Would you say that tranquil thoughts about periodontology while on a scenic lake are an apple and oranges comparison?
David J. Pippin, DDS
The sun was warm on the back of my neck and glinted and sparkled off the water of the lake nestled deep in the forest. I watched the fly on the end of my line drift lazily along. My attention drifted as I basked in the mountain scenery around me. A massive variety of green plants surrounded the lake, soaking up the sunshine and creating a web of life linking plants, birds, animals, insects, and fungi together.
The conditions here comprising light, soil, rainfall, and varying temperatures made a habitat, and the living organisms in it constituted an ecological community bound together in harmony and balance, and all interdependent.
The sunlight penetrated the lake as well, nourishing all the green plants growing beneath its surface, illuminating the multitude of species feeding on them, amongst them, and on each other - insects, snails, amphibians, crustaceans, and, of particular interest to me as I made my next cast, fish. The whole dynamic composition, lake and forest, was dependent on each other in their ecosystem.
But this ecological web did not just burst forth fully formed. It evolved to its present mature state over a period of time.
The periodontal ecosystem
An area of bare ground begins with simple plants like lichens and mosses which, depending on climate and other variables, give way to grasses, then bushes and shrubs, and the final climax stage of trees. Other species, requiring specific ecological niches, follow along with everything affecting everything else. Any ecosystem experiences this phenomenon where different species move in, compete, become more numerous, establish themselves, and enrich the complexity of the system in a process known as ecological succession.
A periodontal pocket is a habitat too, like the lake and forest. A major feature of this habitat is a smoothly flowing stream, the sulcular fluid, complete with nutrients. The ecosystem which becomes established in this habitat is a microbial world subject to the same dynamic processes that apply to any other ecosystem.
The first bacteria ("bugs" in a microbiologist`s slang) to appear on a clean tooth surface are streptococci, early colonizers which can glue themselves to the tooth with extracellular adhesives (dextrans and levans). The filamentous actinomyces then thicken the microbial mat. Other species begin to appear, snuggle into the mat, and proliferate - ecological succession in the microbial world.
Out in the stream, things are also happening. The stream in the periodontal pocket is about 0.25 mm wide. This may not seem like much, but to a 5 micron bacteria, it`s an ocean. That wide ocean is home to organisms which can swim - motile bacteria like vibrios, spirochetes, gliding roads, and organisms with flagella.
As the ecological succession progresses in the microbial ecosystem, the microorganisms become increasingly interdependent and interrelated, a process known as ecological synergism. In the semi-permeable matrix of plaque, oxygen tensions change as streptococci and other facultative organisms use up the available oxygen, thus ensuring an oxygen-free environment for anaerobic organisms. Nutritional factors change as metabolic by-products are concentrated in the mature plaque matrix. Metabolic interrelationships develop based on the ability of one organism to evolve substrates and growth requirements necessary for another. A diptheroid species, for example, produces a vitamin K analogue needed by bacteroides.
The bad news bugs
As the microbial ecology becomes more and more complex with changing environmental conditions of their own and their host`s making, eventually some 200 species and strains may come to inhabit the mature plaque, a veritable zoo of microorganisms. At some point near the climax stage of the ecological succession the periodontal pathogens appear - the bad news bugs in the microbial zoo.
In the specific plaque hypothesis, the late colonizing periodontal pathogens are suspected specific organisms which have the potential to gradually produce collagenase, proteases, chondroitin sulfatase, hyaluronidase, and endotoxins capable of causing direct damage to host tissues. They also may trigger destructive aspects of the host immune system, for example, by activating the complement cascade to generate biologically active substances.
Evidence is mounting to implicate some ten or so microorganisms. In our microbial zoo, several inhabitants are hanging around with blood on their jowls, highly suspicious characters like Porphyromonas gingivalis, Bacteroides forsythus, Actinobacillus actinomycetemcomitans, Prevotella intermedia, Fusobacterium nucleatum, Eikenella corrodens, Campylobacter recta, Selenomonas, and others.
The host immune system`s cellular and humoral components does protect us from this onslaught. If it didn`t, we would all die of horrible, fulminating gingival infections. But it is a two-edged sword. It protects us, but it also possesses the potential to produce a great deal of tissue damage.
Polymorphonuclear leukocytes emigrate from gingival vessels through the connective tissue and into the sulcus where they form a protective barrier, phagocytizing gluttonously. However, in this milieu their lysosomes degranulate, releasing potent lysosomal enzymes such as collagenase, proteases, acid hydrolases, esterases, lipases, and a long list of others, capable of degrading all organic macromolecules. When this occurs in gingival tissues, inadvertent degradation of host gingival tissues takes place on a widespread and sustained basis.
Offering both protection and destruction
Other aspects of the immune system may also contribute to both protection and destruction. Macrophages may function in an immunoregulatory fashion. They also phagocyose microorganisms and debris. Stimulation of macrophages, however, may cause them to produce cytotoxic products that may cause localized tissue destruction and alveolar bone resorption.
Lymphocytes produce biologically active lymphokines such as lymphotoxin, interleukins, and macrophage activating factor (MAF). T-lymphocytes give rise to the dreaded Killer T-cell. B-lymphocytes may convert to plasma cells, the body`s antibody factories. Antibodies may act as opsonins or be directly bacteriocidal. Antibodies may also combine with complement to produce cytolytic complement-antibody complexes and generate biologically active components of the complement cascade. These biologically active fragments are powerful mediators of inflammation and may set up cyclic episodes of tissue destruction.
So the contribution of the host immune system is conceptually important to the pathogenesis of periodontal disease. It has a role in combating the organisms of microbial plaque, yet there is a potential for localized or widespread, cyclic, or sustained degradation of the gingival connective tissues, alveolar bone, and the periodontal attachment apparatus.
Left undisturbed, microbial plaque undergoes an ecological succession with a shift from aerobic Gram-positive species to anaerobic Gram-negative species, as well as to motile organisms and periodontal pathogens.
At some point, the host immune system is activated. From the initial activation, a complex interplay of host immunological components and microorganisms of microbial plaque results in an escalation of inflammatory processes leading to a chronic inflammatory state with its attendant destructive attributes. It all takes time, and it all progresses in an escalating step-like fashion.
What if the plaque is disturbed? Then the carefully progressing layers of interdependence are toppled, everything is shifted back to the left and it all begins again with Gram-positive aerobic early colonizers and a cooling of the inflammatory response.
We hope that patients do this on a daily basis and keep out of trouble. We call it oral hygiene, brushing and flossing, or plaque control, and it is certainly not a new thought. In the 1890s, C.C. Bass and G.V. Black said plaque causes disease, and it must be removed. In the 1960s, evangelists of preventive dentistry like Bob Barkley, Simon Katz, and Sumter Arnim advocated zero plaque scores. In the 1990s, familiar names like Sigmund Socransky, Max Listgarten, and Max Goodson speak in ecological terms of reducing the degree of organization of plaque, of maintaining a "healthy" plaque composed of a scant, Gram-positive, aerobic indigenous flora.
The goals are the same: disruption of the ecological succession and a shift in the amount and composition of the flora to a plaque compatible with health.
Disruption in the ecosystem
What happens to the patients who don`t hear or heed the message and develop periodontal pockets? Brushes and floss will not reach to the depths of a 6 mm pocket where the plaque is snug, warm, and undisturbed, but dentists and hygienists can. The goal has not changed. Disrupt the degree of organization and shift the plaque composition to Gram- positive aerobes.
The philosophy of non-surgical periodontics and periodontal maintenance rests firmly on the belief that it takes time for plaque to mature, for the host immune system to become involved and for disease to develop. It follows that if we can stir up the plaque on a consistently routine basis we can halt the progression of the disease.
If we visualize this concept, we can imagine a graph. The horizontal axis would be "time." The vertical axis would be "complexity of microbial flora." A hazy horizontal line would divide the graph equally. The lower half would be labeled "health," while the upper half would be marked as "disease."
As time progresses, ecological succession progresses, and the line following the time axis reaches upward and outward. With time, the "bugs" change, the immune system is activated, and eventually the state of the tissues reaches the limits of health, crossing through the hazy border into disease.
Clinically, if you can catch the patient at just that stage, and then scale and debride the pocket subgingivally (whether there is calculus there or not), plaque will return to zero complexity, until it starts all over gain with its slow rise upwards.
Poisoning at the right time
It doesn`t always have to be a scaler with which the plaque is disturbed. If the fish in my mountain lake are poisoned on a routine basis, a population of fish will never become established.
There is a search underway in periodontics for the ideal "poison" for subgingival plaque. A variety of chemotherapeutic agents have been tried including stannous fluoride, chlorhexidine, alexidine, sanguinarine, and others. Effective delivery may be made by irrigation via a blunt side-vent needle placed well into the pocket and connected to a syringe or irrigation device. Slow-release fibers designed to be placed subgingivally and liberate high concentrations of tetracycline into the pocket`s micro-environment are available for clinical use. Other antibiotics in similar slow-release subgingival forms are currently being investigated and also look promising.
The imaginary graph above, of course, is too vague about the exact amount of time it takes to move from a clean tooth to one harboring periodontal pathogens. Unfortunately, no one quite knows. The popularity of three-month recalls in periodontal circles provides evidence that a three-month interval will keep most patients in the zone of health. It is clear, however, that for some patients, based on their clinical symptoms, three months is too long and empirically derived shorter recall periods are necessary. Definitive means of determining the ideal interval between recall visits eludes researches and clinicians, but there are exciting concepts just over the horizon.
Speaking of horizons, the sun, once sparkling on my alpine lake, had just slipped behind the mountains while my thoughts drifted along drawing parallels between the ecology of lakes and forests and periodontal pockets. The calm, smooth lake surface belied the complexity and activity under the water. Like the lake, the important things in periodontal pockets are also going on below the surface, out of sight. It takes patience, persistence, and perhaps a certain dedication to the sport to be successful with fishing and also in periodontal therapy. I pulled my day?s catch out of the water and eyed them critically. Not bad, and they were going to taste delicious cooked over an open campfire.
David J. Pippin, DDS, MS, is an assistant professor in the department of periodontology at the University of Missouri Kansas City School of Dentistry.
