Background: Epidemiological studies have demonstrated deteriorating effects of smoking on periodontal tissue. The aims of this study were to compare oxygen saturation of hemoglobin in the gingiva (GSo2) of smokers and non-smokers and to evaluate the chronic effect of smoking on gingival oxygen sufficiency.
Methods: GSo2 was determined using tissue reflectance spectrophotometry in 110 papillary gingival sites of 62 smokers and 100 sites of 60 non-smokers.
Results: No significant difference was found in GSo2 between smokers and non-smokers. In the model of ANOVA with covariates, age (P= 0.0048) and probing depth (P= 0.0012) had significant effects on GSo2. No significant effect was found in either smoking status (P= 0.3557) or the modified gingival index (MGI) (P= 0.3824). The interaction effect between smoking status and the MGI was highly significant (P = 0.0003) indicating that the effect of smoking status on the GSo2 should be compared at each level of the MGI score. GSo2 in healthy gingiva was significantly lower in smokers than non-smokers (P = 0.0014), while smokers showed higher GSo2 than non-smokers in moderately inflamed gingiva (P = 0.0356). The GSo2 in inflamed gingiva was significantly decreased compared with healthy gingiva in non-smokers (P = 0.0044), while smokers showed no significant difference between healthy and inflamed gingiva (P= 0.2772 to 0.8665). GSo2 in smokers was consistently and significantly lower than that of healthy gingiva of non-smokers (P = 0.0391 to 0.0004).
Conclusions: Smokers exhibit possibly lower function of oxygen sufficiency in healthy gingiva and reduced ability to adapt the function in inflamed gingiva than non-smokers. This suggests that smokers have functional impairments in the gingival microcirculation.
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http://dx.doi.org/10.1902/jop.2000.71.12.1846 | DOI Listing |
JCO Precis Oncol
January 2025
Karmanos Cancer Institute and Department of Oncology, Wayne State University School of Medicine, Detroit, MI.
Purpose: Although lung cancer is one of the most common malignancies, the underlying genetics regarding susceptibility remain poorly understood. We characterized the spectrum of pathogenic/likely pathogenic (P/LP) germline variants within DNA damage response (DDR) genes among lung cancer cases and controls in non-Hispanic Whites (NHWs) and African Americans (AAs).
Materials And Methods: Rare, germline variants in 67 DDR genes with evidence of pathogenicity were identified using the ClinVar database.
Thorac Cancer
January 2025
Department of Thoracic Surgery and Lung Transplantation, The Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong, China.
Background: The mycobiome in the tumor microenvironment of non-smokers with early-stage lung adenocarcinoma (ES-LUAD) has been minimally investigated.
Methods: In this study, we conducted ultra-deep metagenomic and transcriptomic sequencing on 128 samples collected from 46 nonsmoking ES-LUAD patients and 41 healthy controls (HC), aiming to characterize the tumor-resident mycobiome and its interactions with the host.
Results: The results revealed that ES-LUAD patients exhibited fungal dysbiosis characterized by reduced species diversity and significant imbalances in specific fungal abundances.
Dent J (Basel)
December 2024
Department of Biostatistics, Faculty of Medicine, Izmir Katip Celebi University, 35620 Izmir, Turkey.
Oral hygiene is a key factor for dental and periodontal diseases and the prognosis of any treatment to restore their consequences. The present survey aimed to evaluate how well informed patients in Albania are on oral hygiene, given the scarce evidence on this topic. This survey was performed using a Google Forms questionnaire on oral hygiene habits, type and technique of instruments used, and frequency of dental recall visits.
View Article and Find Full Text PDFFront Oncol
January 2025
Department of Otorhinolaryngology, Head and Neck Surgery, University Hospital Schleswig-Holstein, Kiel, Germany.
Introduction: Several aspects of the involvement of HPV in the pathogenesis of HPV-associated diseases remain poorly understood including mechanistic aspects of infection and the question of why the majority of HPV-positive HNSCC-patients are non-smokers, whereas HPV-negatives are smokers. Our previous research, based on 1,100 patient samples, hypothesized an explanation for this phenomenon: Smoking induces upregulation of a mucosal protective protein (SLPI), which competes with HPV for binding to Annexin A2 (AnxA2), pivotal for HPV cell entry. Here we investigate the mechanistic aspects of our hypothesis using transfection assays.
View Article and Find Full Text PDFCureus
December 2024
Clinical Research, Shaukat Khanum Memorial Cancer Hospital and Research Centre, Lahore, PAK.
Background Lung cancer is the most frequent cause of cancer-related deaths and the most common type of cancer globally. It is generally classified into two main histologic subtypes: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). NSCLC is the most prevalent type and is enriched with genetic and molecular diversity.
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