Cervical cancer is a malignant epithelial tumor that affects the vaginal part of the cervix or cervical canal, and nowadays about 500.000 new cases of cervical cancer are registered worldwide annually (Cervical cancer, 2012). The development of the illness can be provoked by the background diseases which lead to the transformation of the vaginal part of the cervix: polyps, papillomas, cervicitis, erosions and others (Badretdinova, Gantsev, & Trubin, 2014).
The pathological processes that lead to the transformation of cervical epithelium are regarded as precancerous conditions which can be provoked by the viral infections, such as human papillomaviruses (HPVs), and consequent chronic inflammations.
Viral Infection
The viral nature of a number of human malignant tumors is proved by clinical research. Recent research data demonstrates that over 90% of cervical cancers contain high-risk HPVs including HPV 16, 18,31, 33, 45 (Bulkmans et al., 2007). All papillomaviruses have similar genetic structure and morphology. They contain three types of capsid proteins and complexes of closed circular DNA with a histone cell (Miller, Puricelli, & Stack, 2012). It is observed that HPV DNA may persist in the cells of the basal layer of epithelium for a significant period, and then it can progress through the inclusion of HPV DNA into the cellular genome and can be developed as the malignant transformation of epithelium (Miller et al., 2012).
HPV enters the basal cells of epithelium through micro traumas formed during the sexual contacts. Viral DNA integrates into the cellular nucleus and, while being present in the basal layer in a small number of copies, HPV cannot be detected. During the further HPV expression, the subclinical and clinical stages of the disease commence developing. At this stage, the cytopathic effect of HPV, koilocytosis, occurs in the surface layers of epithelium while the cellular core takes an irregular shape and becomes hyperchromatic due to the accumulation of virion therein (Miller et al., 2012).
Despite their high-risk potential, the progression HPV pathogenic effect is conditional. Carriage of HPV shows no malignant process as such, but the risk of cancer development can be increased. Factors that modify the pathogenic effects of HPV and provoke the consequent growth of tumor may include the immune deficiency, other infections, and viruses, or cervical traumas. For example, it is observed that the combination of HIV and HPV increases the risk of malignancy (Isaakidis et al., 2013).
The rapid rise of HPV infection occurs among women of 15-25 years old, i.e. after the onset of sexual activity (Bell et al., 2011). The risk factors of infection include the features of reproductive behavior. The research findings make it clear that the number of sexual partners is correlated with HPV infection (Bell et al., 2011). Therefore, the methods for the prevention of HPV infection are the intervention of reproductive behavior and regular clinical examination.
For a long time, the only method of HPV detection was the cytological screening based on the identification of cytological transformations of epithelium associated with the infection. However, the results of cytological testing are often misleading, and their interpretation is highly subjective. HPV diagnosis became credible only with the advent of reliable methods based on the detection of nucleic acid – DNA hybridization and polymerase chain reaction (PCR) (Zappacosta et al., 2013).
HPV genetic screening has an important clinical significance because HPV detection helps to identify a group of women at high risk of cervical cancer development. According to recent research findings, the early signs of precancerous lesions develop in nearly 15-50% of HPV-positive women with normal cervical epithelium, and these morphological transformations can occur within a few years or even months (Zappacosta et al., 2013). The incidence of cervical cancer development in women infected with high-risk HPVs is higher than in the non-infected population. Thus, the especially careful monitoring for HPV diagnosis is required.
Chronic Inflammation
The major causes of chronic inflammation development, such as cervicitis, are various genital infections. Inflammation can be provoked by mycoplasmosis, HPV, herpes, etc. (Veríssimo Fernandes et al., 2015). Due to the fact that the mentioned infections are rarely limited merely by the cervical lesion and usually spread to other organs as well, cervicitis cannot be regarded as an independent disease, but only as one of many manifestations of genital infections.
Chronic cervicitis and other types of inflammations imply that the infection which provoked the inflamatory process penetrated the organism a long time ago and slowly progresses gradually destructing the cervical tissues (Veríssimo Fernandes et al., 2015). When a patient lacks the adequate treatment of chronic inflammation and other concomitant infections, the risk of cervical cancer occurrence drastically increases.
It is possible to prevent inflammations through the correction of reproductive behavior and enhancement of gynecological hygiene. The gynecological examination helps to detect the disease and assess the condition of the cervix. The presence of bad-smelling discharge, persistent irritation, or pyorrhea are the most common symptoms of inflammation (Sharp, 2011). Since the occurrence of chronic inflammation is associated with other infections, the PCR analysis for genital viruses may be required as well.
References
Badretdinova, F., Gantsev, S. K., & Trubin, V. B. (2013). Optimization Program of Diagnostic, Therapeutic, and Rehabilitation Measures for the Cervical Background Diseases and Precancer. Clinical Ovarian and Other Gynecologic Cancer, 6(1-2), 7-10. Web.
Bell, M. C., Schmidt-Grimminger, D., Jacobsen, C., Chauhan, S. C., Maher, D. M., & Buchwald, D. S. (2011). Risk factors for HPV infection among American Indian and white women in the Northern Plains. Gynecologic Oncology, 121(3), 532-536. Web.
Bulkmans, N. W. J., Berkhof, J., Bulk, S., Bleeker, M. C. G., van Kemenade, ,F.J., Rozendaal, L.,… C, J. L. M. M. (2007). High-risk HPV type-specific clearance rates in cervical screening. The British Journal of Cancer, 96(9), 1419-1424. Web.
Cervical cancer: Estimated incidence, mortality and prevalence worldwide in 2012. (2012). Web.
Isaakidis, P., Pimple, S., Varghese, B., Khan, S., Mansoor, H., Ladomirska, J.,… Alders, P. (2013). HPV infection, cervical abnormalities, and cancer in HIV-infected women in Mumbai, India: 12-month follow-up. International Journal of Women’s Health IJWH, 487. Web.
Miller, D. L., Puricelli, M. D., & Stack, M. S. (2012). Virology and molecular pathogenesis of HPV (human papillomavirus)-associated oropharyngeal squamous cell carcinoma. The Biochemical Journal, 443(2), 339-353. Web.
Sharp, K. A. (2011). Cervicitis. In L. J. Fundukian (Ed.), The Gale Encyclopedia of Medicine (4th ed., Vol. 2, p. 926). Detroit: Gale. Web.
Veríssimo Fernandes, J., De Medeiros Fernandes, T. A., Veríssimo De Azevedo, J. C., Oliveira Cobucci, R. N., Freire De Carvalho, M. G., Sousa Andrade, V., & Galvão De Araújo, J. M. (2015). Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review). Oncology Letters, 9(3), 1015-1026. Web.
Zappacosta, R., Caraceni, D., Ciccocioppo, L., Rotondo, T., Capanna, S., Gatta, D. M.,… Rosini, S. (2013). Implementing specificity of HPV-DNA primary screening in a successful organised cervical cancer prevention programme. Gynecologic Oncology, 128(3), 427-432. Web.