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nicotine osteoblast alveolar bone

Beom-Su Kim, Su-Jin Kim, Hyung-Jin Kim, Seung-Jin Lee, Yoon-Jeong Park, Jun Lee, Hyung-Keun You
AIMS: Nicotine is a risk factor for various diseases, including osteoporosis, oral cancer, and periodontal disease. Numerous studies have elucidated the effects of nicotine on cell proliferation and differentiation. The purpose of this study was to determine the effects of nicotine on the proliferation and osteoblast differentiation of human alveolar bone marrow-derived mesenchymal stem cells (hABMMSCs). MAIN METHODS: In this study, we treated hABMMSCs with different doses (1 μM to 5 mM) of nicotine...
January 16, 2012: Life Sciences
Giscard José Ribeiro Machado, Sheila Mônica Damásio Dias, Alvaro Fancisco Bosco, Tetuo Okamoto, João César Bedran de Castro, Rita Cássia Menegati Dornelles
PURPOSE: The purpose of this study was to evaluate the effects of nicotine and ovariectomy on alveolar bone regeneration after exodontias in rats. MATERIALS AND METHODS: For 30 days, sham ovariectomized (OVX)/NaCl, sham OVX/nicotine, OVX/NaCl, and OVX/nicotine animals were given 2 daily injections of saline or hemisulfate of nicotine. After this period, exodontic procedures were carried out and treatment continued up to the time of euthanasia on days 7 and 14 when the alveoli were removed for further analyses...
November 2010: Journal of Oral and Maxillofacial Surgery
Tomoko Katono, Takayuki Kawato, Natsuko Tanabe, Hideki Tanaka, Naoto Suzuki, Satoshi Kitami, Toyoko Morita, Masafumi Motohashi, Masao Maeno
OBJECTIVE: Lipopolysaccharide (LPS) from periodontopathic bacteria can initiate alveolar bone loss through the induction of host-derived cytokines. Smoking increases the risk and severity of periodontitis. We examined the effects of nicotine and LPS on the expression of matrix metalloproteinases (MMPs), plasminogen activators (PAs), and their inhibitors, including tissue inhibitors of metalloproteinases (TIMPs) and PA inhibitor-1 (PAI-1), in osteoblasts. METHODS: The cells were cultured with or without 10(-4) M nicotine and 100 ng/ml LPS for 12 days or with 100 microg/ml polymyxin B, 10(-4) M D-tubocurarine, 10 micromol/ml NS398, or 10(-6) M celecoxib in the presence of either nicotine or LPS for 12 days...
February 2009: Archives of Oral Biology
Maiko Shoji, Natsuko Tanabe, Narihiro Mitsui, Naoto Suzuki, Osamu Takeichi, Tomoko Katono, Akira Morozumi, Masao Maeno
Previous studies have indicated that lipopolysaccharide (LPS) from Gram-negative bacteria in plaque induces the release of prostaglandin E(2) (PGE(2)), which promotes alveolar bone resorption in periodontitis, and that tobacco smoking might be an important risk factor for the development and severity of periodontitis. We determined the effect of nicotine and LPS on alkaline phosphatase (ALPase) activity, PGE(2) production, and the expression of cyclooxygenase (COX-1, COX-2), PGE(2) receptors Ep1>4, and macrophage colony stimulating factor (M-CSF) in human osteoblastic Saos-2 cells...
March 2007: Acta Biochimica et Biophysica Sinica
Hideki Tanaka, Natsuko Tanabe, Maiko Shoji, Naoto Suzuki, Tomoko Katono, Setsuko Sato, Masafumi Motohashi, Masao Maeno
Several studies have indicated that one of the causes of alveolar bone destruction with periodontitis is lipopolysaccharide (LPS) from the cell wall of Gram-negative bacteria in plaque and that tobacco smoking may be an important risk factor for the development and severity of periodontitis. The present study was undertaken to determine the effect of nicotine and LPS on the expression of macrophage colony-stimulating factor (M-CSF), osteoprotegerin (OPG), and prostaglandin E2 (PGE2) in osteoblasts, and the indirect effect of nicotine and LPS on the formation of osteoclast-like cells...
March 6, 2006: Life Sciences
Bruno Braga Benatti, João Batista César-Neto, Patrícia Furtado Gonçalves, Enílson Antônio Sallum, Francisco Humberto Nociti
This study aimed to evaluate in rats the impact of cigarette smoke inhalation (CSI) and nicotine administration (NA) on a periodontal healing model in the absence of a plaque biofilm. Wistar rats (n = 42) were assigned to three groups: Group 1, control (n = 14); Group 2, NA (3 mg kg(-1)) (n = 14); and Group 3, CSI (n = 14). Thirty days after CSI and NA exposure, fenestration defects were created buccally to the distal root of the first mandibular molar. The animals were killed 21 d later and their mandibles were processed for histological examination...
October 2005: European Journal of Oral Sciences
Juliana B Saldanha, Suzana P Pimentel, Marcio Z Casati, Enilson A Sallum, Deise Barbieri, Heitor Júnior Moreno, Francisco H Júnior Nociti
BACKGROUND: A series of animal and in vitro data confirms that nicotine impairs bone healing, diminishes osteoblast function, and causes autogenous bone graft morbidity. Therefore, this study aimed to investigate the impact of nicotine on the healing of bone defects treated by the guided bone regeneration (GBR) principle. METHODS: Sixteen mongrel dogs were used. One defect was surgically created bilaterally and randomly assigned as an expanded polytetrafluoroethylene (ePTFE) membrane site or a non-membrane control site...
April 2004: Journal of Periodontology
W K Ramp, L G Lenz, R J Galvin
Use of smokeless tobacco is associated with various oral lesions including periodontal damage and alveolar bone loss. This study was performed to test the effects of nicotine on bone-forming cells at concentrations that occur in the saliva of smokeless tobacco users. Confluent cultures of osteoblast-like cells isolated from chick embryo calvariae were incubated for 2 days with nicotine added to the culture medium (25-600 micrograms/ml). Nicotine inhibited alkaline phosphatase in the cell layer and released to the medium, whereas glycolysis (as indexed by lactate production) was unaffected or slightly elevated...
May 1991: Proceedings of the Society for Experimental Biology and Medicine
M A Fang, P J Frost, A Iida-Klein, T J Hahn
We examined the effect of nicotine on cellular proliferation, as measured by [3H]thymidine (TdR) incorporation and cell count, and on alkaline phosphatase activity in UMR 106-01 rat osteoblastic osteosarcoma cells. The cells were cultured with varying concentrations of nicotine in serum-free medium for 2 to 72 hours. Nicotine produced a dose-dependent suppression of TdR incorporation, with maximum suppression seen at 10 mM (7% of control); the EC50 for suppression of TdR incorporation was 10 microM. 1 microM nicotine decreased cell number by 20% to 30%...
1991: Bone
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