This comparative clinical investigation was conducted in accordance with the Declaration of Helsinki (revised 2013) and Good Clinical Practice guidelines.^[27] The Institutional Ethics Committee, Bhopal, Madhya Pradesh, India, approved the study protocol. All participating subjects received detailed oral and written explanations of the study objectives and provided signed voluntary informed consent prior to enrollment.

A total of 1,250 adult participants aged between 20 and 60 years were recruited from the Outpatient Department of Periodontics, People's Dental Academy, Bhopal. The participants were assigned to three defined, mutually exclusive clinical cohorts:

Control Group (Group A,n = 250): Periodontally healthy subjects presenting with probing pocket depths ≤ 3 mm, absence of clinical attachment loss, and bleeding on probing at less than 10% of examined sites.^[8]

Pre-Treatment Test Group (Group B, n=500): Patients presenting with active, untreated generalized chronic periodontitis, characterized by probing pocket depths ≥4 mm and clinical attachment loss in more than 30% of examined clinical sites.^{[7, 8]}

Post-Treatment Test Group (Group C, n=500): Patients previously diagnosed with generalized chronic periodontitis who had completed full-mouth non-surgical mechanical periodontal therapy (quadrant-wise scaling and root planing using ultrasonic instrumentation and area-specific Gracey curettes) and supportive periodontal care at least six months prior to clinical evaluation.^{[20, 21, 22]}

To minimize confounding influences on periodontal indices, systemic inflammation, and psychological stress profiles, strict eligibility criteria were enforced:

Inclusion Criteria: Adult male and female subjects aged 20–60 years having a minimum of 20 functional natural teeth (excluding third molars).

Exclusion Criteria: Current or former users of any form of smoked or smokeless tobacco; patients diagnosed with systemic medical disorders known to influence periodontal status or host immunity (including diabetes mellitus, cardiovascular conditions, autoimmune disorders, and hepatic/renal disease); pregnant or lactating females; patients who had used systemic antimicrobial, corticosteroid, or non-steroidal anti-inflammatory agents within the preceding six months; and individuals receiving active psychiatric counseling or psychopharmacological therapy.

All clinical examinations were conducted by a single, calibrated periodontal examiner. The assessment covered six sites per tooth (mesio-buccal, mid-buccal, disto-buccal, mesio-lingual/palatal, mid-lingual/palatal, and disto-lingual/palatal) for all functional natural teeth, excluding third molars, using a standardized UNC-15 periodontal probe and a mouth mirror under adequate operatory illumination.

The recorded parameters comprised:

Simplified Oral Hygiene Index (OHI-S): Assessing debris and calculus accumulation.^[4]

Gingival Index (GI): Assessing the severity and qualitative extent of gingival inflammation.^[5]

Probing Pocket Depth (PD): Measured from the gingival margin to the base of the pocket, rounded to the nearest millimeter.

Clinical Attachment Level (CAL): Measured from the cemento-enamel junction (CEJ) to the base of the pocket.

Bleeding on Probing (BOP): Evaluated dichotomously (presence or absence of bleeding within 30 seconds of gentle probing with approximately 0.25 N force).^[1]

The anatomical quantification of oral inflammatory burden was computed using the mathematical algorithms established by Nesse et al. (2008).^[1]

Full-mouth CAL and recession values were used to compute the Periodontal Epithelial Surface Area (PESA) for each tooth, utilizing Humphrey’s mean root surface area coefficients.^[1]

The PISA for each specific tooth site was derived by multiplying the individual PESA by the site-specific dichotomous BOP score (0 for non-bleeding, 1 for bleeding):

The individual site PISA values were summed across all examined teeth to yield the total full-mouth PISA value in square centimeters (cm²), reflecting the total vascularized ulcerated epithelial wound surface area.^[1]

Subjective chronic psychological stress over the preceding 30 days was measured using the validated 10-item Perceived Stress Scale (PSS-10) originally formulated by Cohen et al.^{[2, 3]} The instrument assesses how unpredictable, uncontrollable, and overloaded respondents find their lives.^[2]

Items were scored on a 5-point Likert scale ranging from 0 (never) to 4 (very often). Positively framed items (Questions 4, 5, 7, and 8) were reverse-coded before summing all ten responses, producing a composite continuous score ranging from 0 to 40.^{[2, 3]} Stress scores were further classified into standard categories:^[2]

Low Stress: 0–13

Moderate Stress: 14–26

High Stress: 27–40

Data were tabulated in Microsoft Excel and analyzed using SPSS Version 26.0 (IBM Corp., Armonk, NY). Continuous variables were summarized as mean ± standard deviation (SD), and categorical variables were expressed as frequencies and percentages.

Inter-group baseline demographic comparability was evaluated using one-way ANOVA for continuous variables and Chi-square (χ²) tests for categorical distributions. Differences in clinical periodontal parameters and PSS-10 scores between cohorts were assessed using one-way ANOVA followed by Tukey’s Honest Significant Difference (HSD) post-hoc test for multiple comparisons.

Direct comparisons between the pre-treatment (Group B) and post-treatment (Group C) cohorts were verified using independent two-tailed Student’s t-tests, with Cohen’s d calculated to determine effect size. Bivariate associations between PSS-10 scores and PISA within each cohort were evaluated using Pearson’s correlation coefficient (r). Statistical significance was set at α=0.05.

The study population comprised 1,250 participants with a mean age of 38.5±12.3 years. Analysis of baseline demographics confirmed that the cohorts were well-matched, with no statistically significant differences in age (p=0.21), sex distribution (p=0.87), or composite socioeconomic status (p=0.93), confirming inter-group comparability (Table 1).

Table 1: Baseline Demographic Characteristics Across Study Cohorts

Evaluation of clinical parameters revealed significant improvements in the post-treatment cohort (Group C) compared to the untreated periodontitis cohort (Group B) (p<0.001 for all variables; Table 2).

Mean full-mouth PISA values decreased from 12.5±4.3 cm² in Group B to 4.6±2.1 cm² in Group C, representing a mean difference of 7.90 cm² (95% CI: 7.44 to 8.36 cm²) and an overall 63.2% reduction in ulcerated inflammatory surface area.

Similarly, marked reductions were noted in mean OHI-S (2.3±0.6 vs. 1.2±0.4), GI (2.1±0.5 vs. 1.1±0.3), PD (4.8±1.2 mm vs. 2.5±0.7 mm), and CAL (3.5±1.0 mm vs. 1.6±0.5 mm). Cohen’s d values for all periodontal indices exceeded 2.0, demonstrating substantial clinical effect sizes following mechanical intervention.

Table 2: Comparison of Clinical Periodontal Metrics and Inflammatory Surface Area Between Pre- and Post-Treatment Cohorts

Mean PSS-10 scores were significantly lower in the post-treatment cohort (17.2±4.5) than in the untreated periodontitis cohort (22.7±5.1, t=18.09, p<0.001; Table 3), showing a large effect size (Cohen’s d=1.14).

Categorical redistribution of stress severity revealed that patients classified with high stress dropped from 24.0% (n=120) in Group B to 7.4% (n=37) in Group C (OR=0.25, 95% CI: 0.17 to 0.38, p<0.001). Concurrently, the proportion of individuals in the low-stress category rose from 3.6% (n=18) in Group B to 22.4% (n=112) in Group C (OR=7.72, 95% CI: 4.61 to 12.92, p<0.001).

Table 3: Redistribution of Perceived Stress Severity Categories Following Periodontal Therapy

In active, untreated chronic periodontitis (Group B), bivariate correlation analysis demonstrated a statistically significant, moderate-to-strong positive correlation between PSS-10 and PISA (r=0.62, r²=0.384, p<0.001; Table 4).

However, in the post-treatment cohort (Group C), this correlation was markedly attenuated and lacked statistical significance (r=0.11, r²=0.012, p=0.142). In periodontally healthy controls (Group A), the correlation was similarly non-significant (r=0.08, p=0.207).

Table 4: Bivariate Pearson Correlation Between PSS-10 and PISA Across Cohorts

The reduction in mean PISA from 12.5±4.3 cm² in untreated disease to 4.6±2.1 cm² following therapy represents the elimination of approximately 7.9 cm² of ulcerated pocket epithelium. In biological terms, an active inflammatory surface area exceeding 12 cm² represents an open, chronically bleeding wound roughly equivalent to the size of an adult human palm.^[1]

This ulcerated barrier allows continuous systemic entry of subgingival periopathogens, lipopolysaccharides (LPS), and inflammatory cytokines.^{[18, 19, 23]} By disrupting subgingival biofilms and eliminating calculus, non-surgical mechanical instrumentation permits pocket epithelial re-adaptation, junctional epithelial adhesion, and microvascular resolution.^{[20, 22]} This structural healing limits systemic bacteremia, dampens low-grade vascular inflammation, and resolves local tissue edema.^{[18, 19]}

The parallel reduction in mean PSS-10 scores from 22.7±5.1 to 17.2±4.5 (p<0.001), accompanied by a notable decline in high-stress individuals (24.0% to 7.4%), suggests that effective periodontal debridement may positively influence patient psychological well-being. This response can be understood through two interconnected pathways:

Somatic and Functional Relief: Advanced untreated periodontitis produces distinct physical symptoms, including spontaneous gingival bleeding, persistent halitosis, tooth mobility, and masticatory pain. These symptoms can cause social embarrassment, self-consciousness, and reduced self-esteem.^{[25, 26]} By eliminating bleeding, halitosis, and gingival soreness, successful therapy improves oral health-related quality of life (OHRQoL), alleviating daily disease-related emotional distress.^{[25, 26]}

Attenuation of the Systemic Neuro-Inflammatory Loop: Pro-inflammatory cytokines generated within the ulcerated periodontium (such as IL-1beta, IL-6, and TNF-α) enter the systemic circulation and can interact with the central nervous system.^{[18, 23]} These circulating mediators can stimulate the vagus nerve and alter blood-brain barrier transport, activating hypothalamic microglial cells and neuroendocrine pathways associated with sickness behavior, fatigue, and dysphoria. By resolving this inflammatory focus, mechanical therapy dampens systemic cytokine spillover, which may help relieve inflammatory signaling that contributes to heightened stress perception.^{[18, 24]}

A primary finding of this study is the loss of a statistically significant correlation between PSS-10 and PISA in the treated cohort (r=0.11, p=0.142), contrasting sharply with the strong positive correlation observed in active untreated disease (r=0.62, p<0.001). These untreated findings corroborate observations by Parihar et al. (2024),^[12] Coelho et al. (2020),^[13] Varma et al. (2023),^[14] Balaji et al. (2018),^[15] Abe et al. (2020),^[16] and Macri et al. (2024).^[17]

This finding illustrates that psychological distress alone is insufficient to sustain extensive pocket ulceration in the absence of an organized subgingival microbial biofilm. Chronic stress acts as a disease modifier rather than a primary initiator^{[10, 13]}. In untreated periodontitis, neuroendocrine dysregulation (HPA-axis glucocorticoid receptor resistance and SAM-mediated vasoconstriction) impairs the host's cellular defenses, allowing subgingival pathogens to proliferate and accelerate tissue breakdown^[24].

However, once root surfaces are debrided and subgingival dysbiosis is suppressed, background psychological stress no longer finds an active microbial nidus to amplify into severe epithelial ulceration. This supports the clinical principle that mechanical biofilm disruption remains the foundation of periodontal therapy, even in patients under ongoing psychological strain^{[21, 22]}.

Methodological strengths of this study include the large sample size (N=1,000 across pre- and post-treatment cohorts), the use of PISA as a continuous biological metric of inflammatory wound size, the application of a validated psychometric instrument (PSS-10), and strict exclusion criteria eliminating major confounders such as tobacco use, diabetes mellitus, and psychiatric medication^{[1, 2, 3]}.

Several limitations should be noted. First, the study employed a cross-sectional comparative design across distinct pre-treatment and post-treatment cohorts rather than a longitudinal design following the same individuals over time. While the cohorts were demographically well-matched, longitudinal intervention trials tracking serial post-therapy intervals are recommended to clarify the precise temporal sequence of stress and inflammatory resolution. Second, psychological distress was measured using self-reported psychometrics without accompanying biochemical stress markers, such as salivary cortisol or alpha-amylase. Future interventional studies incorporating systemic cytokine profiling, salivary neuroendocrine assays, and microbial sequencing will further elucidate the molecular pathways governing this response.

This comparative clinical investigation evaluated the therapeutic impact of non-surgical mechanical periodontal therapy on active oral inflammatory burden, quantified via the Periodontal Inflamed Surface Area (PISA), and perceived psychological stress, assessed via the 10-item Perceived Stress Scale (PSS-10), in adult patients with chronic periodontitis.

Evaluating 500 untreated periodontitis patients (Group B) alongside 500 patients who had received non-surgical mechanical debridement and supportive maintenance (Group C) demonstrated that mechanical instrumentation achieved a 63.2% reduction in vascularized ulcerated epithelial wound area, with mean PISA decreasing from 12.5±4.3 cm² to 4.6±2.1 cm² (p<0.001).

Concurrently, perceived stress scores declined significantly from 22.7±5.1 to 17.2±4.5 (p<0.001), with high-stress categorizations falling from 24.0% to 7.4%. Importantly, the moderate-to-strong positive correlation between stress and inflammatory surface area observed during active untreated disease (r=0.62, p<0.001) was absent following mechanical therapy (r=0.11, p=0.142), reflecting successful clinical healing and disease stabilization.