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Advisor(s)
Abstract(s)
O carcinoma pavimento-celular oral (CPCO) é a forma mais frequente de cancro da cavidade oral e está intimamente associado a fatores de risco modificáveis, como o tabagismo e o consumo excessivo de álcool, cuja combinação exerce um efeito sinérgico na sua patogénese. Outros elementos contribuintes incluem infeções virais, nomeadamente pelo vírus do papiloma humano (HPV), más condições de saúde oral, deficiências nutricionais e infeções fúngicas crónicas como a candidíase. Apesar de ser considerado um cancro amplamente evitável, o CPCO pode também surgir em indivíduos fora dos grupos clássicos de risco, o que sublinha a importância do rastreio e do diagnóstico precoce.
A imunossupressão, seja decorrente de terapêuticas farmacológicas utilizadas em contexto de transplantes e doenças autoimunes, seja resultante de imunodeficiências primárias ou adquiridas, constitui um fator de risco significativo para o desenvolvimento de neoplasias. A redução da vigilância imunológica facilita a sobrevivência e proliferação de células com mutações genéticas, bem como a reativação de infeções virais oncogénicas. Evidência proveniente de recetores de transplante renal e de células hematopoiéticas confirma um aumento consistente no risco de tumores sólidos, incluindo carcinomas da cavidade oral, sobretudo em doentes expostos a regimes prolongados de imunossupressão e na presença de doença crónica do enxerto contra o hospedeiro.
A relação entre imunossupressão e cancro oral traduz-se numa maior suscetibilidade à transformação maligna de lesões potencialmente malignas e ao desenvolvimento de CPCO. Este efeito não decorre apenas da diminuição da vigilância tumoral, mas também da facilitação de coinfeções virais e fúngicas, como HPV e Candida spp., que atuam como cofatores na carcinogénese. Assim, a imunossupressão prolongada deve ser entendida como um determinante central no desenvolvimento de cancro oral, reforçando a necessidade de estratégias de prevenção adaptadas e de uma vigilância clínica contínua em populações de risco.
Oral squamous cell carcinoma (OSCC) is the most frequent form of cancer of the oral cavity and is strongly associated with modifiable risk factors such as tobacco use and excessive alcohol consumption, whose combination exerts a synergistic effect on its pathogenesis. Other contributing elements include viral infections, particularly human papillomavirus (HPV), poor oral health conditions, nutritional deficiencies, and chronic fungal infections such as candidiasis. Although OSCC is considered a largely preventable cancer, it can also occur in individuals outside the classical risk groups, highlighting the importance of screening and early diagnosis. Immunosuppression, whether resulting from pharmacological therapies used in transplantation and autoimmune diseases or from primary or acquired immunodeficiencies, represents a significant risk factor for the development of neoplasms. The reduction of immune surveillance facilitates the survival and proliferation of genetically altered cells, as well as the reactivation of oncogenic viral infections. Evidence from kidney and hematopoietic cell transplant recipients confirms a consistent increase in the risk of solid tumors, including oral carcinomas, particularly in patients exposed to prolonged immunosuppressive regimens and in the presence of chronic graftversus- host disease. The relationship between immunosuppression and oral cancer translates into a greater susceptibility to the malignant transformation of potentially premalignant lesions and the development of OSCC. This effect arises not only from reduced tumor surveillance but also from the facilitation of viral and fungal coinfections, such as HPV and Candida spp., which act as cofactors in carcinogenesis. Thus, prolonged immunosuppression should be understood as a central determinant in the development of oral cancer, reinforcing the need for adapted preventive strategies and continuous clinical surveillance in at-risk populations.
Oral squamous cell carcinoma (OSCC) is the most frequent form of cancer of the oral cavity and is strongly associated with modifiable risk factors such as tobacco use and excessive alcohol consumption, whose combination exerts a synergistic effect on its pathogenesis. Other contributing elements include viral infections, particularly human papillomavirus (HPV), poor oral health conditions, nutritional deficiencies, and chronic fungal infections such as candidiasis. Although OSCC is considered a largely preventable cancer, it can also occur in individuals outside the classical risk groups, highlighting the importance of screening and early diagnosis. Immunosuppression, whether resulting from pharmacological therapies used in transplantation and autoimmune diseases or from primary or acquired immunodeficiencies, represents a significant risk factor for the development of neoplasms. The reduction of immune surveillance facilitates the survival and proliferation of genetically altered cells, as well as the reactivation of oncogenic viral infections. Evidence from kidney and hematopoietic cell transplant recipients confirms a consistent increase in the risk of solid tumors, including oral carcinomas, particularly in patients exposed to prolonged immunosuppressive regimens and in the presence of chronic graftversus- host disease. The relationship between immunosuppression and oral cancer translates into a greater susceptibility to the malignant transformation of potentially premalignant lesions and the development of OSCC. This effect arises not only from reduced tumor surveillance but also from the facilitation of viral and fungal coinfections, such as HPV and Candida spp., which act as cofactors in carcinogenesis. Thus, prolonged immunosuppression should be understood as a central determinant in the development of oral cancer, reinforcing the need for adapted preventive strategies and continuous clinical surveillance in at-risk populations.
Description
Dissertação para obtenção do grau de Mestre no Instituto Universitário Egas Moniz
Keywords
Imunossupressão Cancro oral Fatores de risco HSCT
