## 1 Introduction  
Oral Squamous Cell Carcinoma (OSCC) represents 90% of lip and oral cancers. OSCC is considered the twelfth most prevalent cancer worldwide. Lip and oral cancer, as one of the Head and Neck Cancers (HNCs) subtypes, is considered the 16 th most commonly diagnosed cancer worldwide in both sexes. In 2018, the annual estimated number of incident cases with oral and lip cancer was 354,864 cases worldwide and 3967 cases in Italy. The annual estimated number of deaths due to oral and lip cancer was 177,384 cases worldwide and 1489 cases in Italy [1; 2; 3; 4].  
The exact pathogenesis of HNCs is not fully clear. It has been suggested to consider HNCs as complex multifactorial disorders [5]. Since cancer cells show genetic damage (e.g., gene mutations) that may be resulted from exposure to carcinogens, it is recommended to study different carcinogens and to understand the associated risk factors in order to plan preventive and management measures of this disease [6; 7].  
Many risk factors have been linked to oral cancer; such as human papillomavirus infection [8], local chronic trauma [9], exposure to ultraviolet radiations [10], low-antioxidants diet [11], immunosuppression [6] and Oral Potentially Malignant Lesions (OPMLs) [12]. Tobacco smoking and alcohol consumption are the most common associated risk factors of OSCC. They are the major risk factors in 74% of cases with OSCC in the western world [13].  
Tobacco products are responsible for causing a variety of cancers including the oral cavity due to the exposure to carcinogens contained in tobacco products. More than 60 known carcinogens in smoke tobacco and about 16 in unburned tobacco have been detected. The concentration and potency of these carcinogens vary according to the type of tobacco product and its method of consumption. In several studies, sufficient evidence has been provided for the carcinogenicity of many of these detected carcinogens; such as tobacco-specific nitrosamines, polycyclic aromatic hydrocarbons and aromatic amines [14].  
Alcohol is directly related to 4.2% of cancer deaths worldwide [15]. Alcohol is linked to 26.4% of all lip and oral cavity cancers worldwide [16]. The main metabolites of ethanol are considered as a class 1 carcinogen [5; 17]. These metabolites play a direct effect in carcinogenesis by causing a disturbance of DNA synthesis and repair, formation of DNA adducts and alteration of oncogenes expression by DNA hypomethyllation [18]. In addition, alcohol metabolites have an indirect role through acting as a solvent and making the mucosa more permeable to other carcinogens such as tobacco carcinogens [17].  
There are conflicting opinions on the role of Family History of Cancer (FHC) on oral cancers. Some authors believe that there is no evidence of a clear hereditary trait for oral cancers, since different hereditary cancer syndromes, except for some Cowden Syndrome cases, have not been reported with oral cancers [6]. Several epidemiological studies have assessed the familial risks for oral cancers. Many of them have suggested the possible correlation between FHC and oral cancer [19; 20; 21; 22].  
The variation in the strength of association of tobacco and alcohol with oral cancers among previous studies and the presence of conflicting opinions in considering the FHC as a risk factor of oral cancers, have signified the need for further studies for comparison.  
This study is carried out to observe retrospectively the association of tobacco and alcohol with OSCC. In addition, the correlation between OSCC and Family History of Cancer (FHC) is analyzed through observing the Family History of Head and Neck Cancer (FHHNC) and General Family History of Cancer (GFHC); including the First-Degree Family History (FDFH) and Second-Degree Family History (SDFH).