______________________________________________ Oral Cancer and Complications of Cancer Therapies
Increasing age is another risk factor in the development of oral cancer, with a peak incidence in individuals 63 years of age; however, it is now occurring more frequently in younger individuals [2; 6]. The exact causes for this are not yet clear, but there appear to be associations between young men and women who use conventional “smokeless” chewing or spit tobacco [2]. Historically, the incidence of oral cancer in the Black population has been twice that of the White population, but 2024 data from the National Cancer Institute indicates that the incidence in the White population has surpassed that of the Black population for both men and women [2; 3; 6]. Incidence of oral cancer is nearly as high in the American Indian/Alaska Native population as it is among the White population. A strong gender differentiation has also been noted historically, as men developed oral cancer with a frequency that was more than six times that of women. The ratio is now one woman to every three men, likely due to the increase in women who smoke since the 1950s [2]. It is thought that lifestyle choices (e.g., tobacco use, particularly in combination with the consumption of alcohol), rather than genetics, are responsible for these various disparities. Chronic tissue trauma from ill-fitting prostheses, such as den- tures or partial dentures, may predispose tissues to malignant change, though as a whole, there is no heightened risk for those with dentures [4]. However, patients who utilize these devices should be educated that any area of irritation should be examined and the corresponding adjustment should be made by a dentist. Sore spots that cannot be eliminated after adjustments, relines of the existing prosthesis, or the fabrica- tion of a completely new prosthesis should be monitored very closely. If the prosthesis is not worn and the sore spot remains, a biopsy of the area is indicated. In one study, HPV type 16 (HPV16) was found to account for approximately 55% of oral cancer cases in the absence of any other risk factors [7]. While HPV16 and HPV18 infections are widely recognized as a main cause of cervical cancers in women, they are also increasingly linked to oral cancer in those younger than 40 years of age [3; 4]. The increase of oral cancer cases in this population is associated with the spread of HPV and is strongly correlated to having multiple oral sex partners [2; 3; 7]. Autoimmune factors, complex genetic mechanisms (individually or collectively), and other viral agents, such as herpes simplex virus, may also be etiologic risk factors in this group ( Table 1 ).
ORAL CANCER RISK FACTORS
Tobacco use Alcohol use
Cannabis use Family history Advanced age Male gender Poor oral hygiene
Poor nutrition HPV infection Human herpesvirus infection Immunosuppression (including HIV infection) Source: [2; 4; 5; 7; 8; 9]
Table 1
Excessive, chronic ultraviolet light exposure has been linked to cancers of the lip, particularly in individuals who work outdoors [4]. Other documented or researched causes include poor nutrition (i.e., lack of fruits/vegetables), lichen planus, and graft-versus-host disease. Oral cancer may also develop in the absence of known risk factors. Approximately 25% of patients with oral cancer have no identified risk factors for the disease [10]. Most of these patients are younger than 40 years of age, well below the age distribution for this disease [2; 11]. THE DEVELOPMENT OF ORAL CANCER A discussion of the histologic basis for normal, healthy oral mucosa is required before an understanding of the stages that lead to the development of an oral malignancy can be appre- ciated. Also, some of the problems that develop after radio- therapy and chemotherapy have a cellular basis in these tissues. The oral mucous membrane does not have the same surface consistency throughout the oral cavity. The oral mucosa is classified into three types: • Masticatory mucosa: It has a firm texture that comprises the hard palate and the gingiva. This tissue is bound to the bone and has a minimal capacity to stretch. • Specialized (sensory) mucosa: Located on the dorsum of the tongue, it contains the taste buds. • Lining (reflecting) mucosa: The vast majority of the oral mucosa is lining (reflecting) mucosa. It is easily flexible and distensible. Common to all three mucosal types is an outermost cellular layer composed of stratified squamous epithelium. Some of the stratified squamous epithelium, specifically the masticatory mucosa, may be keratinized. All of these surface cells are pro- duced from a deeper layer of cells called basal cells. This cellular layer consists of cells that are active in deoxyribonucleic acid (DNA) synthesis and undergo mitosis. The cells that replace the outer squamous layer every three to four days originate
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