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Benefits of early systemic antibiotics in localized aggressive periodontitis: a retrospective study
Author(s) -
Beliveau Dennis,
Magnusson Ingvar,
Bidwell John A.,
Zapert Edward F.,
Aukhil Ikramuddin,
Wallet Shan M.,
Shaddox Luciana M.
Publication year - 2012
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/jcpe.12001
Subject(s) - medicine , bleeding on probing , concomitant , antibiotics , retrospective cohort study , regimen , aggressive periodontitis , periodontitis , systemic antibiotics , antibiotic therapy , surgery , microbiology and biotechnology , biology
Abstract Background Treatment of localized aggressive periodontitis ( LAP ) may include systemic antibiotics, yet it is unclear at what stage of treatment planning antibiotics are most effective. Aim This retrospective analysis compared immediate versus delayed antibiotic therapy on clinical parameters and gingival crevicular fluid ( GCF ) inflammatory mediators. Material and Methods At baseline, 3 months and 6 months after treatment, clinical parameters [probing depth ( PD ), clinical attachment level ( CAL ), bleeding on probing ( BoP ) and plaque] and GCF were collected from LAP participants, who received a 7‐day antibiotic regimen immediately ( ImA ) or 3 months following ( DelA ) mechanical therapy. Results Although both groups presented significant CAL reductions at 6 months, only ImA resulted in a reduction in mean PD at both 3 and 6 months, along with reductions in CAL and BoP at 3 months following therapy. In addition, GCF mediators were higher in DelA group at 3 months post mechanical treatment, but were significantly reduced 6 months following antibiotic therapy. Conclusions ImA and DelA regimens were both effective in improving CAL by 6 months post therapy. However, ImA allowed for better improvement in overall clinical parameters early in the course of treatment, concomitant with lower levels of inflammatory mediators within the GCF .

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