Effects of nicotine on proliferation and extracellular matrix production of human gingival fibroblasts in vitro.

David Tipton, M. K. Dabbous

Research output: Contribution to journalArticle

174 Citations (Scopus)

Abstract

Normal function of gingival fibroblasts is essential for maintenance of the gingival extracellular matrix (ECM), but under inflammatory conditions in gingival tissue which may occur with tobacco use, they can also act in its destruction. The purpose of this study was to determine the effects of nicotine, a major component of tobacco, on gingival fibroblast proliferation, the production of fibronectin (FN), and the production and breakdown of type I collagen to elucidate its role in periodontal destruction associated with its use. A human gingival fibroblast strain derived from a healthy individual with non-inflamed gingiva was used in this study. Nicotine at concentrations > 0.075% caused cell death, and at 0.075% and 0.05% it caused transient vacuolization of the fibroblasts. At concentrations of 0.001% to 0.075%, nicotine significantly inhibited proliferation (P < or = 0.03), measured by the incorporation of [3H]-thymidine into DNA. The production of FN and type I collagen was significantly inhibited by nicotine at > or = 0.05% (P < or = 0.001), measured using specific ELISAs. On the other hand, nicotine at > or = 0.025% significantly increased collagenase activity (P < or = 0.008), using [3H]-gly and [14C]-pro-labeled type I collagen gels as substrate. The results show that, in vitro, nicotine inhibits the growth of gingival fibroblasts and their production of FN and collagen, while also promoting collagen breakdown. This suggests that nicotine itself may augment the destruction of the gingival ECM occurring during periodontal inflammation associated with smokeless tobacco use.

Original languageEnglish (US)
Pages (from-to)1056-1064
Number of pages9
JournalJournal of Periodontology
Volume66
Issue number12
DOIs
StatePublished - Jan 1 1995

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Nicotine
Extracellular Matrix
Fibroblasts
Tobacco Use
Collagen Type I
Fibronectins
Collagen
Smokeless Tobacco
Gingiva
Collagenases
Tobacco
Cell Death
Gels
Maintenance
In Vitro Techniques
Inflammation
Growth

All Science Journal Classification (ASJC) codes

  • Periodontics

Cite this

Effects of nicotine on proliferation and extracellular matrix production of human gingival fibroblasts in vitro. / Tipton, David; Dabbous, M. K.

In: Journal of Periodontology, Vol. 66, No. 12, 01.01.1995, p. 1056-1064.

Research output: Contribution to journalArticle

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abstract = "Normal function of gingival fibroblasts is essential for maintenance of the gingival extracellular matrix (ECM), but under inflammatory conditions in gingival tissue which may occur with tobacco use, they can also act in its destruction. The purpose of this study was to determine the effects of nicotine, a major component of tobacco, on gingival fibroblast proliferation, the production of fibronectin (FN), and the production and breakdown of type I collagen to elucidate its role in periodontal destruction associated with its use. A human gingival fibroblast strain derived from a healthy individual with non-inflamed gingiva was used in this study. Nicotine at concentrations > 0.075{\%} caused cell death, and at 0.075{\%} and 0.05{\%} it caused transient vacuolization of the fibroblasts. At concentrations of 0.001{\%} to 0.075{\%}, nicotine significantly inhibited proliferation (P < or = 0.03), measured by the incorporation of [3H]-thymidine into DNA. The production of FN and type I collagen was significantly inhibited by nicotine at > or = 0.05{\%} (P < or = 0.001), measured using specific ELISAs. On the other hand, nicotine at > or = 0.025{\%} significantly increased collagenase activity (P < or = 0.008), using [3H]-gly and [14C]-pro-labeled type I collagen gels as substrate. The results show that, in vitro, nicotine inhibits the growth of gingival fibroblasts and their production of FN and collagen, while also promoting collagen breakdown. This suggests that nicotine itself may augment the destruction of the gingival ECM occurring during periodontal inflammation associated with smokeless tobacco use.",
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