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Several years ago, Dr Herb Bader wrote: \u201cThe literature supports the advantages of determining the causative organisms in the biofilm, that induces the destructive inflammatory response (Haffajee, Tanner, Teles andSocransky, 2006). In addition, there is a considerable body of evidence supporting the accuracy and sensitivity of salivary testing as being virtually identical to sulcular samples. Work by Giannoble, Wong and others (2008) have confirmed this. Data from thousands of such tests has shown that patients are rarely infected with a single pathogen. The overwhelming majority of tests show anywhere from three or more organisms involved. These findings are significant in targeting adjunctive antibiotic therapy, since different combinations of organisms are susceptible to different antibiotic combinations (Van Winkelhoff, et al). Having established the critical importance of looking at the biologic phenotype underneath the clinical expression, through testing, it now becomes obvious that the only way to truly determine the efficacy of the therapy is by post treatment pathogen testing. Results from the post treatment test in combination with clinical evaluation, gives the clinician an opportunity to determine if a truly successful endpoint has been reached, for long term resolution of the inflammatory and bacterial burden.\u201d<\/p>\n
Our challenge, as the treating clinicians, is how to explain to our patients the less than anticipated improvement of the bacteria profile after treatment. Let\u2019s consider one possible treatment outcome: Our patient returns for a re-evaluation and the clinical (visual) parameters of periodontal disease control are evident. The gingival tissue is pink, firm and healthy with no bleeding on probing and daily oral hygiene seems to be keeping biofilm, plaque and calculus accumulations well controlled; however, the post treatment MyPerioPath\u00ae report shows persistent high levels of pathogenic bacteria. Clinicians and patients alike seem to immediately ask, \u201cwhat went wrong?\u201d forgetting that periodontal disease is a complex interplay of bacterial and host response that is also modified by behavioral and genetic factors.<\/p>\n
When we see great clinical improvement with persistent (unchanged) or worse bacteria levels, we should focus on the tremendous value of this MyPerioProgess\u00ae test information. Without the follow up evidence of persistent bacteria, clinical improvement may give a false sense of \u201csuccess\u201d. This second MyPerioPath\u00ae, MyPerioProgress\u00ae report clearly tells us we have not reached a clinical endpoint and ongoing care is indicated \u2013 this patient is not ready to be placed into a maintenance program of care. We can explain to our patient that the good news is the pre-treatment inflammation is improving and healing is initiated. Now is the time to take a closer look at other contributing factors. We know that our immune system is the first line of defense against pathogenic organisms, so we should consider this patient\u2019s genotype.\u00a0 Do they have a genetic profile, such as DEFB1 G\/A, that makes it harder for their immune system to recognize and fight off pathogens, therefore making it harder for the patient to achieve and maintain a balance of commensal (good) bacteria? (Consider testing with Celsus One \u2122 to determine Genetic Risk)\u00a0 If the results show that the patient has this genetic profile, how can we support this patient in the healing process? We can focus our continued care on modifiable contributing factors such as nutrition, stress levels, compliance with oral care, and compliance with systemic antibiotics or other prescribed products. We can discuss and explore reinfection from family members, or poor dental work, which serves as a reservoir for bacteria to thrive. MyPerioPath\u00ae testing before and after treatment is not a pass or fail report card.\u00a0 Rather, it is a road map that directs us to consider ongoing care and treatment options.<\/p>\n
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