Cervical cancer and use of hormonal contraceptives: a systematic review

Abstract Background Previous studies indicated an impact of hormonal contraceptive use on oral health. This systematic review aimed to investigate the evidence supporting the impact of the use of hormonal contraceptives and periodontal diseases. Methods This study is based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and based on the PECO acrostic. Inclusion criteria comprised observational studies including women (P), which evaluated hormonal contraceptive users (E) and hormonal contraceptive non-users (C), to verify the association between this hormonal therapy and the periodontal diseases (O). Searches were performed on 5 databases: PubMed, Scopus, Web of Science, Cochrane Library, LILACS and grey literature (OpenGrey and Google Scholar). After the selection process, the included studies were evaluated qualitatively. Moreover, quantitative data were analyzed in two meta-analyses for clinical attachment loss (CAL) and probing depth (PD). Finally, the level of certainty was measured with the GRADE (Grading of Recommendations Assessment, Development, and Evaluation) tool between periodontal clinical parameters. Results 18 articles were eligible for the qualitative synthesis and 7 of them were selected for quantitative analysis. Hence, 15 of the eligible articles reported an association between the use of hormonal contraceptives and severity of periodontal disease. However, 6 articles demonstrated high risk of bias and were excluded from quantitative synthesis. The meta-analysis showed a statistically significant difference for CAL (MD 0.24 [0.09, 0.40]; p = 0.002), but in PD (MD 0.05 [− 0.05, 0.15]; p = 0.33) such difference was not identified. A very low level of evidence was found between the clinical parameters. Conclusions The use of hormonal contraceptives may be associated to severity of periodontal diseases. However, the quantitative analysis points to an inconclusive outcome due to the high level of heterogeneity. The association is biologically plausible, however additional studies are warranted to better elucidate the clinical significance of this possible association.

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HPV and Other Microbiota; Who’s Good and Who’s Bad: Effects of the Microbial Environment on the Development of Cervical Cancer—A Non-Systematic Review

Cells ◽

10.3390/cells10030714 ◽

2021 ◽

Vol 10 (3) ◽

pp. 714

Author(s):

Matthias Läsche ◽

Horst Urban ◽

Julia Gallwas ◽

Carsten Gründker

Keyword(s):

Systematic Review ◽

Cervical Cancer ◽

High Risk ◽

Cervical Carcinoma ◽

Hpv Infection ◽

Human Papillomaviruses ◽

Inflammatory Reactions ◽

Metabolic Signalling ◽

Microbial Environment ◽

High Risk Hpv

Cervical cancer is responsible for around 5% of all human cancers worldwide. It develops almost exclusively from an unsolved, persistent infection of the squamocolumnar transformation zone between the endo- and ecto-cervix with various high-risk (HR) human papillomaviruses (HPVs). The decisive turning point on the way to persistent HPV infection and malignant transformation is an immune system weakened by pathobionts and oxidative stress and an injury to the cervical mucosa, often caused by sexual activities. Through these injury and healing processes, HPV viruses, hijacking activated keratinocytes, move into the basal layers of the cervical epithelium and then continue their development towards the distal prickle cell layer (Stratum spinosum). The microbial microenvironment of the cervical tissue determines the tissue homeostasis and the integrity of the protective mucous layer through the maintenance of a healthy immune and metabolic signalling. Pathological microorganisms and the resulting dysbiosis disturb this signalling. Thus, pathological inflammatory reactions occur, which manifest the HPV infection. About 90% of all women contract an HPV infection in the course of their lives. In about 10% of cases, the virus persists and cervical intra-epithelial neoplasia (CIN) develops. Approximately 1% of women with a high-risk HPV infection incur a cervical carcinoma after 10 to 20 years. In this non-systematic review article, we summarise how the sexually and microbial mediated pathogenesis of the cervix proceeds through aberrant immune and metabolism signalling via CIN to cervical carcinoma. We show how both the virus and the cancer benefit from the same changes in the immune and metabolic environment.

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