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Departments / Periodontics
 
Dana T. Graves, DDS
gravesdt@umdnj.edu
Phone: 973-972-1350
Fax: 973-972-3884
Name Dana Graves
Academic rank Professor
Undergraduate education (degree & name of institution)

BA in Chemistry, SUNY at Binghamton

Undergraduate dental school education (degree & name of institution)

DDS,  Columbia University

Postgraduate dental education (degree/certificate, name of institution)

CAGS, Periodontlogy, Harvard University

Advanced degrees other than D.M.D. or D.D.S. (degree & name of institution)

DMSc, Harvard University

Research interests

Host-bacteria interactions and the impact of diabetes on inflammation, cell death, bone and periodontal disease

Grants received

NIH: “Diabetes-enhanced Experimental Periodontitis”
NIH: “Recognition of Commensal and Pathogenic Bacteria By Oral Epithelium”
NIH: “Molecular Mechanisms of Skeletal Repair”

Clinical interests Pathogenesis and treatment of periodontal disease
Journal articles or abstracts published within the past five years

Lu, H, Kraut, D, Gerstenfeld, LC, and Graves DT. Diabetes interferes with the bone formation by affecting the expression of transcription factors that regulate osteoblast differentiation.  Endocrinology. 144:346-52, 2003.

Alikhani, M, Alikhani, Z, He, H, Liu, R, Popek BI and Graves DT. Lipopolysaccharides indirectly stimulate apoptosis and global induction of apoptotic genes in fibroblasts. J Biol Chem. 278: 52901-8, 2003.

Gerstenfeld, LC, Cho, TJ, Kon, T, Aizawa, T, Tsay, A, Fitch, J, Barnes, GL, Graves, DT and Einhorn TA. Impaired facture healing the absence of TNF-alpha signaling: the role of TNF-alpha in endochondral cartilage resorption. J Bone Miner Res. 18: 1584-92. 2003

Gerstenfeld LC, Cullinane DM, Barnes GL, Graves DT, Einhorn TA. Fracture healing as a post-natal developmental process; molecular, spatial, and temporal aspects of its regulation. J Cell Biochem. 88:873-84. 2003.

Santana, RB, Xu, L, Chase, HB, Amar, S, Graves DT and Trackman, PC. A role for advanced glycation end products in diminished bone healing in type 1 diabetes. Diabetes. 52:1502-10. 2003.

Lu, H, Raptis, M, Black, E, Stan, M, Amar, S and Graves DT. Influence of diabetes on the exacerbation of an inflammatory response in cardiovascular tissue. Endocrinology. 145:4934-4939, 2004.

Naguib, G, Al-Mashat, H, Desta, T, Graves, DT. Diabetes prolongs the inflammatory response to a bacterial stimulus through cytokine dysregulation.  Invest Dermatol. 123:87-92. 2004.

Liu, R, Desta, T, He, H and Graves, DT. Diabetes alters the response to bacteria by enhancing fibroblast apoptosis. Endocrinology.145:2997-3003. 2004.

He, H, Liu, R, Desta, T, Leone C, Gerstenfeld, LC and Graves DT. Diabetes causes decreased osteoclastogenesis, reduced bone formation, and enhanced apoptosis of osteoblastic cells in bacteria stimulated bone loss. Endocrinology. 145:447-52. 2004

.Graves, DT, Naguib, G, Lu, H, Leone, C, Hsue, H and Krall, E.Inflammation is more persistent in type 1 diabetic mice. J Dent Res. 84:324-8, 2005.

Graves, DT, Naguib, G, Lu, H, Desta, T and Amar S.  Porphyromonas gingivalis fimbriae are proinflammatory but do not play a prominent role in the innate immune response to P. gingivalis. J Endotoxin Res. 11:13-8. 2005.

Alikhani, Z, Alikhani, M, Boyd, C, Nagao, K, Trackman, PC and Graves DT. Advanced glycation endproducts enhance expression of pro-apoptotic genes and stimulate fibroblast apoptosis through cytoplasmic and mitochondrial pathways.J Biol Chem. 280:12087-95 2005

Alikhani, M, Alikhani, Z and Graves, DT. FOXO1 functions as a master switch that regulates gene expression necessary for TNF-induced fibroblast apoptosis. J Biol Chem. 280:12096-102. 2005.

Lehmann W, Edgar CM, Wang K, Cho TJ, Barnes GL, Kakar S, Graves DT, Rueger JM, Gerstenfeld LC, Einhorn TA. Tumor necrosis factor (TNF-alpha) coordinately regulates the expression of specific matrix metalloproteinases (MMPS) and angiogenic factors during fracture healing. Bone. 36:300-10. 2005.

Liu, R,  Bal, HS, Desta, T, Behl, Y and Graves DT. Tumor necrosis factor mediates diabetes-enhanced apoptosis of matrix producing cells and impairs diabetic healing. Am J Pathol. 168:757-64.2006.

Al-Mashat, HA, Kandru, S, Liu, R, Behl, Y, Desta, T and Graves DT. Diabetes enhances mRNA levels of pro-apoptotic genes and caspase activity which contribute to impaired healing. Diabetes.55:487-95. 2006.

Leone, CW, Bokhadhoor, H, Kuo, D, Desta, T, Yang, J, Siqueira, MF, Amar, S and Graves DT. Immunization enhances inflammation and tissue destruction in response to P. gingivalis. Infect Immun. 74:2286-92. 2006.

Liu, R,  Bal, HS, Desta, T,  Krothapalli, N, Alyassi, M, Luan, Q and Graves, DT. Diabetes enhances periodontal bone loss through enhanced resorption and diminished bone formation. J Dent Res. 85:510-4. 2006.

Gerstenfeld LC, Alkhiary YM, Krall EA, Nicholls FH, Stapleton SN, Fitch JL, Bauer M, Kayal R, Graves DT, Jepsen KJ, Einhorn TA. Three-dimensional reconstruction of fracture callus morphogenesis. J Histochem Cytochem. 54:1215-28. 2006

Alikhani M, Alikhani Z, Boyd C, Maclellan CM, Raptis M, Liu R, Pischon N, Trackman PC, Gerstenfeld L, Graves DT. Advanced glycation end products stimulate osteoblast apoptosis via the MAP kinase and cytosolic apoptotic pathways. Bone. 40:345-53. 2007.

Kayal RA, Tsatsas D, Bauer MA, Allen B, Al-Sebaei MO, Kakar S, Leone CW, Morgan EF, Gerstenfeld L, Einhorn TA, Graves DT. Diminished Bone Formation during Diabetic Fracture Healing is Related to the Premature Resorption of Cartilage Associated with Increased Osteoclast Activity. J Bone Miner Res. 22:560-82007.

Desta T, Graves DT. Fibroblast apoptosis induced by Porphyromonas gingivalis is stimulated by a gingipain and caspase-independent pathway that involves apoptosis-inducing factor.Cell Microbiology. 2007

Graves DT, Kayal RA. Diabetic complications and dysregulated innate immunity. Front Biosci. 3:1227-39. 2008

Luan Q, Desta T, Chehab L, Sanders VJ, Plattner J, Graves DT. Inhibition of experimental periodontitis by a topical boron-based antimicrobial. J Dent Res. 87:148-52, 2008.

Behl Y, Krotahapalli P, Desta T, DiPiazza A, Roy S, Graves DT. Diabetes-enhanced tumor necorosis factor-alpha production promotes apoptosis and the loss of retinal microvascular cells in type 1 and type 2 models of diabetic retinopathy. Am J Pathol. 172:1411-8, 2008.

Liu R, Desta T, Raptis M, Darveau RP, Graves DT. P. gingivalis and E. coli lipopolysaccharides exhibit different systemic but similar local induction of inflammatory markers. J Periodontol. 79:1241-7. 2008.

Ai-Aql ZS, Alagl AS, Graves DT, Gerstenfeld LC, Einhorn TA.Molecular mechanisms controlling bone formation during fracture healing and distraction osteogenesis. J Dent Res.;87:107-18. 2008.

Behl Y, Siqueira M, Ortiz J, Li J, Desta T, Faibish D, Graves DT. Activation of the acquired immune response reduces coupled bone formation in response to a periodontal pathogen. J Immunol. 12:8711-8. 2008

Gerstenfeld LC, Sacks DJ, Pelis M, Mason ZD, Graves DT, Barrero M, Ominsky MS, Kostenuik PJ, Morgan EF, Einhorn TA. Comparison of Effects of the Bisphosphonate Alendronate Versus the RANKL Inhibitor Denosumab on Murine Fracture Healing. J Bone Miner Res.  2008

Kayal RA, Alblowi J, McKenzie E, Krothapalli N, Silkman L, Gerstenfeld L, Einhorn TA, Graves DT. Diabetes causes the accelerated loss of cartilage during fracture repair which is reversed by insulin treatment.  Bone. 2008.

Yang J, Siqueira MF, Behl Y, Alikhani M, Graves DT. The transcription factor ST18 regulates proapoptotic and proinflammatory gene expression in fibroblasts. FASEB  J. 22:3956-67, 2008.

Liu R, Desta T, Raptis M, Darveau RP, Graves DT. P. gingivalis and E. coli lipopolysaccharides exhibit different systemic but similar local induction of inflammatory markers. J Periodontol. 79:1241-7. 2008

Behl Y, Krothapalli P, Desta T, DiPiazza A, Roy S, Graves DT. Diabetes-enhanced tumor necrosis factor-alpha production promotes apoptosis and the loss of retinal microvascular cells in type 1 and type 2 models of diabetic retinopathy. Am J Pathol. 172:1411-8. 2008

Behl, Y, Krothapalli, P,  Desta T, Roy,  S and Graves, DT. FOXO1 plays an important role in enhanced microvascular cell apoptosis and microvascular cell loss in type 1 and type 2 diabetic rats. Diabetes, in press.

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