Nicotine stimulates osteoclast resorption in a porcine marrow cell model

Claudia L. Henemyre, Donald K. Scales, Steven D. Hokett, Michael F. Cuenin, Mark E. Peacock, Merle H Parker, Phyllis D. Brewer, Augustine H. Chuang

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

Background: Combustible tobacco use is generally linked with accelerated periodontal bone loss and diminished post-surgical wound healing; however, the pathogenesis of this process at the cellular level remains unclear. Nicotine is known to affect human gingival fibroblast orientation, attachment, and β1 integrin expression, yet little is known about its effects on osteoclasts, the cells most responsible for bone resorption. The purpose of this study was to determine the effects of physiologically relevant nicotine levels on porcine osteoclast function as measured by resorption of calcium phosphate. Methods: Pure nicotine was diluted in medium to the following concentrations: 0.03 μM, 0.15 μM, 0.30 μM, 0.60 μM and 1.50 μM. Porcine osteoclasts were seeded onto calcium phosphate multi-test slides and incubated at 37°C with half media changes every 24 hours. Cells received 0, 0.15, 0.30, 0.60, and 1.50 μM nicotine, or 25 nM parathyroid hormone (PTH). Osteoclast resorption was quantified by measuring the resorbed surface area of the calcium phosphate substrate. Results: Osteoclast cultures resorbed bone slices and calcium phosphate substrate. All nicotine concentrations and PTH resulted in statistically significantly greater mean percent resorptions than the control group (P <0.05). However, no statistical difference was found between the various nicotine doses or PTH. The number of osteoclasts increased in a linear relationship to the increasing nicotine concentrations; however, no correlation was found between osteoclast number and the amount of resorption. Conclusions: Nicotine is non-toxic to osteoclasts at the clinically relevant levels tested. Nicotine appears to stimulate osteoclast differentiation and resorption of calcium phosphate, the major component of bone. Nicotine-modulated osteoclast stimulation may, in part, explain the increased rapidity of periodontal bone loss and refractory disease incidence in smokers.

Original languageEnglish (US)
Pages (from-to)1440-1446
Number of pages7
JournalJournal of Periodontology
Volume74
Issue number10
DOIs
StatePublished - Oct 1 2003

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Osteoclasts
Nicotine
Swine
Bone Marrow
Parathyroid Hormone
Alveolar Bone Loss
Bone and Bones
Tobacco Use
Bone Resorption
Integrins
Wound Healing
Fibroblasts
calcium phosphate
Control Groups
Incidence

Keywords

  • Bone resorption
  • Calcium phosphate
  • Nicotine/adverse effects
  • Osteoclasts
  • Smoking/adverse effects

ASJC Scopus subject areas

  • Periodontics

Cite this

Nicotine stimulates osteoclast resorption in a porcine marrow cell model. / Henemyre, Claudia L.; Scales, Donald K.; Hokett, Steven D.; Cuenin, Michael F.; Peacock, Mark E.; Parker, Merle H; Brewer, Phyllis D.; Chuang, Augustine H.

In: Journal of Periodontology, Vol. 74, No. 10, 01.10.2003, p. 1440-1446.

Research output: Contribution to journalArticle

Henemyre, CL, Scales, DK, Hokett, SD, Cuenin, MF, Peacock, ME, Parker, MH, Brewer, PD & Chuang, AH 2003, 'Nicotine stimulates osteoclast resorption in a porcine marrow cell model', Journal of Periodontology, vol. 74, no. 10, pp. 1440-1446. https://doi.org/10.1902/jop.2003.74.10.1440
Henemyre, Claudia L. ; Scales, Donald K. ; Hokett, Steven D. ; Cuenin, Michael F. ; Peacock, Mark E. ; Parker, Merle H ; Brewer, Phyllis D. ; Chuang, Augustine H. / Nicotine stimulates osteoclast resorption in a porcine marrow cell model. In: Journal of Periodontology. 2003 ; Vol. 74, No. 10. pp. 1440-1446.
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abstract = "Background: Combustible tobacco use is generally linked with accelerated periodontal bone loss and diminished post-surgical wound healing; however, the pathogenesis of this process at the cellular level remains unclear. Nicotine is known to affect human gingival fibroblast orientation, attachment, and β1 integrin expression, yet little is known about its effects on osteoclasts, the cells most responsible for bone resorption. The purpose of this study was to determine the effects of physiologically relevant nicotine levels on porcine osteoclast function as measured by resorption of calcium phosphate. Methods: Pure nicotine was diluted in medium to the following concentrations: 0.03 μM, 0.15 μM, 0.30 μM, 0.60 μM and 1.50 μM. Porcine osteoclasts were seeded onto calcium phosphate multi-test slides and incubated at 37°C with half media changes every 24 hours. Cells received 0, 0.15, 0.30, 0.60, and 1.50 μM nicotine, or 25 nM parathyroid hormone (PTH). Osteoclast resorption was quantified by measuring the resorbed surface area of the calcium phosphate substrate. Results: Osteoclast cultures resorbed bone slices and calcium phosphate substrate. All nicotine concentrations and PTH resulted in statistically significantly greater mean percent resorptions than the control group (P <0.05). However, no statistical difference was found between the various nicotine doses or PTH. The number of osteoclasts increased in a linear relationship to the increasing nicotine concentrations; however, no correlation was found between osteoclast number and the amount of resorption. Conclusions: Nicotine is non-toxic to osteoclasts at the clinically relevant levels tested. Nicotine appears to stimulate osteoclast differentiation and resorption of calcium phosphate, the major component of bone. Nicotine-modulated osteoclast stimulation may, in part, explain the increased rapidity of periodontal bone loss and refractory disease incidence in smokers.",
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AU - Henemyre, Claudia L.

AU - Scales, Donald K.

AU - Hokett, Steven D.

AU - Cuenin, Michael F.

AU - Peacock, Mark E.

AU - Parker, Merle H

AU - Brewer, Phyllis D.

AU - Chuang, Augustine H.

PY - 2003/10/1

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N2 - Background: Combustible tobacco use is generally linked with accelerated periodontal bone loss and diminished post-surgical wound healing; however, the pathogenesis of this process at the cellular level remains unclear. Nicotine is known to affect human gingival fibroblast orientation, attachment, and β1 integrin expression, yet little is known about its effects on osteoclasts, the cells most responsible for bone resorption. The purpose of this study was to determine the effects of physiologically relevant nicotine levels on porcine osteoclast function as measured by resorption of calcium phosphate. Methods: Pure nicotine was diluted in medium to the following concentrations: 0.03 μM, 0.15 μM, 0.30 μM, 0.60 μM and 1.50 μM. Porcine osteoclasts were seeded onto calcium phosphate multi-test slides and incubated at 37°C with half media changes every 24 hours. Cells received 0, 0.15, 0.30, 0.60, and 1.50 μM nicotine, or 25 nM parathyroid hormone (PTH). Osteoclast resorption was quantified by measuring the resorbed surface area of the calcium phosphate substrate. Results: Osteoclast cultures resorbed bone slices and calcium phosphate substrate. All nicotine concentrations and PTH resulted in statistically significantly greater mean percent resorptions than the control group (P <0.05). However, no statistical difference was found between the various nicotine doses or PTH. The number of osteoclasts increased in a linear relationship to the increasing nicotine concentrations; however, no correlation was found between osteoclast number and the amount of resorption. Conclusions: Nicotine is non-toxic to osteoclasts at the clinically relevant levels tested. Nicotine appears to stimulate osteoclast differentiation and resorption of calcium phosphate, the major component of bone. Nicotine-modulated osteoclast stimulation may, in part, explain the increased rapidity of periodontal bone loss and refractory disease incidence in smokers.

AB - Background: Combustible tobacco use is generally linked with accelerated periodontal bone loss and diminished post-surgical wound healing; however, the pathogenesis of this process at the cellular level remains unclear. Nicotine is known to affect human gingival fibroblast orientation, attachment, and β1 integrin expression, yet little is known about its effects on osteoclasts, the cells most responsible for bone resorption. The purpose of this study was to determine the effects of physiologically relevant nicotine levels on porcine osteoclast function as measured by resorption of calcium phosphate. Methods: Pure nicotine was diluted in medium to the following concentrations: 0.03 μM, 0.15 μM, 0.30 μM, 0.60 μM and 1.50 μM. Porcine osteoclasts were seeded onto calcium phosphate multi-test slides and incubated at 37°C with half media changes every 24 hours. Cells received 0, 0.15, 0.30, 0.60, and 1.50 μM nicotine, or 25 nM parathyroid hormone (PTH). Osteoclast resorption was quantified by measuring the resorbed surface area of the calcium phosphate substrate. Results: Osteoclast cultures resorbed bone slices and calcium phosphate substrate. All nicotine concentrations and PTH resulted in statistically significantly greater mean percent resorptions than the control group (P <0.05). However, no statistical difference was found between the various nicotine doses or PTH. The number of osteoclasts increased in a linear relationship to the increasing nicotine concentrations; however, no correlation was found between osteoclast number and the amount of resorption. Conclusions: Nicotine is non-toxic to osteoclasts at the clinically relevant levels tested. Nicotine appears to stimulate osteoclast differentiation and resorption of calcium phosphate, the major component of bone. Nicotine-modulated osteoclast stimulation may, in part, explain the increased rapidity of periodontal bone loss and refractory disease incidence in smokers.

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