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 endoplas...

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Detalles Bibliográficos
Autores: Pelechá-Salvador M, López-Domènech S, Márquez-Arrico CF, Fernández-Reyes M, Perea-Galera L, Hermenejildo J, Morillas C, Fernández-Collazo P, Silvestre-Rangil J, Víctor VM, Silvestre FJ, Rocha M
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2026
País:España
Institución:INCLIVA
Repositorio:r-INCLIVA. Repositorio Institucional de Producción Científica de INCLIVA
OAI Identifier:oai:incliva.fundanetsuite.com:p20752
Acceso en línea:https://incliva.portalinvestigacion.com/publicaciones/20752
Access Level:acceso abierto
Palabra clave:endoplasmic reticulum stress
gingivitis
polycystic ovary syndrome
unfolded protein response
oxidative stress
Descripción
Sumario: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),clini-cal 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-eIF2 alpha), 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-eIF2 alpha 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-eIF2 alpha 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.