NYMC > Faculty > Faculty Profiles > By School > School of Medicine(SOM)/Graduate School BMS(GSBMS) > Pharmacology > Amar, Salomon

Salomon Amar, D.D.S., Ph.D.

Salomon Amar Ph.D.Senior Vice President for Research Affairs, Touro College and University System
Vice President for Research, New York Medical College 
Professor of Pharmacology and Microbiology and Immunology, New York Medical College
Professor of Dental Medicine, Touro College of Dental Medicine at NYMC


Sunshine Cottage Administration Building, Suite 209
New York Medical College
40 Sunshine Cottage Road
Valhalla, NY 10595

Email: Salomon_Amar@nymc.edu
(914) 594-3036



Aquiba School, Strasbourg, France

B.S., Mathematics and Physics


Louis Pasteur, Strasbourg, France



Louis Pasteur, Strasbourg, France

Certificate, Histology Cytology


Louis Pasteur, Strasbourg, France

M.S., Skeletal Tissues and Apatites


Louis Pasteur, Strasbourg, France

Certificate, Periodontology


Louis Pasteur, Strasbourg, France

Ph.D., Developmental Biology


Northwestern University, Chicago, Illinois, USA

Postdoctoral Fellow,Biochemistry-Molecular Biology


Eastman Dental Center, Rochester, New York, USA  

Certificate, Periodontology


Boston University, Boston, Massachusetts, USA


Industry Interests:

  • Research
  • Education/Learning
  • Health Care

Area of Expertise:

  • Inflammation, Molecular Immunology, Biotechnology, Pharmacology, Periodontal Disease, Clinical Trials

Hospital Affiliation:

  • Tel Aviv Ichilov Medical Center, Tel Aviv Israel


Wall Street Journal Seeks Opinion of Dr. Salomon Amar

  • Discusses research on the link between oral and overall health in the Wall Street Journal article Poor Oral Health Is Linked To Deadly Pancreatic Cancer January 23, 2007. Amar's study, to be completed in 2009, suggests treating gum disease may decrease inflammation throughout the body and improve heart health. "All kinds of answers are going to come out of this," Amar says in the article. "I think historically the mouth was never considered an important part of the body."

Dr. Salomon Amar Referenced in Los Angeles Times

  • An April 16, 2007 Los Angeles Times article on the relationship between gum disease and overall health seeks the opinion of Dr. Salomon Amar, associate dean for research, on the treatment and symptoms of gum disease. "For years the mouth was never considered a part of the body," says Amar. "Gum disease was not considered something that could have any impact." Amar is currently analyzing the effect of aggressive gum disease treatment on heart problems in people with gum disease and heart disease as part of the study Systemic Endothelial Consequences of Periodontal Disease.

Weakened Antibacterial Immunity Linked to Obesity

The Body’s Ecosystem:  

Research Interests

My research team has a long-standing interest in periodontal tissue homeostasis and mechanisms of inflammatory bone loss. Both basic immunological and translational research (including clinical trials) have been used to dissect molecular immune mechanisms and test them in animal models and ultimately in clinical trials. Our work has led to seminal observations in periodontal systemic diseases especially cardiovascular diseases or obesity leading to innovative approaches in public health aspects of these diseases. Our publication record includes several papers with an impact extending beyond the periodontal research field (e.g., in PNAS; J. Immunol. Circulation) and our work is highly cited (Google Scholar citation counter: Citations= 7153, H-Index=45; i10-index=87). Concepts first identified in the context of periodontal inflammation and immune tolerance have found application in other fields; for instance, our observation that high fat diet modulate the immune system in periodontal disease was extended to obesity to explain the diet induced immune dysregulation mediated by TLR2. I have successfully directed several NIH-supported projects that have implicated important components of innate immunity (Toll-like receptors and NOD) in novel mechanisms of inflammation and periodontal disease pathogenesis.  We gained over the years, expertise in innate immunity, inflammation and obesity and contributed to the understanding of the role of infection in the modulation of Obesity, Cardiovascular disease, and Diabetes with a seminal paper in 2007 demonstrating that obesity interferes with the ability of the immune system to appropriately respond to infection. 

Contributions to Science

Identification, Cloning and Characterization of a novel transcription factor affecting TNF named LITAF: Our work identified a novel LPS-induced TNF Alfa factor (LITAF) working with NFkB to drive the transcription of inflammatory cytokines. The generation of whole body and macrophage specific LITAF-deficient animals facilitated the characterization of LITAF as a factor overexpressed in inflammatory condition. Animal deficient of LITAF were found immune to LPS shock and inflammatory conditions such as infective arthritis and possibly Crohn’s disease. This led us to develop novel optimized anti-LITAF compounds currently being tested in models of acute and chronic inflammation (PD, RA and CD). LITAF was found more recently involved in tumor growth a mechanisms possibly implicating dysregulated inflammation in cancer development.

Host response in experimental periodontitis and wound healing: This work was instrumental in demonstrating the role of pro-inflammatory cytokines in primate experimental periodontitis and periodontal wound healing. Soluble decoy receptors to TNF and IL-1 were found to significantly reduce inflammation and bone loss in experimental periodontitis and promote a more optimal healing after periodontal surgery. This work paved the way for the widespread usage of these molecules in the treatment of RA and more recently being tested in the treatment of atherosclerosis. This concept was extended recently extended using RANKL soluble receptors in the treatment of experimental periodontitis.

Oral Microorganisms involved in atherothrombosis: This seminal work was the first demonstration in an animal model of the involvement of P. gingivalis in the aggravation of atherothombosis lesions. The signal transduction pathway activated by P. gingivalis in macrophages was mapped to include TLR2 and more recently the inflammasome element NOD2. The role of IL-1 in the inflammatory reaction to HFD and P. gingivalis was also demonstrated and Through collaborative research with laboratories with complementary expertise the findings of this work has served in the development of clinical trials testing the effect of IL-1 inhibition in atherothrombosis and testing the effect of periodontal microbial eradication in the improvement of cardiovascular parameters.  

Macrophage involvement in inflammatory and regenerative processes: This work first demonstrated the deleterious role of dysregulated macrophage function in inflammatory diseases. The signal transduction pathway activated in macrophages was identified along with a profiling of cytokines differentially expressed by macrophages upon various bacterial products stimuli. This worked was successfully extended in other systems especially lung macrophages and with macrophage polarization in testing improve outcomes in regenerative medicine (i.e. PD and Orthopedics). 

Obesity and High Fat Diet as modulator of host-parasite interaction: This work was crucial in demonstrating the deleterious role of chronic exposure to HFD in the modulation of host-P. gingivalis interaction. The immune system was found significantly affected by the chronic exposure to free fatty acids that promiscuously signals through TLR2 thereby tolerazing the receptor to future bacterial product signaling. on While Moderate exercise and diet control restore the identified defects (iNOS , PPARγ and Akt) TLR2 was not able to be restored. Therapeutic interventions involving TLRs are unrealistic given their pleotropism. We have therefore engaged in a new program to define achievable and optimal pharmacotherapeutic interventions to be tested in the restoration of the immune function in periodontal infection.  

Selected Bibliography:

  1. Assuma R., Oates T., Cochran D., Amar S. and Graves D.T.: IL-1 and TNF antagonists inhibit the inflammatory response and bone loss in experimental periodontitis. J. Immunol. 160:403-409, 1998.PMID: 9551997
  2. Graves D.T., Delima A., Assuma R. , Amar S, Oates T., and Cochran D. : IL-1 and TNF  antagonists inhibit the progression of inflammatory cell infiltration toward alveolar bone in experimental periodontitis. J Periodont. 69:1419-1424, 1998. PMID: 9926773
  3. Myokai F., Takashiba S., Lebo R. and Amar S.: A novel LPS-induced transcription factor regulating TNF-a gene expression: Molecular cloning, sequencing, characterization, and chromosomal assignment. Proc. Natl. Acad. Sci. 96: 4518-4523, 1999. PMCID: PMC16364
  4. Li L., Messas E., Batista E. L. Levine R.A. and Amar S.: Porphyromonas gingivalis infection accelerates the progression of atherosclerosis in an Apoe (+/-) murine model. Circulation 105: 861-867, 2002. PMID: 11854128
  5. Delima A.J., Karatzas S., Amar S. and Graves D.T.: Inflammation and tissue loss caused by periodontal pathogens is reduced by interleukin-1 antagonists.: J. Infect. Dis. 186:511-516, 2002. PMID: 12195378
  6. Amar S., Gokce N., Morgan S., Loukideli M., Van Dyke T.E. and Vita J.A.: Periodontal disease is associated with brachial artery endothelial dysfunction and systemic inflammation. Thromb. Vasc. Biol. 23:1245-1249, 2003. PMID: 12763762
  7. Chi , Messas E., Levine RA., Graves D.T., and Amar S.: lnterleukin-1 receptor signaling mediates atherosclerosis associated with bacterial exposure and/or high-fat diet in a murine ApoE heterozygote model: pharmacotherapeutic implications. Circulation 110:1678-1685, 2004. PMID: 15353494
  8. Zhang X., Kohli M., Zhou Q., Graves D.T, and Amar S.: Short- and long-term effects of IL-1 and TNF antagonists on periodontal wound healing. J. Immunol. 173:3514-3523, 2004 PMID: 15322216
  9. Zhou Q., Desta T., Graves D.T. and Amar S.: Cytokine profiling of macrophages exposed to Porphyromonas gingivalis, its LPS or its FimA. Infect Immun. 73:935-43, 2005. PMCID: PMC547047
  10. Tang X., Metzger, D., Leeman S.E. and Amar S.: Macrophage-specific LITAF-deficient mice express reduced LPS-induced cytokine profiling: Further evidence for LITAF-dependent LPS signaling pathways. Proc. Natl. Acad. Sci. U S A. 103:13777-13782, 2006. PMCID: PMC1560089
  11. Stucchi A., Reed K., O'Brien M., Cerda S., Andrews C., Gower A., Bushell K., Amar S., Leeman S. and Becker J.: A New Transcription Factor that regulates TNF-a gene expression, LITAF (Lipopolysaccharide Induced TNF-a. Factor) is Increased in Intestinal Tissues from Patients with Crohn's Disease and Ulcerative Colitis. lnflamm Bowel Dis. 12:581-587, 2006. PMCID: PMC3184169
  12. Amar S., Zhou Q., Shaik-Dasthagirisaheb Y. and Leeman S.: Diet-induced obesity (DIO) in mice causes changes in immune responses and bone loss manifested by bacterial challenge. Proc. Natl. Acad. Sci. USA.104: 20466–20471; 2007. Featured in “The cover of PNAS”. PMCID: PMC2154454
  13. Zhou Q. and Amar S.: Identification of Signaling Pathways of Human Macrophages in Response to P. gingivalis infection and to its purified components stimulation. J. Immunol. 179: 7777-7790; 2007. PMID: 18025224
  14. Amar S., Wu S.C. and Madan M.: Is gingivalis cell invasion required for atherogenesis? Pharmacotherapeutic implications. J. Immunol. 182: 1584-1592; 2009. PMID: 19155507
  15. Zhou Q., Leeman S.E. and Amar S.: Signaling mechanisms involved in altered function of macrophages from diet induced obese mice. Proc. Natl. Acad. Sci. USA. 106:10740-10745; 2009. PMCID: PMC2697902
  16. Wilson A.A., Murphy G.J., Hamakawa H., Kwok L.W., Srinivasan S., Hovav A.H., Mulligan R.C., Amar S., Suki B. , and Kotton D.N.: Amelioration of emphysema in mice via lentiviral transduction of long-lived pulmonary alveolar macrophages. J. Clin. Invest. 120:379-89; 2010. PMCID: PMC2798672
  17. Zhou and Amar S.: Obesity and Immune Functions. pp 111-131 In "Dietary Components and Immune Function" Ed: Ronald Ross Watson, Sherma Zibadi, Victor R. Preedy; Humana Press. 2010.
  18. Yuan H., Gupte, R., Zelkha S. and Amar S.: RANKL antagonists inhibit tissue inflammation and bone loss in experimental periodontitis: J. Clin. Periodontol. 38: 1029–1036 2011. PMID: 22092474
  19. Zhou Q., Leeman S.E. and Amar S.: Signaling mechanisms in the restoration of impaired immune function due to diet induced obesity. Proc. Natl. Acad. Sci. USA. 108:2867-2872. 2011. PMCID: PMC3041076
  20. Yuan H., Gupte, R., Zelkha S. and Amar S.: RANKL antagonists inhibit tissue inflammation and bone loss in experimental periodontitis: J. Clin. Periodontol. 38: 1029–1036 2011. PMID: 22092474
  21. Merrill J.C., You J., Constable C., Leeman S.L. and Amar S.: Whole-body deletion of LPS-induced TNF-α factor (LITAF) markedly improves experimental endotoxic shock and inflammatory arthritis. Proc. Natl. Acad. Sci. USA. 108:21247-52. 2011. PMCID: PMC3248491
  22. Zhou J., Yang Z., Tsuji T., Gong J., Xie J., Chen C., Li W., Amar S. and Luo Z.: LITAF and TNFSF15, two downstream targets of AMPK, exert inhibitory effects on tumor growth. Oncogene; doi:10.1038/onc.2010.575. 2011. PMCID: PMC3431012
  23. Brown B.N., Ratner B.D., Goodman S.B., Amar S. and Badylak S.F.: Macrophage polarization: An opportunity for improved outcomes in biomaterials and regenerative medicine. Biomaterials. 33:3792-802. 2012. PMCID: PMC3727238
  24. Liu B,. Faller L.L., Klitgord N, Mazumdar V., Ghodsi M., Sommer D.D., Gibbons T.R., Treangen T.J., Chang Y.C., Li S., Stine O.C., Hasturk H., Kasif S., Segrè D., Pop M., Amar S.: Deep sequencing of the oral microbiome reveals signatures of periodontal disease. PLoS ONE 7: e37919. doi:10.1371/journal.pone.0037919. 2012. PMID: 22675498.
  25. Yuan H, Zelka S, Burkatovskaya M, Gupte R, Leeman SE and Amar S.: Pivotal role of NOD2 in inflammatory processes affecting atherosclerosis and periodontal bone loss. Proc. Natl. Acad. Sci. USA. 110(52): E5059-68. 2013. PMCID: PMC3876260
  26. Richard G., Trivedi N., Belta C. and Amar S.: Partial Restoration of Macrophage Alteration from Diet-induced obesity in Response to Porphyromonas gingivalis Infection. PLoS One. 8:e70320. doi: 10.1371/journal.pone.0070320. 2013. PMCID: PMC3726386
  27. Amar S. and Leeman : Periodontal Innate Immune Mechanisms Relevant to Obesity. Mol. Oral Microbiol. 28:331-41. 2013. PMID: 23911141

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