Persistence of extracrevicular bacterial reservoirs after treatment of aggressive periodontitis

Jason D. Johnson, Ruoqiong Chen, Patricia A Lenton, Guizhen Zhang, James E Hinrichs, Joel D Rudney

Research output: Contribution to journalArticle

56 Citations (Scopus)

Abstract

Background: The purpose of this study was to test the hypothesis that periodontal pathogens associated with aggressive periodontitis persist in extracrevicular locations following scaling and root planing, systemic antibiotics, and antimicrobial rinses. Methods: Eighteen patients with aggressive periodontitis received a clinical examination during which samples of subgingival plaque and buccal epithelial cells were obtained. Treatment consisted of full-mouth root planing, systemic antibiotics, and chlorhexidine rinses. Clinical measurements and sampling were repeated at 3 and 6 months. Quantitative polymerase chain reaction determined the number of Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Prevotella intermedia, Porphyromonas gingivalis, Tannerella forsythia (previously T. forsythensis), and Treponema denticola in the plaque. Fluorescence in situ hybridization and confocal microscopy determined the extent of intracellular invasion in epithelial cells. Results: Clinical measurements improved significantly following treatment. All bacterial species except P. gingivalis were significantly reduced in plaque between baseline and 3 months. However, all species showed a trend to repopulate between 3 and 6 months. This increase was statistically significant for log T. denticola counts. All species were detected intracellularly. The percentage of cells infected intracellularly was not affected by therapy. Conclusions: The 6-month increasing trend in the levels of plaque bacteria suggests that subgingival recolonization was occurring. Because the presence of these species within epithelial cells was not altered after treatment, it is plausible that recolonization may occur from the oral mucosa. Systemic antibiotics and topical chlorhexidine did not reduce the percentage of invaded epithelial cells. These data support the hypothesis that extracrevicular reservoirs of bacteria exist, which might contribute to recurrent or refractory disease in some patients.

Original languageEnglish (US)
Pages (from-to)2305-2312
Number of pages8
JournalJournal of periodontology
Volume79
Issue number12
DOIs
StatePublished - Dec 1 2008

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Aggressive Periodontitis
Epithelial Cells
Treponema denticola
Root Planing
Aggregatibacter actinomycetemcomitans
Porphyromonas gingivalis
Chlorhexidine
Anti-Bacterial Agents
Prevotella intermedia
Bacteria
Cheek
Mouth Mucosa
Therapeutics
Fluorescence In Situ Hybridization
Confocal Microscopy
Mouth
Polymerase Chain Reaction

Keywords

  • Aggressive periodontitis
  • Antibiotic
  • Bacteria
  • Intracellular
  • Mouth mucosa
  • Treponema denticola

Cite this

Persistence of extracrevicular bacterial reservoirs after treatment of aggressive periodontitis. / Johnson, Jason D.; Chen, Ruoqiong; Lenton, Patricia A; Zhang, Guizhen; Hinrichs, James E; Rudney, Joel D.

In: Journal of periodontology, Vol. 79, No. 12, 01.12.2008, p. 2305-2312.

Research output: Contribution to journalArticle

Johnson, Jason D. ; Chen, Ruoqiong ; Lenton, Patricia A ; Zhang, Guizhen ; Hinrichs, James E ; Rudney, Joel D. / Persistence of extracrevicular bacterial reservoirs after treatment of aggressive periodontitis. In: Journal of periodontology. 2008 ; Vol. 79, No. 12. pp. 2305-2312.
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abstract = "Background: The purpose of this study was to test the hypothesis that periodontal pathogens associated with aggressive periodontitis persist in extracrevicular locations following scaling and root planing, systemic antibiotics, and antimicrobial rinses. Methods: Eighteen patients with aggressive periodontitis received a clinical examination during which samples of subgingival plaque and buccal epithelial cells were obtained. Treatment consisted of full-mouth root planing, systemic antibiotics, and chlorhexidine rinses. Clinical measurements and sampling were repeated at 3 and 6 months. Quantitative polymerase chain reaction determined the number of Aggregatibacter actinomycetemcomitans (previously Actinobacillus actinomycetemcomitans), Prevotella intermedia, Porphyromonas gingivalis, Tannerella forsythia (previously T. forsythensis), and Treponema denticola in the plaque. Fluorescence in situ hybridization and confocal microscopy determined the extent of intracellular invasion in epithelial cells. Results: Clinical measurements improved significantly following treatment. All bacterial species except P. gingivalis were significantly reduced in plaque between baseline and 3 months. However, all species showed a trend to repopulate between 3 and 6 months. This increase was statistically significant for log T. denticola counts. All species were detected intracellularly. The percentage of cells infected intracellularly was not affected by therapy. Conclusions: The 6-month increasing trend in the levels of plaque bacteria suggests that subgingival recolonization was occurring. Because the presence of these species within epithelial cells was not altered after treatment, it is plausible that recolonization may occur from the oral mucosa. Systemic antibiotics and topical chlorhexidine did not reduce the percentage of invaded epithelial cells. These data support the hypothesis that extracrevicular reservoirs of bacteria exist, which might contribute to recurrent or refractory disease in some patients.",
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