Understanding the physiologic process of cervical maturation during adolescence and young adulthood may give us insight into the epidemiologic observation that adolescents and young adults appear vulnerable to certain pathogens. Women ages 15–24 years have the highest age-specific rates of reportable sexually transmitted infections (STIs) including Chlamydia trachomatis, Neisseria gonorrhoeae,
and human papillomavirus (HPV).(1
) This vulnerability is often attributed to risky sexual behaviors, but biologic factors including the epithelial topography of the cervix during this time period may also be contributory. During fetal development, the cervical epithelium is composed of a single layer of Mullerian columnar cells that are partially replaced by urogenital stratified squamous epithelium.(3
) An abrupt squamo-columnar junction is seen on the neonatal ectocervix. The epithelium remains relatively quiescent until puberty, when uncommitted basal cells of the columnar epithelium transform into squamous cells in a physiologic process termed “squamous metaplasia”.(4
) This epithelial area of transformation is referred to as the “transformation zone”. Over time, a new squamo-columnar junction is typically formed more proximally at the endocervix as the topography of the ectocervix transforms from a predominant columnar epithelium (considered to be more immature) to a predominant squamous epithelium (more mature). The cervical epithelium is the primary site of infection for common STIs. Columnar epithelial cells are known targets for C. trachoma
tis and N. gonorrhoeae
) whereas the active transformation zone is an ideal host for HPV as host cell replication and differentiation is required for HPV growth. Understanding the natural history of cervical maturation may assist us in identifying factors that exacerbate or minimize the vulnerability of the epithelium to infection.
Unfortunately, few studies have examined the maturation process of the cervical epithelium in adolescents.(4
) Some cross sectional studies have reported associations between greater cervical maturation and higher numbers of years sexually active and numbers of sexual partners.(8
) These behavioral factors may represent biological factors such as an increased exposure to infections or cervical trauma. Cervicitis has been associated with a loss of cervical columnar cells, a typical feature of the maturational process.(11
) Consequently, STIs have been hypothesized to promote maturation via the induction of inflammation and subsequent cellular repair. In contrast, hormonal contraception has been linked to increased cervical ectopy (or less cervical maturation).(12
) Some have suggested that the appearance of increased immaturity is due to hormonal contraception causing tissue edema and eversion of the endocervix. However, more recent studies showed no association.(15
)Squamous metaplasia itself is thought to be triggered by the shift of the vaginal pH from the pre-pubertal level of >4.7 to the more acidic pubertal level of <4.5. In theory, maturation could be slowed or reversed by alkaline disturbances, as in bacterial vaginosis or with frequent exposure to semen which is strongly alkaline. Cigarette smoking is another possible influence since nicotine and its metabolites are detectable in cervical mucous.(18
) Interestingly, both hormonal contraception and smoking have long been associated with an increased risk for cervical cancer,(20
) and HPV infection is common during adolescence and young adulthood.(2
) As the cervical epithelium changes during this age, the possible relationships between hormonal contraception, smoking, and maturational activity could influence one’s vulnerability to HPV and other STIs. Since prior studies of cervical maturation were retrospective, cross-sectional, or case-control, it is difficult if not impossible to identify causal dynamic relationships.
The aims of this study were to: 1) examine the changes in epithelial topography of the cervix in healthy young women in a longitudinal design, and 2) determine the sociodemographic, behavioral, and biological factors associated with the rate of cervical epithelial maturation.