The Effect of Periodontal Treatment on Hemoglobin A1c Levels of Diabetic Patients: A Systematic Review and Meta-Analysis

<div><p>Background</p><p>There is growing evidence that periodontal treatment may affect glycemic control in diabetic patients. And several systematic reviews have been conducted to assess the effect of periodontal treatment on diabetes outcomes. Researches of this aspect are widely concerned, and several new controlled trials have been published. The aim of this study was to update the account for recent findings.</p><p>Methods</p><p>A literature search (until the end of January 2014) was carried out using various databases with language restriction to English. A randomized controlled trial (RCT) was selected if it investigated periodontal therapy for diabetic subjects compared with a control group received no periodontal treatment for at least 3 months of the follow-up period. The primary outcome was hemoglobin A1c (HbA1c), and secondary outcomes were periodontal parameters included probing pocket depth (PPD) and clinical attachment level (CAL).</p><p>Results</p><p>Ten trials of 1135 patients were included in the analysis. After the follow-up of 3 months, treatment substantially lowered HbA1c compared with no treatment after periodontal therapy (–0.36%, 95%CI, −0.52% to −0.19%, <i>P</i><0.0001). Clinically substantial and statistically significant reduction of PPD and CAL were found between subjects with and without treatment after periodontal therapy (PPD −0.42 mm, 95%CI: −0.60 to −0.23, <i>P</i><0.00001; CAL −0.34 mm, 95%CI: −0.52 to −0.16, <i>P</i> = 0.0002). And there is no significant change of the level of HbA1c at the 6-month comparing with no treatment (–0.30%, 95%CI, −0.69% to 0.09%, <i>P</i> = 0.13).</p><p>Conclusions</p><p>Periodontal treatment leads to the modest reduction in HbA1c along with the improvement of periodontal status in diabetic patients for 3 months, and this result is consistent with previous systematic reviews. And the effect of periodontal treatment on HbA1c cannot be observed at 6-month after treatment.</p></div

Forest plot presenting change in HbA1c (%) at 6-month.

<p>Forest plot presenting change in HbA1c (%) at 6-month.</p

Judgements about each risk of bias item for each included study.

<p>Judgements about each risk of bias item for each included study.</p

Forest plot presenting change in HbA1c (%) at 3-month.

<p>Forest plot presenting change in HbA1c (%) at 3-month.</p

Forest plot presenting change in PPD (mm) at 3-month.

<p>Forest plot presenting change in PPD (mm) at 3-month.</p

Each risk of bias item presented as percentages across all included studies.

<p>Each risk of bias item presented as percentages across all included studies.</p

Flow diagram of the trials search and selection process.

<p>Flow diagram of the trials search and selection process.</p

Characteristics of included trials.

<p>PI, plaque index; GI, gingival index; PPD, probing pocket depth; CAL, clinical attachment loss; GR, gingival recession; BOP, bleeding on probing; NA, not available; CHX, chlorhexidine gluconate; OH, oral hygiene; SRP, scaling and root planning.</p><p>*reported in a graph.</p>†<p>data obtained by calculation.</p><p>Characteristics of included trials.</p

Funnel plot presenting change in HbA1c (%) at 3-month.

<p>Funnel plot presenting change in HbA1c (%) at 3-month.</p

Cascade-Targeted Nanoplatforms for Synergetic Antibiotic/ROS/NO/Immunotherapy against Intracellular Bacterial Infection

Intracellular bacteria in dormant states can escape the immune response and tolerate high-dose antibiotic treatment, leading to severe infections. To overcome this challenge, cascade-targeted nanoplatforms that can target macrophages and intracellular bacteria, exhibiting synergetic antibiotic/reactive oxygen species (ROS)/nitric oxide (NO)/immunotherapy, were developed. These nanoplatforms were fabricated by encapsulating trehalose (Tr) and vancomycin (Van) into phosphatidylserine (PS)-coated poly[(4-allylcarbamoylphenylboric acid)-ran-(arginine-methacrylamide)-ran-(N,N′-bisacryloylcystamine)] nanoparticles (PABS), denoted as PTVP. PS on PTVP simulates a signal of “eat me” to macrophages to promote cell uptake (the first-step targeting). After the uptake, the nanoplatform in the acidic phagolysosomes could release Tr, and the exposed phenylboronic acid on the nanoplatform could target bacteria (the second-step targeting). Nanoplatforms can release Van in response to infected intracellular overexpressed glutathione (GSH) and weak acid microenvironment. l-arginine (Arg) on the nanoplatforms could be catalyzed by upregulated inducible nitric oxide synthase (iNOS) in the infected macrophages to generate nitric oxide (NO). N,N′-Bisacryloylcystamine (BAC) on nanoplatforms could deplete GSH, allow the generation of ROS in macrophages, and then upregulate proinflammatory activity, leading to the reinforced antibacterial capacity. This nanoplatform possesses macrophage and bacteria-targeting antibiotic delivery, intracellular ROS, and NO generation, and pro-inflammatory activities (immunotherapy) provides a new strategy for eradicating intracellular bacterial infections