Changes in inflammatory mediators in experimental periodontitis in the rhesus monkey

M. A. Smith, L. D. Braswell, J. G. Collins, D. L. Boyd, M. K. Jeffcoat, M. Reddy, K. L. Li, S. Wilensky, Richard Vogel, M. Alfano, S. Offenbacher

Research output: Contribution to journalArticle

Abstract

Ligature-induced periodontitis was monitored for 6 months in eight Macaca mulatta monkeys to examine clinical status, radiographic bone level, and crevicular fluid (CF) levels of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), interleukin-1β (IL-1β), tumor necrosis factor alpha, and leukotriene B4 (LTB4). A split-mouth design was used, with eight ligated teeth and eight contralateral nonligated teeth which develop soft-chow- promoted (spontaneous) disease. Ligated sites experienced an average attachment loss of 0.94 mm per site and linear bone loss of 0.88 mm per site, with spontaneous-periodontitis sites experiencing approximately half the loss of ligated sites. The CF mediator levels showed increased levels of PGE2 and TxB2 at the ligated sites, as compared with the spontaneous sites, with no significant contralateral differences in the IL-1β or LTB4 responses. The concentrations of LTB4 in CF reached an early threefold peak over the baseline level at 1 month. By 2 months there was a statistically significant threefold elevation in CF-PGE2 in the ligated sites and a twofold elevation in the spontaneous sites as compared to the baseline level (P = 0.041 and 0.008, respectively). The monocyte product IL-1β increased sharply at 2 months and returned to the baseline level by 6 months at both ligated and nonligated sites. Tumor necrosis factor alpha in CF was below the limit of detection at all sites throughout the experiment (i.e., <2 ng/ml). The selective elevation of both PGE2 and TxB2 in ligated sites, compared with levels in spontaneous sites, in the presence of similar levels of LTB4 and IL-1β provides further evidence that these molecules regulate the magnitude of the tissue-destructive response in progressive periodontitis.

Original languageEnglish (US)
Pages (from-to)1453-1459
Number of pages7
JournalInfection and Immunity
Volume61
Issue number4
StatePublished - 1993

Fingerprint

Leukotriene B4
Periodontitis
Macaca mulatta
Interleukin-1
Dinoprostone
Thromboxane B2
Tooth
Tumor Necrosis Factor-alpha
Bone and Bones
Haplorhini
Ligation
Mouth
Limit of Detection
Monocytes
prostaglandin B2

ASJC Scopus subject areas

  • Immunology

Cite this

Smith, M. A., Braswell, L. D., Collins, J. G., Boyd, D. L., Jeffcoat, M. K., Reddy, M., ... Offenbacher, S. (1993). Changes in inflammatory mediators in experimental periodontitis in the rhesus monkey. Infection and Immunity, 61(4), 1453-1459.

Changes in inflammatory mediators in experimental periodontitis in the rhesus monkey. / Smith, M. A.; Braswell, L. D.; Collins, J. G.; Boyd, D. L.; Jeffcoat, M. K.; Reddy, M.; Li, K. L.; Wilensky, S.; Vogel, Richard; Alfano, M.; Offenbacher, S.

In: Infection and Immunity, Vol. 61, No. 4, 1993, p. 1453-1459.

Research output: Contribution to journalArticle

Smith, MA, Braswell, LD, Collins, JG, Boyd, DL, Jeffcoat, MK, Reddy, M, Li, KL, Wilensky, S, Vogel, R, Alfano, M & Offenbacher, S 1993, 'Changes in inflammatory mediators in experimental periodontitis in the rhesus monkey', Infection and Immunity, vol. 61, no. 4, pp. 1453-1459.
Smith MA, Braswell LD, Collins JG, Boyd DL, Jeffcoat MK, Reddy M et al. Changes in inflammatory mediators in experimental periodontitis in the rhesus monkey. Infection and Immunity. 1993;61(4):1453-1459.
Smith, M. A. ; Braswell, L. D. ; Collins, J. G. ; Boyd, D. L. ; Jeffcoat, M. K. ; Reddy, M. ; Li, K. L. ; Wilensky, S. ; Vogel, Richard ; Alfano, M. ; Offenbacher, S. / Changes in inflammatory mediators in experimental periodontitis in the rhesus monkey. In: Infection and Immunity. 1993 ; Vol. 61, No. 4. pp. 1453-1459.
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abstract = "Ligature-induced periodontitis was monitored for 6 months in eight Macaca mulatta monkeys to examine clinical status, radiographic bone level, and crevicular fluid (CF) levels of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), interleukin-1β (IL-1β), tumor necrosis factor alpha, and leukotriene B4 (LTB4). A split-mouth design was used, with eight ligated teeth and eight contralateral nonligated teeth which develop soft-chow- promoted (spontaneous) disease. Ligated sites experienced an average attachment loss of 0.94 mm per site and linear bone loss of 0.88 mm per site, with spontaneous-periodontitis sites experiencing approximately half the loss of ligated sites. The CF mediator levels showed increased levels of PGE2 and TxB2 at the ligated sites, as compared with the spontaneous sites, with no significant contralateral differences in the IL-1β or LTB4 responses. The concentrations of LTB4 in CF reached an early threefold peak over the baseline level at 1 month. By 2 months there was a statistically significant threefold elevation in CF-PGE2 in the ligated sites and a twofold elevation in the spontaneous sites as compared to the baseline level (P = 0.041 and 0.008, respectively). The monocyte product IL-1β increased sharply at 2 months and returned to the baseline level by 6 months at both ligated and nonligated sites. Tumor necrosis factor alpha in CF was below the limit of detection at all sites throughout the experiment (i.e., <2 ng/ml). The selective elevation of both PGE2 and TxB2 in ligated sites, compared with levels in spontaneous sites, in the presence of similar levels of LTB4 and IL-1β provides further evidence that these molecules regulate the magnitude of the tissue-destructive response in progressive periodontitis.",
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AU - Smith, M. A.

AU - Braswell, L. D.

AU - Collins, J. G.

AU - Boyd, D. L.

AU - Jeffcoat, M. K.

AU - Reddy, M.

AU - Li, K. L.

AU - Wilensky, S.

AU - Vogel, Richard

AU - Alfano, M.

AU - Offenbacher, S.

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N2 - Ligature-induced periodontitis was monitored for 6 months in eight Macaca mulatta monkeys to examine clinical status, radiographic bone level, and crevicular fluid (CF) levels of prostaglandin E2 (PGE2), thromboxane B2 (TxB2), interleukin-1β (IL-1β), tumor necrosis factor alpha, and leukotriene B4 (LTB4). A split-mouth design was used, with eight ligated teeth and eight contralateral nonligated teeth which develop soft-chow- promoted (spontaneous) disease. Ligated sites experienced an average attachment loss of 0.94 mm per site and linear bone loss of 0.88 mm per site, with spontaneous-periodontitis sites experiencing approximately half the loss of ligated sites. The CF mediator levels showed increased levels of PGE2 and TxB2 at the ligated sites, as compared with the spontaneous sites, with no significant contralateral differences in the IL-1β or LTB4 responses. The concentrations of LTB4 in CF reached an early threefold peak over the baseline level at 1 month. By 2 months there was a statistically significant threefold elevation in CF-PGE2 in the ligated sites and a twofold elevation in the spontaneous sites as compared to the baseline level (P = 0.041 and 0.008, respectively). The monocyte product IL-1β increased sharply at 2 months and returned to the baseline level by 6 months at both ligated and nonligated sites. Tumor necrosis factor alpha in CF was below the limit of detection at all sites throughout the experiment (i.e., <2 ng/ml). The selective elevation of both PGE2 and TxB2 in ligated sites, compared with levels in spontaneous sites, in the presence of similar levels of LTB4 and IL-1β provides further evidence that these molecules regulate the magnitude of the tissue-destructive response in progressive periodontitis.

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