Giacomo Ori - Academia.edu (original) (raw)
Papers by Giacomo Ori
The International journal of prosthodontics/The international journal of prosthodontics, Feb 21, 2024
Atla-alternatives To Laboratory Animals, May 1, 1999
Alternatives to Laboratory Animals, 1999
Tobacco smoke is considered to be a major risk factor in the development of cardiac diseases and ... more Tobacco smoke is considered to be a major risk factor in the development of cardiac diseases and lung cancer. It has also been shown that periodontitis is more prevalent and more severe in smokers than in non-smokers. Nicotine, the major pyridine alkaloid in tobacco, has been shown to participate in periodontal disease, exerting both local and systemic effects. In the present study, the effects of nicotine (6µg/ml, 60µg/ml and 600µg/ml) on human gingival fibroblasts (HGF) were assessed by using various exposure protocols. The responses of HGF cultures obtained from smokers and non-smokers were compared to those found when using a continuous cell line (L-929). Neutral red uptake (NRU) and the measurement of DNA content with bis-benzimide dye were used to assess cell viability and cell number, respectively. NRU was the most sensitive technique for the detection of cytotoxic effects. L-929 cells were found to be affected by nicotine in the NRU assay, with a strong cytotoxic effect with 600µg/ml nicotine, and a "response" with 60µg/ml nicotine when prolonged or double challenge was applied. Nonsmoker HGF and smoker HGF reacted to nicotine in different ways, depending on the concentrations and the exposure times used, but had identical reactions following double exposure. With the Hoechst DNA assay, 600µg/ml nicotine was found to affect the growth of non-smoker HGF after long or repeated exposure, while smoker HGF were affected only by repeated exposure; growth of L-929 cells was not affected. It was concluded that HGF from smokers are able to sustain higher concentrations of nicotine without adverse effects than are non-smoker HGF and L-929 cells. If this occurs in vivo, nicotine would not be considered to be a major toxicant to HGF in smokers.
Journal of Clinical Periodontology, 1999
. The aim of the present study was to examine: (1) the effects of nicotine on human gingival fibr... more . The aim of the present study was to examine: (1) the effects of nicotine on human gingival fibroblasts (HGF); (2) differences between smokers (≥10 cigarettes/day at least for 5 years) and non‐smokers; (3) differences between patients of different age. HGF were obtained, through biopsies during periodontal surgical procedures, from 15 patients which were divided in 4 groups: 4 patients, smokers aged ≤25 years; 4 patients, non‐smokers aged ≤25 years; 3 patients, smokers aged ≥40 years; 4 patients, non‐smokers aged ≥40 years. Nicotine has been tested in 3 different concentrations: 6 μg/ml; 60 μg/ml; 600 mg/ml. To assess cells viability, the neutral red (NR) test was used; to evaluate cell proliferation, the Hoechst test was employed. After 48 h of nicotine exposure, it was found that 600 mg/ml nicotine was strongly cytotoxic to HGF of all groups, with a significant reduction of both proliferation and viability of cells versus control. Comparison between groups of the same age: when comparing untreated HGF (i.e., control values) of smokers ≤25 years versus non‐smokers ≤25 years, cell proliferation, but not viability, was found to be increased in smokers. Both viability and proliferation of control cells of smokers ≥40 years were increased versus non‐smokers ≥40 years. HGF of non‐smokers ≤25 years, when exposed to nicotine 600 μg/ml, have less viability and proliferation than HGF of smokers of the same age. Comparison between groups of different age: In the smoker group, untreated HGF (i.e., control values) had similar viability and proliferation, irrespective of age, but nicotine 600 μg/ml kills more HGF in smokers ≤25 years than in smokers ≥40 years. In non‐smokers, untreated HGF ≤25 years replicate less, but are not less viable than HGF ≥40 years. When challenged with nicotine 600 μg/ml, HGF ≤25 years were less viable than HGF ≥40 years. From this study, it appears that the smoking history and the patient age could be relevant for final evaluation of the results, since HGF from smokers are less sensitive to nicotine than HGF from non‐smokers, and cells from older donors are more resistant to nicotine than cells from younger donors.
The International journal of prosthodontics/The international journal of prosthodontics, Feb 21, 2024
Atla-alternatives To Laboratory Animals, May 1, 1999
Alternatives to Laboratory Animals, 1999
Tobacco smoke is considered to be a major risk factor in the development of cardiac diseases and ... more Tobacco smoke is considered to be a major risk factor in the development of cardiac diseases and lung cancer. It has also been shown that periodontitis is more prevalent and more severe in smokers than in non-smokers. Nicotine, the major pyridine alkaloid in tobacco, has been shown to participate in periodontal disease, exerting both local and systemic effects. In the present study, the effects of nicotine (6µg/ml, 60µg/ml and 600µg/ml) on human gingival fibroblasts (HGF) were assessed by using various exposure protocols. The responses of HGF cultures obtained from smokers and non-smokers were compared to those found when using a continuous cell line (L-929). Neutral red uptake (NRU) and the measurement of DNA content with bis-benzimide dye were used to assess cell viability and cell number, respectively. NRU was the most sensitive technique for the detection of cytotoxic effects. L-929 cells were found to be affected by nicotine in the NRU assay, with a strong cytotoxic effect with 600µg/ml nicotine, and a "response" with 60µg/ml nicotine when prolonged or double challenge was applied. Nonsmoker HGF and smoker HGF reacted to nicotine in different ways, depending on the concentrations and the exposure times used, but had identical reactions following double exposure. With the Hoechst DNA assay, 600µg/ml nicotine was found to affect the growth of non-smoker HGF after long or repeated exposure, while smoker HGF were affected only by repeated exposure; growth of L-929 cells was not affected. It was concluded that HGF from smokers are able to sustain higher concentrations of nicotine without adverse effects than are non-smoker HGF and L-929 cells. If this occurs in vivo, nicotine would not be considered to be a major toxicant to HGF in smokers.
Journal of Clinical Periodontology, 1999
. The aim of the present study was to examine: (1) the effects of nicotine on human gingival fibr... more . The aim of the present study was to examine: (1) the effects of nicotine on human gingival fibroblasts (HGF); (2) differences between smokers (≥10 cigarettes/day at least for 5 years) and non‐smokers; (3) differences between patients of different age. HGF were obtained, through biopsies during periodontal surgical procedures, from 15 patients which were divided in 4 groups: 4 patients, smokers aged ≤25 years; 4 patients, non‐smokers aged ≤25 years; 3 patients, smokers aged ≥40 years; 4 patients, non‐smokers aged ≥40 years. Nicotine has been tested in 3 different concentrations: 6 μg/ml; 60 μg/ml; 600 mg/ml. To assess cells viability, the neutral red (NR) test was used; to evaluate cell proliferation, the Hoechst test was employed. After 48 h of nicotine exposure, it was found that 600 mg/ml nicotine was strongly cytotoxic to HGF of all groups, with a significant reduction of both proliferation and viability of cells versus control. Comparison between groups of the same age: when comparing untreated HGF (i.e., control values) of smokers ≤25 years versus non‐smokers ≤25 years, cell proliferation, but not viability, was found to be increased in smokers. Both viability and proliferation of control cells of smokers ≥40 years were increased versus non‐smokers ≥40 years. HGF of non‐smokers ≤25 years, when exposed to nicotine 600 μg/ml, have less viability and proliferation than HGF of smokers of the same age. Comparison between groups of different age: In the smoker group, untreated HGF (i.e., control values) had similar viability and proliferation, irrespective of age, but nicotine 600 μg/ml kills more HGF in smokers ≤25 years than in smokers ≥40 years. In non‐smokers, untreated HGF ≤25 years replicate less, but are not less viable than HGF ≥40 years. When challenged with nicotine 600 μg/ml, HGF ≤25 years were less viable than HGF ≥40 years. From this study, it appears that the smoking history and the patient age could be relevant for final evaluation of the results, since HGF from smokers are less sensitive to nicotine than HGF from non‐smokers, and cells from older donors are more resistant to nicotine than cells from younger donors.