Chronic non-communicable diseases (NCDs) have gained increasing significance due to their rising prevalence. Among the 57 million global deaths, 36 million (63%) were attributed to NCDs, with chronic respiratory diseases accounting for 11.7% of these deaths. It is estimated that NCDs are responsible for 53% of all fatalities in India, and chronic obstructive pulmonary disease (COPD), a major health concern, is projected to become the third leading cause of death globally by 2030, surpassing heart disease [1-3].

COPD patients exhibit an abnormal inflammatory response influenced by various genetic and environmental factors that are complex and multifactorial, affecting the progression of other diseases either directly or indirectly. Smoking and bacterial infections are commonly recognized as key risk factors for COPD [4]. Additionally, periodontitis, an inflammatory condition resulting from bacterial infections, has been associated with several systemic complications, including renal dysfunction, cardiovascular diseases, metabolic disorders, and chronic respiratory diseases [5-8].

Chronic periodontitis is primarily viewed as a neutrophil-mediated disorder, involving intricate interactions between cytokines and various cell types. The accumulation of plaque leads to the growth of anaerobic microorganisms, which subsequently activate neutrophils. This activation causes an excessive breakdown of connective tissue by neutrophil enzymes [9]. In COPD, neutrophil responses are dysregulated and correlate with the severity or progression of the disease. Although the underlying triggers may differ, both chronic periodontitis and COPD share a pathogenic pathway that involves the activation and action of neutrophils and proteinases. The release of neutrophil molecules, proteinases, and dysfunction can result in similar degenerative processes across various tissues [10].

The 2013 proposal by the European Federation of Periodontology and the American Academy of Periodontology suggests that the homogenous diffusion of inflammatory mediators and microorganisms from periodontal tissues can influence the inflammatory state of COPD [11]. Therefore, in COPD patients with chronic periodontitis, managing periodontal inflammation through therapy may help prevent significant lung function decline and reduce the frequency of exacerbations [12]. Leuckfeld et al. [13] in 2008 highlighted that periodontitis is a common complication in individuals with severe COPD, serving as an independent risk factor for the condition. Furthermore, Deo et al. [14] in 2009 observed a marked increase in COPD severity with greater periodontal attachment loss.

Although several studies have indicated a positive association between COPD and periodontitis, the ongoing debate revolves around whether this relationship is genuine or the result of confounding factors. Consequently, this study aimed to compare the periodontal health of COPD patients with age- and gender-matched controls in Indian subjects.

A case–control investigation was implemented to evaluate and contrast the periodontal health profile of individuals diagnosed with COPD and that of matched controls by age and sex.

An initial pilot assessment involving 15 individuals from each group (cases and controls) was undertaken, which revealed a mean periodontal index difference of 0.6 between the groups, corresponding to an effect size of 0.2998 within a 95% confidence interval. Based on these preliminary results, the minimum calculated sample size was determined to be 175 subjects per group. Participants were eligible for inclusion as cases if they were over 30 years of age, had at least 20 natural teeth, had received a clinical diagnosis of COPD, and provided informed consent. COPD severity classification followed the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria [11], dividing patients into mild (FEV1/FVC ≥ 0.70 and FEV1 ≥ 80%), moderate (FEV1/FVC ≥ 0.70 and FEV1 between 50% and 80%), and severe (FEV1/FVC ≥ 0.70 and FEV1 between 30% and 50%, or with chronic respiratory compromise). Healthy individuals accompanying COPD patients, matched for age and sex, were enrolled as controls. Exclusion criteria included prior periodontal therapy within the preceding three months, presence of systemic conditions with potential periodontal impact, and use of medications likely to alter periodontal outcomes.

The data collection tool consisted of a structured, self-administered questionnaire designed to capture demographic characteristics, socioeconomic indicators using the Kuppuswamy classification, behavioral risk factors (such as smoking and alcohol consumption), and oral hygiene routines. Oral hygiene was evaluated through the Simplified Oral Hygiene Index (OHI-S) developed by Greene and Vermillion [15]. Periodontal conditions were recorded using the Community Periodontal Index (CPI) and the Loss of Attachment (LOA) index, in accordance with the World Health Organization's 1997 oral health survey guidelines [16].

Data were processed using the SPSS, version 23. Chi-square testing was employed to assess associations between categorical variables. For group comparisons, statistical methods included analysis of variance (ANOVA), post hoc testing, Mann–Whitney U-test, and independent t-tests. The relationship between COPD status and periodontal disease was further explored using logistic regression modeling. A significance threshold of P < 0.05 was applied throughout the analysis.

The periodontal status among individuals with varying severities of COPD demonstrated a notable trend, particularly in oral hygiene and attachment loss parameters. As illustrated in Table 1, a statistically significant difference was observed in OHI-S and LOA scores across mild, moderate, and severe COPD groups, with higher severity associated with worsening periodontal indicators. The CPI, however, did not show a statistically significant variation across COPD severity levels, indicating that while plaque accumulation and periodontal destruction progressed with COPD severity, gingival and periodontal pocket depths were comparatively consistent.

Table 1: Comparison of periodontal status according to severity of COPD

A comparison between case and control groups further highlighted the disparity in periodontal health, with cases exhibiting significantly higher mean scores in OHI-S, CPI, and LOA (p < 0.01 for all variables), as presented in Table 2. This suggests that individuals diagnosed with COPD tend to have poorer oral hygiene, more severe periodontal disease, and greater attachment loss compared to non-COPD controls.

Table 2: Comparison of OHI-S, CPI, LOA scores between cases and controls groups

Sociodemographic variables also influenced periodontal outcomes, as detailed in Table 3. Increasing age among cases was associated with progressively elevated odds of periodontal disease, especially notable in the 40–49 age group (OR: 4.29), and remaining consistently high in subsequent older age groups. Male gender was significantly associated with increased risk (p = 0.001), while socioeconomic status (SES) demonstrated an inverse relationship, with upper-lower and lower-middle SES categories showing reduced odds compared to the lower SES reference group. However, these associations were not statistically significant in controls, indicating a possible interaction between COPD status and sociodemographic risk modifiers.

Table 3: Logistic regression analysis by sociodemographic variables for periodontal disease

Logistic regression analysis further established the predictive value of oral health parameters in relation to COPD status (Table 4). After adjustment, fair to poor oral hygiene was strongly associated with higher odds of being in the COPD group (AOR: 2.74, p < 0.001). Similarly, elevated CPI scores and LOA codes were also significant predictors (AOR: 3.39 and 2.20 respectively; p < 0.001 for both), underscoring the robust association between deteriorating periodontal health and the presence of COPD.

Table 4: Logistic regression analysis by oral health

In the current investigation, patients diagnosed with chronic obstructive pulmonary disease (COPD) were stratified into mild, moderate, and severe categories in accordance with the GOLD guidelines [11]. A greater proportion of individuals in this study exhibited either mild or moderate disease severity. Comparable distributions have been noted in earlier research [17,18]. Sapey et al. [19] documented a predominance of moderate-to-severe COPD in their cohort, a disparity possibly attributable to cultural context or differing participant characteristics.

Evidence from various investigations has highlighted a trend of suboptimal dental hygiene behaviors among individuals with COPD, which may act as a confounding factor in assessing this association [19–21]. The development of plaque biofilm can disrupt microbial equilibrium, leading to neutrophil activation, a process integral to the pathogenesis of both periodontal disease and COPD. In the present dataset, elevated mean scores for debris and calculus were observed among the COPD group, despite comparable oral hygiene routines and frequency of dental visits when contrasted with control subjects. This pattern implies a possible underlying mechanistic relationship between oral and respiratory health. Similar trends in diminished oral hygiene status among COPD patients have been noted in prior studies [18,21–23].

An increase in oral hygiene index scores was directly correlated with the progression in COPD severity. These outcomes align with a systematic review by Kelly et al. [24], which identified a link between exacerbations of COPD and poor oral hygiene. Additionally, research by Zhou et al. [25] and Kucukcoskun et al. [26] demonstrated that periodontal therapy was associated with improved pulmonary metrics and reduced frequency of COPD flare-ups. Nevertheless, these observations are not consistent with the findings reported by Baldomero et al. [27].

Although a rising trend in Community Periodontal Index (CPI) scores was noted with increasing COPD severity, this change lacked statistical significance. Similar nonsignificant relationships were reported by Bergström et al. [28] and Hyman and Reid [29]. This lack of association is also in line with data from Liu et al. [30], while Shen et al. [31] described a modestly elevated but statistically insignificant odds ratio (1.19) for this association.

Likewise, clinical attachment loss (LOA) scores were markedly elevated among COPD cases, with values increasing proportionally to disease severity. These findings corroborate those of Bhavsar et al. [21], Peter et al. [17], and Gupta et al. [32]. A case–control analysis from China reported that the COPD group retained fewer teeth overall, with a majority demonstrating clinical attachment loss exceeding 4 mm [20]. Furthermore, a meta-analysis encompassing ten separate studies reported significantly higher mean CAL in individuals with COPD [23]. The likelihood of LOA exceeding 3 mm was estimated at 1.86 among COPD patients, consistent with the present observations.

Nonetheless, this study is subject to certain constraints. First, not all possible confounding variables were accounted for. Second, the duration of COPD in study participants was not evaluated. Third, there is potential for Berksonian bias in the case–control selection process. Therefore, to clarify the causal pathways linking COPD and periodontal disease, further longitudinal research is warranted.

Among the various factors analyzed, sex, tobacco usage, alcohol intake, and the diagnosis of COPD emerged as significant determinants influencing periodontal health. In summary, the study identified a robust correlation between chronic obstructive pulmonary disease and periodontal pathology. Furthermore, deterioration in oral hygiene and the progression of periodontal disease were found to be more pronounced with increasing COPD severity.

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