached the end-points of therapy, the
need for retreatment, or referral. Clinical researchers and the dental industry recognize
the need to enhance the traditional tools for assessing periodontal disease status. It is
essential to include the host component in an evaluation of each patient's present
periodontal condition, in addition to detecting/identifying bacteria, examining for
bleeding on probing and loss of attachment, and other clinical criteria. Without an
assessment of host immune response to oral microbial challenge throughout the mouth as
well as at specific periodontal sites, a major piece of the periodontal management puzzle
is missing. For example, if we know that the detection of past attachment/bone loss does
not necessarily mean that site will experience further breakdown in the future, we cannot
assume that all patients with six millimeter pockets require surgical therapy to eliminate
the pocket. These pockets must be carefully monitored; however, if they are now
stabilized, maintenance therapy to reduce the bacterial challenge may be all that is
necessary.
The detection and measuring of matrix metalloproteinases or neutral protease enzymes,
include collagenase, is one modality for evaluating host immune response that is now
available to dentists and hygienists. As noted previously, these enzymes in sufficient
concentrations are one indicator of active disease and can help distinguish between simple
inflammation and potential destructive periodontitis. An assay for these enzymes can be
conducted at chairside and the results can be entered into the patient's record for future
reference.
Enzyme assays as well as other methods for evaluating host response will be
increasingly utilized by dental professionals, as these modalities represent a major step
forward in the management of periodontal disease on a personalized and site-specific basis
for each patient. As our understanding of periodontal disease increases, there is little
doubt that these and future assessment techniques will help redefine the standard of care
for periodontal patients.
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