Comparison of light transmittance and color changes between polyurethane and copolyester retainer materials after staining and destaining.

BACKGROUND: Retainers are the only effective approach to prevent orthodontic relapse. The aim of this study was to compare the changes in color and light-transmittance of rough and smooth thermoformed polyurethane and copolymer retainer samples after staining in different solutions and destaining with different approaches. METHODS: Four hundred copolyester (Essix® ACE) and 400 polyurethane (Zendura®) samples with different surface textures, smooth and rough, were stained in 4 different solutions (n = 100 per solution) over 28 days. Each of the four groups of 100 stained samples of each material was subdivided into 5 groups of 20 samples and subjected to different destaining solutions. Light transmittance and color changes were evaluated using a spectrometer and a spectrophotometer. Mean differences were compared using a two-way analysis of variance (ANOVA) and posthoc multiple comparison tests at P = 0.05. RESULTS: No significant differences in light transmittance were found between both untreated materials. Both materials were stained in a similar fashion and showed no significant differences between two materials after staining. Coffee and tea stained both materials more significantly than wine, but there was a significant difference of changes of color and light transmittance between rough and smooth surfaces during the destaining in coffee- and tea-stained samples of copolyester material. All destaining solutions were effective at removing all stains on the samples. The surface roughness of the material plays a significant role in the ability of the materials to be destained, demonstrating a more significant greater effect on cleaning rough samples for improvements in light-transmittance and greater changes in color. CONCLUSIONS: This study concluded that the surface of materials plays a significant role in the material destaining and staining. In addition, the different polymers used for retainer fabrication exhibited different responses during the destaining process depending on types of stains.

Controversy of physiological vs. pharmacological effects of BMP signaling: Constitutive activation of BMP type IA receptor-dependent signaling in osteoblast lineage enhances bone formation and resorption, not affecting net bone mass.

Bone morphogenetic proteins (BMPs) were first described over 50 years ago as potent inducers of ectopic bone formation when administrated subcutaneously. Preclinical studies have extensively examined the osteoinductive properties of BMPs in vitro and new bone formation in vivo. BMPs (BMP-2, BMP-7) have been used in orthopedics over 15 years. While osteogenic function of BMPs has been widely accepted, our previous studies demonstrated that loss-of-function of BMP receptor type IA (BMPR1A), a potent receptor for BMP-2, increased net bone mass by significantly inhibiting bone resorption in mice, indicating a positive role of BMP signaling in bone resorption. The physiological role of BMPs (i.e. osteogenic vs. osteoclastogenic) is still largely unknown. The purpose of this study was to investigate the physiological role of BMP signaling in endogenous long bones during adult stages. For this purpose, we conditionally and constitutively activated the Smad-dependent canonical BMP signaling thorough BMPR1A in osteoblast lineage cells using the mutant mice (Col1CreER™:caBmpr1a). Because trabecular bones were largely increased in the loss-of-function mouse study for BMPR1A, we hypothesized that the augmented BMP signaling would affect endogenous trabecular bones. In the mutant bones, the Smad phosphorylation was enhanced within physiological level three-fold while the resulting gross morphology, bodyweights, bone mass/shape/length, serum calcium/phosphorus levels, collagen cross-link patterns, and healing capability were all unchanged. Interestingly, we found; 1) increased expressions of both bone formation and resorption markers in femoral bones, 2) increased osteoblast and osteoclast numbers together with dynamic bone formation parameters by trabecular bone histomorphometry, 3) modest bone architectural phenotype with reduced bone quality (i.e. reduced trabecular bone connectivity, larger diametric size but reduced cortical bone thickness, and reduced bone mechanical strength), and 4) increased expression of SOST, a downstream target of the Smad-dependent BMPR1A signaling, in the mutant bones. This study is clinically insightful because gain-of-function of BMP signaling within a physiological window does not increase bone mass while it alters molecular and cellular aspects of osteoblast and osteoclast functions as predicted. These findings help explain the high-doses of BMPs (i.e. pharmacological level) in clinical settings required to substantially induce a bone formation, concurrent with potential unexpected side effects (i.e. bone resorption, inflammation) presumably due to a broader population of cell-types exposed to the high-dose BMPs rather than osteoblastic lineage cells.