OBJECTIVE: To evaluate site-related changes in periodontal pocket depth (PPD) after non-surgical periodontal therapy and to identify predictors for PPD changes in a retrospective patient data analysis.
METHODS: PPD, clinical attachment level, bleeding on probing, tooth mobility (TM), furcation involvement (FI), abutment status, adherence to supportive periodontal care (SPC) and SPC follow-ups were obtained from fully documented patient data before periodontal therapy (baseline, T0), after active periodontal therapy (APT, T1) and during SPC (T2). PPD changes were classified into deteriorated or unchanged/improved at the site level. Multi-level logistic regression analysis was performed to identify factors influencing PPD changes during SPC.
RESULTS: This retrospective study included 51 females and 65 males (mean T0 age: 54.8 ± 10.1 years, 25 smokers, 12 diabetics) suffering from Stage III/IV periodontitis. Evaluation outcome: T0/16,044 sampling sites/2674 teeth; T1/15,636/2606; T2/14,754/2459. During 9.0 ± 2.3 years SPC, PPD decreased (-1.33 ± 0.70 mm) by 21.8% of the sites, remained unchanged by 41.4% and increased (1.40 ± 0.78 mm) by 36.8%. Distopalatal FI (p < .001, odds ratio [OR]: 0.252, 95% confidence interval [CI] for OR: 0.118-0.540), residual pockets (p < .001, OR: 0.503, 95% CI: 0.429-0.590) and TM Degrees I-III (Degree I: p = .002, OR: 0.765, 95% CI: 0.646-0.905; Degree II: p = .006, OR: 0.658, 95% CI: 0.489-0.886; Degree III: p = .023, OR: 0.398, 95% CI: 0.180-0.879) correlated significantly with increasing PPD.
CONCLUSIONS: Over 75% of PPD remained unchanged or increased during SPC. Distopalatal FI, TM Degrees I-III and residual pockets after APT lead to worsening of periodontal pockets.

OBJECTIVE: This Bayesian network meta-analysis of randomized controlled trials assessed the effect of adjuvant periodontal treatment in both periodontal and HbA1c outcomes in adult individuals with type 2 diabetes (T2DM).
METHODS: A systematic search was done up to February 2023 comparing sub-gingival debridement (SD) in combination with local or systemic adjuvant treatment with SD alone for individuals with T2DM. The primary outcomes were changes in absolute HbA1c levels and full-mouth probing depth reported at 3- to 6-month post-treatment.
RESULTS: Seventy-two eligible publications evaluating 27 adjuvant treatments were retrieved. The combination of SD and systemic antibiotic metronidazole or SD and antioxidant alpha lipoic acid provided, respectively, 1.4% (95% credible interval [CrI] 0.48; 2.20) and 2.4% (95% CrI 1.50; 3.30) more significant improvement on HbA1c levels, and 0.89 mm (95% CrI 0.23; 1.50) and 0.92 mm (95% CrI 0.02; 0.92) greater periodontal probing depth reductions. Other adjuvant treatments provided added benefit to the periodontal outcomes without discernible effects on HbA1c.
CONCLUSIONS: Adjuvant use of metronidazole or alpha lipoic acid was the best adjunct option to provide clinically meaningful HbA1c levels and probing depth reductions. However, no strong recommendation can be drawn due to the scarcity of studies for each adjuvant treatment and the low certainty of the resultant evidence.

BACKGROUND: This study was designed to assess the influence of non-surgical periodontal therapy (NSPT) on gingival crevicular fluid (GCF) levels of semaphorin-4D (SEMA-4D), peptidylarginine deiminase-2 (PAD-2), and matrix metalloproteinase-8 (MMP-8) levels in periodontally healthy, Stage III periodontitis non-smoker and smoker patients.
METHODS: Sixty patients were equally divided into three groups, Group I: Periodontally healthy, Group II: Non-smokers with Stage III periodontitis, and Group III: Smokers with Stage III periodontitis. The patients underwent NSPT with clinical and biochemical parameters examined at baseline and 3 months post therapy. GCF was collected for levels of SEMA-4D, PAD-2, and MMP-8 through enzyme-linked immunosorbent assay (ELISA).
RESULTS: Greater values of PPD (8.06 ± 0.19 mm), CAL (8.94 ± 0.19 mm), PI (2.58 ± 0.19) while lower PBI (1.39 ± 0.19%) and GI (1.72 ± 0.19) scores were seen in Group III as compared to Group II, which reduced significantly from baseline to 3 months in both the groups after NSPT. Minimum values of SEMA-4D, PAD-2, and MMP-8 levels in GCF were seen for Group I, which increased incrementally to Group II and III. Also, among Group II and III the SEMA-4D, PAD-2, and MMP-8 levels in GCF reduced from baseline to 3 months indicating a favorable response within the tissues.
CONCLUSIONS: Greater levels in GCF of Levels of SEMA-4D, PAD-2, and MMP-8 in Group II and III, which reduced significantly post NSPT, implied that these biomarkers play a pivotal role in the inflammatory process and can be utilized for early diagnosis.

The aim of the study was to assess the effect of non-surgical periodontal therapy (NSPT) on periodontal and cardiac parameters as well as on the expression of calprotectin and periostin levels in periodontitis patients with and without coronary artery disease (CAD).
Ninety subjects were categorised into three groups: Group H: periodontally and systemically healthy subjects, Group P: stage III grade B periodontitis subjects with no associated systemic diseases and Group P + CAD: stage III grade B periodontitis subjects diagnosed with CAD. Demographic, periodontal and cardiac parameters were recorded at baseline (0 day) and on the 180th day after NSPT. Gingival crevicular fluid was collected from all participants at baseline (0 day) and after the 180th day. Calprotectin and periostin expression were reassessed.
A significant increase in the levels of calprotectin (34.05 ± 11.72) was seen at baseline in the P + CAD group, whereas on the contrary, a decreased periostin (1.59 ± 0.41) was also noted at baseline. The study also showed a significant improvement in periodontal and cardiac parameters on the 180th day following NSPT.
Detection of calprotectin and periostin expression in GCF samples could represent a link to the association of periodontitis and CAD.