A Review of the Nonsurgical Treatment of Oral Leukoplakia

The aim of this paper was to assess the nonsurgical treatment of oral leukoplakia (OL). A medline search from 1983 to 2009 was conducted. The topical or systemic nonsurgical treatments or combination of both was reviewed. The primary outcomes of interest were clinical resolution, malignant transformation, follow-up, and recurrence of OL. Studies showed a rate higher than 50% of clinical resolution with photodynamic therapy, beta-carotene, lycopene, or vitamin A. Few studies reported rates of recurrence from 5 to 67% and of malignant transformation from 8 to 23%. There is a lack of randomized clinical trials that assess the effectiveness of nonsurgical treatment of OL. At this time, randomized controlled trials for nonsurgical treatment of OL demonstrate no evidence of effective treatment in preventing malignant transformation and recurrence. It reinforces that even after clinical resolution, OL should be regularly followed

Rheumatoid arthritis associated with the occurrence, severity and extension of periodontitis : a case-control study

Emerging evidence pointed to a potential association between periodontitis (PE) and rheumatoid arthritis (RA), based on shared characteristics and similarities in risk factors, immunogenetics and pathways of tissue destruction. The aim of this study was

Periodontitis and type 2 diabetes among women with previous gestational diabetes: epidemiological and immunological aspects in a follow-up of three years

Periodontitis can contribute to the development of insulin resistance. Gestational diabetes is a risk factor for type 2 diabetes. Therefore, periodontitis, when associated with gestational diabetes, could increase the risk for the development of type 2 diabetes after pregnancy. Objective The aim of this study was to verify the incidence on the development of type 2 diabetes in women with previous gestational diabetes with and without periodontitis after a three-year time interval. Material and Methods Initial sample of this follow-up study consisted of 90 women diagnosed with gestational diabetes who underwent periodontal examination. After three years, 49 women were subjected to new periodontal examination and biological, behavioral, and social data of interest were collected. Additionally, the quantification of the C-reactive protein in blood samples was performed. Fasting glucose and glycated hemoglobin levels were requested. Saliva samples were collected for quantification of interleukin 6 and 10, tumor necrosis factor α, matrix metalloproteinase 2 and 9. Results The incidence of type 2 diabetes mellitus was 18.4% and of periodontitis was 10.2%. There was no significant difference in the incidence of type 2 diabetes mellitus among women with and without periodontitis. It was observed impact of C-reactive protein in the development of type 2 diabetes mellitus. However, it was not observed impact of periodontitis on the development of type 2 diabetes mellitus among women with previous gestational diabetes. Conclusions It was not observed impact of periodontitis on the development of type 2 diabetes among women with previous gestational diabetes. The impact of C-reactive protein in the development of type 2 diabetes mellitus highlights the importance of an inflammatory process in the diabetes pathogenesis

Periodontal disease, peri-implant disease and levels of salivary biomarkers IL-1β, IL-10, RANK, OPG, MMP-2, TGF-β and TNF-α: follow-up over 5 years

Objective: The aim of this study was to evaluate the levels of salivary biomarkers IL-1β, IL-10, RANK, OPG, MMP-2, TG-β and TNF-α in individuals with diagnosis of peri-implant mucositis in the absence or presence of periodontal and peri-implant maintenance therapy (TMPP) over 5 years. Material and Methods: Eighty individuals diagnosed with peri-implant mucositis were divided into two groups: one group that underwent periodontal and peri-implant regularly maintenance therapy, called GTP (n=39), and a second group that received no regular maintenance GNTP (n=41). Each participant underwent a complete periodontal and peri-implant clinical examination. Collection of saliva samples and radiographic examination to evaluate peri-implant bone levels were conducted at two times: initial examination (T1) and after 5 years (T2). The salivary samples were evaluated through ELISA for the following markers: IL-1β, IL-10, RANK, OPG, MMP-2, TGF and TNF-α. Results: A higher incidence of peri-implantitis was observed in the GNTP group (43.9%) than in the GTP group (18%) (p=0.000). All individuals (n=12) who presented peri-implant mucositis and had resolution at T2 were in the GTP group. After 5 years, there was an increase in the incidence of periodontitis in the GNTP group compared to the GTP group (p=0.001). The results of the study revealed an increase in the salivary concentration of TNF-α in the GNTP group compared to the GTP group. The other salivary biomarkers that were evaluated did not show statistically significant differences between the two groups. Conclusions: The salivary concentration of TNF-α was increased in individuals with worse periodontal and peri-implant clinical condition and in those with a higher incidence of peri-implantitis, especially in the GNTP group. Longitudinal studies in larger populations are needed to confirm these findings and elucidate the role of this biomarker in peri-implant disease

Subgingival Microbiota Dysbiosis in Systemic Lupus Erythematosus: Association with Periodontal Status

Background Periodontitis results from the interaction between a subgingival biofilm and host immune response. Changes in biofilm composition are thought to disrupt homeostasis between the host and subgingival bacteria resulting in periodontal damage. Chronic systemic inflammatory disorders have been shown to affect the subgingival microbiota and clinical periodontal status. However, this relationship has not been examined in subjects with systemic lupus erythematosus (SLE). The objective of our study was to investigate the influence of SLE on the subgingival microbiota and its connection with periodontal disease and SLE activity. Methods We evaluated 52 patients with SLE compared to 52 subjects without SLE (control group). Subjects were classified as without periodontitis and with periodontitis. Oral microbiota composition was assessed by amplifying the V4 region of 16S rRNA gene from subgingival dental plaque DNA extracts. These amplicons were examined by Illumina MiSeq sequencing. Results SLE patients exhibited higher prevalence of periodontitis which occurred at a younger age compared to subjects of the control group. More severe forms of periodontitis were found in SLE subjects that had higher bacterial loads and decreased microbial diversity. Bacterial species frequently detected in periodontal disease were observed in higher proportions in SLE patients, even in periodontal healthy sites such as Fretibacterium, Prevotella nigrescens, and Selenomonas. Changes in the oral microbiota were linked to increased local inflammation, as demonstrated by higher concentrations of IL-6, IL-17, and IL-33 in SLE patients with periodontitis. Conclusions SLE is associated with differences in the composition of the microbiota, independently of periodontal status. Electronic supplementary material The online version of this article (doi:10.1186/s40168-017-0252-z) contains supplementary material, which is available to authorized users

Alloxan-induced diabetes delays repair in a rat model of closed tibial fracture

A closed fracture was performed on the left tibia of 3-month-old Wistar rats weighing 250 to 350 g that were either healthy (N = 24) or made diabetic with alloxan (N = 24) to investigate the effect of alloxan-induced diabetes on the course of bone fracture healing. Histomorphometric analysis of the fracture site was performed at 7, 14, 25, and 35 days. After 7 days, diabetic rats had significantly less cartilage (P = 0.045) and greater fibrous connective (P = 0.006) tissue formation at the fracture site compared to controls. In contrast, marked callus formation was seen in diabetic rats with significant osteogenesis (P = 0.011, P = 0.010, P = 0.010, respectively, for 14, 25, and 35 days) and chondrogenesis (P = 0.028, P = 0.033, P = 0.019) compared to controls. Radiographic analysis revealed a displaced fracture with poor bone fragment alignment and delayed consolidation at these times in the diabetic group. The levels of alkaline phosphatase were significantly higher in diabetic rats at 25 days (P = 0.009). These results suggest that the initial excessive formation of fibrous connective tissue associated with delay in chondrogenesis and osteogenesis may not provide suitable stability of the fractured site, contributing to the inappropriate alignment of fragments and an increase in the volume of callus in later stages of repair. The resulting displaced fracture in diabetic rats requires long periods for remodeling and complete bone consolidation

A Controversial Role for IL-12 in Immune Response and Bone Resorption at Apical Periodontal Sites

Periapical lesions are inflammatory conditions of tooth periapical tissues, triggered by dental pulp infection and characterized by exudation of immune cells to the affected tissues and production of inflammatory mediators such as cytokines. The inflammatory periapical reaction is mainly driven by Th1, Th2, and Th17 responses, and such polarization may modulate progression of the disease and expression of bone proresorptive cytokines. IL-12 is a potent inducer of IFN-γ production, which stimulates Th1 effector cells. Many evidences have shown a positive correlation between the bone resorptive cytokine IL-1β and the production of IL-12 and IFN-γ. Furthermore, IL-12 may have a potential role in the release of bone resorptive mediators and blockade of Th2 cytokines, affecting the progression of periapical bone loss. Nevertheless, IL-12 and IFN-γ have also been described as suppressors of osteoclast differentiation and activation, favoring bone maintenance. This paper focuses on the controversial roles of IL-12 in periapical lesions

Composite-derived monomers affect cell viability and cytokine expression in human leukocytes stimulated with Porphyromonas gingivalis

Objectives:  Dental composites release unreacted resin monomers into the oral environment, even after polymerization. Periodontal cells are, therefore, exposed to substances that potentially elicit the immune inflammatory response. The underlying molecular mechanisms associated with the interaction between resin monomers and human immune cells found in the gingival crevicular fluid are not fully understood yet. This study investigated the ability of bisphenol A-glycidyl methacrylate (BISGMA), urethane dimethacrylate (UDMA) and triethylene glycol dimethacrylate (TEGDMA) to induce apoptosis and cytokine release by human leukocytes stimulated with a periodontal pathogen. Methodology: Peripheral blood mononuclear cells (PBMC) from 16 healthy individuals were included in this study. To determine the toxicity, the PBMC were incubated for 20 hours, with monomers, for the analysis of cell viability using MTT assay. To evaluate cell death in the populations of monocytes and lymphocytes, they were exposed to sub-lethal doses of each monomer and of heat-inactivated Porphyromonas gingivalis (P. gingivalis) for 5 hours. Secretions of IL-1β, IL-6, IL-10 and TNF-α were determined by ELISA after 20 hours. Results: UDMA and TEGDMA induced apoptosis after a short-time exposure. Bacterial challenge induced significant production of IL-1β and TNF-α (p<0.05). TEGDMA reduced the bacterial-induced release of IL-1β and TNF-α, whereas UDMA reduced IL-1β release (p<0.05). These monomers did not affect IL-10 and IL-6 secretion. BISGMA did not significantly interfere in cytokine release.  Conclusions: These results show that resin monomers are toxic to PBMC in a dose-dependent manner, and may influence the local immune inflammatory response and tissue damage mechanisms via regulation of bacterial-induced IL-1β and TNF-α secretion by PBMC

Dysbiotic oral microbiota contributes to alveolar bone loss associated with obesity in mice

Periodontal diseases (PD) are inflammatory conditions that affect the teeth supporting tissues. Increased body fat tissues may contribute to activation of the systemic inflammatory response, leading to comorbidities. Some studies have shown that individuals with obesity present higher incidence of PD than eutrophics. Objective: To investigate the impact of obesity on periodontal tissues and oral microbiota in mice. Methodology: Two obesity mice models were performed, one using 12 weeks of the dietary protocol with a high-fat (HF) diet in C57BL/6 mice and the other using leptin receptor-deficient mice (db/db-/-), which became spontaneously obese. After euthanasia, a DNA-DNA hybridization technique was employed to evaluate the microbiota composition and topical application of chlorhexidine (CHX), an antiseptic, was used to investigate the impact of the oral microbiota on the alveolar bone regarding obesity. Results: Increased adipose tissue may induce alveolar bone loss, neutrophil recruitment, and changes in the oral biofilm, similar to that observed in an experimental model of PD. Topical application of CHX impaired bone changes. Conclusion: Obesity may induce changes in the oral microbiota and neutrophil recruitment, which are associated with alveolar bone loss