Improved methods are needed to assess the structure and activity of lesions on root surfaces in order to improve clinical decision making. Conventional visual and tactile methods for assessing lesion activity are not reliable, and the clinician is often unable to evaluate if the lesion is progressing or has remineralized. An important marker of an arrested lesion is a highly mineralized surface zone that forms when mineral is deposited in the outer layer of the lesion. In vitro studies have shown that a mineralized surface zone influences the kinetics of water evaporation and the surface temperature while drying. Temperature changes can be monitored by measuring the thermal emission with thermal imaging. Studies have also shown that the depth and severity of demineralization and the thickness of the highly mineralized transparent surface zone on arrested lesions can be measured nondestructively with optical coherence tomography (OCT). Thermal imaging at 8-µm to 13-µm wavelengths was completed on 30 test subjects with a suspected active root caries lesion by monitoring thermal emission from the tooth surfaces during 30 s of air drying. Lesions were also evaluated using cross-polarization OCT (CP-OCT) during lesion dehydration to identify transparent surface zones indicative of arrested lesions and determine if shrinkage occurred during drying. The overall thermal emission recorded during drying was significantly different ( P < 0.001) when comparing sound tooth surfaces, lesion areas identified as arrested, and lesion areas identified as active, demonstrating that thermal imaging is a promising approach for the clinical assessment of lesion activity on root surfaces. Ten of the lesions in this study had distinct areas with transparent surface zones that were visible in CP-OCT images. Shrinkage was detected with CP-OCT during drying for 12 lesions. This study confirms that these novel approaches for assessing lesion activity on root surfaces can be implemented in vivo.
Transparent remineralized surface zones found on natural caries lesions may reduce the permeability to water and plaque generated acids. Near-IR (NIR) reflectance imaging coupled with dehydration can be used to measure changes in the fluid permeability of lesions in enamel and dentin. Previous work demonstrated a negative association between the surface zone thickness and the rate of dehydration in simulated enamel lesions. In this study, the rates of dehydration and thickness of transparent surface layer of coronal lesions of extracted teeth were measured and correlated. Reflectance imaging at NIR wavelengths from 1695–1750 nm, which coincides with higher water absorption and manifests the greatest sensitivity to contrast changes during dehydration measurements, was used to image these enamel lesions. The remineralized surface layer thickness was determined using optical coherence tomography (OCT).
Objective Ultraviolet (UV) and infrared (IR) lasers can be used to specifically target protein, water, and mineral, respectively, in dental hard tissues to produce varying changes in surface morphology, permeability, reflectivity and acid resistance. The purpose of this study was to explore the influence of laser irradiation and topical fluoride application on the surface morphology, permeability, reflectivity, and acid resistance of enamel and dentin to shed light on the mechanism of interaction and develop more effective treatments. Methods Twelve bovine enamel surfaces and twelve bovine dentin surfaces were irradiated with various combinations of lasers operating at 0.355 (Freq.-tripled Nd:YAG (UV) laser), 2.94 (Er:YAG laser), and 9.4 μm (CO2 laser), and surfaces were exposed an acidulated phosphate fluoride gel and an acid challenge. Changes in the surface morphology, acid resistance, and permeability were measured using digital microscopy, polarized light microscopy, near-IR reflectance, fluorescence, polarization sensitive-optical coherence tomography (PS-OCT), and surface dehydration rate measurements. Results Different laser treatments dramatically influenced the surface morphology and permeability of both enamel and dentin. CO2 laser irradiation melted tooth surfaces. Er:YAG and UV lasers, while not melting tooth surfaces, showed markedly different surface roughness. Er:YAG irradiation led to significantly rougher enamel and dentin surfaces and led to higher permeability. There were significant differences in acid resistance among the various treatment groups. Conclusion Surface dehydration measurements showed significant changes in permeability after laser treatments, application of fluoride and after exposure to demineralization. CO2 laser irradiation was most effective in inhibiting demineralization on enamel while topical fluoride was most effective for dentin surfaces.
Periodontal disease is driven by dysbiosis in the oral microbiome, resulting in over-representation of species that induce the release of pro-inflammatory cytokines, chemokines, and tissue-remodeling matrix metalloproteinases (MMPs) in the periodontium. These chronic tissue-destructive inflammatory responses result in gradual loss of tooth-supporting alveolar bone. The oral spirochete Treponema denticola (T. denticola), is consistently found at significantly elevated levels in periodontal lesions. Host-expressed Toll-Like Receptor 2 (TLR2) senses a variety of bacterial ligands, including acylated lipopolysaccharides and lipoproteins. T. denticola dentilisin, a surface-expressed protease complex comprised of three lipoproteins has been implicated as a virulence factor in periodontal disease, primarily due to its proteolytic activity. While the role of acylated bacterial components in induction of inflammation is well-studied, little attention has been given to the potential role of the acylated nature of dentilisin. The purpose of this study was to test the hypothesis that T. denticola dentilisin activates a TLR2-dependent mechanism, leading to upregulation of tissue-destructive genes in periodontal tissue. RNA-sequencing of periodontal ligament cells challenged with T. denticola bacteria revealed significant upregulation of genes associated with extracellular matrix organization and degradation including potentially tissue-specific inducible MMPs that may play novel roles in modulating host immune responses that have yet to be characterized within the context of oral disease. The Gram-negative oral commensal, Veillonella parvula, failed to upregulate these same MMPs. Dentilisin-induced upregulation of MMPs was mediated via TLR2 and MyD88 activation, since knockdown of expression of either abrogated these effects. Challenge with purified dentilisin upregulated the same MMPs while a dentilisin-deficient T. denticola mutant had no effect. Finally, T. denticola-mediated activation of TLR2/MyD88 lead to the nuclear translocation of the transcription factor Sp1, which was shown to be a critical regulator of all T. denticola-dependent MMP expression. Taken together, these data suggest that T. denticola dentilisin stimulates tissue-destructive cellular processes in a TLR2/MyD88/Sp1-dependent fashion.
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