I was disappointed by the lack of accuracy of many of the comments and the misinterpretation of our published data in "Efficacy of Subantimicrobial Dosing With Doxycycline: Point/Counterpoint" by Drs. Gary Greenstein and Ira Lamster (April JADA). I plan on publishing an article with other academics and clinicians addressing each of these points in detail.
However, challenging each point is not possible in a rapidly published, and by necessity brief, letter to the editor, so at this time I will restrict my comments to the last section of their article, "Update: An Additional Clinical Trial."
The authors’ statement that the data in my recent publication1 "contradicts the usual findings in the periodontal literature" clearly indicates that the authors completely misunderstood a major goal of our study. Our study was designed to be different from most other longitudinal studies described in the periodontal literature.
As a unique aspect of our study, we deliberately selected for measurement only those pockets that repeatedly exhibited pathologically elevated, host-derived collagenase activity (that is, at the prescreening, then two weeks later at the screening, then two weeks later at the baseline appointments). Based on our working definition of active pockets, these pockets lost an average of about 0.8 millimeters of clinical attachment in only six to nine months in spite of repeated (twice in six months) scaling and prophylaxis.
In contrast, those patients, who received subantimicrobial doxycycline (Periostat [CollaGenex]) periodically (three months on, then three months off, then three months back on the daily regimen) adjunctive to supra- and subgingival scaling, did not lose significant attachment during this nine-month double-blind, placebo-controlled study. Inexplicably, the authors made no mention of any of these unique aspects of our study in their article.
To the best of our knowledge, no study has attempted to select "active" pockets by repeatedly detecting elevated host-derived proteinase in the same lesion, although several notable studies have succeeded in characterizing active pockets by detecting elevated levels of gingival crevicular fluid enzymes such as elastase, collagenase and gelatinase.2–5
However, most traditional periodontal studies (and in particular those referred to by the authors) use only baseline probing depth (and clinical indexes of inflammation) measurements as an entry criterion into a longitudinal study. It is likely that many of these pockets (the majority?) are inactive lesions. In fact, many of these pockets show improvement (that is, attachment gain and decreased pocket depth) even with no treatment (placebo/control group), the well-known Hawthorne effect.
Therefore, in our study of operationally defined active pockets, subantimicrobial doxycycline as adjunctive therapy was significantly more effective than repeated scaling alone, and the authors clearly misunderstood the purpose of our study.
While scaling and root planing have repeatedly been shown to be an effective therapy, many patients treated with a mechanical approach alone continue to show progression of disease. In our study,1 unlike most longitudinal studies of chronic periodontitis, a biological diagnostic marker was used to aid in the identification of actively destructive pockets. Subantimicrobial doxycycline adjunctive to supra- and subgingival scaling was clearly more effective than mechanical débridement alone in preventing disease progression.
If periodontitis is to be considered a serious disease (the major cause of tooth loss in the adult population worldwide and a significant risk factor for serious systemic diseases such as cardiovascular disease, stroke, bacterial pneumonia, low birthweight babies, less manageable diabetes—that is, "periodontal medicine"), then the two-pronged approach of an antimicrobial combined with host modulation therapy must be given serious consideration in light of the wealth of data for its support.6–9
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