Trends over time in the incidence of cervical neoplasia in comparison to trends over time in human papillomavirus infection.

INTRODUCTION: The establishment of human papillomavirus (HPV) infection as a major cause of cervical neoplasia has resulted in major efforts to develop prophylactic HPV vaccines for prevention of cervical neoplasia. Cervical cancer and the other HPV-associated cancers constitute a major public health burden and eradication of the major causative infection is certainly the most appealing long-term preventive measure. Nevertheless, the effects of preventive HPV vaccination will need to be estimated and compared for (cost-) efficacy with other primary prevention and with secondary prevention programs. However, estimating the effects of preventing a causative exposure is complicated when the exposure is a transmissible infection. The spread of the epidemic is dynamic and may change over time depending e.g. on the changes in human behavior. Depending on the circumstances, prevention of an infection may have either greater or lesser effects than the prevention of a non-infectious exposure. Estimating the time trends in HPV infections and the underlying trends in the risk of cervical neoplasia is important for estimating effects of interventions.
METHOD: A literature review on recent evidence on time trends in cervical neoplasia, compared with evidences on time trends in HPV infections and interactions between different types of HPV infections.
RESULTS: In Finland, there has between 1991 and 1995 been a 60% increase in the incidence of cervical cancer among women <55 years of age. Trends in detection rates of cervical cancer precursor lesions are consistent with an increase in the background cervical cancer risk. From the 1960s to 1980s, there has been a major increase in HPV seroprevalences over time in the Nordic countries. Increasing trends are also seen for other sexually transmitted diseases and smoking. Several studies indicate the existence of interaction between benign and oncogenic HPV types, thus making the relationship between the incidences in HPV infections and in cervical neoplasia complex.
CONCLUSION: The increase in cervical cancer is paralleled by increases in HPV infection, other STDs and smoking and changes in screening practices, all of which may have contributed. Prediction of the effect on cervical cancer incidence of changes in HPV incidences is complicated by the existence of several risk factors, the protective effect of screening and by the population dynamics of HPV infections.