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ISSN: 2376-032X

JBR Journal of Interdisciplinary Medicine and Dental Science
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Research Article

Two Case Reports on Refractory Periodontitis: Systemic Implications and a Potential New Therapeutic Strategy

Michael B Goldberg1*, Lorne M Golub2, Hsi-ming Lee3 and Howard C Tenenbaum1,2,3,4

1Department of Periodontics, Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada.

2Department of Oral Biology and Pathology, School of Dental Medicine, Stony Brook University, State University of New York (S.U.N.Y.), Stony Brook, NY, USA.

3Maurice and Gabriella Goldschleger School of Dental Medicine, Tel Aviv University, Tel Aviv, Israel.

4Department of Laboratory Medicine and Pathology, Faculty of Medicine, University of Toronto, Toronto, Ont., Canada.

*Corresponding Author:
Dr. Michael B Goldberg
University of Toronto Faculty of Dentistry
Room 349A, 124 Edward Street
Toronto, Ontario, Canada
Tel: (416) 979- 4928-4502
E-mail: [email protected]

Received Date: October 08, 2013; Accepted Date: November 14, 2013; Published Date: November 18, 2013

Citation: Goldberg MB, Golub LM, Hsi-ming L, Tenenbaum HC (2013) Two Case Reports on Refractory Periodontitis: Systemic Implications and a Potential New Therapeutic Strategy. J Interdiscipl Med Dent Sci 1:101. doi: 10.4172/2376-032X.1000101

Copyright: © 2013 Goldberg MB, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Two cases of Refractory Periodontitis (RP) were studied over an 8-month time period. Both received a novel regimen of “combination” Host-Modulation Therapy (HMT) (subantimicrobial-dose doxycycline plus low-dose flurbiprofen adjunctive to traditional non-surgical periodontal therapy. Prior to beginning “combination” HMT, Case #1 was characterized by progressive periodontal deterioration; dramatically elevated levels of inflammatory mediators (IL-1β) and tissue-destructive enzymes (collagenase activity) in periodontal pockets (GCF); and evidence of systemic inflammation (high serum levels of hs-C-reactive protein), and mildly elevated LDL and total levels of cholesterol, indicating an increased risk for cardiovascular disease (CVD). In contrast, Case #2 exhibited undetectable levels of local biomarkers of inflammation and tissue destruction in their periodontal pockets (GCF), and much lower levels of both serum hs-CRP and cholesterol indicating lower risk for CVD. Both cases, however, demonstrated the characteristics of RP including progressive loss of bone and attachment despite repeated periodontal therapy. During the 12-month regimen of, Case #1, who exhibited much higher levels of local and systemic biomarkers, responded much more dramatically to the “combination” therapy than Case #2. We suggest that this novel “combination” therapy may be particularly useful in a sub-set of RP patients who exhibit evidence of systemic inflammation in their serum (or plasma) samples indicating increased risk for CVD; in these patients “combination” therapy may dramatically reduce both periodontal disease activity and CVD risk. In order to test this hypothesis, which proposes the development of more individualized therapeutic strategies, it clearly must be validated in future randomized clinical trials.

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