ABSTRACT
PURPOSE: The aim of this study was to define a color space of non-vital teeth and to compare it with the color space of matched vital teeth, recorded in the same patients. MATERIALS AND METHODS: In a group of 218 patients, with the age range from 17 to 70, the middle third of the buccal surface of 359 devitalized teeth was measured using a clinical spectrophotometer (Vita Easyshade Advance). Lightness (L*), chromatic parameters (a*, b*), chroma (C*), hue angle (h) and the closest Vita shade in Classical and 3D Master codifications were recorded. For each patient, the same data were recorded in a vital reference tooth. The measurements were performed by the same operator with the same spectrophotometer, using a standardized protocol for color evaluation. RESULTS: The color coordinates of non-vital teeth varied as follows: lightness L*: 52.83–92.93, C*: 8.23–58.90, h: 51.20–101.53, a*: −2.53–24.80, b*: 8.10–53.43. For the reference vital teeth, the ranges of color parameters were: L*: 60.90–97.16, C*: 8.43–39.23, h: 75.30–101.13, a*: −2.36–9.60, b*: 8.36–39.23. The color differences between vital and non-vital teeth depended on tooth group, but not on patient age. CONCLUSION: Non-vital teeth had a wider color space than vital ones. Non-vital teeth were darker (decreased lightness), more saturated (increased chroma), and with an increased range of the hue interval. An increased tendency towards positive values on the a* and b* axes suggested redder and yellower non-vital teeth compared to vital ones.
Subject(s)
Humans , Tooth , Tooth, NonvitalABSTRACT
OBJECTIVE: Retinal dehydrogenase 1 (RALDH1) is a cytosolic enzyme which acts both as a source of retinoic acid (RA) and as a detoxification enzyme. RALDH1 has key functions in the midbrain dopaminergic system, which influences motivation, cognition, and social behavior. Since dopamine has been increasingly linked to autism spectrum disorder (ASD), we asked whether RALDH1 could contribute to the autistic phenotype. Therefore, we investigated for the first time the levels of RALDH1 in autistic patients. To further assess the detoxification function of RALDH1, we also explored 4-hydroxynonenal protein adducts (4-HNE PAs) and reduced glutathione (GSH) levels. Moreover, considering the effect of testosterone on RALDH1 expression, we measured the second to fourth digit ratio (2D:4D ratio) for both hands, which reflects exposure to prenatal testosterone. METHODS: Male patients with ASD (n=18; age, 62.9±4.3 months) and healthy controls (n=13; age, 78.1±4.9 months) were examined. Erythrocyte RALDH1, serum 4-HNE PAs and erythrocyte GSH levels were measured using colorimetric assays, and digit lengths were measured using digital calipers. RESULTS: We found significantly lower (−42.9%) RALDH1 levels in autistic patients as compared to controls (p=0.032). However, there was no difference in 4-HNE PAs levels (p=0.368), GSH levels (p=0.586), or 2D:4D ratios (p=0.246 in the left hand, p=0.584 in the right hand) between healthy controls and autistic subjects. CONCLUSION: We concluded that a subset of autistic patients had a low RALDH1 level. These results suggest that low RALDH1 levels could contribute to the autistic phenotype by reflecting a dopaminergic dysfunction.