Associate Member of the Staff
Department of Periodontology
email:
University of Istanbul, D.D.S., MSc., 1991, Dentistry
University of Istanbul, Ph.D., 1998, Periodontology
Boston University Goldman School of Dental Medicine, CAGS, 2004, Periodontology
A Diplomate of the American Board of Periodontology and the current President of the Periodontal Research Group of the International Association for Dental Research, Dr. Kantarci focuses on improving periodontal and systemic health through the integration of clinical and laboratory research. His main interest is the characterization of inflammatory pathways of periodontal disease and utilization of this knowledge for development of novel therapeutic strategies to restore the homeostasis of periodontium.
Research in the Kantarci lab focuses on investigation of the molecular mechanisms and resolution pathways of oral inflammation in patients with periodontitis, diabetes, and HIV infection. Inflammation research is the center of Dr. Kantarci’s studies and he has extensive experience in using experimental animal models for these diseases. Specifically, Dr. Kantarci focuses on the signal transduction mediated by lipids and various proteins in neutrophils and monocytes and their interaction with other cells of the oral cavity. He has developed several in vitro assays and applications of high-throughput analysis (e.g. xMAP Multiplexing) to translational clinical research. To this end, he is testing the inflammatory mediator content in various milieu such as gingival crevicular fluid, saliva and serum. Recently, he has been focused on various the impact of hypoxia on cell functions. Inflammation-mediated hypoxia is an important mechanism in various pathological processes such as periodontitis (and at large in inflammatory diseases).
Dr. Kantarci has been working on the clinical characterization and the mechanism of fibrotic changes in gingival tissues as a side effect of various medications. This is an important phenomenon caused by cyclosporin-A (an immunosuppressant widely used in solid organ transplants), phenytoin (an anti-epileptic medication), and various calcium channel blockers used to control hypertension. Common to all these medications, significant and debilitating fibrotic enlargements of the gingival tissues pose a major problem to patients and affect the quality of life. In collaboration with Dr. Philip Trackman, Dr. Kantarci has identified multiple mechanisms for the fibrotic enlargements of the gingival tissues. The ultimate goal of these studies is to develop therapeutic strategies to control and prevent such pathologies, which are currently treated by surgical techniques and in most cases recur.
Dr. Kantarci has been leading a series of studies on the osteoblast and osteoclast activity in alveolar bone in response to orthodontic tooth movement with or without various methods to enhance the speed of the movement and the bone turnover. This line of research focuses on techniques to improve the outcomes for orthodontic patients and speed recovery time. Recent work from Dr. Kantarci’s laboratory has shown that tooth movement was significantly accelerated—a 3 to 4-fold increase—over traditional orthodontic treatment. The experimental model used in these studies clearly shows that surgical or non-surgical techniques increase the magnitude and rate of the tooth movement compared to the conventional technique in vivo. The benefits of this type of tooth movement will be especially important for adults because they often require surgical treatment.
Liang Y, Hasturk H, Elliot J, Noronha A, Liu X, Wetzler LM, Massari P, Kantarci A, Winter HS, Farraye FA, Ganley-Leal LM. 2011. Toll-like receptor 2 induces mucosal homing receptor expression and IgA production by human B cells. Clin. Immunol. 138(1):33-40.:15.
Ayilavarapu S, Kantarci A, Fredman G, Turkoglu O, Omori K, Liu H-S, Iwata T, Yagi M, Hasturk H, Van Dyke TE. 2010. Diabetes-induced oxidative stress is mediated by iPLA2 in neutrophils. J. Immunol. 184:1507-1515.
Shaik-Dasthagirisaheb Yazdani B, Kantarci A, Gibson FC. 2010. Immune response of macrophages from young and aged mice to the oral pathogenic bacterium Porphyromonas gingivalis Immun. Ageing 29
El-Sharkawy H, Aboelsaad N, Eliwa M, Darweesh M, Alshahat M, Kantarci A, Hasturk H, Van Dyke TE. 2010. Adjunctive treatment of chronic periodontitis with daily dietary supplementation with omega-3 fatty acids and low-dose aspirin. J. Periodontol. 81:1635-1643.
Jagannathan M, McDonnell M, Liang Y, Hasturk H, Hetzel J, Rubin D, Kantarci A, Van Dyke TE, Ganley-Leal LM, Nikolajczyk BS. 2010. Toll-like receptors regulate B cell cytokine production in patients with diabetes. Diabetologia 53:1461-1471.
Zawawi KH, Kantarci A, Schulze-Späte U, Fujita T, Batista Jr, EL, Amar S, Van Dyke TE. 2010. Moesin-induced signaling in response to lipopolysaccharide in macrophages. J. Periodontal Res.45:589-601.
Yagi M, Kantarci A,Iwata T, Omori K, Ayilavarapu S, Ito K, Hasturk H, Van Dyke TE. 2009. PDK1 regulates chemotaxis in human neutrophils. J. Dent. Res. 88:1119-1124.
Iwata T, Kantarci A,Yagi M, Jackson T, Hasturk H, Kurihara H, Van Dyke TE. 2009.Ceruloplasmin induces PMN priming in LAP. J. Periodontol.80:1300-1306.
Omori K, Ohira T, Uchida Y, Ayilavarapu S, Batista Jr EL, Yagi M, Iwata T, Liu H, Hasturk H, Kantarci A, Van Dyke TE. 2008. Priming of neutrophil oxidative burst in diabetes requires pre-assembly of the NADPH oxidase. J. Leukoc. Biol. 84:292-301.
Nassar H, Kantarci A,Van Dyke TE. 2007. Diabetic periodontitis: A model for activated innate immunity and impaired resolution of inflammation. Periodontol 2000 43:233-244.
Ding Y, Kantarci A,Badwey JA, Hasturk H, Malabanan A, Van Dyke TE. 2007. Phosphorylation of pleckstrin increases proinflammatory cytokine secretion by mononuclear phagocytes in diabetes mellitus. J. Immunol.179:647-654.
Hasturk H, Kantarci A,Goguet-Surmenian E, Blackwood A, Andry C,Serhan CN, Van Dyke TE. 2007. Resolvin E1 regulates inflammation at the cellular and tissue level and restores tissue homeostasis in vivo. J. Immunol. 179:7021-7029.
Kantarci A, Augustijn P, Firatli E, Sheff MC, Hasturk H,Graves DT, Trackman PC. 2007. Apoptosis in gingival overgrowth tissues. J. Dent. Res. 86(9):888-892.A
