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1.
Tob Induc Dis ; 21: 101, 2023.
Article in English | MEDLINE | ID: mdl-37533959

ABSTRACT

INTRODUCTION: Smoking is known to alter the regenerative and immunomodulatory properties of many types of mesenchymal stem cells (MSCs). This study investigates the impact of cigarette smoke exposure on the regenerative potential of dental pulp stem cells (DPSCs). METHODS: DPSCs were treated with various doses of cigarette smoke condensate (CSC) or nicotine. Cell proliferation and survival were evaluated by a water-soluble tetrazolium salt (WST-1) and a survival assay. DPSC migration, cytokine expression, mutagenesis, and the signaling pathway were also measured during CSC and nicotine treatment. RESULTS: Low concentrations of CSC and nicotine did not impair cell proliferation, but higher concentrations reduced cell proliferation. CSC and nicotine could impede DPSC survival and migration in a dose-dependent manner. In addition, the cytokine secretion expression profile was altered with CSC or nicotine treatments. In particular, secretion of IL-6, TNF-α, and IL-10 significantly increased, while TGF-ß1 levels showed different patterns after exposure to CSC or nicotine, as shown by ELISA and quantitative PCR. Nicotine treatment increased AKT (also known as protein kinase B) and extracellular signal-regulated kinase (ERK) phosphorylation. Finally, CSC induced higher levels of mutagenicity than nicotine, as shown by the Ames test. CONCLUSIONS: These findings suggest that cigarette smoke exposure alters the regenerative abilities of DPSCs in various ways. Future studies are warranted to further characterize the underlying molecular mechanisms of smoking-mediated damage to DPSCs, which will guide the personalized stem cell treatment plan for smoking patients.

2.
Am J Physiol Cell Physiol ; 320(2): C175-C181, 2021 02 01.
Article in English | MEDLINE | ID: mdl-33175571

ABSTRACT

The persistent prevalence of cigarette smoking continues to contribute to preventable disease and death in the United States. Although much is known about the deleterious systemic effects of cigarette smoke and nicotine, some clinically relevant areas, such as the impact of cigarette smoke and nicotine on stem cells and the subsequent implications in regenerative medicine, still remain unclear. This review focuses on recent studies on the effect of cigarette smoke and one of its deleterious components, nicotine, on mesenchymal stem cells, with an emphasis on dental stem cells.


Subject(s)
Dental Pulp/cytology , Dental Pulp/drug effects , Mesenchymal Stem Cells/drug effects , Nicotiana/adverse effects , Smoke/adverse effects , Animals , Cell Differentiation/drug effects , Cell Differentiation/physiology , Cells, Cultured , Dental Pulp/physiology , Humans , Mesenchymal Stem Cells/physiology
3.
Microb Cell ; 6(4): 197-208, 2019 Mar 11.
Article in English | MEDLINE | ID: mdl-30956972

ABSTRACT

Chlamydia pneumoniae is an airborne, Gram-negative, obligate intracellular bacterium which causes human respiratory infections and has been associated with atherosclerosis. Because individuals with periodontitis are at greater risk for atherosclerosis as well as respiratory infections, we in-vestigated the role of C. pneumoniae in inflammation and periodontal dis-ease. We found that C. pneumoniae was more frequently found in subgingival dental plaque obtained from periodontally diseased sites of the mouth versus healthy sites. The known periodontal pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were also found in the plaque. In addition, C. pneumoniae could efficiently invade human gingival epithelial cells (GECs) in vitro, causing translocation of NF-κB to the nucleus along with increased secretion of mature IL-1ß cytokine. Supernatants collected from C. pneumoniae-infected GECs showed increased activation of caspase-1 protein, which was significantly reduced when nlrp3 gene expression was silenced using shRNA lentiviral vectors. Our results demonstrate that C. pneumoniae was found in higher levels in periodontitis patients compared to control pa-tients. Additionally, C. pneumoniae could infect GECs, leading to inflammation caused by activation of NF-κB and the NLRP3 inflammasome. We propose that the presence of C. pneumoniae in subgingival dental plaque may contribute to periodontal disease and could be used as a potential risk indicator of perio-dontal disease.

4.
Microbes Infect ; 14(9): 684-9, 2012 Aug.
Article in English | MEDLINE | ID: mdl-22484385

ABSTRACT

Porphyromonas gingivalis is a major pathogen implicated in chronic periodontitis. We examined whether P. gingivalis affected the secretion of the pro-inflammatory cytokine interleukin-18 (IL-18) in macrophage-like THP-1 cells and in monocytic THP-1 cells in suspension. Live P. gingivalis-induced significant IL-18 secretion. Heat-inactivation of P. gingivalis greatly reduced the IL-18 stimulation; the IL-18 levels were similar to that observed with P. gingivalis LPS alone. Live P. gingivalis caused a cytotoxic effect that was reduced greatly by heat-inactivation. Our observations indicate that P. gingivalis specifically stimulates the production and release of the active form of IL-18, which may contribute to the progression of periodontitis.


Subject(s)
Interleukin-18/metabolism , Monocytes/immunology , Monocytes/microbiology , Porphyromonas gingivalis/immunology , Cell Line , Humans
5.
Arch Oral Biol ; 52(11): 1102-8, 2007 Nov.
Article in English | MEDLINE | ID: mdl-17586460

ABSTRACT

The study aim was to determine whether prostaglandin E(2) (PGE(2)) in gingival crevicular fluid (GCF) could serve as a risk factor for periodontitis in human immunodeficiency virus-positive (HIV(+)) patients. Clinical measurements, including gingival index (GI), plaque index, bleeding index, probing depth (PD), attachment loss (AL) and GCF samples were taken from two healthy sites (including sites with gingival recession, GI=0; PD< or =3 mm; AL< or =2 mm), three gingivitis sites (GI>0; PD< or =3 mm; AL=0) and three periodontitis sites (GI>0; PD> or =5 mm; AL> or =3 mm) of each of the 30 patients at baseline and 6-month visits. GCF samples were also taken by means of paper strips. GCF PGE(2) levels were determined by a sandwich ELISA. The progressing site was defined as a site which had 2 mm or more attachment loss during the 6-month study period. The mean amounts of PGE(2) were significantly higher in gingivitis and periodontitis sites than in healthy sites (p<0.0001). GCF levels of PGE(2) were significantly correlated with probing depth, attachment loss, CD4(+) cells, viral load, age and smoking pack-years at baseline and 6-month visits (0.0001

Subject(s)
Dinoprostone/analysis , Gingival Crevicular Fluid/chemistry , HIV Infections/complications , Periodontitis/complications , Adult , Age Factors , Analysis of Variance , CD4-Positive T-Lymphocytes/immunology , Disease Progression , Gingivitis/complications , Gingivitis/metabolism , HIV Infections/immunology , HIV Infections/metabolism , Humans , Longitudinal Studies , Lymphocyte Count , Male , Middle Aged , Periodontal Index , Periodontitis/metabolism , Risk Factors , Smoking/adverse effects , Viral Load
6.
J Periodontal Res ; 39(3): 149-57, 2004 Jun.
Article in English | MEDLINE | ID: mdl-15102043

ABSTRACT

OBJECTIVE: The purpose of this study was to identify risk factors for periodontitis associated with human immunodeficiency virus (HIV) infection. METHODS: A total of 152 HIV(+) patients were recruited from the CARE clinic at the University of the Pacific School of Dentistry. Clinical measurements (gingival index, plaque index, bleeding index, probing depth, and attachment loss), gingival crevicular fluid (GCF) and subgingival plaque samples were taken from eight sites of each patient at baseline and 6-month visits. GCF neutrophil elastase was determined by measurement of p-nitroanalide resulting from hydrolysis of an elastase-specific peptide. GCF beta-glucuronidase was determined by release of 4-methylumbelliferone from hydrolysis of a specific substrate. A bacterial concentration fluorescence immunoassay was used to detect periodontopathic bacteria in subgingival plaque samples. RESULTS: Viral load, age, smoking pack-years, Fusobacterium nucleatum, Prevotella intermedia, Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, neutrophil elastase, and beta-glucuronidase were significantly correlated with clinical measurements (0.0001 < p < 0.05). Significantly higher levels of elastase, beta-glucuronidase, F. nucleatum, P. intermedia, and A. actinomycetemcomitans were found at progressing sites than in non-progressing sites (0.001 < p < 0.05). CONCLUSIONS: These data indicate that age, smoking pack-years, viral load, F. nucleatum, P. intermedia, A. actinomycetemcomitans, elastase, and beta-glucuronidase are risk factors for periodontitis in HIV(+) patients.


Subject(s)
HIV Infections/complications , Periodontitis/etiology , Adolescent , Adult , Age Factors , Analysis of Variance , Bacteria, Anaerobic/pathogenicity , Dental Plaque/microbiology , Gingival Crevicular Fluid/enzymology , Glucuronidase/analysis , Humans , Leukocyte Elastase/analysis , Male , Middle Aged , Odds Ratio , Regression Analysis , Risk Factors , Smoking/adverse effects , Statistics, Nonparametric , Viral Load
7.
Ann Periodontol ; 7(1): 8-16, 2002 Dec.
Article in English | MEDLINE | ID: mdl-16013212

ABSTRACT

BACKGROUND: Necrotizing ulcerative periodontitis (NUP) is a painful and potentially debilitating affliction that affects about 2% to 6% of HIV-positive subjects. NUP may be caused by specific microorganisms that are presently unknown or by microbial species not usually thought to cause periodontal infections. The purpose of this study was to define the bacterial species associated with NUP in HIV-positive patients. METHODS: 16S rRNA bacterial genes of DNA isolated from subgingival plaque of 8 HIV-positive subjects with NUP were amplified by polymerase chain reaction (PCR) and cloned into Escherichia coli. The sequences of cloned inserts were used to determine species identity or closest relatives by comparison with known sequences. The microbial profiles in subgingival plaque of subjects with NUP, chronic periodontitis, and periodontal health were compared using a battery of over 200 oligonucleotide probes in a PCR-based, reverse-capture, checkerboard DNA-DNA hybridization assay. RESULTS: Sequence analysis of over 400 clones revealed 108 species; 65 were "uncultivable" phylotypes, of which 26 were novel to NUP subjects. Species or phylotypes most commonly detected were Bulleidia extructa, Dialister, Fusobacterium, Selenomonas, Peptostreptococcus, Veillonella, and the phylum TM7. Based on sequence analysis and checkerboard analysis, NUP did not possess the classical periodontal pathogens such as Porphyromonas gingivalis. Otherwise, the microbial profiles of NUP and periodontitis had many similarities. The microbial profiles of subgingival plaque from periodontally healthy subjects were different and less complex in comparison to the profiles of both disease groups. CONCLUSIONS: Certain species appear to be associated with health and periodontal diseases. The putative pathogens associated with periodontal disease in HIV-negative subjects are not associated with NUP in HIV-positive subjects.


Subject(s)
Bacterial Typing Techniques/methods , Dental Plaque/microbiology , Gingivitis, Necrotizing Ulcerative/microbiology , HIV Seropositivity/microbiology , Adult , DNA, Bacterial/analysis , Female , Gingivitis, Necrotizing Ulcerative/complications , HIV Seropositivity/complications , Humans , Male , Oligonucleotide Array Sequence Analysis/methods , RNA, Ribosomal, 16S/genetics , Sequence Analysis, DNA
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