The prevalence rate of periodontal pathogens and its association with oral squamous cell carcinoma.

Mounting evidence suggests a causal relationship between specific bacterial infections or microbial compositions and the development of certain malignant neoplasms. In this study, we performed research through 16S rRNA amplicon sequencing, qPCR and fluorescence in situ hybridization to certify the relationship between periodontal pathogens and oral squamous cell carcinoma (OSCC). Subgingival plaque, cancer and paracancerous tissues from 6 patients with OSCC were selected for mapping bacterial profiles by 16S rRNA amplicon sequencing. The research showed that periodontal pathogens were enriched in cancer and paracancerous tissues, while the bacterial profiles were similar between the cancer tissues and subgingival plaque. Furthermore, the relative abundance of Porphyromonas gingivalis, Fusobacterium nucleatum and Streptococcus sanguinis was detected in 61 cancer tissues, paracancerous tissues and subgingival plaque samples and in 30 normal tissues by qPCR. The results revealed that P. gingivalis and F. nucleatum existed at higher levels in cancer tissue than in normal tissues and were correlated with subgingival plaques. P. gingivalis was detected using a special oligonucleotide probe in 60.7% of OSCC tissues, 32.8% of paracancerous tissues and 13.3% of normal tissues. Relevance analysis showed that P. gingivalis infection was positively associated with late clinical staging, low differentiation and lymph node metastasis in patients with OSCC, which was accompanied by deeper periodontal pockets, severe clinical attachment loss and loss of teeth. This study revealed that there might be a close relationship between oral microorganisms, particularly periodontal pathogens, and OSCC, which might enrich the pathogenesis of oral squamous carcinoma.

An Antibacterial Strategy of Mg-Cu Bone Grafting in Infection-Mediated Periodontics.

Periodontal diseases are mainly the results of infections and inflammation of the gum and bone that surround and support the teeth. In this study, the alveolar bone destruction in periodontitis is hypothesized to be treated with novel Mg-Cu alloy grafts due to their antimicrobial and osteopromotive properties. In order to study this new strategy using Mg-Cu alloy grafts as a periodontal bone substitute, the in vitro degradation and antibacterial performance were examined. The pH variation and Mg2+ and Cu2+ release of Mg-Cu alloy extracts were measured. Porphyromonas gingivalis (P. gingivalis) and Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), two common bacteria associated with periodontal disease, were cultured in Mg-Cu alloy extracts, and bacterial survival rate was evaluated. The changes of bacterial biofilm and its structure were revealed by scanning electron microscopy (SEM) and transmission electronic microscopy (TEM), respectively. The results showed that the Mg-Cu alloy could significantly decrease the survival rates of both P. gingivalis and A. actinomycetemcomitans. Furthermore, the bacterial biofilms were completely destroyed in Mg-Cu alloy extracts, and the bacterial cell membranes were damaged, finally leading to bacterial apoptosis. These results indicate that the Mg-Cu alloy can effectively eliminate periodontal pathogens, and the use of Mg-Cu in periodontal bone grafts has a great potential to prevent infections after periodontal surgery.

Porphyromonas gingivalis Infection Promoted the Proliferation of Oral Squamous Cell Carcinoma Cells through the miR-21/PDCD4/AP-1 Negative Signaling Pathway.

Recent epidemiological studies have revealed that Porphyromonas gingivalis, a major pathogen in periodontal disease, is associated with the development of oral squamous cell carcinoma (OSCC). However, the underlying mechanisms induced by P. gingivalis have not been well-defined. We aimed to determine the role of P. gingivalis in OSCC proliferation and the relevant molecular mechanisms. A cellular proliferation model of OSCC Tca8113 cells infected by P. gingivalis at a multiplicity of infection (MOI) of 50 was established. Cell proliferation was drastically increased in the infected cells compared with the control cells, while the proportion of cells in S phase was increased and the proportion of cells in G1 phase was decreased in the infected cells compared with the control cells. Additionally, the levels of activator protein 1 (AP-1; c-Jun and c-Fos) and its target gene cyclin D1 were increased in P. gingivalis-infected Tca8113 cells compared with control cells. miR-21 expression was elevated when programmed cell death 4 (PDCD4) expression was downregulated. Cyclin D1 expression was regulated by miR-21, PDCD4, and AP-1. The disruption of the pathway by silencing c-Jun, blocking miR-21 expression, or overexpressing PDCD4 led to decreased cyclin D1 expression and inhibited cell proliferation. P. gingivalis DNA levels were positively correlated with miR-21 and c-Jun expression and negatively correlated with PDCD4 expression in clinical OSCC samples. Our findings indicated that P. gingivalis might promote OSCC proliferation by regulating cyclin D1 expression via the miR-21/PDCD4/AP-1 negative feedback signaling pathway.

[Effect of non-surgical periodontal therapy on glycemic control and the level of serum IL-6 in type 2 diabetic patients with chronic periodontitis].

OBJECTIVE: To evaluate the effect of non-surgical periodontal therapy on periodontal status, glycemic control and the level of serum interleukin (IL)-6 in type 2 diabetic patients with chronic periodontitis (DMCP). METHODS: Fifty-five DMCP and 55 systemically healthy patients with chronic periodontitis (CP) were recruited in this study. The diabetes were classified into two groups, the well-controlled group [glycated hemoglobin (HbA1c) < 7.00%] and the poorly controlled group (HbA1c ≥ 7.00%). All subjects received non-surgical periodontal therapy. Periodontal clinical parameters including periodontal probing depth(PD), attachment loss (AL), bleeding index (BI) and plaque index (PLI) were recorded at baseline, 6 weeks and 3 months after the treatment. Fasting plasma glucose (FPG), HbA1c and the concentration of serum IL-6 were measured. RESULTS: At 6 weeks and 3 months after treatment, PD, AL, BI, PLI and the concentration of serum IL-6 of both groups significantly reduced (P < 0.05). The level of IL-6 in diabetic patients reduced significantly from (3.47 ± 0.33) ng/L to (3.21 ± 0.66) ng/L and to(3.03 ± 0.54) ng/L. The HbA1c of diabetic patients reduced significantly 3 months after treatment [(6.80 ± 1.21%] compared with the baseline [(7.35 ± 1.73)%, P < 0.05]. HbA1c of the poorly controlled group reduced significantly (P < 0.05), while HbA1c of the well-controlled diabetes did not show any apparent reduction (P > 0.05). CONCLUSIONS: Non-surgical periodontal therapy can effectively reduce the concentration of serum IL-6, thereby improving glycemic control in type 2 diabetes patients with chronic periodontitis. However, there was no any significant reduction of HbA1c in the well-controlled diabetes.