RESUMEN
BACKGROUND: Although both animal and human studies suggested the association between placenta growth factor (PlGF) and chronic obstructive pulmonary disease (COPD), especially lung emphysema, the role of PlGF in the pathogenesis of emphysema remains to be clarified. This study hypothesizes that blocking PlGF prevents the development of emphysema. METHODS: Pulmonary emphysema was induced in PlGF knock-out (KO) and wild type (WT) mice by intra-tracheal instillation of porcine pancreatic elastase (PPE). A group of KO mice was then treated with exogenous PlGF and WT mice with neutralizing anti-VEGFR1 antibody. Tumor necrosis factor alpha (TNF-alpha), matrix metalloproteinase-9 (MMP-9), and VEGF were quantified. Apoptosis measurement and immunohistochemical staining for VEGF R1 and R2 were performed in emphysematous lung tissues. RESULTS: After 4 weeks of PPE instillation, lung airspaces enlarged more significantly in WT than in KO mice. The levels of TNF-alpha and MMP-9, but not VEGF, increased in the lungs of WT compared with those of KO mice. There was also increased in apoptosis of alveolar septal cells in WT mice. Instillation of exogenous PlGF in KO mice restored the emphysematous changes. The expression of both VEGF R1 and R2 decreased in the emphysematous lungs. CONCLUSION: In this animal model, pulmonary emphysema is prevented by depleting PlGF. When exogenous PlGF is administered to PlGF KO mice, emphysema re-develops, implying that PlGF contributes to the pathogenesis of emphysema.
Asunto(s)
Pulmón/metabolismo , Proteínas Gestacionales/deficiencia , Enfisema Pulmonar/prevención & control , Animales , Apoptosis , Modelos Animales de Enfermedad , Pulmón/patología , Metaloproteinasa 9 de la Matriz/metabolismo , Ratones , Ratones Noqueados , Elastasa Pancreática , Factor de Crecimiento Placentario , Proteínas Gestacionales/genética , Enfisema Pulmonar/inducido químicamente , Enfisema Pulmonar/metabolismo , Enfisema Pulmonar/patología , Factor de Necrosis Tumoral alfa/metabolismo , Factor A de Crecimiento Endotelial Vascular/metabolismo , Receptor 1 de Factores de Crecimiento Endotelial Vascular/metabolismo , Receptor 2 de Factores de Crecimiento Endotelial Vascular/metabolismoRESUMEN
Because of its close proximity to teeth and periodontium, gingival squamous cell carcinoma (SCC) can sometimes mimic tooth-related benign inflammatory conditions, resulting in misdiagnosis. In this study we report a case of gingival SCC that mimicked a dentoalveolar abscess of endodontic origin in its early presentation. The course and treatment of this case is discussed and a brief review of the literature is presented. Because many patients with gingival SCC visit dentists as their initial professional contact, it is hoped that the case can serve as a reminder for dentists to keep the possibility of carcinoma in mind when examining intraoral lesions.
Asunto(s)
Carcinoma de Células Escamosas/patología , Neoplasias Gingivales/patología , Absceso Periapical/diagnóstico , Carcinoma de Células Escamosas/cirugía , Diagnóstico Diferencial , Femenino , Neoplasias Gingivales/cirugía , Humanos , Metástasis Linfática , Persona de Mediana Edad , Disección del CuelloRESUMEN
OBJECTIVES: The issue of existence of malignancy within oral leukoplakia has seldom been addressed in Taiwan. The aims of this study were to investigate the prevalence of carcinoma and dysplasia within oral leukoplakia at the time of clinical diagnosis and to identify the associated risk factors in Taiwan. STUDY DESIGN: The prevalence rate of malignancy and dysplasia in 1046 oral leukoplakias at a university hospital was calculated. Univariate and multivariate analyses by the Mantel-Haenszel method and multiple logistic regression model were performed to examine risk factors associated with the presence of carcinoma and dysplasia within the lesions. RESULTS: The prevalence rate of carcinoma was 12.9%. The relative risks for the presence of malignancy in leukoplakias on the tongue/floor of mouth and with nonhomogeneous appearance were 2.72- and 28.13-fold by multivariate logistic regression analysis, when compared with those on buccal mucosa and lesions having homogeneous surface (both P < .05). In contrast, patients who both smoked and chewed betel quid had a significantly lower risk for carcinoma than the abstainers (P < .05). A synergistic effect between the 2 major risk factors of clinical appearance and lesion site was evident. Nonhomogeneous leukoplakia on tongue/floor of mouth had a 43.10-fold higher risk compared to homogeneous lesions located on buccal mucosa or other sites (P < .05). However, homogeneous leukoplakia in buccal mucosa or other sites of the oral cavity still had the possibility of having carcinoma within the lesion. The prevalence of dysplasia was 45.6% among the noncancerous leukoplakias with risk factors similar to those for carcinoma. CONCLUSIONS: Our results demonstrate that some leukoplakias contain a malignant component. Lesions with certain features are more prone to carcinoma, but no clinical attributes can bring certitude. Therefore, all oral leukoplakias should be submitted to microscopic analysis before any definite treatment or long-term follow-up.
Asunto(s)
Carcinoma de Células Escamosas/epidemiología , Leucoplasia Bucal/epidemiología , Neoplasias de la Boca/epidemiología , Lesiones Precancerosas/epidemiología , Adulto , Anciano , Anciano de 80 o más Años , Análisis de Varianza , Areca/efectos adversos , Carcinoma de Células Escamosas/etiología , Carcinoma de Células Escamosas/patología , Carcinoma Verrugoso/epidemiología , Carcinoma Verrugoso/etiología , Carcinoma Verrugoso/patología , Transformación Celular Neoplásica , Femenino , Humanos , Leucoplasia Bucal/etiología , Leucoplasia Bucal/patología , Modelos Logísticos , Masculino , Persona de Mediana Edad , Mucosa Bucal/patología , Neoplasias de la Boca/etiología , Neoplasias de la Boca/patología , Oportunidad Relativa , Lesiones Precancerosas/etiología , Lesiones Precancerosas/patología , Prevalencia , Factores de Riesgo , Razón de Masculinidad , Encuestas y Cuestionarios , Taiwán/epidemiologíaRESUMEN
OBJECTIVE: The aim of the study was to examine the expressions of p53 and proliferating cell nuclear antigen (PCNA) in oral lichen planus (OLP) in relation to its clinical behavior and the patients' oral habits. STUDY DESIGN: Immunohistochemical study was carried out to investigate the expressions of p53 and PCNA in 56 OLP specimens. The results were correlated with the clinical behavior of the disease and the patients' oral habits. The expression rates were further compared with those of normal oral mucosa (NOM), epithelial hyperkeratosis (EH), epithelial dysplasia (ED), and squamous cell carcinoma (SCC). RESULTS: The staining rate of p53 (28.6%) and PCNA labeling index (LI) (27.6 +/- 8.8%) in OLP were similar to those in EH ( P = .868, .074, respectively), but higher than those of NOM and lower than those of ED and SCC (all P < .05). In OLP, no significant correlations were found between p53 or PCNA expression and the patients' age, gender, lesion duration, location, size, number of site, presence of pain, presence of local irritant, and the habits of alcohol drinking and cigarette smoking (all P > .05). In addition, the mean PCNA LI of p53+ cases was close to that of p53- cases (P = .38). However, the staining rate of p53 in OLP was higher in areca quid (AQ) chewers compared to abstainers (P = .001), and the mean PCNA LI in atrophic cases was higher than that in hypertrophic cases (P = .029). Interestingly, the staining rate of p53 and mean PCNA LI were significantly increased in AQ chewers with atrophic OLP (100%, 36.7% +/- 9.0%, respectively), which were similar to those in ED and SCC (all P > .05). CONCLUSIONS: Although this study could not confirm the precancerous nature of OLP by the relatively low p53 and PCNA expression, the results do suggest that atrophic form OLP and patients with AQ chewing habit may have a higher disease activity in view of higher expression rates of p53 and PCNA in the lesions.