For periodontist in Houston, TX successful intervention in a disease process requires that the practitioner understand the disease process fully. An example of this is our new understanding of duodenal ulcer pathogenesis, which has led to a paradigm shift in treatment of ulcers away from medications affecting acid production to treatment with antibiotics. Without an understanding of the role of Heliobacter pylorii in the pathogenesis, a rationale for treatment with antibiotics was non-existent.
Our understanding of periodontal diseases has developed slowly. In a series of papers, Low established the role of oral hygiene in the prevention of gingivitis and implicated bacteria in the development of gingivitis (I). This finding provided support for several approaches to treatment. First, it supported the concept that removal of bacteria from the root surface was a critical step in controlling periodontal disease, thus leading the way for scaling and root planning as a cornerstone of periodontal disease treatment. Second, it supported the role for 'treating periodontal disease with antibiotics. We have since found that both of these approaches have limitations. To a degree, these limitations are defined by our incomplete understanding of the disease process.
Currently, our model explaining the pathogenesis of periodontal disease is significantly different from what it was 5 years ago(2l. We now think that health exists as a homeostatic condition between oral bacteria and host defenses. Alterations in host defenses can lead to establishment of an "eco-system" of bacteria capable of supporting periodontal pathogens. Subsequently, these bacteria stimulate the host immune system. To a great extent, this response of the immune system determines the level of tissue destruction that occurs in periodontal diseases.
The purpose of this paper is to present the current theories of periodontal disease pathogenesis. This discussion will provide the groundwork for understanding the relationship between systemic diseases and periodontal diseases. In addition, understanding these new concepts of the disease process will clarify the limitations of currently used treatment modalities and provide a basis for future treatment protocols.
Bacteria in the periodontal pocket exist in a biofilm.
Most bacteria implicated in the pathogenesis of periodontal disease are anaerobic(2-4). Currently, Porphyromonas gingival is, Bacteriodes forsythus, and Actinobacillus actinomycetemcomitans are thought to cause the majority of periodontal diseases (4). Exxposure to oxygen leads to the death of most of these microorganisms. This characteristic was the basis for the Keyes technique using sodium bicarbonate (baking soda) and hydrogen peroxide. Although the technique was effective at controlling superficial bacteria, its application to patients with moderate to advanced periodontal disease had little effect. This limitation was probably due to failure of the agents to reach the bacteria, primarily because the bacteria are at too deep a sulcular depth in more advanced disease and secondly because the bacteria exist in a biofilm which limited exposure to chemicals in the periodontal pocket.
The term biofilm refers to a glycoprotein matrix containing bacterial4J• Often, numerous strains of bacteria exist in the biofilm in a symbiotic relation. Thus, species A of bacteria may require an element or metabolite for its growth, that is deleterious to species B. By utilizing all of the available element/metabolite, species A promotes the growth of B. In other cases, a waste product of species A may be critical for the growth of species B. This symbiotic interaction is a hallmark of biofilms. The glycoprotein matrix serves an important function by limiting diffusion and aiding in the establishment of concentration gradients.
In addition to aiding the development of concentration gradients for periodontist in Houston, TX, the biofilm provides a protective barrier for bacteria from host defenses. The biofilm limits the exposure of bacteria to crevicular fluid. Thus, bacteria in a biofilm have a greatly limited exposure to serum factors including antibodies as well as antibiotics. A good example of this characteristic is to picture Jello gelatin as the biofilm. Water poured onto the jello will not penetrate into the jello due to limited diffusion. Penetration of antibiotics into the biofilm can be thought to have diffusion characteristics similar to that of water. Thus, the majority of bacteria in the biofilm would not be exposed to the antibiotic. This model provides a better understanding of our failure to treat periodontal diseases with antibiotics alone.
Another function of the biofilm is to limit access of the host defense cells to the bacteria. In a patient with severe gingivitis, as many as 10 million neutrophils (PMNs) traverse the gingival sulculus each minute. Although these cells may recognize and respond to bacteria on the surface of the biofilm, bacteria deeper in the biofilm will not be recognized. Thus, if these cells are provided the nutrients required for their growth, survival of the species is ensured and continued exposure of the host to bacterial challenge occurs. Together, this information will prove to be critical in predicting patient outcomes, and genetic tests will become important tools in treatment planning for periodontist Houston, TX.
bibliography
I. Low H, Theilade E, Jensen S. Experiimental gingivitis in man. J Periodontol 1965;36: I 77-187.
2. The pathogenesis of periodontitis. Ediitors- R. Page and K. Komman. Periodontollogy 2000; 1997; Vol 14.
3. Page R, Offenbacher S, Schroeder H, Seymour G, Kornman K. Advances in the pathogenesis of periodontitis: summary of developments, clinical implications and future directions. Periodontology 2000 1997; 14: 216-248.
4. Darveau R, Tanner A, Page R. The microbial challenge in periodontitis. Periiodontology 2000; 1997; 14; 12-32.
5. Dennison D, VanDyke T. The acute inflammatory response and the role of phhagocytic cells in periodontal health and disease. Periodontology 2000 1997; 14:54478.
6. Dennison D, GOllsegen R, Rose L. Position paper- American Academy of Peeriodontology. Diabetes and Periodontal Diseases. J. Periodontol 1996; 67:166-176. 7. Taylor L, Burt J, Becker L , Genco R, Shlossman M, Knowler J, Pettitt L. Severe periodontitis and risk for poor glycemic control in patients with non-insulin depenndent diabetes mellitus. J. Periodontol. 1996; 67: 1085- J093.
8. Beck J, Garcia R, Heiss G. Vokonas P,Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol 1996; 67:1123-1137.
9. Loesche W, Schork A, Terpenning M. Chen Y, Dominguez L, Grossman N. Assessing the relationship between dental disease and coronary heart disease in eldderly US veterans. JADA 1998; 129:301 3lJ
This series of articles outlining recent progress in periodontology was first introduced in the GHDS Journal issue of March 1998.