Drs. Gary Greenstein and Ira Lamster present an inaccurate analysis of the published literature and a biased viewpoint concerning the safety and efficacy of subantimicrobial dose doxycycline, or SDD, as an adjunct to scaling and root planing in the treatment of chronic periodontitis ("Efficacy of Subantimicrobial Dosing with Doxycycline: Point/Counterpoint," April JADA).
Comparing scaling and root planing in a group receiving SDD to a group receiving placebo, the study by Caton and colleagues1 clearly demonstrates the statistical superiority using patient-derived means and the clinical significance using site-based frequency distributions of the group receiving SDD. Furthermore, Greenstein and Lamster cite a study by Walker and colleagues2 as not supporting these differences, but fail to point out that Walker and colleagues studied the lack of antimicrobial effect of SDD, and this study was not powered sufficiently nor intended to demonstrate clinical differences.
A comprehensive body of research and clinical data has confirmed that the use of SDD carries no risk of alterations in the composition or susceptibility of the host microflora.2,3 Again Greenstein and Lamster make several factual errors in their discussion of the data presented by prior authors in this discussion.
Gingival crevicular fluid, or GCF, concentration of doxycycline following administration of SDD has not been determined directly. However, other studies have suggested that total GCF doxycycline concentrations may be about 70 percent of serum levels.4,5 Mean maximum total serum concentration of doxycycline following administration of SDD varies from 0.6 to 0.8 micrograms per milliliter, or µg/mL,2 which is well below the threshold concentration known to be antimicrobial (1 µg/mL). However, the amount of doxycycline available to exert an antimicrobial effect may be as little as about 10 percent of that observed in high performance liquid chromotography assays for total doxycycline, due to extensive protein binding.
Greenstein and Lamster concluded that "the evidence ... indicates that suppression of the bacterial challenge and subsequent reduction of the host response is the most efficient way to control periodontal disease." We would agree with this statement and would recommend the use of SDD to modulate the host response and restore the natural balance of enzymes and cytokines as an adjunct to scaling and root planing in patients with chronic periodontitis.
We would also agree that it is critically important to assess new therapies for patient management prior to their introduction. In this particular case, controlled clinical trials conducted in accord with rigorous protocols have clearly established the value of SDD as an adjunct to scaling and root planing in the treatment of chronic periodontitis and demonstrated beyond reasonable doubt that the risks are minimal.
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