Background: Periodontitis and type 2 diabetes mellitus (T2DM) share a bidirectional relationship mediated through chronic inflammation and altered host immune responses. Diabetes adversely influences periodontal healing and may affect treatment outcomes following periodontal therapy.
Aim: To compare periodontal clinical outcomes following non-surgical periodontal therapy in patients with periodontitis with and without T2DM over a 12-month follow-up period. Materials and Methods: This prospective cohort study included 100 patients diagnosed with Stage II–III periodontitis. Fifty patients with controlled T2DM constituted Group A, while 50 systemically healthy patients formed Group B. All participants underwent scaling and root planing with oral hygiene reinforcement. Clinical parameters including Plaque Index (PI), Gingival Index (GI), Probing Pocket Depth (PPD), and Clinical Attachment Level (CAL) were recorded at baseline, 3, 6, 9, and 12 months. Statistical analysis was performed using repeated measures ANOVA and independent t-tests. A p-value <0.05 was considered statistically significant. Results: Both groups demonstrated significant improvements in all periodontal parameters throughout follow-up. However, non-diabetic patients exhibited significantly greater reductions in PPD and gains in CAL at 6, 9, and 12 months (p<0.05). At 12 months, mean PPD reduction was 2.91±0.54 mm in non-diabetic patients compared with 2.38±0.62 mm among diabetic patients (p<0.001). CAL gain was also significantly higher among non-diabetic individuals (2.54±0.57 mm vs 2.05±0.60 mm, p=0.001). Conclusion: Non-surgical periodontal therapy effectively improved periodontal health in both cohorts; however, patients without T2DM achieved superior clinical outcomes. Diabetes may negatively influence periodontal healing despite adequate periodontal treatment.
Periodontitis is a chronic multifactorial inflammatory disease characterized by progressive destruction of tooth-supporting tissues, leading to periodontal pocket formation, clinical attachment loss, alveolar bone destruction, and eventual tooth loss if left untreated [1]. It remains one of the most prevalent oral diseases worldwide and significantly impacts oral health-related quality of life.
Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by chronic hyperglycemia resulting from insulin resistance and impaired insulin secretion. The global prevalence of diabetes continues to rise, making it a major public health challenge [2]. Substantial evidence has established a bidirectional relationship between diabetes and periodontal disease. Patients with diabetes are more susceptible to periodontal destruction, while severe periodontitis adversely affects glycemic control [3].
Several biological mechanisms explain the increased severity of periodontitis in diabetic individuals. Chronic hyperglycemia promotes the formation of advanced glycation end products (AGEs), which interact with their receptors and trigger enhanced inflammatory responses, oxidative stress, and tissue destruction [4]. Furthermore, impaired neutrophil function, altered collagen metabolism, vascular changes, and dysregulated immune responses contribute to delayed periodontal healing among diabetic patients [5].
Non-surgical periodontal therapy, primarily scaling and root planing (SRP), remains the cornerstone of periodontal treatment and has been shown to reduce periodontal inflammation and improve clinical outcomes [6]. Previous studies have demonstrated improvements in probing pocket depth and clinical attachment level following SRP in both diabetic and non-diabetic populations [7]. However, variations in healing responses and long-term treatment outcomes have been reported.
Understanding differences in periodontal treatment outcomes between diabetic and non-diabetic patients is clinically important for developing individualized treatment strategies and improving long-term prognosis [8]. Longitudinal studies evaluating periodontal healing over extended follow-up periods provide valuable information regarding disease progression and treatment effectiveness [9].
The present prospective cohort study was conducted to compare clinical periodontal outcomes following non-surgical periodontal therapy in patients with periodontitis with and without T2DM over a 12-month follow-up period. The null hypothesis stated that there would be no significant differences in periodontal outcomes between the two groups after treatment [10].
Study Design and Setting A prospective cohort study was conducted in the Department of Periodontology over a period of 18 months following approval from the Institutional Ethics Committee. Study Population One hundred patients diagnosed with generalized Stage II–III periodontitis according to the 2018 classification of periodontal diseases were recruited. Group A (T2DM group): 50 patients with diagnosed Type 2 Diabetes Mellitus. Group B (Control group): 50 systemically healthy patients without diabetes. Inclusion Criteria • Age between 35 and 65 years. • Presence of at least 20 natural teeth. • Generalized Stage II or III periodontitis. • HbA1c ≤8% among diabetic participants. • No periodontal treatment during the preceding 6 months. Exclusion Criteria • Smokers and tobacco users. • Pregnancy and lactation. • Immunocompromised conditions. • Antibiotic therapy within previous 3 months. • Uncontrolled systemic diseases. Clinical Examination The following clinical parameters were recorded at baseline, 3, 6, 9, and 12 months: • Plaque Index (PI) • Gingival Index (GI) • Probing Pocket Depth (PPD) • Clinical Attachment Level (CAL) Treatment Protocol All participants received: • Oral hygiene instructions. • Full-mouth scaling and root planing. • Reinforcement of oral hygiene measures at every follow-up vsisit. Statistical Analysis Data were analyzed using SPSS version 26.0. Continuous variables were expressed as mean ± standard deviation. Intergroup comparisons were performed using independent t-tests. Intragroup comparisons across time intervals were analyzed using repeated measures ANOVA. Statistical significance was set at p<0.05.
Table 1. Baseline Characteristics of Study Participants
|
Variable |
T2DM Group (n=50) |
Non-Diabetic Group (n=50) |
p-value |
|
Age (years) |
49.8 ± 7.2 |
48.6 ± 6.8 |
0.381 |
|
Male/Female |
29/21 |
27/23 |
0.688 |
|
HbA1c (%) |
7.2 ± 0.6 |
5.4 ± 0.3 |
<0.001 |
|
Baseline PI |
2.21 ± 0.39 |
2.17 ± 0.35 |
0.594 |
|
Baseline GI |
2.08 ± 0.36 |
2.02 ± 0.32 |
0.398 |
|
Baseline PPD (mm) |
5.62 ± 0.78 |
5.55 ± 0.74 |
0.647 |
|
Baseline CAL (mm) |
6.28 ± 0.81 |
6.20 ± 0.76 |
0.612 |
As shown in Table 1, both groups were comparable at baseline regarding age, gender distribution, and periodontal parameters (p>0.05). Expectedly, HbA1c values were significantly higher among diabetic patients (p<0.001).
Table 2. Comparison of Plaque Index and Gingival Index During Follow-Up
|
Time |
PI (T2DM) |
PI (Control) |
p-value |
GI (T2DM) |
GI (Control) |
p-value |
|
Baseline |
2.21±0.39 |
2.17±0.35 |
0.594 |
2.08±0.36 |
2.02±0.32 |
0.398 |
|
3 Months |
1.46±0.28 |
1.38±0.25 |
0.134 |
1.29±0.24 |
1.21±0.22 |
0.087 |
|
6 Months |
1.18±0.22 |
1.09±0.20 |
0.036* |
0.98±0.18 |
0.90±0.17 |
0.024* |
|
9 Months |
1.01±0.19 |
0.91±0.17 |
0.008* |
0.82±0.15 |
0.74±0.14 |
0.007* |
|
12 Months |
0.90±0.17 |
0.81±0.15 |
0.005* |
0.71±0.13 |
0.63±0.12 |
0.002* |
Table 2 demonstrates progressive reductions in plaque accumulation and gingival inflammation in both groups. Non-diabetic patients exhibited significantly lower PI and GI values from the 6-month follow-up onward (p<0.05).
Table 3. Comparison of Mean Probing Pocket Depth (PPD)
|
Time |
T2DM Group (mm) |
Control Group (mm) |
p-value |
|
Baseline |
5.62 ± 0.78 |
5.55 ± 0.74 |
0.647 |
|
3 Months |
4.68 ± 0.71 |
4.42 ± 0.65 |
0.058 |
|
6 Months |
4.01 ± 0.66 |
3.68 ± 0.59 |
0.009* |
|
9 Months |
3.52 ± 0.61 |
3.05 ± 0.57 |
<0.001* |
|
12 Months |
3.24 ± 0.58 |
2.64 ± 0.51 |
<0.001* |
As presented in Table 3, significant reductions in probing depth occurred in both groups throughout the study period. However, non-diabetic participants demonstrated significantly greater pocket reduction at 6, 9, and 12 months (p<0.05), indicating superior periodontal healing.
Table 4. Comparison of Clinical Attachment Level (CAL)
|
Time |
T2DM Group (mm) |
Control Group (mm) |
p-value |
|
Baseline |
6.28 ± 0.81 |
6.20 ± 0.76 |
0.612 |
|
3 Months |
5.52 ± 0.74 |
5.28 ± 0.70 |
0.098 |
|
6 Months |
4.98 ± 0.69 |
4.61 ± 0.63 |
0.006* |
|
9 Months |
4.48 ± 0.65 |
4.01 ± 0.58 |
<0.001* |
|
12 Months |
4.23 ± 0.60 |
3.66 ± 0.54 |
0.001* |
Table 4 demonstrates substantial attachment gain following treatment in both groups. Nevertheless, non-diabetic individuals exhibited significantly greater CAL improvement from 6 months onward compared with diabetic patients (p<0.05), suggesting more favorable tissue healing following periodontal therapy.
The present prospective cohort study evaluated periodontal clinical outcomes following non-surgical periodontal therapy in patients with periodontitis with and without T2DM over a 12-month follow-up period. The findings demonstrated significant improvements in all periodontal parameters in both groups following scaling and root planing. However, non-diabetic patients consistently exhibited superior clinical outcomes, particularly in terms of probing pocket depth reduction and clinical attachment gain. The baseline demographic and periodontal characteristics of both groups were statistically comparable, minimizing the influence of confounding variables and allowing a more reliable assessment of the impact of diabetes on periodontal healing. Similar baseline comparability has been reported by Taylor et al., who emphasized that matching periodontal severity between diabetic and non-diabetic subjects is critical when evaluating treatment outcomes [11]. Both cohorts demonstrated significant reductions in plaque index and gingival index during follow-up. These findings indicate that oral hygiene reinforcement combined with non-surgical periodontal therapy effectively reduced microbial burden and gingival inflammation irrespective of diabetic status. Grossi et al. reported comparable improvements in plaque control among diabetic and non-diabetic individuals after periodontal treatment, highlighting the importance of patient compliance and maintenance therapy [12]. Despite improvements in oral hygiene parameters, diabetic patients showed comparatively higher plaque and gingival scores during later follow-up periods. This observation may be attributed to altered host inflammatory responses associated with chronic hyperglycemia. Diabetes promotes increased production of pro-inflammatory cytokines including interleukin-1β, tumor necrosis factor-α, and prostaglandin E2, resulting in persistent inflammatory activity within periodontal tissues [13]. One of the most clinically significant findings of the present study was the greater reduction in probing pocket depth observed among non-diabetic participants. At 12 months, the mean probing depth was significantly lower in the control group compared with the T2DM group. These results are consistent with the findings of Christgau et al., who reported enhanced pocket reduction among systemically healthy individuals following scaling and root planing compared with diabetic patients [14]. Several biological mechanisms may explain this difference. Chronic hyperglycemia contributes to the accumulation of advanced glycation end products (AGEs) within periodontal tissues. Interaction between AGEs and their cellular receptors stimulates oxidative stress, matrix degradation, and inflammatory cytokine production, ultimately impairing tissue repair mechanisms [15]. Consequently, diabetic individuals may experience delayed resolution of inflammation and slower periodontal healing following therapy. Clinical attachment level improvement is considered one of the most important indicators of successful periodontal treatment. In the present study, both groups exhibited significant attachment gain; however, non-diabetic patients achieved significantly greater CAL improvement from six months onward. Similar findings were reported by Tervonen and Karjalainen, who observed reduced attachment gain among diabetic individuals despite adequate periodontal treatment and maintenance care [16]. The impaired attachment gain observed in diabetic patients may be associated with altered collagen metabolism. Hyperglycemia adversely affects fibroblast proliferation and collagen synthesis while simultaneously increasing collagen degradation. These changes compromise connective tissue remodeling and regeneration following periodontal therapy [17]. Furthermore, microvascular alterations commonly associated with diabetes reduce blood supply to periodontal tissues, thereby limiting nutrient delivery and wound healing capacity. The current findings also support the concept that glycemic status influences periodontal treatment outcomes. Previous studies have shown that controlled diabetic patients respond more favorably to periodontal therapy than poorly controlled individuals, although their outcomes may still remain inferior to those of systemically healthy subjects [18]. The diabetic participants included in the present study had relatively acceptable glycemic control; therefore, even greater differences might be expected among patients with poorly controlled diabetes. Long-term follow-up is essential for evaluating periodontal stability following treatment. The present study demonstrated sustained improvements over a 12-month period, emphasizing the effectiveness of supportive periodontal care and regular maintenance visits. Similar long-term benefits have been reported by Faria-Almeida et al., who demonstrated that diabetic patients receiving structured maintenance therapy could achieve significant periodontal improvements despite exhibiting somewhat reduced healing responses compared with healthy controls [19]. The clinical implications of the present findings are noteworthy. Periodontists should recognize diabetes as a significant modifying factor affecting treatment response and prognosis. Comprehensive periodontal care for diabetic patients should include close collaboration with physicians, reinforcement of oral hygiene practices, regular periodontal maintenance, and optimization of glycemic control. Such multidisciplinary management may enhance periodontal healing and improve long-term treatment outcomes[20-23]. The strengths of this study include its prospective design, equal sample size in both groups, multiple follow-up intervals, and standardized clinical measurements. Nevertheless, certain limitations should be acknowledged. Glycemic control was assessed primarily through baseline diabetic status, and changes in HbA1c throughout follow-up were not evaluated. Additionally, microbiological and inflammatory biomarkers were not assessed. Future studies incorporating larger multicenter cohorts and biochemical analyses may provide deeper insights into the mechanisms linking diabetes and periodontal healing [24,25].
Non-surgical periodontal therapy resulted in significant improvements in periodontal health among both diabetic and non-diabetic patients with periodontitis. However, individuals without Type 2 Diabetes Mellitus demonstrated significantly greater reductions in probing pocket depth and superior clinical attachment gain throughout the 12-month follow-up period. These findings suggest that diabetes adversely affects periodontal healing despite appropriate periodontal treatment. Regular periodontal maintenance, meticulous plaque control, and optimization of glycemic status remain essential components in the management of periodontitis among diabetic patients. Further longitudinal studies are warranted to evaluate the influence of long-term glycemic control on periodontal treatment outcomes.