Evaluation of periodontal status in women with polycystic ovary syndrome versus healthy women: a cross-sectional study

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J Yeungnam Med Sci. 2023;40(Suppl):S17-S22

Publication date (electronic) : 2023 May 8

doi : https://doi.org/10.12701/jyms.2023.00143

Sandhya Pavankumar^,1, Pavan Kumar Yellarthi², Sandeep JN³, Ramanarayana Boyapati⁴, Trinath Kishore Damera¹, Naveen Vital Kumar G¹

¹Department of Periodontics, GITAM Dental College and Hospital, Visakhapatnam, India

²Department of Oral Medicine and Radiology, GITAM Dental College and Hospital, Visakhapatnam, India

³Department of Periodontics, V.S Dental College and Hospital, Bengaluru, India

⁴Department of Periodontics, Sibar Institute of Dental Sciences, Guntur, India

Corresponding author: Sandhya Pavankumar, MDS Department of Periodontics, GITAM Dental College and Hospital, Rushikonda, Visakhapatnam, Andhra Pradesh 530045, India Tel: +91-891-2840351 • Fax: +91-891-2790033 • E-mail: sandhyapavankumar25@gmail.com

Received 2023 February 4; Revised 2023 March 29; Accepted 2023 April 4.

Abstract

Introduction

Polycystic ovary syndrome (PCOS) is a highly common condition affecting approximately 4% to 12% of females of reproductive age [1,2]. Although this syndrome is heterogeneous in nature, chronic anovulation and hyperandrogenism are its hallmarks. In 1935, Stein and Leventhal were among the first to describe this condition. Later, great progress was made in understanding the pathogenesis of PCOS owing to its neuroendocrine underpinnings [3] and the link between insulin resistance, obesity, and PCOS [4]. Given the present knowledge of PCOS, it is important that the treatment approach should not only treat infertility and hirsutism but also consider the long-term hazards related to insulin resistance [1].

Metabolic abnormalities such as dyslipidemia, type 2 diabetes mellitus, endometrial carcinoma, and cardiovascular disease seem to be associated with PCOS. However, obesity (abdominal phenotype), insulin resistance, altered lipid levels, and hyperinsulinemia are primary characteristic features of PCOS [5,6].

Hyperinsulinemia and insulin resistance play critical roles in PCOS pathogenesis. The initiation and maintenance of hyperandrogenism are closely associated with obesity and hyperinsulinemia [7]. Increased androgen levels affect insulin sensitivity in target tissues, leading to an insulin-resistant state. The presence of low-grade inflammation due to insulin resistance explains the increased levels of C-reactive protein (CRP) seen in this syndrome [8-10].

Periodontitis, a chronic inflammatory disease initiated by lipopolysaccharides produced by periodontopathic bacteria, eventually leads to attachment loss and alveolar bone loss [11]. Elevated CRP levels have been observed in patients with periodontitis. Hence, the increased CRP level associated with low-grade chronic inflammation is emerging as a plausible etiological mechanism linking systemic and periodontal diseases [12].

Increased levels of proinflammatory cytokines such as interleukin (IL)-1 and tumor necrosis factor-α (TNF-α) observed in the serum and gingival crevicular fluid of patients with periodontitis [13] might also contribute to insulin resistance [14]. The pathognomonic states of PCOS and chronic periodontitis may explain the association between these conditions.

Therefore, this study aimed to compare the prevalence of periodontal disease in women with PCOS and healthy women.

Methods

Results

The age distribution among patients with PCOS and those who were healthy ranged from 17 to 45 years. The groups did not differ significantly (p=0.740) in age (Table 1).

Table 1.

Distribution of age among individuals with PCOS and those who are healthy

1. Oral hygiene index-simplified

When the mean OHI-S scores were compared between the PCOS (2.10±0.70) and healthy (2.10±0.70) groups, oral hygiene status was not significantly different (p=0.997) between them (Table 2).

Table 2.

Comparison of OHI-S, GI, CPI, and LA scores between women with PCOS and those who are healthy

Discussion

PCOS is a complex and heterogeneous endocrinopathy characterized by a wide array of clinical symptoms. A single causative factor cannot fully account for the entire range of irregularities associated with this disorder [1]. After Stein and Leventhal described this syndrome in 1935, extensive research was conducted linking PCOS and systemic ailments, such as type 2 diabetes mellitus and cardiovascular diseases [16]. A chronic inflammatory state due to insulin resistance and hyperinsulinemia has been observed in patients with PCOS. Hence, females with PCOS demonstrate higher serum levels of CRP, TNF-α, and IL-6 compared to those individuals who are healthy [17].

Gingivitis and periodontitis are common chronic inflammatory conditions caused by periodontopathic bacteria and are associated with elevated levels of systemic and local proinflammatory cytokines, such as CRP, TNF-α, IL-1, and IL-6 [13,18]. This increased concentration of proinflammatory mediators contributes to insulin resistance and creates chronic inflammatory conditions [14]. A common pathophysiological pathway connecting these disorders might exist because both PCOS and periodontal disease are associated with systemic inflammation and insulin resistance. It can be hypothesized that increased levels of proinflammatory cytokines due to low-grade chronic inflammation in PCOS may increase the incidence of periodontal disease and that elevated levels of proinflammatory cytokines in chronic periodontitis might further contribute to insulin resistance in patients with PCOS.

However, very few studies have focused on periodontal parameters in women with PCOS. This cross-sectional study aimed to compare the prevalence of periodontal disease between women with PCOS and healthy women.

A total of 196 women (98 per group in the PCOS and healthy groups) aged 17 to 45 years participated in this cross-sectional study. OHI-S, GI, CPI, and LA scores were recorded for all participants. The Student t-test was used to analyze the data.

The results showed that the study groups were adjusted for age (p=0.740). Despite similar plaque scores (p=0.977), women with PCOS had significantly higher GI scores than those who were healthy (p<0.001). These findings agree with those of an earlier study [19] that also showed increased gingival inflammation in the PCOS group. This effect may be attributed to endocrinological changes, such as increased levels of testosterone, epiandrostenedione, luteinizing hormone, and estrogen [20]. It is well documented that estrogen promotes the growth of periodontal pathogens, especially Prevotella intermedia, increases cellular proliferation in blood vessels, and decreases keratinization [21] which may have contributed to the increased gingival inflammation in the PCOS group.

This study also showed that the CPI and LA scores were higher in the PCOS group than in the healthy group (p<0.001). Our findings are in accordance with those of earlier studies [22,23], which demonstrated that patients with PCOS had increased pocket depth, clinical attachment loss, and bleeding sites on probing. In contrast to the present study, Isik et al. [24] demonstrated no significant difference (p>0.05) in periodontal parameters, GI, percentage of bleeding on probing, and clinical attachment level (except for increased probing depth) in subjects with PCOS compared to healthy women. That study only included women of early reproductive age and those recently diagnosed with PCOS; the periodontal examination was also performed only on the Ramfjord teeth. These selection criteria may have been critical to the observed disparity in the results [24].

The increased vulnerability of patients with PCOS to periodontal disease can be explained by the following mechanisms: (1) increased CRP levels; (2) elevated levels of proinflammatory chemokines and cytokines such as IL-17 [25], IL-18, IL-6, TNF-α, macrophage inflammatory protein-1, and monocyte chemoattractant protein-1; (3) substantial increases in the levels of monocytes and lymphocytes [26-28]; (4) abnormal endothelial function and marked elevation of numerous markers of endothelial inflammation such as soluble intercellular adhesion molecule-1, endothelin-1, plasminogen activator inhibitor-1, soluble vascular cell adhesion molecule-1, and asymmetric dimethylarginine [26,29,30]; (5) increased oxidative stress [26,31,32]; (6) reduced glutathione, and decreased levels of haptoglobin, a protein with antioxidant properties, hence resulting in low total antioxidant status [26,33,34]; and (7) elevated levels of advanced glycation end-products [26,35,36]. However, longitudinal studies with larger sample sizes are required to confirm this interpretation.

This study had certain limitations as body mass index (BMI), waist circumference, waist-to-hip ratio, and metabolic parameters were not assessed. The PCOS population has a higher prevalence of abdominal fat than individuals matched for weight [37]. Additionally, there is increased production of proinflammatory cytokines due to this fat [38], which increases the systemic inflammatory load that in turn enhances the initiation and progression of periodontal diseases.

Within the limitations of this study, women with PCOS had a higher prevalence of periodontitis than women who were healthy. There appears to be an interaction between PCOS and periodontitis that may have a synergistic effect on the production of proinflammatory mediators. Hence, education on periodontal health, early detection, and intervention for periodontal diseases are of paramount importance in patients with PCOS to maintain both periodontal and systemic health. Long-term studies are needed to elucidate the relationship between PCOS and periodontal disease. Future studies should include parameters such as waist-to-hip ratio, waist circumference, and BMI and should evaluate the effects of different drugs and periodontal therapies on patients with PCOS.

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