A comparison of resin infiltration and microabrasion for postorthodontic white spot lesion.

INTRODUCTION: The objective of this research was to evaluate and compare the effectiveness of microabrasion and resin infiltration for white spot lesions (WSLs). METHODS: Patients with postorthodontic WSLs were enrolled and randomly assigned to the control, microabrasion, and resin-infiltration groups. Intraoral photographs were taken before and after (6 months later) treatment. WSL sizes were determined through ImageJ (Wayne Rasband, Kensington, Md). Integrated optical density (IOD) was determined for a WSL and its surrounding normal enamel through Image-Pro Plus (version 6.0; Media Cybernetics, Rockville, Md), and their differences of IOD were considered as the IOD surrogate for that WSL. The color change of WSL were measured through ΔE. RESULTS: A total of 27 eligible patients were enrolled; 9 subjects were assigned to each group, resulting in 56 teeth in the control group, 72 in the microabrasion group, and 58 in the resin-infiltration group. The ratios of WSL size (after/before) were similar between the microabrasion and resin-infiltration group (43.94 ± 0.03% vs 45.02 ± 0.03%; P = 0.96 > 0.05), but those of the 2 groups were significantly lower than those of the control group (92.15 ± 0.02%) (P <0.001). Moreover, the ratios of IOD (after/before) were significantly lower in the resin-infiltration group (22.94 ± 0.02%) than in the microabrasion (78.11 ± 0.03%) and control (83.79 ± 0.02%) (P <0.001) groups. The highest ΔE improvement was obtained by infiltration, but there was no significant difference between microabrasion and control group. CONCLUSIONS: Resin infiltration and microabrasion are comparably effective in reducing the sizes of WSL, but resin infiltration enjoys an esthetic advantage over microabrasion.

The rostromedial tegmental nucleus: a key modulator of pain and opioid analgesia.

A recently defined structure, the rostromedial tegmental nucleus (RMTg; aka tail of the ventral tegmental area [VTA]), has been proposed as an inhibitory control center for dopaminergic activity of the VTA. This region is composed of GABAergic cells that send afferent projections to the ventral midbrain and synapse onto dopaminergic cells in the VTA and substantia nigra. These cells exhibit µ-opioid receptor immunoreactivity, and in vivo, ex vivo, and optogenetic/electrophysiological approaches demonstrate that morphine excites dopamine neurons by targeting receptors on GABAergic neurons localized in the RMTg. This suggests that the RMTg may be a key modulator of opioid effects and a major brake regulating VTA dopamine systems. However, no study has directly manipulated RMTg GABAergic neurons in vivo and assessed the effect on nociception or opioid analgesia. In this study, multiplexing of GABAergic neurons in the RMTg was achieved using stimulatory Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) and inhibitory kappa-opioid receptor DREADDs (KORD). Our data show that locally infused RMTg morphine or selective RMTg GABAergic neuron inhibition produces 87% of the maximal antinociceptive effect of systemic morphine, and RMTg GABAergic neurons modulate dopamine release in the nucleus accumbens. In addition, chemoactivation of VTA dopamine neurons significantly reduced pain behaviors both in resting and facilitated pain states and reduced by 75% the dose of systemic morphine required to produce maximal antinociception. These results provide compelling evidence that RMTg GABAergic neurons are involved in processing of nociceptive information and are important mediators of opioid analgesia.

Developing myelin specific promoters for schwannoma gene therapy.

BACKGROUND: Schwannomas are peripheral nerve sheath tumors composed entirely of Schwann-lineage cells that cause pain and sensory-motor dysfunction through compression of peripheral nerves, the spinal cord, and/or the brain stem. Treatment of schwannoma is largely limited to resection which itself has limited value. The goal of this study is to establish a technique to identify the most efficient and tissue-specific promoter for use in a schwannoma gene therapy construct. NEW METHOD: This work involves transfection of schwannoma cells with adeno-associated viral vector plasmids expressing GFP under different myelin cell specific promoters. The transfected cells were evaluated for green fluorescence intensity in vitro, and in vivo after implantation into sciatic nerves of nude mice. RESULTS: Our data demonstrate that myelin protein zero (MPZ, P0) and peripheral myelin protein 22 (PMP22) promoters produce greater GFP expression in schwannoma cell lines than myelin basic protein (MBP) promoter. In vitro, P0 promoter activity in schwannoma cell lines was shown to be less active than the cytomegalovirus and chicken ß-actin (CBA) promoter. However, we did not observe any significant difference between the activity of the CBA and P0 promoters in a xenograft schwannoma model. COMPARISON WITH EXISTING METHODS(S): We show here the influence of the peripheral nerve microenvironment on promoter efficacy in expressing transgenes using simple transfection by lipofection followed by prompt implantation of the transfected cells into the sciatic nerve of nude mice. CONCLUSIONS: We demonstrate that of the myelin specific promoters evaluated, P0 is optimal for driving expression of transgenes in schwannoma cells.