31 Mar Complement inhibitor reverses periodontitis
MedicalResearch.com interview with:
Dr. George Hatisengallis
George Hatzisengallis, DDS, Ph.D.,
Thomas W. Evans Centennial Professor
University of Pennsylvania
Penn Dental Medicine – Microbiology
Philadelphia, PA 19104-6030
MedicalResearch.com: What is the background for this study? What are the main findings?
Dr. Hatsengallis: The present study is the result of eight years of collaboration with my colleague at Penn Medicine, Dr. John D. Lambris. In our previous mechanistic studies, we showed that complement, a system of innate immunity and inflammation, is critically involved in the pathogenesis of periodontitis, an oral inflammatory disease that leads to the destruction of the tissues (gums and bones) that support the teeth. . C3 is the central component of the complement system, where all activation pathways converge. Therefore, we reasoned that blocking C3 with a suitable inhibitor could prevent the development of periodontitis. The results of this study confirmed our hypothesis. Indeed, by administering the C3 Cp40 inhibitor to periodontal tissue only once a week, it reversed naturally occurring chronic periodontitis in a preclinical model. Specifically, Cp40 inhibited pre-existing gingival inflammation (as determined by both clinical and laboratory evaluation) and the formation of osteoclasts, the cells involved in bone resorption. If you suffer from something like periodontitis, then you may want to consider getting treatment for it. For more information on what this type of treatment could be, you can always do research bone surgery.
MedicalResearch.com: What should clinicians and patients take away from your report?
Dr. Hatisengallis: Although in this study Cp40 was successfully applied as a stand-alone therapy, it can be considered as an adjunctive therapy in the management of human chronic periodontitis. Cp40 has now been developed for human clinical applications (AMY-101; Amyndas Pharmaceuticals). Future clinical trials could investigate the potential of Cp40/AMY-101 to inhibit periodontal inflammation and bone loss compared to scaling and root planing, while in very severe cases of the disease, the drug could be combined with scaling and root planing and compared to periodontal surgery in an attempt to avoid the need for a surgical approach.
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Dr. Hatsengallis: There are different candidate approaches to treating periodontitis. Our current work shows that strategies aimed at controlling the host inflammatory response have great therapeutic potential. Future research should focus on translating important findings from preclinical models to the clinic. Dissecting the mechanisms of disease is very important, but translating this type of research into new and effective treatments is even more important.
MedicalResearch.com: Is there anything else you would like to add?
Dr. Hatsengallis: As I mentioned earlier, Cp40/AMY-101 has great potential as a novel anti-inflammatory treatment for periodontitis. Periodontitis has a serious public health impact and economic burden, therefore, we need innovative treatments complementary to existing treatments – such as mechanical removal of tooth-associated biofilm – that are not always sufficient to control periodontitis. This drug could not necessarily be applied in a therapeutic setting (as used in our study), but could also be given on a preventive basis to people at high risk for periodontitis, such as cigarette smokers and diabetic patients. Since Cp40/AMY-101 is intended for topical treatment of human periodontitis, potential safety considerations are unlikely to apply, although of course this should be verified. It should be noted, however, that no adverse effects were observed in preclinical studies.
MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.
Reference:
J Clin Periodontol. 2016 Mar;43(3):238-49. doi: 10.1111/jcpe.12507. Epub 2016 Mar 3.
Inhibition of pre-existing natural periodontitis in non-human primates by a topical C3 complement peptide inhibitor.
Maekawa T1,2Briones RA3Resuello RR4Tuplano JV4Hatsengalis E5Kajikawa T1Koutsogiannakis S6Garcia CA3Ricklin D6Brilliant JD6Hatjisengallis G1.
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Last updated on 31 March 2016 by Marie Benz MD FAAD
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