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O. Toti and . Huck, Implication des microvésicules d'origine endothéliale induites par l'infection par Porphyromonas gingivalis dans l'inflammation endothéliale. Congrès de la SFPIO -Société Française de Parodontologie et d'Implantologie Orale, pp.13-15, 2019.

I. M. Bugueno, L. Keller, F. Batool, S. Kuchler-bopp, N. Benkirane-jessel et al., A new 3D in vitro model of gingival tissue to assess host-pathogen interactions

. Europerio9, , pp.20-23, 2018.

I. M. Bugueno, F. Batool, N. Benkirane-jessel, and O. Huck,

A. Londres, I. M. Bugueno, L. Keller, F. Batool, S. Kuchler-bopp et al., Porphyromonas gingivalis modulates Ox-LDL pre-treated endothelial cell death". 26 es Journées Européennes de la Societé Française de Cardiologie (JESFC). 14-16 janvier, 103th Annual meeting American Academy of Periodontology. 5-12 septembre 2017, pp.25-28, 2016.

, Congrès de la Société Française de Parodontologie et d'Implantologie Orale (SFPIO). 6-9 Juin, 2016.

I. M. Bugueno, J. L. Davideau, H. Tenenbaum, N. Jessel, I. M. Huck-o-;-v-bugueno et al., « Modulation de la voie liée à l'apoptosome Apaf-1 par Porphyromonas gingivali », 2016.

, Annexe nº1

L. Korah, N. Amri, I. M. Bugueno, E. Hotton, H. Tenenbaum et al., Experimental periodontitis in Msx2 mutant mice induces alveolar bone necrosis, Journal of Periodontology, 2019.

O. Lapérine, A. Cloitre, J. Caillon, O. Huck, I. M. Bugueno et al.,

J. L. Davideau, V. Geoffroy, J. Guicheux, S. Beck-cornier, and P. Lesclous, Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis, PLoS ONE, vol.11, issue.12, p.168080
URL : https://hal.archives-ouvertes.fr/inserm-01562952

. Vi, Annexe nº4

A. Cloitre, B. Halgand, S. Sourice, J. Caillon, O. Huck et al.,

V. Geoffroy and P. Lesclous, IL-36? is a pivotal inflammatory player in periodontitis-associated bone loss, Scientific Reports, vol.9, 2019.
URL : https://hal.archives-ouvertes.fr/hal-02418941

, L'infection chronique a été décrite comme un mécanisme potentiel impliqué dans l'aggravation de l'athérothrombose. A l'heure actuelle, le rôle joué par Porphyromonas gingivalis (P.gingivalis) est considéré comme majeur dans les phénomènes associés, tels que sa capacité à perturber la barrière épithéliale ainsi que l'endothélium vasculaire, l'induction d'une réponse inflammatoire soutenue contribuant à la destruction tissulaire, Les mécanismes impliqués dans l'initiation et le développement des parodontites, ainsi que la dissémination des parodontopathogènes via la circulation systémique et ses effets au niveau vasculaire

, Nous avons mis en évidence que P.gingivalis est capable d'activer l'inflammation et la réponse du système immunitaire entraînant la destruction du parodonte en modulant différentiellement des processus biologiques primordiaux tels que l'apoptose (modulation de l'apoptosome Apaf-1 et son inhibiteur XIAP), le cycle cellulaire (P53, P21, CDK4), l'inflammation (modulation des TLR-2, TLR-4 et ses adaptateurs MAL et TRAM et des protéines inflammatoires telles que TNF-?), lui permettant d'échapper au système immunitaire, de contribuer à la destruction parodontale et sa dissémination systémique et d'exercer des effets sur l'endothélium, de microtissus (MT), ainsi que dans des cellules endothéliales (EC). Finalement, nous avons évalué son rôle dans la réponse inflammatoire liée à la signalisation via les TLR-2 et TLR-4 et cinq protéines adaptatrices contenant le domaine du récepteur Toll/interleukine-1 (TIR)