Detection of Cytomorphological Changes in Oral Mucosa among Alcoholics and Cigarette Smokers

Smoking has become general habits in social life. One popular kind is filtered cigarette. As the base component is tobacco without clove and separated by the filter on it. Long irritation from heat and a toxic component of cigarette changed in oral mucosa epithelial. This condition can stimulate the increase of progenitor cells, which is marked by immunohistochemistry staining method of cytokeratin 19. This descriptive study is to find the expression of cytokeratin 19 in oral mucosa cytoplasm epithelial of filter cigarette smokers. There were 30 smokers which were selected with certain criteria. Samples were taken from a cytological smear of mucosa epithelial then stained with immunohistochemistry method. Analysis has taken by calculating the number of cells in the cytological smear. Then the immunoexpression of cytokeratin 19 was known from the percentage of cytoplasm cells which have brown colour compared with a total number of cells. In conclusion, the smoking filter cigarette would increase the number of progenitor cells from chronic inflammation, which is marked by cytokeratin 19 expression in oral mucosa cytoplasm epithelial of smokers.

Download Full-text

Cytopathological Effects Of Smoking On Clinically Normal Oral Mucosa

IIUM Medical Journal Malaysia ◽

10.31436/imjm.v16i2.1056 ◽

2017 ◽

Vol 16 (2) ◽

Author(s):

Ghasak Ghazi Faisal ◽

Faridah Md Khalid ◽

Yusri Yazid

Keyword(s):

Oral Cancer ◽

Oral Mucosa ◽

Oral Disease ◽

Control Group ◽

Cigarette Smokers ◽

Mild Dysplasia ◽

Normal Oral Mucosa ◽

Floor Of The Mouth ◽

Clinically Normal ◽

Cytological Changes

Introduction: Smoking is a well-known cause of oral disease and oral cancer. Several dysplastic cytological changes occur before the appearance of the clinical lesion. This study aimed to investigate the cytopathological effects of smoking in clinically normal oral mucosa of cigarette smokers. Materials and Methods: A total of 40 cigarette smokers and 40 nonsmokers (control group) were included in this study. All participants had clinically normal oral mucosa. Oral smears were obtained from the side of the tongue and floor of the mouth using a Cytobrush. The smears were stained by Papanicolaou stain and examined under light microscope for inflammation, hyperkeratinization and dysplasia. Results: There was a significantly higher rate(p<0.005) of inflammation 63%, hyperkeratiniztion 62% and mild dysplasia 26% among smokers than non-smokers where the rates were 35%, 12% and 2% respectively. Conclusion: Smoking causes significant cytopathological changes in normal oral mucosa, the detection of which is important to prevent progression into carcinoma. The procedure is fast, painless and inexpensive.

Download Full-text

Cytological Evaluation of Cellular Atypia in the Oral Mucosa of Active and Passive Cigarette Smokers

Dental Clinical and Experimental Journal ◽

10.5812/dcej.66710 ◽

2019 ◽

Vol 4 (1) ◽

Author(s):

Maryam Shahsavari ◽

Siavash Azizi

Keyword(s):

Oral Mucosa ◽

Cigarette Smokers ◽

Cellular Atypia ◽

Cytological Evaluation

Download Full-text

Induction and Differentiation of Dental Epithelium in Vivo and in Vitro

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100053425 ◽

1982 ◽

Vol 40 ◽

pp. 142-145

Author(s):

E. J. Kollar

Keyword(s):

Connective Tissue ◽

Oral Mucosa ◽

Basal Lamina ◽

Functional Derivatives ◽

Specific Source ◽

Dental Epithelium ◽

Connective Tissue Stroma

The differentiation and maintenance of many specialized epithelial structures are dependent on the underlying connective tissue stroma and on an intact basal lamina. These requirements are especially stringent in the development and maintenance of the skin and oral mucosa. The keratinization patterns of thin or thick cornified layers as well as the appearance of specialized functional derivatives such as hair and teeth can be correlated with the specific source of stroma which supports these differentiated expressions.

Download Full-text