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A Randomized, Placebo‐Controlled Trial of Doxycycline: Effect on the Microflora of Recurrent Periodontitis Lesions in High Risk Patients
Author(s) -
Kulkarni Gajanan V.,
Lee Wilson K.,
Aitken Sharon,
Birek Peter,
McCulloch Christopher A.
Publication year - 1991
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.1991.62.3.197
Subject(s) - doxycycline , placebo , actinobacillus , eikenella corrodens , fusobacterium nucleatum , medicine , gastroenterology , periodontitis , bacteroides , randomized controlled trial , clinical attachment loss , antibiotics , porphyromonas gingivalis , microbiology and biotechnology , pathology , biology , bacteria , genetics , alternative medicine
T wenty‐seven patients with a recent history of periodontal abscesses and/or loss of gingival attachment level (GAL) despite active periodontal therapy were enrolled in a double‐blind, randomized, placebo‐controlled trial. Clinical measurements and subgingival scaling were performed every 2 months. When a site exhibited ≥ 2 mm loss of GAL or a periodontal abscess, patients were administered either doxycycline at a dosage of 200 mg to start and 100 mg per day for 3 weeks, or a placebo. Clinical measurements of GAL and microbial analysis of subgingival plaque at study and control sites were made at the time of active disease and at intervals of 1 week and 7 months after completion of the drug regime. Plaque samples were screened for the presence of Actinobacillus actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Bacteroides intermedius (Bi), Eikenella corrodens (Ec) and Fusobacterium nucleatum (Fn) by indirect immunofluorescence antibody technique and for spirochetes (Sp) using Ryu's stain. Based on presence or absence analysis of the sum scores of the 6 pathogens, both the placebo (n = 10) and the doxycycline groups (n = 17) exhibited similar scores at the time of detection of active disease (x placebo = 2.38 ± 0.32; x doxycycline = 2.95 ± 0.27; P = 0.18). One week after treatment, the probability of detection was unchanged in the placebo group (x placebo = 3.14 ± 0.47), but was significantly reduced in the doxycycline group (x doxycycline = 1.77 ± 0.26; P = 0.0002). Study (active) sites exhibited scores 2 to 3 times higher than control (inactive) sites before doxycycline treatment. After doxycycline treatment, scores for control sites did not change significantly. The species most reduced by doxycycline were Pg, Bi, Fn, and Sp, while Aa and Ec exhibited no consistent decrease. Patients treated with doxycycline demonstrated no further disease activity for up to 7 months, while all but 2 of the placebo‐treated patients showed further active disease. However, there was no significant difference ( P = 0.82) of bacterial scores between the doxycycline and placebo groups at 7 months. Consistent with low in vitro inhibition of whole plaque samples at the dosages used here, the clinical efficacy of doxycycline in vivo over the long‐term may not be mediated solely by suppression of the periodontopathic microflora. J Periodontal 1991; 62:197–202 .