Diabetes Prevents Periodontitis-Induced Increases in Gingival Platelet Derived Growth Factor-B and Interleukin 1-Beta in a Rat Model

D. L. Doxey, Christopher W Cutler, A. M. Iacopino

Research output: Contribution to journalArticle

34 Citations (Scopus)

Abstract

PERIODONTITIS IS A CHRONIC INFLAMMATORY disease characterized by a progression that is very much dependent on host response. The gingiva can be considered to be in a constant state of wounding (pathologic wounding by bacterial plaque) and a constant state of maintenance/repair. In this context, any metabolic disturbance in the host which compromises tissue repair/wound healing will exacerbate the progression of periodontitis. Diabetes presents an interesting example because two major complications of diabetes are delayed wound healing and periodontitis. Our previous studies indicate that delayed wound healing and periodontitis may be manifestations of a general systemic deficit in diabetes involving alteration of macrophage cytokine gene expression. The present study was designed to determine whether: 1) diabetes-induced metabolic alterations affect gingival cytokine levels; and 2) diabetes-induced metabolic alterations modify the gingival cytokine profile in periodontitis. Sprague-Dawley rats (N = 12/group) were injected with streptozotocin (65 mg/kg) into the tail vein to induce diabetes (defined by blood glucose levels > 250 mg/dl) or received the injection vehicle or no treatment as controls. Periodontitis was induced in additional groups of diabetic and control rats by gavage with Porphyromonas gingivalis A7436. After 90 days, serum glucose was analyzed to document diabetes; alveolar bone level was measured to document severity of periodontitis; gingiva was harvested circumferentially from the first and second molars; and cytokines in gingival homogenates were assayed by ELISA using commercial kits. Cytokine levels were expressed as mean ± SEM pg/μg protein. Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1β), transforming growth factor-beta (TGF-β), and tumor necrosis factor-alpha (TNF-α). Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1β. Diabetes superimposed on periodontitis prevented these increases. Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1β.

Original languageEnglish (US)
Pages (from-to)113-119
Number of pages7
JournalJournal of Periodontology
Volume69
Issue number2
DOIs
StatePublished - Jan 1 1998
Externally publishedYes

Fingerprint

Proto-Oncogene Proteins c-sis
Periodontitis
Interleukin-1beta
Cytokines
Wound Healing
Gingiva
Porphyromonas gingivalis
Diabetes Complications
Streptozocin
Transforming Growth Factor beta
Sprague Dawley Rats
Blood Glucose
Tail
Veins
Chronic Disease
Tumor Necrosis Factor-alpha

Keywords

  • Animal studies
  • Cytokines
  • Diabetes mellitus/complications
  • Gingiva/anatomy and histology
  • Periodontitis/histology
  • Wound healing

ASJC Scopus subject areas

  • Periodontics

Cite this

Diabetes Prevents Periodontitis-Induced Increases in Gingival Platelet Derived Growth Factor-B and Interleukin 1-Beta in a Rat Model. / Doxey, D. L.; Cutler, Christopher W; Iacopino, A. M.

In: Journal of Periodontology, Vol. 69, No. 2, 01.01.1998, p. 113-119.

Research output: Contribution to journalArticle

@article{9558ede2329f47f2949cba3a233dae33,
title = "Diabetes Prevents Periodontitis-Induced Increases in Gingival Platelet Derived Growth Factor-B and Interleukin 1-Beta in a Rat Model",
abstract = "PERIODONTITIS IS A CHRONIC INFLAMMATORY disease characterized by a progression that is very much dependent on host response. The gingiva can be considered to be in a constant state of wounding (pathologic wounding by bacterial plaque) and a constant state of maintenance/repair. In this context, any metabolic disturbance in the host which compromises tissue repair/wound healing will exacerbate the progression of periodontitis. Diabetes presents an interesting example because two major complications of diabetes are delayed wound healing and periodontitis. Our previous studies indicate that delayed wound healing and periodontitis may be manifestations of a general systemic deficit in diabetes involving alteration of macrophage cytokine gene expression. The present study was designed to determine whether: 1) diabetes-induced metabolic alterations affect gingival cytokine levels; and 2) diabetes-induced metabolic alterations modify the gingival cytokine profile in periodontitis. Sprague-Dawley rats (N = 12/group) were injected with streptozotocin (65 mg/kg) into the tail vein to induce diabetes (defined by blood glucose levels > 250 mg/dl) or received the injection vehicle or no treatment as controls. Periodontitis was induced in additional groups of diabetic and control rats by gavage with Porphyromonas gingivalis A7436. After 90 days, serum glucose was analyzed to document diabetes; alveolar bone level was measured to document severity of periodontitis; gingiva was harvested circumferentially from the first and second molars; and cytokines in gingival homogenates were assayed by ELISA using commercial kits. Cytokine levels were expressed as mean ± SEM pg/μg protein. Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1β), transforming growth factor-beta (TGF-β), and tumor necrosis factor-alpha (TNF-α). Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1β. Diabetes superimposed on periodontitis prevented these increases. Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1β.",
keywords = "Animal studies, Cytokines, Diabetes mellitus/complications, Gingiva/anatomy and histology, Periodontitis/histology, Wound healing",
author = "Doxey, {D. L.} and Cutler, {Christopher W} and Iacopino, {A. M.}",
year = "1998",
month = "1",
day = "1",
doi = "10.1902/jop.1998.69.2.113",
language = "English (US)",
volume = "69",
pages = "113--119",
journal = "Journal of Periodontology",
issn = "0022-3492",
publisher = "American Academy of Periodontology",
number = "2",

}

TY - JOUR

T1 - Diabetes Prevents Periodontitis-Induced Increases in Gingival Platelet Derived Growth Factor-B and Interleukin 1-Beta in a Rat Model

AU - Doxey, D. L.

AU - Cutler, Christopher W

AU - Iacopino, A. M.

PY - 1998/1/1

Y1 - 1998/1/1

N2 - PERIODONTITIS IS A CHRONIC INFLAMMATORY disease characterized by a progression that is very much dependent on host response. The gingiva can be considered to be in a constant state of wounding (pathologic wounding by bacterial plaque) and a constant state of maintenance/repair. In this context, any metabolic disturbance in the host which compromises tissue repair/wound healing will exacerbate the progression of periodontitis. Diabetes presents an interesting example because two major complications of diabetes are delayed wound healing and periodontitis. Our previous studies indicate that delayed wound healing and periodontitis may be manifestations of a general systemic deficit in diabetes involving alteration of macrophage cytokine gene expression. The present study was designed to determine whether: 1) diabetes-induced metabolic alterations affect gingival cytokine levels; and 2) diabetes-induced metabolic alterations modify the gingival cytokine profile in periodontitis. Sprague-Dawley rats (N = 12/group) were injected with streptozotocin (65 mg/kg) into the tail vein to induce diabetes (defined by blood glucose levels > 250 mg/dl) or received the injection vehicle or no treatment as controls. Periodontitis was induced in additional groups of diabetic and control rats by gavage with Porphyromonas gingivalis A7436. After 90 days, serum glucose was analyzed to document diabetes; alveolar bone level was measured to document severity of periodontitis; gingiva was harvested circumferentially from the first and second molars; and cytokines in gingival homogenates were assayed by ELISA using commercial kits. Cytokine levels were expressed as mean ± SEM pg/μg protein. Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1β), transforming growth factor-beta (TGF-β), and tumor necrosis factor-alpha (TNF-α). Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1β. Diabetes superimposed on periodontitis prevented these increases. Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1β.

AB - PERIODONTITIS IS A CHRONIC INFLAMMATORY disease characterized by a progression that is very much dependent on host response. The gingiva can be considered to be in a constant state of wounding (pathologic wounding by bacterial plaque) and a constant state of maintenance/repair. In this context, any metabolic disturbance in the host which compromises tissue repair/wound healing will exacerbate the progression of periodontitis. Diabetes presents an interesting example because two major complications of diabetes are delayed wound healing and periodontitis. Our previous studies indicate that delayed wound healing and periodontitis may be manifestations of a general systemic deficit in diabetes involving alteration of macrophage cytokine gene expression. The present study was designed to determine whether: 1) diabetes-induced metabolic alterations affect gingival cytokine levels; and 2) diabetes-induced metabolic alterations modify the gingival cytokine profile in periodontitis. Sprague-Dawley rats (N = 12/group) were injected with streptozotocin (65 mg/kg) into the tail vein to induce diabetes (defined by blood glucose levels > 250 mg/dl) or received the injection vehicle or no treatment as controls. Periodontitis was induced in additional groups of diabetic and control rats by gavage with Porphyromonas gingivalis A7436. After 90 days, serum glucose was analyzed to document diabetes; alveolar bone level was measured to document severity of periodontitis; gingiva was harvested circumferentially from the first and second molars; and cytokines in gingival homogenates were assayed by ELISA using commercial kits. Cytokine levels were expressed as mean ± SEM pg/μg protein. Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1β), transforming growth factor-beta (TGF-β), and tumor necrosis factor-alpha (TNF-α). Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1β. Diabetes superimposed on periodontitis prevented these increases. Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1β.

KW - Animal studies

KW - Cytokines

KW - Diabetes mellitus/complications

KW - Gingiva/anatomy and histology

KW - Periodontitis/histology

KW - Wound healing

UR - http://www.scopus.com/inward/record.url?scp=0031989767&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031989767&partnerID=8YFLogxK

U2 - 10.1902/jop.1998.69.2.113

DO - 10.1902/jop.1998.69.2.113

M3 - Article

C2 - 9526909

AN - SCOPUS:0031989767

VL - 69

SP - 113

EP - 119

JO - Journal of Periodontology

JF - Journal of Periodontology

SN - 0022-3492

IS - 2

ER -