D Kalash1, A Vovk1, H Huang1, I Aukhil1, S M Wallet2, L M Shaddox3. 1. Department of Periodontology, the College of Dentistry, University of Florida, Gainesville, Fla., USA. 2. Department of Periodontology and Department of Oral Biology, the College of Dentistry, University of Florida, Gainesville, Fla., USA. 3. Department of Periodontology and Department of Oral Biology, the College of Dentistry, University of Florida, Gainesville, Fla., USA. lshaddox@dental.ufl.edu.
Abstract
PURPOSE: A previous study has shown that children with localized aggressive periodontitis (LAP) demonstrate a lipopolysaccharide (LPS) hyper-responsiveness in addition to elevated levels of systemic LPS when compared to periodontally healthy children. The purpose of this study was to evaluate whether periodontal therapy modulates systemic lipopolysaccharide levels and whether these levels may influence clinical outcomes. METHODS: Peripheral blood samples and clinical parameters (probing depth [PD], clinical attachment levels [CAL], percent sites greater than four mm, bleeding on probing [BoP], and visible plaque [P]) were collected from 29 LAP patients prior to and at three, six, and 12 months following scaling and root planning and systemic antibiotics. Serum LPS levels were quantified using a chromogenic assay. RESULTS: Twenty-five patients were compliant with the prescribed antibiotic treatment and demonstrated a significant reduction in LPS as well as overall PD, CAL, and plaque at all time points post-therapy. Additionally LPS reductions correlated with reductions in PD, CAL, and plaque. CONCLUSIONS: Localized aggressive periodontitis therapy with antibiotics plays an important role in reducing systemic lipopolysaccharide levels. Since LPS is a key mediator of the LAP hyperinflammatory response, its systemic reduction is especially important for the successful management of these children.
PURPOSE: A previous study has shown that children with localized aggressive periodontitis (LAP) demonstrate a lipopolysaccharide (LPS) hyper-responsiveness in addition to elevated levels of systemic LPS when compared to periodontally healthy children. The purpose of this study was to evaluate whether periodontal therapy modulates systemic lipopolysaccharide levels and whether these levels may influence clinical outcomes. METHODS: Peripheral blood samples and clinical parameters (probing depth [PD], clinical attachment levels [CAL], percent sites greater than four mm, bleeding on probing [BoP], and visible plaque [P]) were collected from 29 LAP patients prior to and at three, six, and 12 months following scaling and root planning and systemic antibiotics. Serum LPS levels were quantified using a chromogenic assay. RESULTS: Twenty-five patients were compliant with the prescribed antibiotic treatment and demonstrated a significant reduction in LPS as well as overall PD, CAL, and plaque at all time points post-therapy. Additionally LPS reductions correlated with reductions in PD, CAL, and plaque. CONCLUSIONS:Localized aggressive periodontitis therapy with antibiotics plays an important role in reducing systemic lipopolysaccharide levels. Since LPS is a key mediator of the LAP hyperinflammatory response, its systemic reduction is especially important for the successful management of these children.
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