by Deborah M. Lyle, RDH, MS
The idea that periodontal disease is an infection mediated by bacteria is not new. The etiology of periodontal infections has been studied since the late 1800s. Researchers tried to isolate the organisms responsible for periodontal diseases and found this task to be extremely difficult. Clinicians have focused on the removal of plaque as a key factor in treatment and prevention, regardless of research, but have often encountered frustration when therapy and recommended self-care were not producing healthy outcomes.
This article will explain why it is difficult to identify the etiological agents for periodontal diseases and help us understand their role in the disease process.
It began in the golden age of microbiology (1880-1920) with the discovery of many etiological agents responsible for systemic infections. During the same time period and into the 1930s, researchers tried to identify the agent responsible for periodontal disease. The result was the identification of four distinct groups of microorganisms as possible etiological agents: amebae, spirochetes, fusiforms, and streptococci. These groups were identified based on their apparent association with periodontal lesions.1
Keep in mind that microbial techniques were limited and consisted of wet mount or stained smear microscopy and limited cultural techniques. These organisms were suspected because they could be isolated from individuals with periodontal disease and were either non-existent or in significantly lower proportions in healthy mouths.
Some researchers during this time believed that periodontal infections were the result of multiple organisms or "mixed" infections. This hypothesis was started in part by the work of M. H. Vincent who identified pseudo-membraneous lesions of the oral cavity and the role of fusiforms and spirochetes. We know it as necrotizing ulcerative gingivitis, but it was originally known as Vincent's infection.2
Interest in the etiological agent of periodontal disease began to wane in the mid 1930s, giving way to the belief that the etiology was due to some defect on the part of the patient, to occlusal trauma, atrophy, or a combination of these factors. Bacteria was relegated to a back seat and thought to be a secondary invader.2
By the 1950s, the focus shifted back to bacteria. Clinicians touted the need for plaque control in the prevention and treatment of periodontal disease. This was known as the nonspecific plaque hypothesis, with the belief that any accumulation of bacteria at or below the gingival margin would lead to inflammation, and it was the quantity and not the quality of the plaque that was important.
Toward the end of the 1960s and continuing through the 1980s, the specific plaque hypothesis developed, with research focusing once again on specific organisms and their potential for initiation and progression of periodontal disease. These studies were aided by the development of newer methods of microbial analysis that included darkfield microscopy, scanning electron microscopy, transmission electron microscopy, DNA probes, BANA hydrolysis and immunoassay.3 The belief that plaque was similar from patient to patient was disproved as studies began to show that there were significant differences between patients and even between sites in the same patient. Additionally, subgingival plaque samples showed differences when taken from patients with different forms of periodontal disease.
Defining microbial pathogens
Many factors have impacted the ability to identify the etiological agents responsible for periodontal diseases. Haffajee and Socransky outlined many of the reasons, which include:4
• Over 300 species found in periodontal pockets that are difficult to culture
• The presence of opportunistic species
• Physical constraints of the periodontal pocket impacting the sampling process
• Evaluating the role of a single organism in mixed infections
• Breakdown of sites due to different pathogens and the difference in disease activity and inactivity in various sites
• Difference in virulence within strains of bacteria
• Individual host response to the bacteria
Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Bacteroides forsythus are strongly associated with periodontal infections, disease progression, and unsuccessful therapy, and were designated as periodontal pathogens at the 1996 World Workshop of Periodontology.5 The evidence regarding other patho-gens is not as extensive but does show implication in causing periodontal disease. These pathogens include F. nucleatum, Camphylobacter rectus, P. intermedia, and various spirochetes. Recently, viruses such as cytomegalovirus and Epstein-Barr virus have been proposed to play a role in the process, possibly due to impact on host response.
Criteria used to define periodontal pathogens include association, elimination, host response, virulence factors, animal studies, and risk assessment. Association refers to the frequency and numbers of the species present in specific types of periodontal infections. If you eliminate that species, resolution or remission of the infection should be evident. The host response can define a species by the production of antibodies that is directed specifically to that species. Some properties possessed by certain species impact its virulence and can play a role in the disease process. Animal studies are used to identify a possible etiological role of a species, and technology allows for the assessment of specific microorganisms in large numbers of subgingival plaque samples, leading to the assessment of risk in prospective studies.
The current viewpoint is that pathogenic bacteria are necessary — but not sufficient — for the initiation or progression of periodontal disease. The number, type, and location of organisms, as well as the host response play important roles in the process.
Biofilms are everywhere — on the inside of pipes and tubing, on rocks in rivers and streams, on the bottom of boats, in dental unit waterlines, and on teeth and oral soft tissue. Dental plaque is a biofilm. Biofilms are defined as matrix-enclosed bacterial populations that adhere to each other and to surfaces.6 Costerton and colleagues demonstrated in 1991 that bacteria grow in tiny enclaves or microcolonies. The bacterial cells join together and attach themselves to a surface and produce an extracellular matrix that holds the microcolony together. The microcolonies have channels running through them that allow for the passage of nutrients and waste removal. These microcolonies help protect the bacteria from antimicrobials, antibiotics, and host defense mechanisms. Key characteristics of a biofilm are the ability to attach to a solid surface and specific association or co-aggregation of bacteria.7
The viability of a biofilm depends on the ability of the organisms within the biofilm to communicate with one another. One way bacteria communicate is by quorum sensing, or the regulation of expression of specific genes through the accumulation of signaling compounds. They also communicate by the exchange of genetic information between cells of the same species and cross species.8
Biofilms form both supra- and subgingivally. Supragingival biofilms are attached to the tooth surface and are predominated by Actinomyces species. The subgingival biofilms have a tooth-associated and tissue-associated biofilm, separated by loosely bound or planktonic cells. The subgingival biofilms are also dominated by the Actinomyces species, but in significantly higher counts. In disease, the subgingival environment will show a decrease in Actinomyces species and an increase in B. forsythus, P. gingivalis and T. denticola.7
Impact on practice
Do therapy and self-care recommendations change with our understanding of the formation and workings of biofilms? We need to keep in mind that biofilms have large numbers of pathogenic bacteria, are widely distributed in the oral cavity, and exist in an environment that helps protect against antimicrobial agents and the host defense mechanism.
Therapy continues to focus on the mechanical removal of the biofilm, both supra- and subgingivally. Numerous studies have shown positive outcomes from scaling, root planning, and ultrasonic instrumentation. Since the biofilms have the ability to multiply quickly and reinfect, self-care measures are extremely important. Systemic antibiotics have had varying results, which may be due to increased resistance or difficulty in penetrating the biofilm. The use of locally administered antimicrobials has enhanced the ability to control the biofilm, especially when coupled with mechanical debridement.
The challenge is providing patients with the mechanisms to control the biofilm after therapy. Self-care needs to focus on controlling the supra- and subgingival biofilm with brushing, flossing or other interproximal aid, and daily irrigation.
Early studies were done on planktonic bacteria and did not give us insight into the microcolonies within a biofilm. Even when treatment is successful, bacteria will recolonize and increase the patient's risk for disease initiation and breakdown.
Understanding dental biofilms may lead to new treatments that focus on preventing communication or passage of nutrients within the biofilm or modulating the host response to prevent destruction of the periodontium. This information helps dental professionals and researchers focus on research and therapies that improve outcomes, and understand why periodontal therapy is not always successful.
Deborah M. Lyle, RDH, MS, is currently employed by Waterpik Technologies as the manager of professional marketing and education. She has presented numerous continuing education programs both nationally and internationally. Lyle also is a member of the ADHA Council on Education. She may be reached at [email protected].References
1 Meyer KF. The present status of dental bacteriology. J Am Dent Assoc 1917; 4:966-996.
2 Socransky S, Haffajee A. Evidence of bacterial etiology: a historical perspective. Periodontology 2000 1994; 5:7-25.
3 Papapanou PN, Engebretson SP, Lamster IB. Current and future approaches for diagnosis of periodontal diseases, NY State Dent J 1999; 32-39.
4 Haffajee AD, Socransky SS. Microbial etiological agents of destructive periodontal diseases. Periodontology 2000 1994; 5:78-111.
5 Zambon JJ. Periodontal diseases: microbial factors. Ann Periodontol 1996; 1:879-925.
6 Costerton JW et al. Biofilms, the customized microniche. J Bacteriol 1994; 176:2137-2142.
7 Socransky SS, Haffajee AD. Dental biofilms: difficult therapeutic targets. Periodontology 2000 2002; 28:12-55.
8 Prosser JI. Quorum sensing in biofilms. In: Newman HN, Wilson M, ed. Dental plaque revisited. Cardiff: biofilm, 1999; 79-88.