Abstract
OBJECTIVE: To describe sociodemographic variables and verify changes in white blood cells of patients with oral squamous cell carcinoma (OSCC).METHODS: Cross-sectional retrospective study that used secondary data of patients with OSCC, attended at the Oral Medicine Service of the School of Dentistry of ULBRA, between 2010 and 2014.RESULTS: 87.3% of the population were male, white (71%), age superior to 60 years (38.7%), urban worker (61.3%), without changing in the overall health at query time (67.7%) and residents of the municipality of Canoas/RS (93.6%). The most prevalent injuries sites were the buccal floor, alveolar ridge, corners of the mouth and gums (61.3%). 74.2% of the sample were smokers and 45.2% drinkers. As for the WBC, most patients presented values within the normal range: total leukocytes (77.4%), lymphocytes (87.1%) and neutrophils (96.8%). CONCLUSION: The profile of the sample was consistent with literature: white males over the age of 40 years, smokers/former-smokers and alcoholics/ex-alcoholics. The patients did not show changes in the white blood cells (leukogram) values. It is recommended that more research should be conducted in this area of knowledge, due to the importance of the subject.
Highlights
Oral squamous cell carcinoma (OSCC) is the most prevalent malignant neoplasm of the oral cavity (95%), considered to be a heterogeneous disease due to its multifactorial etiology associated with intrinsic and extrinsic factors and its developmental mechanisms
The molecular mechanisms of its carcinogenesis, tumor progression and metastasis are related to multiple genetic alterations caused by chronic exposure to carcinogens such as smoking, alcohol, viral infections (HPV), dietary factors and inflammation [1, 2]
The role of chronic inflammation in carcinogenesis was first proposed by Rudolf Virchow in 1863, when he observed the presence of leukocytes in the neoplastic tissue [5, 6]
Summary
Oral squamous cell carcinoma (OSCC) is the most prevalent malignant neoplasm of the oral cavity (95%), considered to be a heterogeneous disease due to its multifactorial etiology associated with intrinsic and extrinsic factors and its developmental mechanisms. The development of an inflammatory state, or the maintenance of an existing inflammation, promotes cellular changes, causing suppression of immune responses, associated or not with the presence of bacterial or viral agents, and may act as a risk factor for the development of the lesion [3, 4]. If the inflammation is persistent, it will have the ability to induce cell proliferation and promote long cell survival, through the activation of oncogenes and inactivation of tumor suppressor genes. This will result in genetic instability with increased risk of injury. Tumor cells would induce the secretion of inflammatory mediators which, in turn, would promote the proliferation of tumor cells, the tumor progressing rapidly against an intense inflammatory infiltrate and/or its sub-products [4]
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