Gingival fluid IL‐1 and IL‐6 levels in refractory periodontitis

Richard A Reinhardt, M. P. Masada, Wayne Berwyn Kaldahl, L. M. DuBois, K. S. Kornman, J. I. Choi, K. L. Kalkwarf, A. C. Allison

Research output: Contribution to journalArticle

137 Citations (Scopus)

Abstract

Abstract Selected gingival bacteria and cytokine profiles associated with patients who did not respond to conventional periodontal therapy (refractory) were evaluated. 10 subjects with a high incidence of post‐active treatment clinical attachment loss (>2% sites/year lost ≥ 3 mm) were compared to 10 age‐, race‐, and supragingival plaque‐matched patients with low post‐treatment clinical attachment loss (<0.5% sites/year) relative to the following parameters at 2 sites/patient with the deepest probing depths: (1) presence of 3 selected periodontal pathogens (Actinobacillus antinomycetemcomitans, Porphyromonas gingivalis. Eikenella corrodens) in subgingival plaque as determined by selective culturing, and (2) gingival crevicular fluid (GCF) levels of 3 cytokines associated with bone resorption (IL‐1 alpha, IL‐1 beta, IL‐6) as determined by two‐site ELISA. Results indicated no significant differences in any clinical measurement (except incidence of clinical attachment loss), in the presence of any bacterial pathogen, or in GCF cytokine levels between refractory subject sites versus stable subject sites. However, when sites producing the greatest total GCF cytokine/patient were compared, sites from refractory patients produced significantly more IL‐6 (30.1 ± 4.0 versus 15.4 ± 2.8 nM, p<0.01). The subgingival presence of each of the 3 bacterial pathogens was associated with elevated GCF IL‐1 concentrations. These data suggest that gingival IL‐1 and IL‐6 production is different in response to local and systemic factors associated with periodontitis, and that IL‐6 may play a role in the identification and mechanisms of refractory periodontitis.

Original languageEnglish (US)
Pages (from-to)225-231
Number of pages7
JournalJournal of Clinical Periodontology
Volume20
Issue number3
DOIs
StatePublished - Mar 1993

Fingerprint

Periodontitis
Gingival Crevicular Fluid
Interleukin-6
Cytokines
Actinobacillus
Eikenella corrodens
Porphyromonas gingivalis
Incidence
Bone Resorption
Enzyme-Linked Immunosorbent Assay
Bacteria
Therapeutics

Keywords

  • IL‐6
  • gingival crevicular‐fluid
  • interleukin (IL)‐1
  • refractory periodontitis

ASJC Scopus subject areas

  • Periodontics

Cite this

Gingival fluid IL‐1 and IL‐6 levels in refractory periodontitis. / Reinhardt, Richard A; Masada, M. P.; Kaldahl, Wayne Berwyn; DuBois, L. M.; Kornman, K. S.; Choi, J. I.; Kalkwarf, K. L.; Allison, A. C.

In: Journal of Clinical Periodontology, Vol. 20, No. 3, 03.1993, p. 225-231.

Research output: Contribution to journalArticle

Reinhardt, Richard A ; Masada, M. P. ; Kaldahl, Wayne Berwyn ; DuBois, L. M. ; Kornman, K. S. ; Choi, J. I. ; Kalkwarf, K. L. ; Allison, A. C. / Gingival fluid IL‐1 and IL‐6 levels in refractory periodontitis. In: Journal of Clinical Periodontology. 1993 ; Vol. 20, No. 3. pp. 225-231.
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AU - Reinhardt, Richard A

AU - Masada, M. P.

AU - Kaldahl, Wayne Berwyn

AU - DuBois, L. M.

AU - Kornman, K. S.

AU - Choi, J. I.

AU - Kalkwarf, K. L.

AU - Allison, A. C.

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N2 - Abstract Selected gingival bacteria and cytokine profiles associated with patients who did not respond to conventional periodontal therapy (refractory) were evaluated. 10 subjects with a high incidence of post‐active treatment clinical attachment loss (>2% sites/year lost ≥ 3 mm) were compared to 10 age‐, race‐, and supragingival plaque‐matched patients with low post‐treatment clinical attachment loss (<0.5% sites/year) relative to the following parameters at 2 sites/patient with the deepest probing depths: (1) presence of 3 selected periodontal pathogens (Actinobacillus antinomycetemcomitans, Porphyromonas gingivalis. Eikenella corrodens) in subgingival plaque as determined by selective culturing, and (2) gingival crevicular fluid (GCF) levels of 3 cytokines associated with bone resorption (IL‐1 alpha, IL‐1 beta, IL‐6) as determined by two‐site ELISA. Results indicated no significant differences in any clinical measurement (except incidence of clinical attachment loss), in the presence of any bacterial pathogen, or in GCF cytokine levels between refractory subject sites versus stable subject sites. However, when sites producing the greatest total GCF cytokine/patient were compared, sites from refractory patients produced significantly more IL‐6 (30.1 ± 4.0 versus 15.4 ± 2.8 nM, p<0.01). The subgingival presence of each of the 3 bacterial pathogens was associated with elevated GCF IL‐1 concentrations. These data suggest that gingival IL‐1 and IL‐6 production is different in response to local and systemic factors associated with periodontitis, and that IL‐6 may play a role in the identification and mechanisms of refractory periodontitis.

AB - Abstract Selected gingival bacteria and cytokine profiles associated with patients who did not respond to conventional periodontal therapy (refractory) were evaluated. 10 subjects with a high incidence of post‐active treatment clinical attachment loss (>2% sites/year lost ≥ 3 mm) were compared to 10 age‐, race‐, and supragingival plaque‐matched patients with low post‐treatment clinical attachment loss (<0.5% sites/year) relative to the following parameters at 2 sites/patient with the deepest probing depths: (1) presence of 3 selected periodontal pathogens (Actinobacillus antinomycetemcomitans, Porphyromonas gingivalis. Eikenella corrodens) in subgingival plaque as determined by selective culturing, and (2) gingival crevicular fluid (GCF) levels of 3 cytokines associated with bone resorption (IL‐1 alpha, IL‐1 beta, IL‐6) as determined by two‐site ELISA. Results indicated no significant differences in any clinical measurement (except incidence of clinical attachment loss), in the presence of any bacterial pathogen, or in GCF cytokine levels between refractory subject sites versus stable subject sites. However, when sites producing the greatest total GCF cytokine/patient were compared, sites from refractory patients produced significantly more IL‐6 (30.1 ± 4.0 versus 15.4 ± 2.8 nM, p<0.01). The subgingival presence of each of the 3 bacterial pathogens was associated with elevated GCF IL‐1 concentrations. These data suggest that gingival IL‐1 and IL‐6 production is different in response to local and systemic factors associated with periodontitis, and that IL‐6 may play a role in the identification and mechanisms of refractory periodontitis.

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