Dana Graves

Summary

Affiliation: Boston University
Country: USA

Publications

  1. ncbi IL-1 plays a critical role in oral, but not dermal, wound healing
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Immunol 167:5316-20. 2001
  2. ncbi Inflammation is more persistent in type 1 diabetic mice
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Suite W 202D, Boston, MA 02118, USA
    J Dent Res 84:324-8. 2005
  3. ncbi Diabetes-enhanced inflammation and apoptosis--impact on periodontal pathology
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, W 202 D, 700 Albany Street, Boston, MA 02118, USA
    J Dent Res 85:15-21. 2006
  4. pmc Diabetic complications and dysregulated innate immunity
    Dana T Graves
    Boston University School of Dental Medicine, Department of Periodontology and Oral Biology, W 202D, 700 Albany Street, Boston, MA 02118, USA
    Front Biosci 13:1227-39. 2008
  5. pmc The use of rodent models to investigate host-bacteria interactions related to periodontal diseases
    Dana T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Clin Periodontol 35:89-105. 2008
  6. ncbi The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Periodontol 74:391-401. 2003
  7. doi Cytokines that promote periodontal tissue destruction
    Dana Graves
    Division of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, 100 E Newton Street, Boston, MA 02118, USA
    J Periodontol 79:1585-91. 2008
  8. ncbi Porphyromonas gingivalis fimbriae are pro-inflammatory but do not play a prominent role in the innate immune response to P. gingivalis
    Dana T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    J Endotoxin Res 11:13-8. 2005
  9. ncbi Tumor necrosis factor modulates fibroblast apoptosis, PMN recruitment, and osteoclast formation in response to P. gingivalis infection
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, MA 02118, USA
    J Dent Res 80:1875-9. 2001
  10. pmc Diminished bone formation during diabetic fracture healing is related to the premature resorption of cartilage associated with increased osteoclast activity
    Rayyan A Kayal
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Bone Miner Res 22:560-8. 2007

Research Grants

Collaborators

Detail Information

Publications46

  1. ncbi IL-1 plays a critical role in oral, but not dermal, wound healing
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Immunol 167:5316-20. 2001
    ..In a less challenging environment, the production of new connective tissue and its coverage by migrating epithelium are minimally affected by the absence of IL-1 activity...
  2. ncbi Inflammation is more persistent in type 1 diabetic mice
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Suite W 202D, Boston, MA 02118, USA
    J Dent Res 84:324-8. 2005
    ..Both exhibited prolonged TNF-alpha expression compared with controls. These results suggest that diabetes alters bacteria-host interactions by prolonging the inflammatory response...
  3. ncbi Diabetes-enhanced inflammation and apoptosis--impact on periodontal pathology
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, W 202 D, 700 Albany Street, Boston, MA 02118, USA
    J Dent Res 85:15-21. 2006
    ..These findings may shed light on diabetes-enhanced risk of periodontal diseases...
  4. pmc Diabetic complications and dysregulated innate immunity
    Dana T Graves
    Boston University School of Dental Medicine, Department of Periodontology and Oral Biology, W 202D, 700 Albany Street, Boston, MA 02118, USA
    Front Biosci 13:1227-39. 2008
    ..Cause and effect relationship between dysregulation of key components of innate immunity and diabetic complications in many instances have been demonstrated with the use of cytokine blockers and antioxidants...
  5. pmc The use of rodent models to investigate host-bacteria interactions related to periodontal diseases
    Dana T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Clin Periodontol 35:89-105. 2008
    ....
  6. ncbi The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Periodontol 74:391-401. 2003
    ..This destruction may very well represent an overreaction of the host response to periodontal pathogens caused by excessive production of IL-1 and TNF...
  7. doi Cytokines that promote periodontal tissue destruction
    Dana Graves
    Division of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, 100 E Newton Street, Boston, MA 02118, USA
    J Periodontol 79:1585-91. 2008
    ....
  8. ncbi Porphyromonas gingivalis fimbriae are pro-inflammatory but do not play a prominent role in the innate immune response to P. gingivalis
    Dana T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    J Endotoxin Res 11:13-8. 2005
    ..These results indicate that FimA is a potent inducer of inflammatory cytokine expression but, in the context of P. gingivalis infection, it is not a principal stimulator of the innate host response...
  9. ncbi Tumor necrosis factor modulates fibroblast apoptosis, PMN recruitment, and osteoclast formation in response to P. gingivalis infection
    D T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, MA 02118, USA
    J Dent Res 80:1875-9. 2001
    ..Furthermore, this may represent a more general mechanism by which bacterial challenge induces apoptosis of matrix-producing cells through the induction of TNF...
  10. pmc Diminished bone formation during diabetic fracture healing is related to the premature resorption of cartilage associated with increased osteoclast activity
    Rayyan A Kayal
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Bone Miner Res 22:560-8. 2007
    ..Increased cartilage turnover was associated with elevated osteoclast numbers, a higher expression of genes that promote osteoclastogenesis, and diminished primary bone formation...
  11. pmc Diabetes causes the accelerated loss of cartilage during fracture repair which is reversed by insulin treatment
    Rayyan A Kayal
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    Bone 44:357-63. 2009
    ..That insulin reverses these effects demonstrates that they are directly related to the diabetic condition...
  12. pmc Cytokine profiling of macrophages exposed to Porphyromonas gingivalis, its lipopolysaccharide, or its FimA protein
    Qingde Zhou
    Department of Periodontology and Oral Biology, School of Dental Medicine, Boston University Medical Center, 700 Albany Street, W 201E, Boston, MA 02118, USA
    Infect Immun 73:935-43. 2005
    ..These results indicate that host immune cells sense live P. gingivalis and its components differently, which translates into the expression of different inflammatory cytokine profiles...
  13. ncbi Three-dimensional reconstruction of fracture callus morphogenesis
    Louis C Gerstenfeld
    Orthopaedic Research Laboratory, Boston University Medical Center, 715 Albany Street, R 205, Boston, MA 02118, USA
    J Histochem Cytochem 54:1215-28. 2006
    ..These data further show that remodeling of the calcified cartilage produces a trabecular bone structure unique to fracture healing that provides the rapid regain in weight-bearing capacity to the injured bone...
  14. pmc TNF-alpha mediates diabetes-enhanced chondrocyte apoptosis during fracture healing and stimulates chondrocyte apoptosis through FOXO1
    Rayyan A Kayal
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA, USA
    J Bone Miner Res 25:1604-15. 2010
    ..Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-alpha, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation...
  15. pmc Immunization enhances inflammation and tissue destruction in response to Porphyromonas gingivalis
    Cataldo W Leone
    Department of Periodontology and Oral Biology, Boston University Goldman School of Dental Medicine, 700 Albany Street, W 201, Boston, MA 02118, USA
    Infect Immun 74:2286-92. 2006
    ..gingivalis increases the inflammatory and destructive responses which occur in part through up-regulating the innate immune response and enhancing osteoclastogenesis and fibroblast apoptosis...
  16. pmc High levels of tumor necrosis factor-alpha contribute to accelerated loss of cartilage in diabetic fracture healing
    Jazia Alblowi
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts, USA
    Am J Pathol 175:1574-85. 2009
    ....
  17. doi Comparison of effects of the bisphosphonate alendronate versus the RANKL inhibitor denosumab on murine fracture healing
    Louis C Gerstenfeld
    Orthopaedic Research Laboratory, Department of Orthopedic Surgery, Boston University School of Medicine, Boston, Massachusetts 02118, USA
    J Bone Miner Res 24:196-208. 2009
    ..In contrast, strength and stiffness were enhanced in these treatment groups compared with control bones...
  18. ncbi Fracture healing as a post-natal developmental process: molecular, spatial, and temporal aspects of its regulation
    Louis C Gerstenfeld
    Department of Orthopaedic Surgery, Orthopaedic Research Laboratory, Boston University Medical Center, Boston, Massachusetts 02118 2526, USA
    J Cell Biochem 88:873-84. 2003
    ....
  19. ncbi Diabetes causes decreased osteoclastogenesis, reduced bone formation, and enhanced apoptosis of osteoblastic cells in bacteria stimulated bone loss
    Hongbing He
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    Endocrinology 145:447-52. 2004
    ..The uncoupling of bone formation and resorption may be due in part to prolonged apoptosis of bone lining cells...
  20. ncbi Diabetes prolongs the inflammatory response to a bacterial stimulus through cytokine dysregulation
    Ghada Naguib
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    J Invest Dermatol 123:87-92. 2004
    ..These results indicate that cytokine dysregulation associated with prolonged TNF expression represents a mechanism through which bacteria may induce a more damaging inflammatory response in diabetic individuals...
  21. pmc Contribution of interleukin-11 and prostaglandin(s) in lipopolysaccharide-induced bone resorption in vivo
    Li Li
    Department of Periodontology and Oral Biology, School of Dental Medicine, Boston University, Boston, Massachusetts 02118, USA
    Infect Immun 70:3915-22. 2002
    ..IL-11 and PGs mediate LPS-induced bone resorption by enhancing osteoclastogenesis independently of the IL-1 or TNF signaling...
  22. ncbi Diabetes alters the response to bacteria by enhancing fibroblast apoptosis
    Rongkun Liu
    Boston University School of Dental Medicine, W 202D, 700 Albany Street, Boston, Massachusetts 02118, USA
    Endocrinology 145:2997-3003. 2004
    ..Thus, diabetes may impair the healing response to bacteria-induced connective tissue loss by increasing the number of caspase-3-activated fibroblasts, leading to greater apoptosis and reduced numbers of fibroblastic cells...
  23. pmc P. gingivalis and E. coli lipopolysaccharides exhibit different systemic but similar local induction of inflammatory markers
    Rongkun Liu
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Periodontol 79:1241-7. 2008
    ..gingivalis lipopolysaccharide (PgLPS), PgLPS(1435)(/1449) and PgLPS(1690), exhibit differences in their capacity to stimulate systemic versus local responses compared to Escherichia coli lipopolysaccharide (LPS)...
  24. ncbi A role for advanced glycation end products in diminished bone healing in type 1 diabetes
    Ronaldo B Santana
    Goldman School of Dental Medicine, Division of Oral Biology, Boston University, 100 East Newton Street, Boston, MA 02118, USA
    Diabetes 52:1502-10. 2003
    ..05). Evidence for the expression of RAGE was obtained in mouse and rat osteoblastic cultures. These results support the contribution of AGEs to diminished bone healing in type 1 diabetes, possibly mediated by RAGE...
  25. pmc Tumor necrosis factor-alpha mediates diabetes-enhanced apoptosis of matrix-producing cells and impairs diabetic healing
    Rongkun Liu
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    Am J Pathol 168:757-64. 2006
    ..This enhanced healing may in part be explained by block-ing TNF-alpha-induced apoptosis of critical matrix-producing cells...
  26. pmc 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
    Yugal Behl
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    Am J Pathol 172:1411-8. 2008
    ....
  27. ncbi Diabetes interferes with the bone formation by affecting the expression of transcription factors that regulate osteoblast differentiation
    Huafei Lu
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    Endocrinology 144:346-52. 2003
    ....
  28. ncbi Evidence that diabetes mellitus aggravates periodontal diseases and modifies the response to an oral pathogen in animal models
    Dana T Graves
    Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, Boston, Massachusetts, USA
    Compend Contin Educ Dent 25:38-45. 2004
    ..The diminished capacity to form new bone may make it more difficult for diabetics in particular to repair the loss of tissue that occurs in periodontal diseases...
  29. pmc Activation of the acquired immune response reduces coupled bone formation in response to a periodontal pathogen
    Yugal Behl
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    J Immunol 181:8711-8. 2008
    ..These studies give insight into inflammatory bone diseases such as periodontal disease and arthritis were the formation of lytic lesions occurs in conjunction with deficient bone formation and activation of an acquired immune response...
  30. ncbi Inflammation and tissue loss caused by periodontal pathogens is reduced by interleukin-1 antagonists
    Andrew J Delima
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Massachusetts 02118, USA
    J Infect Dis 186:511-6. 2002
    ..The results indicate that inhibition of IL-1 alone significantly reduces inflammation, connective tissue attachment loss, and bone resorption that are induced by periodontal pathogens...
  31. ncbi Diabetes-enhanced inflammation and apoptosis: impact on periodontal pathosis
    Dana T Graves
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA, USA
    Periodontol 2000 45:128-37. 2007
  32. pmc Fibroblast apoptosis induced by Porphyromonas gingivalis is stimulated by a gingipain and caspase-independent pathway that involves apoptosis-inducing factor
    Tesfahun Desta
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    Cell Microbiol 9:2667-75. 2007
    ..gingivalis causes fibroblast apoptosis through a pathway that involves protein kinase A and AIF, is not dependent upon bacterial proteolytic activity and is also independent of the classic apoptotic pathways involving caspase-3...
  33. ncbi Lipopolysaccharides indirectly stimulate apoptosis and global induction of apoptotic genes in fibroblasts
    Mani Alikhani
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 278:52901-8. 2003
    ..Thus, LPS acts to modulate the expression of a large number of genes that favor apoptosis of fibroblastic cells that is dependent upon activation of caspase-8 and is largely mediated by TNF...
  34. ncbi Interleukin-1 receptor signaling mediates atherosclerosis associated with bacterial exposure and/or a high-fat diet in a murine apolipoprotein E heterozygote model: pharmacotherapeutic implications
    Hunghui Chi
    Department of Periodontology and Oral Biology, School of Dental Medicine, Boston University, Boston, MA 02118, USA
    Circulation 110:1678-85. 2004
    ..Studies presented here tested the hypothesis that IL-1 receptor (IL-1R1) signaling plays a crucial role in bacteria- and/or high-fat diet (HFD)-enhanced atherogenesis...
  35. ncbi TNF-alpha in vivo stimulates apoptosis in fibroblasts through caspase-8 activation and modulates the expression of pro-apoptotic genes
    Mani Alikhani
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    J Cell Physiol 201:341-8. 2004
    ..Thus, TNF-alpha acts to modulate the expression of many genes that favors apoptosis of fibroblastic cells, which is dependent mostly upon signaling through caspase-8...
  36. ncbi Diabetes enhances mRNA levels of proapoptotic genes and caspase activity, which contribute to impaired healing
    Hesham A Al-Mashat
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    Diabetes 55:487-95. 2006
    ..Thus, diabetes-enhanced apoptosis represents an important mechanism through which healing is impaired, and this can be explained, in part, by diabetes-increased expression of proapoptotic genes and caspase activity...
  37. ncbi Advanced glycation end products enhance expression of pro-apoptotic genes and stimulate fibroblast apoptosis through cytoplasmic and mitochondrial pathways
    Zoubin Alikhani
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 280:12087-95. 2005
    ..However, the pattern of expression was not identical to the pattern of apoptotic genes induced by tumor necrosis factor alpha...
  38. ncbi FOXO1 functions as a master switch that regulates gene expression necessary for tumor necrosis factor-induced fibroblast apoptosis
    Mani Alikhani
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts 02118, USA
    J Biol Chem 280:12096-102. 2005
    ..siRNA silencing also blocked down-regulation of anti-apoptotic genes. These results indicate that TNF induces activation of the FOXO1 transcription factor, which acts as a master switch to control apoptosis...
  39. pmc FOXO1 plays an important role in enhanced microvascular cell apoptosis and microvascular cell loss in type 1 and type 2 diabetic rats
    Yugal Behl
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, Massachusetts, USA
    Diabetes 58:917-25. 2009
    ..To investigate early events leading to microvascular cell loss in diabetic retinopathy...
  40. pmc Advanced glycation end products stimulate osteoblast apoptosis via the MAP kinase and cytosolic apoptotic pathways
    Mani Alikhani
    Department of Periodontology and Oral Biology, Boston University School of Dental Medicine, Boston, MA 02118, USA
    Bone 40:345-53. 2007
    ..These results indicate that advanced glycation end products, which accumulate in diabetic and aged individuals, may promote apoptosis of osteoblastic cells and contribute to deficient bone formation...
  41. ncbi Short- and long-term effects of IL-1 and TNF antagonists on periodontal wound healing
    Xuemei Zhang
    Department of Periodontology and Oral Biology, School of Dental Medicine, Boston University, Boston, MA 02118, USA
    J Immunol 173:3514-23. 2004
    ..Short-term blockade of IL-1 and TNF may facilitate periodontal wound healing, whereas prolonged blockade may have adverse effects...
  42. ncbi Advanced glycation end products induce apoptosis in fibroblasts through activation of ROS, MAP kinases, and the FOXO1 transcription factor
    Mani Alikhani
    Dept of Periodontology and Oral Biology, Boston Univ School of Dental Medicine, Boston, MA 02118, USA
    Am J Physiol Cell Physiol 292:C850-6. 2007
    ..Together these data support a model in which AGE-induced apoptosis involves the formation of ROS, NO, and ceramide and leads to p38 and JNK MAP kinase activation, which in turn induces FOXO1 and caspase-3...
  43. ncbi Influence of diabetes on the exacerbation of an inflammatory response in cardiovascular tissue
    Huafei Lu
    Boston University School of Dental Medicine, W 202D, 700 Albany Street, Boston, Massachusetts 02118, USA
    Endocrinology 145:4934-9. 2004
    ..Given that infection, bacteremia, and endotoxemia are relatively frequent events in humans, these results identify a putative mechanism for increased cardiovascular heart disease in diabetes...
  44. pmc The transcription factor ST18 regulates proapoptotic and proinflammatory gene expression in fibroblasts
    Julia Yang
    Boston University School of Dental Medicine, 700 Albany St W 202 D, Boston, MA 02118, USA
    FASEB J 22:3956-67. 2008
    ..Taken together, these studies demonstrate that the transcription factor ST18/NZF3 regulates the mRNA levels of proapoptotic and proinflammatory genes in revealing a previously unrecognized function...
  45. ncbi Healing is delayed in oral compared to dermal excisional wounds
    Nasser Nooh
    College of Dentistry, King Saud University, Riyadh, Saudi Arabia
    J Periodontol 74:242-6. 2003
    ..However, the oral environment also presents challenges to healing that include a large commensal flora and trauma from mastication...
  46. ncbi Quantification and localization of platelet-derived growth factor in gingiva of periodontitis patients
    Maria Leticia B Pinheiro
    Graduate Periodontics, Faculdade de Odontologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
    J Periodontol 74:323-8. 2003
    ..The goals of the present study were to test whether PDGF is present at increased levels in inflamed gingiva and to localize its expression in gingival biopsies from individuals with chronic periodontitis...

Research Grants6

  1. Diabetes-enhanced Experimental Periodontitis
    Dana Graves; Fiscal Year: 2007
    ..These studies will use the rat model and TNF blocker described in Aim 1. ..
  2. Recognition of Commensal and Pathogenic Bacteria By Oral Epithelium
    Dana Graves; Fiscal Year: 2007
    ..The goal of this Aim is to investigate whether age-associated acquisition of a commensal flora induces bacterial tolerance. ..