California Continuing Education Credits: 3 units
PIC HOMEPAGE
I. Dental Plaque: Structural, Microbiological and Developmental Characteristics
II. Dental Plaque: Relationship to Dental Diseases
III. Dental Plaque: Recent Reclassification of Periodontal Microorganisms
Our understanding of the relationship between the microorganisms found in dental plaque and the common dental disease of periodontitis has undergone numerous phases historically (Figure 8, Concepts of Bacterial Etiology, adapted from Socransky, 1992). Early in the 19th century, it was felt that, like the situation with diseases such as tuberculosis, a specific bacterial species was responsible for the disease processes. The criteria by which a given bacterial species was associated with disease historically has been through the application of Koch's Postulates. These criteria were developed by Robert Koch in the late 1800's. The criteria are as follows:
1. A specific organism can always be found in association with a given disease.
2. The organism can be isolated and grown in pure culture in the laboratory.
3. The pure culture will produce the disease when inoculated into a susceptible animal.
4. It is possible to recover the organism in pure culture from the experimentally infected animal.
However, the concept that a specific bacterial species was responsible for periodontal diseases fell out of favor for several reasons. First, dispite numerous attempts, a specific bacterial agent was not isolated from diseased individuals. Rather, the organisms found associated with disease were also found associated with health. Good experimental animal model systems of periodontal disease were not available to test the pathogenicity of specific microorganisms (this, in fact, remains problematic today). Further, in the mid 1900's, epidemiological studies indicated that the older an individual was, the more likely they were to have periodontal disease. This led to the concept that the bacterial plaque itself, irrespective of the specific bacteria found in plaque, was associated with disease. This concept, known as the Non-Specific Plaque Hypothesis (Loesche, 1976), held that all bacteria were equally effective in causing disease.
Several important developments caused a change in this thinking. First, it was realized that organisms that are found as part of the "normal" bacterial flora (i.e., found in health), may function as pathogens under certain conditions. These organisms may be altered, or increase significantly in numbers relative to other non-pathogenic species, to function as pathogens. This type of bacterial pathogen is referred to as an endogenous pathogen, in contrast to an organism that is not normally found in healthy states which is termed an exogenous pathogen. Secondly, tremendous advances were made in the 1960's and 1970's in techniques used to culture anaerobic microorganisms (bacterial species that cannot grow in the presence of oxygen). These advances were related to the anaerobic culturing conditions as well as the nutrients required in media to grow anaerobic species, which are typically very fastidious in their nutrient requirements. The growth of anaerobic microorganisms, and examination of their properties using in vitro and in vivo model systems, has now led us back to the understanding that different microorganisms have varying potential to cause disease. Thus, the current concept of the processes involved in the development of periodontal diseases fall under the Specific Plaque Hypothesis (Loesche,1976). The Specific Plaque Hypothesis states that disease results from the action of one or several specific pathogenic species and is often associated with a relative increase in the numbers of these organism found in plaque.
A form of Koch's Postulates specifically oriented to the situation in periodontal diseases has been proposed by a microbiologist by the name of Socransky (Socransky & Haffajee, 1992). Socransky's criteria for periodontal pathogens are as follows:
1. ASSOCIATION: A pathogen should be found more frequently and in higher numbers in disease states than in healthy states
2. ELIMINATION: Elimination of the pathogen should be accompanied by elimination or remission of the disease.
3. HOST RESPONSE: There should be evidence of a host response to a specific pathogen which is causing tissue damage.
4. VIRULENCE FACTORS: Properties of a putative pathogen that may function to damage the host tissues should be demonstrated.
5. ANIMAL STUDIES: The ability of a putative pathogen to function in producing disease should be demonstrated in an animal model system.
The two periodontal pathogens that have most thoroughly fulfilled Socransky's criteria are Actinobacillus actinomycetemcomitans in the form of periodontal disease known as Localized Juvenile periodontitis (LJP), and Porphyromonas gingivalis in the form of periodontal disease known as adult periodontitis. Selected properties of these microorganisms that have been associated with disease are summarized in the following tables.
| Evidence implicating Porphyromonas gingivalis as a periodontal pathogen (Adapted from Socransky, 1992) | |
| CRITERION | OBSERVATIONS |
| Association | Microorganism is elevated in periodontitis lesions Unusual in health or gingivitis |
| Elimination | Suppression or elimination results in clinical resolution Species found in recurrent lesions |
| Host Response | Elevated systemic and local antibody in periodontitis |
| Virulence Factors | Collagenase, trypsin-like enzyme, fibrinolysin, immunoglobulin degrading enzymes, other proteases, phospholipase A, phosphatases, endotoxin, hydrogen sulfate, ammonia, fatty acids and other factors that compromise PMN function |
| Animal Studies | Onset of disease correlated with colonization in monkey model Key role in mixed infections in animal models |
| Evidence implicating Actinobacillus actinomycetemcomitans as a periodontal pathogen (Adapted from Socransky, 1992) |
|
| CRITERION | OBSERVATIONS |
| Association | Elevated in lesions of Juvenile Periodontitis, and some lesions of Adult Periodontitis
Elevated in "active" Localized Juvenile Periodontitis (LJP) lesions Detected in apical region of periodontal pocket or in tissues of LJP lesions Unusual in health or gingivitis |
| Elimination | Elimination associated with clinical resolution of disease Species found in recurrent lesions |
| Host Response | Elevated systemic and local antibody levels in Juvenile Periodontitis |
| Virulence Factors | Leukotoxin, collagenase, endotoxin, epitheliotoxin, fibroblast inhibitory factor, bone resorption-inducing factor |
| Animal Studies | Disease induced in gnotobiotic rats |
Other species that have been implicated as pathogens, including Fusobacterium nucleatum, Prevotella intermedia, Eikenella corrodens, Campylobacter rectus, Bacteroides forsythus, and the oral spirochetes of the genus Treponema. It is important to note that the disease processes involve not only pathogenic microorganisms, but also a susceptible host. Further, many microorganisms function to the benefit of the host, by inhibiting the growth of potential pathogenic species. One example of such an interaction is Streptococcus sanguis, which produces hydrogen peroxide that is lethal for Actinobacillus actinomycetemcomitans.
Despite tremendous increases in our understanding of the pathogenic properties of specific plaque microorganisms and the role of specific microorganisms in the disease process, current therapy in periodontics is largely non-specific. The treatments that we utilize (e.g., oral hygiene measures, debridement by scaling and root planning, or even the currently available mouthwashes) are oriented towards reducing the accumulation of plaque on the teeth. Future developments in periodontics will involve the development of therapies which prevent the colonization or growth of specific microorganisms that are known to function as pathogens in this environment.
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