Diagnostic performance of magnetic resonance imaging for degenerative temporomandibular joint disease.

BACKGROUND: Degenerative joint disease (DJD) of the temporomandibular joint (TMJ) is an important type of temporomandibular disorders (TMDs) potentially leading to orofacial pain and jaw dysfunction. Magnetic resonance imaging (MRI) is important in TMD diagnosis; however, its diagnostic ability for DJD remains unknown. OBJECTIVE: To explore the utility of MRI in diagnosing DJD according to the latest diagnostic criteria for TMD and detecting condylar bone abnormalities and their severity. METHODS: Overall, 122 participants were examined using cone-beam computed tomography (CBCT) and MRI. The sensitivity, specificity and accuracy of MRI for detecting DJD and different types of TMJ condylar bone abnormalities were calculated (considering CBCT as gold standard); in addition, we tested MRI and CBCT's consistency in scoring five types of condylar bone abnormalities. RESULTS: The sensitivity and specificity of MRI for DJD were 95.3% and 43.1%, respectively. The MRI sensitivities for condylar flattening, erosion, osteophytes, sclerosis and cysts were 98.6%, 96.2%, 79.4%, 50%, and 79.2% (specificity, 53.6%, 48.3%, 81.6%, 83.3%, and 88.2%, respectively), respectively. The consistency between MRI and CBCT in assessing the severity of condylar bone abnormalities was fair-to-moderate (kappa coefficient: 0.278-0.491). The inter-observer consistency for CBCT was good, whereas for MRI, it was relatively poor. CONCLUSION: MRI can detect DJD and condylar bone abnormalities. However, MRI could not efficiently detect the severity of condylar bone abnormalities.

The Regulator Gene rnc Is Closely Involved in Biofilm Formation in Streptococcus mutans.

Streptococcus mutans is an important factor in the etiology and pathogenesis of dental caries, largely owing to its ability to form a stable biofilm. Previous animal studies have indicated that rnc could decrease the amount of sulcal caries, and that the downregulation of cariogenicity might be due to its capacity to disrupt biofilm formation. However, the biofunctions by which rnc is involved in biofilm formation remain to be elucidated. In this study, we further investigate the role of rnc based on the study of mature biofilm. Scanning electron microscopy and the crystal violet assay were used to detect the biofilm forming ability. The production and distribution of exopolysaccharides within biofilm was analyzed by exopolysaccharide staining. Gel permeation chromatography was used to perform molecular weight assessment. Its adhesion force was measured by atomic force microscopy. The expression of biofilm formation-associated genes was analyzed at the mRNA level by qPCR. Here, we found that rnc could occur and function in biofilm formation by assembling well-structured, exopolysaccharide-encased, stable biofilms in S. mutans. The weakened biofilm forming ability of rnc-deficient strains was associated with the reduction of exopolysaccharide production and bacterial adhesion. Over all, these data illustrate an interesting situation in which an unappreciated regulatory gene acquired for virulence, rnc, most likely has been coopted as a potential regulator of biofilm formation in S. mutans. Further characterization of rnc may lead to the identification of a possible pathogenic biofilm-specific treatment for dental caries.

The rnc Gene Promotes Exopolysaccharide Synthesis and Represses the vicRKX Gene Expressions via MicroRNA-Size Small RNAs in Streptococcus mutans.

Dental caries is a biofilm-dependent disease that largely relies on the ability of Streptococcus mutans to synthesize exopolysaccharides. Although the rnc gene is suggested to be involved in virulence mechanisms in many other bacteria, the information regarding it in S. mutans is very limited. Here, using deletion or overexpression mutant assay, we demonstrated that rnc in S. mutans significantly positively regulated exopolysaccharide synthesis and further altered biofilm formation. Meanwhile, the cariogenecity of S. mutans was decreased by deletion of rnc in a specific pathogen-free (SPF) rat model. Interestingly, analyzing the expression at mRNA level, we found the downstream vic locus was repressed by rnc in S. mutans. Using deep sequencing and bioinformatics analysis, for the first time, three putative microRNA-size small RNAs (msRNAs) targeting vicRKX were predicted in S. mutans. The expression levels of these msRNAs were negatively correlated with vicRKX but positively correlated with rnc, indicating rnc probably repressed vicRKX expression through msRNAs at the post-transcriptional level. In all, the results present that rnc has a potential role in the regulation of exopolysaccharide synthesis and can affect vicRKX expressions via post-transcriptional repression in S. mutans. This study provides an alternative avenue for further research aimed at preventing caries.

Co-operative effect of exogenous dextranase and sodium fluoride on multispecies biofilms.

BACKGROUND/PURPOSE: The co-operative effect of exogenous dextranase (Dex) and sodium fluoride (NaF) on Streptococcus mutans monospecies biofilms is impressive. Here we investigated the effects of the combination on a mature cariogenic multispecies biofilm and analyzed the potential mechanism. MATERIALS AND METHODS: A multispecies biofilm of S. mutans, Lactobacillus acidophilus, and Actinomyces viscosus was established in vitro. Dex and NaF were added separately or together. The effects of the agents on the biomass were measured. The exopolysaccharide production was determined with the scintillation counting method. The viability and morphology were evaluated using colony forming unit and confocal laser scanning microscopy, respectively. RESULTS: In general, biofilms treated with Dex and a little concentration of NaF exhibited a lower biomass, exopolysaccharide production, and viability compared with the control group (P < 0.05). Confocal laser scanning microscopy using a vital fluorescence technique showed the combination treated biofilms appeared to be loose relatively and single cells could be observed. Furthermore, the thickness and viability were also lower than either of the separate agent groups (P < 0.05). CONCLUSION: Overall, these findings reveal that a combination of 1 U/mL Dex and 80 µg/mL NaF is a promising candidate for disrupting complex cariogenic multispecies biofilms. This feature may be in that Dex loses the structure of biofilms, thereby facilitating NaF penetration and enhancing its antibacterial effects.