Dr. Richard Nagelberg explains that by identifying the bacterial cause of periodontal disease through salivary testing, treatment planning and risk assessment can be applied on the basis of hard data, rather than treatment limited by subjective assessment.
When advancements are developed that simply and affordably enable clinicians to significantly improve the specificity of their treatment plans for patients, and, by extension, the therapeutic outcome, we would reasonably expect them to be accepted and implemented wholeheartedly by the profession. This is the case with salivary identification of periodontal pathogens. Perhaps more importantly, the same technology allows us to assess the risk for the development of periodontal disease for a patient who may have a clinical condition prior to periodontitis; in other words, the patient is periodontally healthy or has gingivitis.
By identifying the cause of periodontal disease, namely the specific periodontal pathogens harbored in a patient’s mouth, treatment planning and risk assessment are facilitated using hard data, rather than a subjective assessment protocol. Other risk elements including genetics, diabetes, smoking, xerostomia, poor oral hygiene, stress, immunocompromise, hormonal variations, or connective tissue diseases, among others, are important to identify and mitigate as much as possible, but they are all contributing factors, not causative. Strange as it may seem, poor oral hygiene on its own cannot cause periodontal disease—nor can smoking, diabetes, xerostomia, etc. Of course, all of these factors increase the likelihood of periodontal disease development, severity, speed of onset, etc., but they are not direct causes.
Our current understanding of the development of periodontal disease requires specific oral bacteria plus the patient’s immuno-inflammatory response in a genetically susceptible individual, period. What is the evidence for this? One piece was provided by the researchers who originally identified the periodontal pathogens. The late Anne Haffajee, DDS, and the late Sigmund (Sig) S. Socransky, DDS, stated, “The ultimate risk factor for an infectious disease is the causative agent of that disease. Without that agent, no disease will take place no matter what [their emphasis]other risk factors the subject may possess.” (1) The causative agents in the case of periodontal disease are the specific bacteria.
The current standard for nonsurgical in-office periodontal therapy includes periodontal evaluation and charting, radiographs, and scaling and root planing with or without the use of various types of antimicrobials. This is the same way we have approached periodontitis for more than 30 years. This protocol isn’t obsolete; it’s just not sufficient at this point because we are leaving too much to chance. Without identifying the specific bacteria that we are attempting to control, we are simply guessing and practicing blindly.
Let’s say the salivary test reveals the presence of several high-risk, highly pathogenic bacteria such as Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), and Treponema denticola (Td). These are highly toxic bugs associated with aggressive forms of periodontal disease. The salivary test report will specifically state which antibiotics are indicated for each bacterial profile. Now, we can develop a treatment plan for the individual patient, rather than providing a one-size-fits-all approach. With highly pathogenic, toxic bacteria, we can anticipate that some areas will not respond to initial therapy. But we can use the powerful information we gain from the salivary testing to decide how to address nonresponding sites should they occur. This may include the use of antioxidants, probiotics, additional biofilm control devices, or other adjunctive therapies.
Similarly, the presence of these high-risk bacteria in a periodontally healthy individual or someone with gingivitis would represent an elevated level of risk for periodontal disease development, especially in the presence of a medical history or a family history of periodontitis. This constitutes a hard data-driven risk assessment. A thorough evaluation and modification of the patient’s home-care regimen, if necessary, would be warranted, followed by annual salivary retesting.
Another scenario includes patients whose bacterial tests reveal the presence of Fusobacterium nucleatum (Fn), P. gingivalis (Pg), and/or Aggregatibacter actinomycetemcomitans (Aa), in addition to T. forsythia and T. denticola, because these bacteria have been identified as directly causative for atherosclerosis development. (2)
So, are we treating mouths, pocket numbers, swelling and BOP, or people? We work between the chin and the nose, but the effect of the therapy we provide or ignore is felt between the bottom of the feet and the top of the head. Figure out what is holding you back from doing the best you can for your patients, get past it, and reach your full potential as a clinician.
Richard H. Nagelberg, DDS, has practiced general dentistry in suburban Philadelphia for more than 30 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact Dr. Nagelberg at email@example.com.
1. Socransky SS, Haffajee AD. Evidence of bacterial etiology: a historical perspective. Periodontol 2000. 1994;5:7-25.
2. Bale BF, Doneen AL, Vigerust DJ. High-risk periodontal pathogens contribute to the pathogenesis of atherosclerosis. Postgrad Med J. 2016. doi: 10.1136/postgrad medj-2016-134279. [Epub ahead of print].