Endoplasmic reticulum stress in women with polycystic ovary syndrome and gingivitis: A case-control study of metabolic-periodontal interplay.

BACKGROUND

Gingival inflammation has been increasingly linked to metabolic and endocrine disorders, such as polycystic ovary syndrome (PCOS). This connection may involve immune system activation and cellular stress mechanisms, particularly the unfolded protein response (UPR), which regulates endoplasmic reticulum (ER) stress.

OBJECTIVES

The aim of the study was to investigate whether gingivitis modulates UPR activation in peripheral blood mononuclear cells (PBMCs) of women with PCOS.

MATERIAL AND METHODS

In this case-control study, female subjects were divided into 2 groups: a control group (n = 48); and a PCOS group (n = 68), which included 24 individuals with gingivitis (PCOS+). Anthropometric, biochemical and periodontal parameters were determined, namely probing pocket depth (PPD), clinical attachment level (CAL), bleeding on probing (BOP), and plaque index. Markers of oxidative stress, including total superoxide and glutathione peroxidase 1 (GPx1), and UPR mediators, such as glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), phosphorylated eukaryotic initiation factor 2 alpha subunit (p-eIF2α), and C/EBP homologous protein (CHOP), were evaluated in PBMCs.

RESULTS

Polycystic ovary syndrome was associated with an increased plaque index and significantly higher BOP in PCOS+. Increased superoxide and reduced GPx1 levels were observed in women with PCOS, with no significant differences between subgroups. Gingivitis in PCOS was correlated with the activation of specific UPR pathways; higher levels of p-eIF2α and CHOP and lower GRP78 levels were detected in PCOS+, while ATF6 was increased in the overall PCOS group. Moreover, BOP demonstrated a direct correlation with p-eIF2α and the plaque index.

CONCLUSIONS

The association of leukocyte ER stress responses in PCOS with gingival inflammation underscores the impact of periodontal disease on modulating systemic cellular stress in the context of multifactorial metabolic disorders.