Spring blooms were a visual delight and welcome distraction for me as I recently made the long drive north from Atlanta to Franklin, Tenn., to attend the Tennessee Dental Hygienists’ Association (TDHA) annual session. Unfortunately, I could stay only one day, but that particular day was chock-full of activity. Tennessee is known for its hospitality, and I could feel the friendliness of the people from the moment I approached the registration table.
The course I attended was presented by Dr. Tom Nabors, a general dentist with a passion for treating periodontal diseases through the application of a pathogen detection system called micro-IDent®, which identifies a handful of tissue-invasive periodontal anaerobic bacteria. The European-based manufacturer of this system has an American distribution company called ADDX, which is owned and operated by Dr. Nabors.
Testing is recommended for conventional, mechanical nonsurgical periodontal therapy. The micro-IDent® system is especially recommended for therapy-resistant and aggressive periodontal diseases, and helps dental team members select a systemic antibiotic based on laboratory results. In addition to micro-IDent, ADDX offers a genetic test called GenoType® PST®, which tests for the overproduction of an inflammatory mediator interleukin-1. Interleukin-1 (IL-1) is one of several genetic variations impacting the host response associated with a more severe form of periodontitis.1
The ADDX diagnostic tools are recommended for determining individual risks of periodontitis or implant loss. Both tests are less expensive than traditional laboratory culturing, and intraoral samples are packaged in colorful kits and mailed to Germany for analysis. Specimen collection is done by sterile paper points, and results for the micro-IDent test include possible systemic antibiotics. To find out more about ADDX, visit the company website at: www.addx.us.
During his presentation, Dr. Nabors talked about virulence (the capacity of gram negative anaerobic bacteria to cause disease) and some of the species that play a role in the etiology and pathogenesis of periodontal diseases. Even so, I still had questions about the timing of various adjunctive agents in disinfecting periodontal pockets, as well as microbial testing in patients with poor treatment response from conventional therapy; I decided to torture myself by reading a lengthy chapter on the variety of microorganisms that live as an intricate and fascinating ecosystem.
Colorful complexes
Drs. Sigmund Socransky and Anne Haffajee wrote an extensive chapter on periodontal microbial ecology, the study of interactions between periodontal pathogens and their environment.2 Grouping the pathogens in color-coded categories, the resulting complexes look like Easter eggs in a coloring book. I will discuss some of these colorful complexes and their habitats, the places where they grow and reproduce, and niches, their function within the habitat. I will limit my focus to clinical applications for those of us who work day after day in the periodontal pocket trenches, cleaning and disinfecting pockets of all depths.
If individuals withdraw from all oral hygiene measures, gingivitis develops in all subjects in 10 to 21 days.2 Early bacterial colonizers include members of the yellow, green and purple complex, along with the actinomyces species.2 The appearance of bacteria in the orange and red complexes denotes the arrival of the king and queen of complexes, and these two complexes predominate. Increased levels of bacteria in the orange and red complexes create a significant change in the habitat, and the clinical result is gingivitis.2
What intrigues me in reading Socransky and Haffajee’s chapter is their discussion about the orange and red complexes. Subgingival biofilms, as compared to supragingival biofilms, exhibit higher proportions of members of these two complexes. In comparing the subgingival environment of periodontally healthy subjects and subjects with periodontitis, subgingival counts of bacteria in the orange and red complexes are much higher in periodontitis subjects.2 In particular, P. gingivalis, T. forsythia and T. denticola, which are members of the red complex, are more numerous in this particular environment.
The anatomy of a deep pocket is critical to our understanding of where the orange and red complexes live. Deep pockets have two biofilms in a single anatomic space - one biofilm
on the tooth/root side and another on the pocket/epithelium side. There’s also a third “zone” of loosely adherent plaque sandwiched between the other two biofilms. Remember that this pocket space is tight and there’s not a lot of wiggle room.
If a deep pocket exhibits inflammation (bleeding), the composition of the microbiota is affected and members of the orange and red complexes are elevated.2 These bacteria feed from gingival crevicular fluid, not saliva, which increases with inflammation and becomes more abundant and destructive. (Red complexes like a rich diet of proteins or peptides, which appear as breakdown products from adjacent tissues.) The king and queen of complexes can now enjoy a perpetual feast. Low gingival crevicular fluid seems to limit the growth of subgingival biofilms, which means that controlling inflammation is key to limiting the invasion of members of the red complex to the deep pocket environment.2
Disrupting the orange/red complex
So, what’s the clinical significance of our newfound knowledge concerning the orange and red complex? Is there anything new or worthwhile to report?
For starters, we know that there is therapeutic value in the dental prophylaxis. As a result of a dental prophylaxis, bacteria are removed nonspecifically and in proportion to their original numbers. As gingivitis develops, the king and queen of complexes (orange and red) make an appearance. In periodontitis, as the total count of orange and red complexes increase, the environment offers the royal family a perpetual inflammatory feast through the gingival crevicular fluid. The deep pocket is a cozy environment for these complexes and, as hygienists, we must use our precision-thin microultrasonics to disrupt these gatherings.
In addition, once the biofilms are disrupted, non-adhering bacteria that remain are more easily phagocytosed by their enemies (white blood cells called PMNs) in the pocket.3 Adjunctive therapies such as locally delivered antimicrobials, host modulation agents and appropriate systemic antibiotics all play a role in modifying the pocket environment and reducing inflammation.
Self-care measures are often forgotten when we focus on professionally administered therapies. Professionally administered therapies such as scaling and root planing and locally delivered antimicrobials generate significant income for private practices, yet sometimes we fail to deliver adequate self-care instructions. If our patients are not lowering bacterial counts regularly at home, we’ll be spinning our wheels trying to modify the pocket environment, not to mention the continuing expense to patients who must be re-treated with expensive debridement procedures and locally delivered antimicrobials.
It is also important to recognize that home irrigation can modify the pocket environment where the loosely attached bacteria in the orange complex reside, and irrigation can reach a depth of six millimeters.4 Explain to patients that the anaerobic bacteria in deep pockets are found in three areas, and that the layers resemble a sandwich: the loosely attached bugs are comfortably sandwiched between bugs (bread) on both the tooth/root and pocket/epithelium side. Tell them to think outside the lunch box and blast those orange critters to smithereens with an oral irrigator!
The unanswered questions
As I faced the long drive back to Atlanta, I thought about how far we’ve come in understanding periodontal diseases. Yet there are many unanswered questions.
For example, how does a clinician choose a periodontal disease risk assessment tool? Do you use a microbiological test like micro-Ident or BANA, or do you measure a genetic inflammatory marker with a test like the GenoType PST? Would it be better to perform a PreViser periodontal risk assessment first, which generates a score based on the patient’s current periodontal disease state and risk for future disease?
The other thought that nags me is the cost of nonsurgical periodontal therapy, and making serious attempts to control those costs while delivering the appropriate therapy. As dental professionals in a service industry that is sometimes encouraged to be profit-driven, a delicate balance is required to treatment plan according to the patient’s best interests, needs and desires.
It’s a confusing time to be an oral health-care professional, especially with the current emphasis on advancing our knowledge of molecular, cell, and connective tissue biology in order to better understand the host immune and inflammatory responses. Researchers are excited about identifying new host modulation drugs and finding ways to slow the inflammatory process.
Just as environmental factors like respiratory infections cause inflammation (swelling) of airways in asthmatics, anaerobes in the orange and red complexes thrive in an inflamed pocket. The amount of inflammation in periodontal pockets is strongly influenced by host, genetic, or environmental factors. Some examples of specific factors that modify the expression of periodontal diseases in a susceptible host are systemic diseases, an immunocompromised state, medications, poor oral hygiene, hormones, stress, and smoking.
We need to approach learning with an open mind. I suggest you read about the various bacterial complexes and stay tuned to Socransky and Haffajee’s continuing discussion in another chapter of Perio 2000, which will be published later this year, where they address periodontal therapy applications based on modification of the periodontal ecosystem. I’ll make sure RDH readers are informed about this chapter and its clinical applications in a future column.
References
1. Schenkein HA: Host responses in maintaining periodontal health and determining periodontal disease. Perio 2000; 2006: 40: 84.
2. Socransky SS, Haffajee AD: Periodontal microbial etiology. Perio 2000; 2005: (38)1: 135.
3. Rhemrev GE, et al: Immediate effect of instrumentation on the subgingival microflora in deep inflamed pockets under strict plaque control. J Clin Periodontol 2006; 33: 42-48.
4. Rose LF, et al. Periodontics: medicine, surgery and implants; Mosby Inc.; 2004:226.
