The influence of nicotine on the population of fibroblasts in cutaneous scars in rats

Biondo-Simões, Maria de Lourdes Pessole; Spelling, Natali Weniger; Ioshii, Sérgio Issamu; Biondo-Simões, Rachel; Repka, João Carlos Domingues

doi:10.1590/s0102-86502009000600008

Cited by 7 publications

(6 citation statements)

References 22 publications

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“…Also Biondo-Simões et al 14 in an experiment to evaluate rats' abdominal cicatrization observed that nicotine provokes a reduction in the fibroblast population, without modifying significantly the collagen density tough.…”

Section: Resultsmentioning

confidence: 99%

“…Sorensen et al Biondo-Simões et al 12 reported in a study in which the cicatrization and collagen deposition were evaluated in rats exposed to nicotine (2mg/kg/day during seven days before surgery was done and kept for seven or 14 days in post-operative) refer to the copious finding of collagen type 3 in the control group, and that may cause cicatricial immaturity 2,10,13 .…”

Section: Resultsmentioning

confidence: 99%

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Evaluation of the abdominal wall cicatrization of rabbits exposed to nicotine and undergone abdominoplasty using nylon thread or cyanoacrylate

Costa¹,

Jardim²,

Macedo³

et al. 2012

Acta Cir. Bras.

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PURPOSE: To compare the wound healing of the abdominal wall of rabbits exposed to nicotine and submitted to abdominoplasty using 2-octyl cyanoacrylate or nylon thread for the surgery suture. METHODS: Thirty two rabbits were used. They were divided in subgroups: A1, A2, B1 e B2. Group A received saline 0.9%; group B received nicotine, both groups for 14 days before surgery. We performed an abdominoplasty with a nylon suture into the A1 and B1 subgroups; as for A2 and B2 groups the suture was performed with cyanoacrylate. The euthanasia happened in the 14th post-operative day. After, we evaluated: swollen process, fibroblast proliferation, collagen, neovascularization, and macroscope and microscope epithelization of the scars. RESULTS: We observed the presence of eosinophils in all scars exposed to the cyanoacrylate, and a significant increase of neovascularization in the subgroup B2 comparing to the A2 one (p=0.037). The other variables haven't showed any statistical difference. CONCLUSIONS: Nicotine hasn't influenced the swollen process, the fibroblast proliferation, the presence of collagen, neither the epithelialization. The neovascularization showed cicatricial immaturity when comparing group A2 to group B2. The eosinophils in the scars repaired with glue showed that the substance has acted as an allergen.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Evaluation of the abdominal wall cicatrization of rabbits exposed to nicotine and undergone abdominoplasty using nylon thread or cyanoacrylate

Costa¹,

Jardim²,

Macedo³

et al. 2012

Acta Cir. Bras.

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“…In this setting, inflammation may be responsible for the decreased healing observed during nicotine treatment (79). Another study demonstrated in vivo that scar tissue healing was unaffected by nicotine (80). These processes are not well understood and require further investigation into the signaling mechanisms induced by nicotine.…”

Section: Nicotine Activates Collagen-producing Cellsmentioning

confidence: 99%

General mechanisms of nicotine‐induced fibrogenesis

et al. 2012

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Cigarette smoking contributes to the development of cancer, and pathogenesis of other diseases. Many chemicals have been identified in cigarettes that have potent biological properties. Nicotine is especially known for its role in addiction and plays a role in other physiological effects of smoking and tobacco use. Recent studies have provided compelling evidence that, in addition to promoting cancer, nicotine also plays a pathogenic role in systems, such as the lung, kidney, heart, and liver. In many organ systems, nicotine modulates fibrosis by altering the functions of fibroblasts. Understanding the processes modulated by nicotine holds therapeutic potential and may guide future clinical and research decisions. This review discusses the role of nicotine in the general fibrogenic process that governs fibrosis and fibrosis-related diseases, focusing on the cellular mechanisms that have implications in multiple organ systems. Potential research directions for the management of nicotine-induced fibrosis, and potential clinical considerations with regard to nicotine-replacement therapy (NRT) are presented.

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“…Nicotine is an alkaloid present in tobacco and accounts for about 0.6–3.0% of the dry tobacco weight. It inhibits fibroblasts via nicotinic acetylcholine receptors and facilitates the invasion of Porphyromonas gingivalis into epithelial cells and human gingival fibroblasts . The amount of nicotine in tobacco is different from the amount of nicotine in cigarettes.…”

mentioning

confidence: 99%

Effect of nicotine on growth and metabolism of Streptococcus mutans

Huang

Gregory

2012

European J Oral Sciences

111

157

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Streptococcus mutans is a key contributor to dental caries. Smokers have a higher number of caries-affected teeth than do nonsmokers, but the association among tobacco, nicotine, caries, and S. mutans growth has not been investigated in detail. Seven S. mutans strains--UA159, UA130, 10449, A32-2, NG8, LM7, and OMZ175--were used in the present study. The minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), minimum biofilm inhibitory concentration (MBIC), planktonic cell growth, biofilm formation, metabolism, and structure (determined using scanning electron microscopy) of the seven strains treated with different concentrations of nicotine (0-32 mg ml(-1)) were investigated. The MIC, MBC, and MBIC were 16 mg ml(-1) (0.1 M), 32 mg ml(-1) (0.2 M), and 16 mg ml(-1) (0.1 M), respectively, for most of the S. mutans strains. Growth of planktonic S. mutans cells was significantly repressed by 2.0-8.0 mg ml(-1) of nicotine. Biofilm formation and metabolic activity of S. mutans was increased in a nicotine-dependent manner up to 16.0 mg ml(-1) of nicotine. Scanning electron microscopy revealed that S. mutans treated with a high concentration of nicotine a had thicker biofilm and more spherical bacterial cells. In summary, nicotine enhances S. mutans biofilm formation and biofilm metabolic activity. These results suggest that smoking can increase the development of caries by fostering increased formation of S. mutans biofilm on tooth surfaces.

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The influence of nicotine on the population of fibroblasts in cutaneous scars in rats

Abstract: Under the conditions of this experiment, nicotine reduced the fibroblast population without modifying collagen density significantly.

Cited by 7 publications

References 22 publications

Evaluation of the abdominal wall cicatrization of rabbits exposed to nicotine and undergone abdominoplasty using nylon thread or cyanoacrylate

Evaluation of the abdominal wall cicatrization of rabbits exposed to nicotine and undergone abdominoplasty using nylon thread or cyanoacrylate

General mechanisms of nicotine‐induced fibrogenesis

Effect of nicotine on growth and metabolism of Streptococcus mutans

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