Chronic Periodontitis linked to Gynecological Disorders such as PCOD and GDM, finds study
A new research has revealed a clear association between chronic periodontitis and gynecological disorders such as PCOD and GDM. This link is supported by significantly elevated levels of the NLRP3 inflammasome and Fretibacterium HOT 360 in patients who have both periodontitis and these gynecological conditions.
Periodontitis is a chronic inflammatory disease that involves the complex interactions between pathogenic periodontal microbiota and the host immune response, modulated by environmental and genetic factors. Due to its chronic inflammatory nature, CP(Chronic periodontitis) is associated with a systemic state of oxidative stress, mitochondrial dysfunction and multiple systemic diseases. Diabetes mellitus is a traditional risk factor for CP and a bidirectional association between the two diseases has already been established. Also, CP has been associated with various insulin-resistance (IR) conditions, including rheumatoid arthritis, PCOS, and cardiovascular disease (CVD). Numerous environmental factors, such as hormone levels, salivary pH, anaerobic conditions, and nutrition, might impact the oral microbiota. Periodontitis has been associated with various risk factors that impact the spontaneous probability of conception, including age, bacterial vaginosis (BV), endometriosis (EM), PCOS, and obesity. The most common plausible etiologic mechanism linking periodontal disease and many systemic diseases are chronic low-grade inflammation.
Recent studies on the intricate molecular pathways behind the inflammatory response have given rise to the concept of the "inflammasome," a multiprotein oligomer molecule that controls inflammation in its early phases. The NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) complex is one of these inflammasomes and is essential to innate immunity and inflammatory processes. It is composed of a Nod-like receptor (NLR) that controls the expression of important proinflammatory cytokines, especially interleukin18 (IL-18), and mediates the activation of protease enzymes (Caspase 1). Periodontal inflammation is caused by the secretion of Interleukin-1β (IL-1β), a major proinflammatory cytokine by host tissues and upregulation of NLRP3 inflammasome has also been reported.
Polycystic ovarian syndrome (PCOS) is an endocrine disorder with multifactorial etiology. The primary cause of infertility in PCOS is hyperandrogenism, which can activate the NLRP3 inflammasome and cause low-grade inflammation and the release of inflammatory mediators. Women with PCOS tend to have increased levels of androgen, oxidative stress, free fatty acid (FFA) and high mobility group box 1 (HMGB1), molecules that serve as danger signals to activate the inflammasomes, especially the NLRP3 inflammasome pathway.
Gestational diabetes mellitus (GDM) refers to glucose intolerance with onset or first recognition during pregnancy. The common feature in both the pathologies is dysregulation of the inflammatory response. Increased production and overexpression of various inflammatory mediators, including matrix metalloproteases (MMP1, MMP9, and MMP13), receptor activator nuclear factor κB ligand (RANKL), prostaglandin E2 (PGE2), cytokines (IL1, IL6, and TNFα), and chemokines (IL8), have been linked to the pathogenic mechanism between diabetes and periodontal disease. In addition, DM increases the overexpression of innate immune mediators including defensins and Toll-like receptors (TLRs) in gingival tissues, aggravating the severity of chronic periodontitis (CP). The inflammasomes activated by metabolic damage and infection have also been proposed to be involved in the pathogenesis of periodontal disease and DM.
According to studies, unculturable bacteria linked to periodontitis may be a significant factor in the development of PLBW and the presence of periodontal infection during pregnancy. Fretibacterium sp. HOT 360, a member of the phylum synergistetes, was chosen for the present study because of its increased prevalence in deep periodontal pockets. Since both the periodontal disease and gynaecological disorders (PCOS & GDM) have an increased inflammatory burden and are more prone to oral dysbiosis, this study evaluated the NLRP3 levels and Fretibacterium HOT 360 in patients with periodontal disease and gynaecological disorders (PCOS&GDM).
Totally 90 subjects were screened and they were categorised into Group 1 (N=45: Patients with gynaecological disorders and without periodontitis) and Group 2 (N=45: Patients with gynaecological disorders + Periodontitis). Saliva samples were collected to assess the levels of NLRP3 inflammasome and Fretibacterium HOT 360 using an ELISA and conventional PCR respectively. Periodontal parameters (Plaque score, PD, CAL, PISA) were evaluated for all the patients
The mean concentration of NLRP3 inflammasome and Fretibacterium HOT 360 was significantly higher in group 2 (Patients with gynaecological disorders and Periodontitis) than group 1 (Patients with gynaecological disorders and without periodontitis) at p< 0.05. In addition, NLRP3 inflammasome and Fretibacterium HOT 360 were positively correlated with all the periodontal parameters (Plaque score, PD, CAL, PISA) in both the groups with the higher value in group 2.
Within the limitations of this study, it can be concluded that there is a definitive association between chronic periodontitis and gynaecological disorders (PCOD&GDM) as demonstrated by the significant levels of NLRP3 inflammasome and Fretibacterium HOT 360 levels in patients with periodontitis and gynaecological disorders.
Source: Devaraj et al. / Indian Journal of Obstetrics and Gynecology Research 2025;12(2):216–222
