Lessons from Detroit

Nov. 1, 2009
About a year ago, I made a promise to David Apsey, DDS, that I would fly to the Detroit area and observe his periodontal protocol.

by Lynne H. Slim, RDH, BSDH, MSDH
[email protected]

About a year ago, I made a promise to David Apsey, DDS, that I would fly to the Detroit area and observe his periodontal protocol. David is one of the few general dentists I've known who, for more than 16 years, has dedicated a large part of his practice mission to the promotion of periodontal health.

David's practice uniqueness is the result of his commitment to microscopic assessment of motile organisms and the presence of white blood cells (WBCs). In addition to probing the gingival sulcus, Dr. Apsey's hygiene department routinely uses a phase contrast microscope during comprehensive periodontal exams.

Periodontal probing, per se, is not the basis for in-office periodontal treatment decisions. Instead, just as Dr. Paul Keyes advocated, hygienists Anna and Stephanie are always on the lookout for microscopic risk factors (elevated WBCs, abundant oral spirochetes and other motile forms). Using standard criteria, Anna and Stephanie examine each patient's slide just as Dr. Keyes did while at NIH.

Anna and Stephanie group patients into those with extensive periodontal breakdown (>5 mm pockets) and those with minimal breakdown. Those patients with a more serious infection are instructed to brush with baking soda and irrigate subgingivally with 0.5% povidone iodine or antimicrobial mouth rinse undiluted once or twice a day. Systemic antibiotics are also part of Dr. Apsey's protocol, and he often prescribes metronidazole. All patients are instructed to return in a month (free recheck) for micro-evaluation.

Dr. Apsey's protocol is different from mainstream practices where probing is “king” in the diagnosis and treatment planning for non-surgical periodontal therapy.

For the most part, Dr. Apsey still adheres to the specific plaque hypothesis, championed by the now-retired Dr. Walter Loesche (University of Michigan School of Dentistry). Many infections can be effectively treated with debridement (SRP) plus systemic antibiotics.1

Dr. Apsey was also influenced by Drs. Keyes and Rams, who demonstrated that microscopic examination of biofilm samples could be used to adjust treatment protocols by monitoring the number of WBCs and motile organisms. If WBCs disappeared and motile organisms were reduced, the number of cocci and rods increased. As patients improve, the number of WBCs and motile organisms decline while health-associated microbes like cocci and rods increase.2 In healthy, disease-free gingival crevices, Drs. Keyes and Rams found low levels of WBCs and motile bacteria, especially spirochetes. Diseased pockets brought under control, as evidenced by microscopic reevaluation, did not harbor these forms.

Is an abnormal white blood cell count a useful marker when assessing a chronic biofilm infection?

In reviewing the literature on biomarkers for periodontitis, there don't seem to be any that are universally accepted at present, even though several individual biomarkers in saliva and gingival crevicular fluid continue to be studied. In 2006, Dr. Apsey was a principal investigator in a clinical study that compared periodontal probing to the BANA test and a phase contrast microscopic examination of WBCs and motile organisms. 2 These three diagnostic models were performed to determine the prevalence of periodontal disease in 1,043 new adult patients. When probing was used as the diagnostic criteria, about 50% of patients needed treatment, but when the same patients were examined microscopically, only 25% needed treatment. The microscope was useful in that 25% of patients thought to need treatment in the probing model did not have evidence of inflammatory disease — thus the microscopic model may provide accuracy in classifying patients with active infections more accurately and avoid overtreatment of patients with pseudo or disease-free pockets.

It disturbs me that so many of today's general practitioners rely solely on periodontal probing depths and radiographic bone loss in making in-office treatment decisions and referrals to periodontists. This “cookie cutter” approach (which is oftentimes prompted by dental insurance coding requirements that define periodontal disease based on probing depths and radiographic bone loss) is unfortunate for a number of reasons. As previously mentioned, pocket depths don't mean a lot on their own, and measurement error is about 40% for an untrained examiner.3,4 As a practicing periodontal therapist (and untrained examiner), I have many well-maintained adult patients with 4 mm to 5 mm probing depths around many teeth. But these are nonbleeding pockets with little attachment loss, and the probing depths don't seem to change over time. If I assess a new adult patient with a history of asthma and mouth breathing and find generalized 3 mm to 4 mm bleeding pockets, I'm more concerned about controlling inflammation in this patient than I would be in a well-maintained patient with deeper probing depths and no significant systemic risk factors. Although the etiology of periodontal disease is bacterial, the pathogenesis is a host inflammatory reaction to bacterial challenge.5 Even gingival inflammation is now considered a risk factor for tooth loss along with many other risk factors like smoking and poorly controlled diabetes. It's also possible, based in new research in medicine and periodontology, that the host inflammatory response sustains the continued presence of periodontopathogens.6 Studies have also shown that once inflammation is controlled pharmacologically in animal models, Porphyromonas gingivalis (a red complex anaerobe) disappears.6 Porphyromonas gingivalis is a periodontal pathogen that is capable of disrupting host epithelial cells and invading into deeper periodontal tissues.7

I am almost certain that Dr. Apsey, Stephanie, and Anna will continue to do what works best for their patients nonsurgically with an emphasis on microscopy (WBC and motile organism sleuthing), excellent self-care, and recare compliance. Let's also add to that winning protocol an interest in identifying individuals with a compromised inflammatory response for a “Wow!” performance.


  1. Loesche WJ. The antimicrobial treatment of periodontal disease: changing the treatment paradigm. Crit Rev Oral Biol Med. 1999; 10:245-275.
  2. Keyes PH, Rams TE. Clinical application of a microbiologically monitored and modulated periodontal therapy. NY State Dent J 1983; 49:478-481.
  3. Apsey DJ, Kaciroti N, Loesche WJ. The diagnosis of periodontal disease in private practice. J Periodontol 2006; 77(9):1572-1581.
  4. Grossi SG et al. Sources of error for periodontal probing measurements. J Periodontal Res. 1996; 31(5):330-336.

    About the Author

    Lynne Slim, RDH, BSDH, MSDH, is an award-winning writer who has published extensively in dental/dental hygiene journals. Lynne is the CEO of Perio C Dent, a dental practice management company that specializes in the incorporation of conservative periodontal therapy into the hygiene department of dental practices. Lynne is also the owner and moderator of the periotherapist yahoo group: www.yahoogroups.com/group/periotherapist. In addition, Lynne is the editor of the Sunstar Americas e-newsletter “:The GUMline.” Lynne speaks on the topic of conservative periodontal therapy and other dental hygiene-related topics. She can be reached at [email protected] or www.periocdent.com.