Antimicrobial photodynamic therapy (aPDT) is an adjuvant treatment to scaling and root planing (SRP) which improves periodontal health. It may be beneficial to patients with systemic diseases, such as type 1 diabetes mellitus.

This randomized clinical trial evaluated the adjunctive effect of aPDT on the periodontal treatment of patients with type 1 diabetes (T1D).

38 patients were included in the study and divided into four groups: DSRP - T1D patients treated with SRP; CSRP - normoglycemic patients treated with SRP; DPDT - T1D patients treated with SRP + aPDT (methylene blue and red laser); CPDT - normoglycemic patients treated with SRP + aPDT. , Periodontal clinical parameters and inflammatory cytokines in crevicular fluid were recorded at baseline and then after 1, 3 and 6 months. The clinical endpoint for treatment was evaluated after 6 months.

Adjuvant aPDT treatment resulted in reduction of probing depth after 3 months (0.38 mm - p<0.05) on T1D patients and in control group after 6 months (0.66 mm - p<0.05). Reduction of clinical attachment levels was similar for both treatments in control patients (p>0.05). There was a significant reduction of TNF-α in crevicular fluid in both groups treated with aPDT (p<0.05). The T1D (65%) and normoglycemic (72%) groups achieved the clinical endpoint after both treatments (p>0.05).

Adjuvant aPDT provided additional benefits in improving periodontal clinical parameters and reducing inflammatory cytokines in both T1D and normoglycemic patients. However, normoglycemic patients showed greater clinical improvements compared to T1D patients following adjuvant aPDT treatment.

Background: Periodontitis and diabetes mellitus (DM) exhibit a bidirectional relationship and are globally significant systemic chronic conditions. The utilization of antibiotics alongside non-surgical periodontal treatment (NSPT) has been a subject of investigation in numerous clinical studies involving human subjects. Thus, the objective of this systematic review is to address the following question: "What is the efficacy of scaling and root planing (SRP) associated with antimicrobials in patients with type 2 DM and periodontitis?". Methods: A systematic review of the literature was conducted encompassing databases such as MEDLINE/PubMed, Scopus, and Web of Science up to July 2024. Additionally, alerts were configured to capture studies published from the initial search until manuscript submission. Randomized clinical trials assessing clinical periodontal parameters in DM patients undergoing SRP and receiving either topical or systemic antibiotics were compared against a control group (SRP only). Two investigators independently screened articles, extracted data, and evaluated their quality. The selection process, study characteristics, risk of bias, impact of antibiotics on clinical parameters, and certainty of evidence were elucidated in both textual and tabular formats. Meta-analysis was performed separately with forest plots generated for treatment modalities, period of evaluation, and type of antibiotics used. Results: Following the analysis of abstracts and full articles, a total of 30 randomized clinical trials were incorporated into this review, comprising 9 studies on the association of topical antibiotics and 21 studies on systemic antibiotic administration. The principal periodontal parameters assessed included probing pocket depth (PPD), clinical attachment level (CAL), plaque index (PI), and bleeding on probing (BoP). Conclusions: Analysis of the results led to the conclusion that adjunctive periodontal treatment with either topical or systemic antibiotics confers subtle clinical benefits. Nevertheless, owing to the heightened emergence of resistant bacteria and potential side effects, the use of antibiotic therapy in periodontal treatment should be judiciously administered.

To improve the clinical and microbiological outcomes of non-surgical mechanical periodontal therapy, the adjunctive use of antimicrobials has been utilized in treating moderate-to-severe periodontitis. In our study, the retrospective design included previously collected health-related patient data, obtained from the printed and digital charts of patients who received systemic or local antibiotic adjuncts to SI (subgingival instrumentation). A total of 34 patients (diagnosed with generalized Stage III/IV periodontitis) met the inclusion and exclusion criteria and were evaluated. The samples were tested for the following bacterial strains: Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Porphyromonas gingivalis (P. gingivalis), Prevotella intermedia (P. intermedia), Tanererella forsythia (T. forsythia), and Treponema denticola (T. denticola). The inter-group comparisons of the bacterial species did not show statistically significant differences between groups. The present study aimed to evaluate the clinical effects after SI and the adjunctive use of systemically administered (SA) AMX (amoxicillin) + MET (metronidazole) (administered for 7 days), with locally delivered (LDD) piperacillin + tazobactam in step 2 of periodontal therapy. Results: Overall, all parameters were improved in the groups, with a significant difference in inter-group comparison regarding the full-mouth bleeding score (FMBS) (p < 0.05) in favor of the SA group, and the p-value < 0.05 was considered to be statistically significant. Statistically significant PPD (probing pocket depth) reductions and CAL (clinical attachment level) gains were observed in both groups at the 3-month follow-up. In conclusion, within the limitations, the outcomes of this study suggest that SI, with adjunctive local or systemic antibiotic therapy, provided comparable clinical improvements. Systemic AMX + MET protocols were more efficacious with regard to the reduction in FMBS. Follow-up studies with larger patient numbers are needed to further investigate this effect.

The control of dental biofilm regrowth after nonsurgical periodontal therapy is associated with better clinical outcomes. However, many patients have difficulty achieving optimal plaque control. Subjects with diabetes, in which immune and wound-healing responses are typically impaired, may benefit from intensive antiplaque control regimens after scaling and root planing (SRP).

This study aimed to evaluate the effects of an intensive, at-home, chemical, and mechanical antiplaque regimen as an adjunct to SRP for the treatment of moderate to severe periodontitis. A secondary objective was to compare responses in subjects with type 2 diabetes and nondiabetics.

This was a 6-mo, single-center, parallel-group, randomized trial. The test group received SRP and oral hygiene instructions, and subjects were instructed to use a 0.12% chlorhexidine gluconate mouthrinse twice a day for 3 mo and utilize rubber interproximal bristle cleaners twice a day for 6 mo. The control group received SRP and oral hygiene instructions. The main outcome was change in mean probing depth (PD) from baseline to 6 mo. Secondary outcomes included change in sites with deep PDs, mean clinical attachment level, bleeding on probing, plaque index, hemoglobin A1C, fasting blood glucose, C-reactive protein, and taste assessment. This study was registered at ClinicalTrials.gov as NCT04830969.

In total, 114 subjects were randomized to either treatment. Eighty-six subjects completed the trial with no missing visits. Neither an intention-to-treat nor a per-protocol analysis showed statistically significant differences between treatment groups in mean PD at 6 mo. In a subgroup analysis, subjects with diabetes in the test group showed a statistically significant greater reduction in mean PD at 6 mo when compared to subjects with diabetes receiving the control treatment (Δ = 0.15, P = 0.04), while there were no differences within nondiabetics (Δ = 0.02, P = 0.75).

Outcomes in subjects with diabetes may be improved by chemo-mechanical antiplaque measures after nonsurgical periodontal therapy.

This study suggests diabetic subjects may benefit from an intensive, at-home, chemical, and mechanical antiplaque regimen to improve nonsurgical periodontal therapy outcomes.

Oral dysbiosis contributes to periodontitis and has implications for systemic diseases. Diabetes mellitus is a common metabolic disorder characterized by impaired glucose regulation. AMP-activated protein kinase (AMPK) plays a vital role in regulating glucose uptake and glycogenesis in the liver. This study aimed to investigate the association between periodontal bacteria and diabetes mellitus. A clinical trial was conducted to explore the association between oral bacteria and hyperglycemia. Additionally, we elucidated the molecular mechanisms by which periodontal bacteria cause insulin resistance. In the clinical trial, we discovered significant alterations in the expression levels of Fusobacterium nucleatum (Fn) and Tannerella forsythia (Tf) in patients with diabetes compared with healthy controls. Furthermore, Fn and Tf levels positively correlated with fasting blood glucose and glycated hemoglobin (HbA1C) levels. Moreover, we explored and elucidated the molecular mechanism by which Fusobacterium nucleatum culture filtrate (FNCF) induces cytokine release via the Toll-like receptor 2 (TLR2) signaling pathway in human gingival epithelial Smulow-Glickman (S-G) cells. This study investigated the effects of cytokines on insulin resistance pathways in liver cells. The use of an extracellular signal-regulated kinase (ERK) inhibitor (U0126) demonstrated that FNCF regulates the insulin receptor substrate 1 and protein kinase B (IRS1/AKT) signaling pathway, which affects key proteins involved in hepatic glycogen synthesis, including glycogen synthase kinase-3 beta (GSK3β) and glycogen synthase (GS), ultimately leading to insulin resistance. These findings suggest that ERK plays a crucial role in hepatocyte insulin resistance.

A growing body of evidence from multiple areas proposes that periodontal disease, accompanied by oral inflammation and pathological changes in the microbiome, induces gut dysbiosis and is involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). A subgroup of NAFLD patients have a severely progressive form, namely nonalcoholic steatohepatitis (NASH), which is characterized by histological findings that include inflammatory cell infiltration and fibrosis. NASH has a high risk of further progression to cirrhosis and hepatocellular carcinoma. The oral microbiota may serve as an endogenous reservoir for gut microbiota, and transport of oral bacteria through the gastro-intestinal tract can set up a gut microbiome dysbiosis. Gut dysbiosis increases the production of potential hepatotoxins, including lipopolysaccharide, ethanol, and other volatile organic compounds such as acetone, phenol and cyclopentane. Moreover, gut dysbiosis increases intestinal permeability by disrupting tight junctions in the intestinal wall, leading to enhanced translocation of these hepatotoxins and enteric bacteria into the liver through the portal circulation. In particular, many animal studies support that oral administration of Porphyromonas gingivalis, a typical periodontopathic bacterium, induces disturbances in glycolipid metabolism and inflammation in the liver with gut dysbiosis. NAFLD, also known as the hepatic phenotype of metabolic syndrome, is strongly associated with metabolic complications, such as obesity and diabetes. Periodontal disease also has a bidirectional relationship with metabolic syndrome, and both diseases may induce oral and gut microbiome dysbiosis with insulin resistance and systemic chronic inflammation cooperatively. In this review, we will describe the link between periodontal disease and NAFLD with a focus on basic, epidemiological, and clinical studies, and discuss potential mechanisms linking the two diseases and possible therapeutic approaches focused on the microbiome. In conclusion, it is presumed that the pathogenesis of NAFLD involves a complex crosstalk between periodontal disease, gut microbiota, and metabolic syndrome. Thus, the conventional periodontal treatment and novel microbiome-targeted therapies that include probiotics, prebiotics and bacteriocins would hold great promise for preventing the onset and progression of NAFLD and subsequent complications in patients with periodontal disease.

This study compared the clinical effects of a full-mouth disinfection (FMD) protocol for the treatment of mild-to-moderate periodontitis in type 2 diabetic and non-diabetic subjects for up to 1 year. Secondary aim was to evaluate the effects of this therapy on the salivary levels of periodontal pathogens between diabetics and non-diabetics.

Twenty-six type 2 diabetic subjects and 28 non-diabetic subjects with mild-to-moderate periodontitis received full-mouth scaling and root planing within 24 h, application of chlorhexidine digluconate (CHX) gel in pockets and tongue plus CHX rinses for 14 days. Clinical monitoring was performed at baseline, 3, 6, and 12 months post-therapy. Salivary levels of red complex bacterial species were evaluated at baseline, 6, and 12 months post-therapy by qPCR.

Intention-to-treat analyses were performed for seven diabetics and three non-diabetics that did not return for the 12-month evaluation. Most clinical parameters improved significantly at 3, 6, and 12 months post-therapies for both groups (p < 0.05). Overall, there were no significant differences in clinical parameters between groups after therapy (p > 0.05). At 1 year, 39.3% and 50.0% of the non-diabetic and diabetic subjects, respectively, achieved the desired clinical endpoint for treatment (≤ 4 sites with probing depth ≥ 5 mm) (primary outcome variable) (p > 0.05). FMD did not promote changes in the salivary levels of pathogens in either of the groups (p > 0.05). Levels of T. forsythia were lower in diabetic than in non-diabetic subjects at 6 months post-therapy (p < 0.05).

Type 2 diabetic subjects and systemically healthy subjects with mild-to-moderate periodontitis responded similarly to the proposed FMD protocol for up to 1 year.

There is a general thought that diabetics do not answer as well as non-diabetics to periodontal treatments. However, this study showed that diabetics and non-diabetics respond equally to the FMD protocol.

ClinicalTrials.gov Identifier: NCT02643771.