Provoked vulvodynia represents a challenging chronic pain condition, characterized by its multifactorial origins. The inherent complexities of human-based studies have necessitated the use of animal models to enrich our understanding of vulvodynia’s pathophysiology. This review aims to provide an exhaustive examination of the various animal models employed in this research domain. A comprehensive search was conducted on PubMed, utilizing keywords such as “vulvodynia”, “chronic vulvar pain”, “vulvodynia induction”, and “animal models of vulvodynia” to identify pertinent studies. The search yielded three primary animal models for vulvodynia: inflammation-induced, allergy-induced, and hormone-induced. Additionally, six agents capable of triggering the condition through diverse pathways were identified, including factors contributing to hyperinnervation, mast cell proliferation, involvement of other immune cells, inflammatory cytokines, and neurotransmitters. This review systematically outlines the various animal models developed to study the pathogenesis of provoked vulvodynia. Understanding these models is crucial for the exploration of preventative measures, the development of novel treatments, and the overall advancement of research within the field.

Provoked vulvodynia (PV) is the leading cause of vulvar pain and dyspareunia. The etiology of PV is multifactorial and remains poorly understood. PV is associated with a history of repeated vulvar inflammation and is often accompanied by sensory neuromodulation as a result of activation of the metabotropic glutamate receptor 5 (mGluR5) in the sensory nerve terminals. Therefore, this study aims to examine the role of glutamate-mGluR5 signaling during the initial inflammatory phase in chronic vulvar pain development in an animal model of PV.Thermal and mechanical vulvar sensitivity was assessed for three weeks following zymosan vulvar challenges. Anxiety-like behavior and locomotor activity were assessed at the end of the experiment. To investigate the role of glutamate mGluR5, the MTEP (mGluR5 antagonist) was injected into the vulva during vulvar inflammation. On the other hand, glutamate or CHPG (mGluR5 agonist) were injected in order to examine the effects of mGluR5 activation. RT-PCR was performed to assess changes in the transcription of genes related to neuroinflammation, neuromodulation, and neuroplasticity in the spinal cord (L6-S3). Zymosan-induced inflammation resulted in a significant thermal and mechanical vulvar hypersensitivity that persisted for over a month after the zymosan injection. However, local treatment with MTEP enhanced the vulvar mechanical and thermal hypersensitivity. On the other hand, activation of the mGluR5 via injection of glutamate or CHPG into the vulva leads to long-lasting vulvar mechanical and thermal hypersensitivity. The activation of the glutamate pathway was found to be accompanied by an increase in the transcription level of genes related to neuroinflammation and neuroplasticity in the sacral spine region. The present findings indicate that vulvar hypersensitivity is mediated by mGluR5 activation during inflammation. Hence, modulation of the mGluR5 pathway during the critical period of inflammation contributes to preventing chronic vulvar pain development. Conversely, activation of the mGluR5 pathway leads to long-lasting mechanical and thermal hypersensitivity.

Objectives: As the COVID-19 pandemic wanes, understanding maternal–fetal antibody transfer remains crucial for optimizing vaccination strategies. This study evaluates anti-SARS-CoV-2 antibody levels in amniotic fluid following maternal BNT162b2 mRNA vaccination and/or COVID-19 infection during early pregnancy, focusing on the first and second trimesters. Methods: A retrospective cohort study was conducted at a tertiary university-affiliated hospital, involving 149 pregnant women who underwent amniocentesis. Anti-SARS-CoV-2 spike IgG levels were measured in amniotic fluid samples. Participants were categorized based on vaccination and infection status: vaccine-only, infection-only, vaccine + infection, and no vaccine/infection. Correlations between antibody levels and the time since vaccination or infection were analyzed. Results: The vaccine + infection group had a higher proportion of positive antibody levels compared to the vaccine-only group (63.6% vs. 35.9%, p = 0.029). Median SARS-CoV-2 IgG levels were significantly higher in the vaccine + infection group (283.0 AU/mL) than in the vaccine-only group (64.1 AU/mL, p = 0.006). Women who received three vaccine doses had higher antibody levels and more positive antibody rates compared to those with one or two doses. A significant negative correlation was found between antibody levels and the interval since the last vaccine dose or infection. Conclusions: Our results indicate the presence of anti-SARS-CoV-2 antibodies in the amniotic fluid, reflecting antibody transfer during early pregnancy. However, a noticeable decrease in immunity was observed, as indicated by declining amniotic fluid antibody levels over time. Further studies are needed to determine the optimal timing and number of boosters required to protect against new variants of SARS-CoV-2.