**[CURRICULUM VITAE]{.underline}**

**[SALOMON AMAR D.D.S., Ph.D.]{.underline}**

**[PERSONAL DATA]{.underline}**

Business Address: Boston University, Department of Periodontology and
Oral Biology,

700 Albany Street, W201E, Boston, MA 02118.

Business Telephone: (617) 638-4983

Fax: (617) 638-4924

**[EDUCATION]{.underline}**

Aquiba School, Strasbourg, France **B.S.:** Mathematics and Physics

Univ. Louis Pasteur, Strasbourg, France **D.D.S.:**

Univ. Louis Pasteur, Strasbourg, France **Certificate:** Histology
Cytology

Univ. Louis Pasteur, Strasbourg, France **M.S.:** Skeletal Tissues and
Apatites

Univ. Louis Pasteur, Strasbourg, France **Certificate:** Periodontology

Univ. Louis Pasteur, Strasbourg, France **Ph.D.:** Developmental Biology

Northwestern University, Chicago, USA **Postdoctoral Fellow:**
Biochemistry-Molecular Biology

Eastman Dental Center, Rochester, USA **Certificate:** Periodontology

Boston University, USA **D.M.D.**

**[EXPERIENCE IN HIGHER EDUCATION]{.underline}**

2001-Present: Boston University Professor of Periodontology

and Oral Biology

2004- present: FDA Member: Dental Product Panel,

> CDRH, FDA.

1997-Present: Boston University Research Associate Professor of
Biochemistry

1996-2004: FDA Consultant: Dental Product Panel,

> CDRH, FDA.

1995-2001: Boston University Associate Professor of Periodontology

and Oral Biology

1992- 1995: Eastman Dental Center Assistant Professor of Periodontology

1994- 1997: University of Rochester Adjunct Assistant Professor of
Pathology

1994- 1997: University of Rochester Adjunct Assistant Professor of
Hematology

1990-1992 Northwestern University Assistant Professor, Oral Biology

> Division and Department of Periodontics.

1990-1992 Northwestern University Coordinator of Continuing Education

1989-1990 Northwestern University Post doctoral Fellow, Department of

Oral Biology

1985-1989 Medical School Strasbourg, France Research Assistant

1985-1986 Dental School Strasbourg, France Instructor

**[HONORS AND AWARDS:]{.underline}**

· Research First Prize of Alpha Omega Fraternity International Division

· Young Investigator Award, IADR-AADR.

. Diplomate of the American Board of Periodontology

. Lady Davis Fellowship

**[EXPERIENCE OTHER THAN HIGHER EDUCATION]{.underline}**

Private Clinical Practice, Epinal, France, 1986 (Part-time).

Private Clinical Practice limited to Periodontics, Epinal France,
1987-1989.

Private Clinical Practice limited to Periodontics, Rochester, NY,
1994-1995.

Private Clinical Practice limited to Periodontics, Boston, MA,
1995-present.

**[Professional Licensure:]{.underline}**

Illinois Temporary Dental Teaching License, Illinois

Illinois Dental License: Active

Illinois Specialty License: Periodontology, Active

New York State Dental License: Active

Massachusetts Dental License: Active

Diplomate of the American Board of Periodontology

**[Hospital Affiliation:]{.underline}**

Attending Dentist: Franciscan Children Hospital

Attending Dentist: Boston Medical Center

**[EDITORIAL BOARDS]{.underline}**

**[Referee in Peer Reviewed Journals]{.underline}**

*Journal of Periodontology*

*Calcified Tissue International.*

*Archives of Oral Biology.*

*Journal of Dental Research.*

*Clinical Oral Implant Research*

*Position Papers, AAP.*

**[Research Interests and Activities]{.underline}**

**1. Research**

[1.1. Inflammation and Host response:]{.underline}

*[1.1.1. Cytokines:]{.underline}*

The host response to infection plays a major role in the resolution
inflammatory diseases and in particular periodontal diseases. However
the overproduction of proinflammatory mediators during this inflammatory
phase is deleterious to the host. Among the proinflammatory mediators
secreted during the inflammatory process the most prominent are IL-1 and
TNF-alpha. Using a TNF and/or IL-1 -deficient mice, we quantified the
relative contribution of each of these mediators in *Porphyromonas
gingivalis*-induced bone resorption. IL-1 was found to be the most
potent while a synergistic effect was observed with TNF-alpha. These
findings led us to propose the hypothesis that if IL-1 and TNF
expression can be suppressed but not eliminated, outcome variables of
the periodontitis could be largely improved. This hypothesis was tested
using an experimental periodontitis monkey model. Local application of
blockers to IL-1 and TNF in the gingiva can prevent bone loss and the
inflammatory reaction, naturally occurring in the animals receiving the
placebo control. These data highlight the important role of IL-1 and TNF
in mediating periodontal inflammation and bone loss and demonstrate for
the first time that bone loss and inflammation in periodontitis can be
controlled by local application of blockers to IL-1 and TNF.

Given that IL-1 and TNF could not account for all the occurring bone
loss, we investigated other mediators. Under the same condition, the
contribution of Prostaglandin's and IL-11 was determined. IL-11 or PG
were found to be the major mediators equally capable of mediating bone
resorption at low doses of *P.g.* LPS while at high doses of *P.g.* LPS
IL-1 and TNF were the major mediators. These data provide for the first
time the relative contribution of each mediator in *P.g.* LPS-induced
bone loss and propose that chronic bone loss (low LPS doses) can be
prevented by indomethacin or anti-IL-11 while acute bone loss (high LPS
doses) can be prevented by blockers to IL-1 and TNF. Should chronic bone
diseases such as Rhumathoid arthritis or Periodontitis progress
continuously a therapeutic approach involving anti-PG's or anti-IL-11
would be better suited whereas if these diseases progress by burst of
acute bone loss, a therapeutic approach involving blockers to IL-1 and
TNF would be more appropriate.

*[1.1.2. Transcriptional Regulation:]{.underline}*

The overexpression of cytokines (IL-1; TNF) in inflammatory processes is
extremely detrimental for the host. Our approach to reduce deleterious
effects associated with the overexpression of these cytokines consisted
in identifying molecular factors controlling cytokine gene expression in
inflammatory processes and particularly in gingivitis and in
periodontitis.

Tumour necrosis factor alpha (TNF-α) is a potent inflammatory mediator
and has been implicated in the pathophysiology of a variety of diseases
including Crohn's disease, inflammatory bowel disease or IBS, multiple
sclerosis and rheumatoid arthritis. We recently cloned a novel
transcription factor that we can show binds to the TNF-α promoter and
regulates transcription in lipopolysaccharide-treated macrophages by
repressing significantly TNF gene expression. Binding of this protein,
which we have named LPS-induced TNF-α factor (LITAF), to its recognition
element in the TNF-α promoter leads to the up-regulation of TNF-α
expression. Thus, pharmacological inhibition of LITAF appears to be an
attractive therapeutic strategy for the treatment of the diseases
mentioned above, as being upstream of TNF-α it would block the
production of this inflammatory cytokine. The inhibition of this factor
has resulted in a substantial reduction of TNF-alpha and could be used
in therapeutic approaches aimed at dampening down excess of TNF-alpha
(i.e. Rheumatoid Arthritis; Crohn's Disease; Periodontal Disease). Given
the role of NFkB in cytokine gene regulation, the discovery of this
novel transcription factor named LITAF controlling TNF gene expression
is viewed as a milestone in the transcriptional regulation of cytokine
genes. We have continued with this project by expressing high levels of
recombinant LITAF that we have purified for structural analysis. We are
currently carrying out structure-function experiments using X-ray
diffraction; a high-resolution structure will enable the design of
efficacious functional inhibitors of LITAF that could represent lead
compounds for use in drug development programs aimed at treating
inflammatory diseases.

*[1.1.3. Atherosclerosis:]{.underline}*

Finally, we have conclusively demonstrated for the first time in a mouse
model that *Porphyromonas gingivalis,* the principal microorganism in
periodontal diseases, can aggravate and even trigger the development of
atherosclerotic lesions. These results provide for the first time a
causal relation between Porphyromonas gingivalis and atherosclerosis and
pave the way for the complete elucidation of bacterial induced
atherosclerosis.

[1.2. Wound healing:]{.underline}

In our wound healing studies we identified several candidate genes
responsible for periodontal regeneration that are now evaluated in
various animal models. These findings establish for the first time the
existence of an adult stem cell in the periodontal compartment (with a
reduced apoptotic rate compared to other cells) and provide new
understanding of periodontal homeostasis and regeneration. Furthermore,
effort was made to identify critical factors involved in driving
periodontal wounds into the regeneration of periodontal structures after
periodontal diseases. Recently using cDNA array technologies we isolated
and cloned a new factor involved in tissue regeneration. The
overexpression of this factor hold promise in regenerating tissues lost
from disease processes.

[1.3. Human Clinical Approach:]{.underline}

At a clinical level, I have contributed to studies aimed a determining
whether chronic inflammatory diseases such as periodontitis can affect
the endothelial function and lead to atherosclerosis.

**2. Teaching**

\* Periodontics, Instructor, 1985-1988, Dental School, Strasbourg
(France), Undergraduate.

\* Periodontics, Instructor, 1990- 1992, Northwestern University Dental
School, Undergraduate.

\* Periodontics II, Lecturer, 1990-1992, Northwestern University Dental
School, Undergraduate.

\* Periodontics III, Lecturer, 1990-1992, Northwestern University Dental
School, Undergraduate.

\* Advanced Periodontics, Lecturer, 1990-1992, Northwestern University
Dental School, Undergraduate.

\* Pathology Review, Course Director, 1990-1992, Northwestern University
Dental School, Graduate Students.

\* Advanced Anatomy and Histology, Course Director, 1991-1992,
Northwestern University Dental School, Graduate Students.

Oral Anatomy and Histology, Lecturer, 1991-1992, Northwestern University
Dental School, Undergraduate Students

\* Current Literature Review Seminar, Course Director, 1991-1992,
Northwestern University Dental School, Graduate Students.

\* Periodontics I, II, III, Lecturer, 1990-1992, Northwestern University
Dental School,

Continuing Education.

\* Research Laboratory teaching, 1989-1992, Oral Biology Division,
Northwestern University, Graduate Students.

\* Research Laboratory teaching, 1992-1995, Department of
Periodontology, Eastman Dental Center, Graduate Students.

\* Biology of the Periodontium: 1993-present, Eastman Dental Center,
Graduate Students

\*Literature Review Seminar, Instructor, 1994-1995, Eastman Dental
Center, Graduate Students.

> \* Clinical Periodontics: Instructor in the Graduate Periodontal
> Clinic, 1994-1995, Eastman Dental Center, Graduate Students.

\* Oral Biology 1: Course Director, 1996-present, Boston University,
Dental Students

\* Literature Review Seminar, Course Director, 1995-present, Boston
University, Graduate Students.

\* Periodontology III: Course Director, 1996-present, Boston University,
Graduate Students.

**[PROFESSIONAL ACTIVITIES]{.underline}**

**[Memberships]{.underline}**

American Dental Association

International Association for Dental Research

American Association for Dental Research

American Association of Oral Biologists

American Academy of Periodontology

International Academy of Periodontology

The Wound Healing Society

International Endotoxin Society

**[Meetings and Conferences]{.underline}**

> Boston University Chairman and PI of the Organizing Committee for the
> NIH-Sponsor Teleconference: "Behavioral Aspect of Dentistry", October
> 16, 1996 Boston, MA.
>
> Scientific Advisory Committee to the NIH-sponsored Meeting: Molecular
> Mechanisms of Host Cell Interactions in Periodontal Diseases; March
> 14-17, 1997, St. Petersburg, Florida.
>
> Guest Editor with Drs. C. Genco and T. E. Van Dyke of Journal of
> Clinical Infectious Diseases Special Issue on "Molecular Mechanisms of
> Host Cell Interactions in Periodontal Diseases"
>
> IADR/AADR Symposium Organizer: Molecular and Cellular aspect of
> Periodontal Wound Healing: March 2000, Washington DC.
>
> Guest Editor for two special issues in wound healing: Journal of
> Parodontologie and Oral Implantologie. Vol 22, 4, November 2003 and
> Vol 23, 1 March 2004.

**[Committee Participation]{.underline}**

Committee on Academic Freedom: Faculty Council Boston University: Member

Committee on Financial Affairs: Faculty Council Boston university:
Member

AADR Constitution Committee: Member 1998-2001

AADR Award and Fellowship: Member 2001-2004

Curriculum Committee: Boston University School of Dental Medicine:
Member

**[Program Presentations]{.underline}**

Non-academic Settings: Lectures, Presentations, Symposia by Invitation:

\- 7th Conference of AIFRO, Paris, May 16, 1988: \"Clinical and
microbiological implications of Localized Juvenile Periodontitis
development\".

\- Second World Dental Conference, Jerusalem, June 30, 1988: \"An
Atypical case of periodontal disease: Orifacial plasmocytosis involving
periodontal soft tissues\".

\- Northwestern University, Oral Biology Seminar, May 25, 1989:
\"Epigenetic control mechanisms leading to ameloblast and odontoblast
differentiation\".

\- Albert Einstein College of Medicine Guest Lecturer, August 31 and
September 1, 1989: \"Dentin Matrix Induced Osteogenesis and its
potential use in oral and maxillofacial surgery\"; \"Bacterial
penetration in soft tissues in case of Localized Juvenile
Periodontitis\".

\- The University of Illinois at Chicago Guest Lecturer, May 4, 1990:
\"Immunolocalization of *Actinobacillus actinomycetemcomitans* in soft
tissues of Localized Juvenile Periodontitis\".

\- University of California at San Francisco Guest Lecturer, May 8,
1990: \"A rat dentin matrix protein triggers chondroblastic
differentiation\".

\- University of Strasbourg (France), Dental School Guest Lecturer,
January 15,1991: \"Dentin Matrix Induced Osteogenesis\".

\- AADR-IADR Meeting, Acapulco (Mexico), \"Induction of cartilage
nodules by dentin matrix protein in long term muscle fibroblast
culture\", April 1991.

\- The American Academy of Periodontology: 77th Annual Meeting,
Vancouver Canada, Continuing Education; \" Dentin-Matrix Induced
Osteogenesis\" October 3, 1991.

\- Midwest Connective Tissue Workshop, Chicago: \" *In vitro* production
of cartilage nodules from CIA-induced fibroblasts\", November 1-2, 1991.

\- University of Michigan Ann Arbor Guest Speaker: November 7, 1991.

\- University of Maryland at Baltimore, Guest Speaker: November 15,
1991.

\- Eastman Dental Center Rochester, Guest Speaker: November 25, 1991.

\- AADR-AAP Joint Symposium, Boston, March 10-14 1992: Contribution of
Cell and Molecular Biology to periodontal regeneration; Featured
Speaker.

\- Gore and Associates Guest Speaker, Flagstaff, April 6-7 1992:
Periodontal Regeneration.

\- French Society of Periodontology, XIIth Conference, Malta, June 4-7,
1992: A rat dentin polypeptide directs muscle fibroblasts into a
chondro-osteogenic pathway: Its potential use in periodontal
regeneration.

\- The American Academy of Periodontology: 79th Annual Meeting, Chicago,
October 1, 1993: Forum For Clinical Innovation; \"Immunodetection of
bone and cementum matrix macromolecules in human periodontal
regeneration\".

\- The International Conference on BMP's: In honor of Marshall Urist;
June 8-11, 1994, Baltimore, Maryland: \"Immunolocalization of
recombinant human bone morphogenetic protein-2 in regenerating
periodontal tissues\".

\- Gordon Research Conference on Periodontal Diseases: June 19-24, 1994;
New England College, Henniker, NH: \"TNF-alpha Receptor 1-deficient mice
in periodontal diseases\".

\- The University of Florida, Gainsville, Guest Speaker: August 15,
1994.

\- The American Academy of Implant Dentistry: October 9-11, 1994, New
Orleans, LA. \"Correlation between scanning electron microscopy and
conventional histology of human osseointegrated plasma-sprayed
implants\".

\- University of California at San Francisco Guest Lecturer, , 1990:
\"TNF-alpha Receptor 1-deficient mice in inflammatory diseases\".

\- University of Paris VII Garanciere: December 7, 1994; Paris, France:
\" Clinical Applications of Molecular and Cellular Biology Advances in
Periodontal Regeneration\".

\- University of California at San Francisco Guest Lecturer, November
14, 1994: \"The role of TNF-alpha in inflammatory diseases\".

\- University Louis Pasteur, Dental School; December 15, 1994;
Strasbourg, France: \" Clinical Applications of Molecular and Cellular
Biology Advances in Periodontal Regeneration\".

\- University of Rochester, Department of Hematology, Research Seminar;
February 28, 1995: \"TNF-alpha Receptor 1-deficient mice in inflammatory
diseases\".

\- New York University Dental School: Postgraduate Oral Biology guest
Speaker; March 15, 1995: : \" Clinical Implication of Molecular and
Cellular Biology Advances in Periodontal Regeneration\".

\- University of Minnesota, Department of Periodontology,
Dentist-Scientist Award Research Seminar; April 27, 1995: \"TNF-alpha
Receptor 1-deficient mice in inflammatory diseases\".

\- Boston University , Department of Oral Biology and Periodontology.
Invited Speaker; May 2, 1995: \"TNF-alpha Involvement in inflammatory
diseases\".

\- COEFI: Les Premieres Journees Franco-Isrëliennes de Paris, May 29 and
30, 1995; Featured Speaker: \"Growth Factors in Tissue Regeneration\";
\"Predictability in regenerating techniques\".

\- International Academy of Periodontology and French Society of
Periodontology Joint Conference; Monaco June 2-4 , 1995: Featured
Speaker: \"Perspectives in Periodontal Tissue Regeneration\".

\- American College of Cardiology: Annual Meeting: *Pophyromonas
gingivalis* accelerates atheroma lesions in an ApoE^(+/-)^ mouse model.
Orlando March 23^rd^, 2001

\- International Academy or Periodontology: Marrakech, June 3^rd^, 2001:
Featured Speaker: "Periodontal Medicine: a New Discipline."

**[GRANTS AND CONTRACTS:]{.underline}**

**[Active]{.underline}**

NIDCR/NIH R01

Role of LITAF in Inflammatory Processes

P.I.: Salomon Amar

NIDCR/NIH R01

Systemic Endothelial Consequences of Periodontal Disease

P.I.: Salomon Amar

NIDCR/NIH R01

> Functional Genomics in Periodontal Host-Parasite interactions

P.I.: Salomon Amar

NIDCR/NIH P01

Modulation of Molecular Pathogenesis in Systemic Diseases

P.I.: C. Genco

P.I. Biological Core: Salomon Amar

Co-Inv. Project 2 and 3. S. Amar

**[PATENTS]{.underline}**

Transcription factor regulating TNF-alpha

Patent: US 6566501-A 2

20-MAY-2003;

**[PUBLICATIONS:]{.underline}**

1\. Textbooks:

\- ROBINSON P. J and **AMAR S**.: Influence of Pregnancy in the Oral
Cavity. Clinical Obstetrics. Vol. 2: Chap. 15, 1-6, 1992.

2\. Refereed Journals

\- **AMAR S**., KARCHER-DJURICIC V., MEYER J.M. and RUCH J.V.: Lingual
(root-analog) and labial (crown- analog) mouse incisor dentin promotes
ameloblast differentiation. Arch. Anat. Microsc. Morphol. Exp. 75:
229-239, 1986.

\- **AMAR S**., KARCHER-DJURICIC V., MEYER J.M., and RUCH J.V.:
Root-analog and crown-analog mouse incisor dentin promotes ameloblast
differentiation: an evidence of absence of heterotypic cell contacts.
Proc. Finn. Dent. Soc. 83:225-236, 1987.

**- AMAR S** and RUCH J.V.: Mouse incisor lingual inner dental
epithelium does not contain potential ameloblasts. Med. Sci. Res.
15:949-950, 1987.

\- TZIAFAS D., **AMAR S**., STAUBLI A., MEYER J.M., and RUCH J.V.:
Effects of glycosaminoglycans on *in vitro* growing mouse dental cell.
Arch. Oral. Biol. 33:735-740, 1988.

\- TENENBAUM H., **AMAR S**., and KLEWANSKY P.: Orificial plasmocytosis:
a periodontal localization. Ann. Derm. Ven. 115:479-482, 1988.

\- **AMAR S**., TENENBAUM H., and CUISINIER F.J.G.: Characteristics of
early onset periodontitis: a report of two cases. J. Parodont. 8:53-59,
1989.

\- **AMAR S**., LUO W., SNEAD M.L., and RUCH J.V.: Amelogenin gene
expression in mouse incisor heterotopic recombinations. Differentiation.
41:56-61, 1989.

\- CUISINIER F.J.G., TENENBAUM H., and **AMAR S**.: Comparative study of
different biological membranes in SEM. J. Parodont. 8:271-278, 1989.

\- VEIS A., SIRES B., CLOHISY J., SABSAY B., and **AMAR S**.: Rat
incisor dentin contains a factor which alters the phenotypic expression
and stimulates chondrogenesis in fibroblast-like cells *in vitro*.
Biomaterials 11:35-37, 1990.

\- **AMAR S**., SIRES B. and VEIS A.: A rat incisor dentin matrix
protein can induce neonatal rat muscle fibroblasts, in culture, to
express phenotypic products of chondroblastic cells. J. Biol. Bucc.
25:55-60, 1991.

\- **AMAR S.**, SIRES B., SABSAY B., CLOHISY J. and VEIS A.: The
isolation and partial characterization of a rat incisor dentin matrix
polypeptide with *in vitro* chondrogenic activity. J. Biol. Chem.
266:8609-8818, 1991.

\- **AMAR S**., FABRE M., and RUCH J.V.: Effects of ascorbate-deficiency
on collagen secretion and resorption on cultured mouse incisor germs.
Connect. Tissue Res. 28:125-142, 1992.

\- YAMADA J., **AMAR S.**, and PETRUNGARO P.: Psoriasis-associated
periodontitis: a case report. J. Periodontol. 63:854-857, 1992.

\- TAKASHIBA S., SHAPIRA L., **AMAR S.**, and VAN DYKE T. E.: Cloning
and characterization of human TNF-α promoter region. Gene 131:307-308,
1993.

\- MASSARAT T., **AMAR S**., VEIS A. and OSETEK E. : Immunolocalization
of phenotypic cartilage macromolecules within fibroblastic cellular
nodules induced by chondrogenic inducing agents in vitro. Northwest Dent
Res 5:25-29, 1994.

\-**AMAR S**. and CHUNG K.M.: Cellular Biology Advances in Periodontal
Regeneration: Clinical Implications. Curr. Opin. Periodont. 2: 128-140,
1994.

\- SHAPIRA L, TAKASHIBA S, **AMAR** S and VAN DYKE T.E.: *Porphyromonas
gingivalis* lipopolysaccharide stimulation of human monocytes:
Dependence on serum and CD14 receptor. Oral Microbiol Immunol.
9:112-117, 1994.

\- SHAPIRA L., TAKASHIBA S., CHAMPAGNE C., **AMAR** S. and VAN DYKE
T.E.: Induction of TNF-α and IL-1β Secretion by Lipopolysaccharide in
Human Adherent Monocytes Requires the Generation of Two Distinct
Intracellular Signals: Involvement of Protein Kinase C and Tyrosine
Kinase. J. Immunol. 153:1818-1824, 1994.

\-**AMAR S** and CHUNG K.M.: Influence of Hormonal Variation on the
Periodontium in Women. Periodontology 2000 6: 79-87, 1994.

\- SHAPIRA L., CHAMPAGNE C., GORDON B., **AMAR** **S**. and VAN DYKE
T.E.: Lipopolysaccharide (LPS) Priming of Superoxide Release by Human
Neutrophils: Role of Membranal CD14 and Serum LPS Binding Protein.
Inflammation 19:289-295, 1995.

\-**AMAR S** and CHUNG K.M.: Molecular and Cellular Biology Research In
Periodontal Regeneration and its Clinical Implication. Ann. Acad. Med.
Singapore, 24:58-67, 1995.

\- TAKASHIBA S., VAN DYKE T.E., SHAPIRA L. and **AMAR** **S**.,:
Lipopolysaccharide-Inducible and Salicylate-Sensitive Nuclear Factor(s)
on Human Tumor Necrosis Factor-Alpha Promoter. Infect. Immun.
63:1529-1534, 1995.

\- **AMAR S**., PETRUNGARO P., AMAR A. and VAN DYKE T.E:
Immunolocalization of Bone Matrix Macromolecules in Human Periodontal
Regeneration Tissues. Arch. Oral. Biol., 40:653-661, 1995.

\- **AMAR S.**: Implications of Cellular and Molecular Biology Advances
in Periodontal Regeneration. Anat. Rec. 245:361-373, 1996.

\- LANDI L., PRETEL R., ROSS K. and **AMAR S.**: Factors responsible for
failures associated with guided tissue regeneration procedures. J.
Parodont. Impl. Oral. 15: 129-151, 1996

\- TAKASHIBA S., VAN DYKE T.E. and . **AMAR** **S**.: Inhibition of
Nuclear Factor Kappa B Subunit p65 mRNA Accumulation in LPS-Stimulated
Human Monocytic Cells Treated with Sodium Salicylate. Oral. Microbiol.
Immunol. 11: 420-424, 1996.

\- **AMAR S.**, VAN DYKE T.E., EUGSTER H.P., SCHULTZE N., KOEBEL P. and
BLÜTHMANN H.: Tumor Necrosis Factor (TNF)-Induced Cutaneous Necrosis is
mediated by TNF Receptor 1. J. Inflam. 47:180-189, 1997.

\- **AMAR S.**, CHUNG K.M., NAM S.H., KARATZAS S. , MYOKAI F. and VAN
DYKE T.E.: Markers of bone and cementum formation accumulate in tissues
regenerated in periodontal defects treated with expanded
polytetrafluoroethylene membranes. J. Perio. Research. 32:148-158, 1997.

\- LANDI L., **AMAR S.**, POLLINS S. and VAN DYKE T.E.: Host mechanisms
in the pathogenesis of periodontal diseases. Curr. Opin. Periodontol.,
4:3-10,1997.

\- 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.

\- SHAPIRA L, CHAMPAGNE C., VAN DYKE T. E. and **AMAR S**:
Strain-dependent activation of monocytes and inflammatory macrophages by
lipopolysaccharide of *Porphyromonas gingivalis*. Infect. Immun.
66:2736-42, 1998.

\- GENCO A.C., VAN DYKE T.E. and **AMAR S.**: Animal models for
*Porphyromonas gingivalis*-mediated periodontal diseases. Trends
Microbiol. 11:444-449, 1998.

\- 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.

\- MYOKAI F., TAKASHIBA S., LEBO R. and **AMAR S.**: A Novel LPS-Induced
Transcription Factor Regulating TNF-α Gene Expression: Molecular
Cloning, Sequencing, Characterization, and Chromosomal Assignment. Proc.
Natl. Acad. Sci. 96: 4518-4523, 1999.

\- KARATZAS S., ZAVRAS A., GREENSPAN D. and **AMAR S**. : Histologic
Observations of Periodontal Wound Healing After Treatment With
PerioGlas™ in Non-Human Primates. Int. J. Perio. Rest. Dent. 19:
489-499, 1999.

\- CHIANG C. Y., KYRITSIS G, GRAVES D.T., and **AMAR S**: IL-1 and TNF
Activity Partially Account for Calvarial Bone Resorption Induced by
Local Injection of LPS. Infect. Immun. 67: 4231-4236, 1999.

\- TOHME Z. N., AMAR S. AND VAN DYKE T. E.: Moesin Functions As An LPS
receptor On Human Monocyte. Infect. Immun. 67: 3215-3220, 1999.

\- TAKASHIBA S., VAN DYKE T.E., **AMAR S**, MURAYAMA Y., SOSKOLNE A. W.
and SHAPIRA L: Differentiation Of Monocytes Into Macrophages Primes The
Cells for Rapid and Enhanced TNF-α Production: Role of Nuclear Factor
kB. Infec. Immun. 67: 5573-5578, 1999.

\- SOOLARI A.S., CHAMPAGNE C., PUNZI J.S., **AMAR S.**, VAN DYKE T.E.:
Serum modulation of neutrophil response to *Porphyromonas gingivalis*
LPS in periodontal disease. J. Int. Acad. Periodontol. 4: 101-109:1999.

\- DELIMA A. J, OATES T., ASSUMA R., SCHWARTZ Z., COCHRAN D, **AMAR S**.
and GRAVES D.T: Soluble Antagonists to Interleukin-1 (IL-1) and Tumor
Necrosis Factor (TNF) Inhibits Loss of Tissue Attachment in Experimental
Periodontitis. J Clin Periodontol. 28:233-240, 2001.

-   **AMAR S.**, OYAISU K., LI L. and VAN DYKE T.E.: Moesin: A Potential
    LPS Receptor on Human Monocytes. J. Endotox. Res. 7:281-286, 2001.

**-** GRAVES D.T., NOOH N., GILLEN T., DAVEY M., PATEL S., COTTRELL D.
and **AMAR S**: Interleukin-1 Plays a Critical Role in Oral but Not
Dermal Wound Healing. J. Immunol. 167:5316-20, 2001.

\- 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.

\- HAN X.Z. BOLCATO A.L. and **AMAR S**.: identification of genes
differentially expressed in cultured human osteoblasts versus human
fibroblasts by DNA microarray analysis. Connec. Tissue Res. 2002;
43:63-75.

\- HAN X.Z. and **AMAR S**.: Identification of genes differentially
expressed in cultured human periodontal ligament fibroblasts versus
human gingival fibroblasts by DNA microarray analysis. J. Dent. Res.
6:399-405, 2002.

\- LI L., KHANSARI A., GRAVES D.T., and **AMAR S**.: Contribution of
Interleukin-11 and Prostaglandin(s) in Lipopolysaccharide-induced Bone
Resorption *in vivo.* Infect. Immun. 70:3915-3922, 2002.

\- **AMAR S.** and HAN X.: Regulation of tumour necrosis factor-α gene
Expression: Applied Genomics and Proteomics 1: 31-45, 2002.

\- 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.

-TANG X. FENTON M. J. and **AMAR S.**: Identification and functional
characterization of a novel binding site on TNF-α promoter. Proc. Natl.
Acad. Sci. U S A.; 100 :4096-4101. 2003.

\- HAN X. Z. and **AMAR S**.: IGF-1 Signaling Enhances Cell Survival in
Periodontal ligament Fibroblasts versus Gingival Fibroblasts. J. Dent.
Res. 82:454-459, 2003.

\- SANTANA R. B., XU L., CHASE B. H., **AMAR S.**, GRAVES D. T., and
TRACKMAN P. C.: A Role for Advanced Glycation End Products in Diminished
Bone Healing in Type I Diabetes. Diabetes. 52:1502-10. 2003.

**- 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. Arterioscler. Thromb. Vasc. Biol.
23:1245-1249, 2003.

\- HAN X. Z. and **AMAR S**.: IGF-1 signaling preferentially enhances
cell survival in cultured periodontal ligament fibroblasts versus
gingival fibroblasts. J. Perio. 74:1176-1182, 2003.

\- **AMAR S.** AND HAN X.: The impact of periodontal infection on
systemic diseases. Med Sci Monit. 9: 291-299; 2003.

\- HAN X. Z. and **AMAR S.**: Secreted Frizzled-Related Protein 1
(sFRP1) Protects Fibroblast From Ceramide-Induced Apoptosis. J. Biol.
Chem. 279 : 2832-2840, 2004

\- BOLCATO-BELLEMIN A. L., MATTEI M.G., LEBO R. and **AMAR S**.:
Molecular cloning and characterization of the mouse LITAF cDNA,
implications in the regulation of the tumor necrosis factor-α (TNF-α)
gene expression. J. Endotox. Res. 10:15-23, 2004.

\- IONTCHEVA I., **AMAR S.**, ZAWAWI K.H., KANTARCI A., and VAN DYKE
T.E.: A Role for Moesin in Lipopolysaccharide Stimulated Signal
Transduction. Infect. Immun. 72: 2312-2320, 2004.