Often the first evidence of variation from normal in human dentition is an observable difference in the color of the teeth. During the past decade, the demand for conservative esthetic dentistry has grown dramatically. Tooth discoloration is a frequent dental finding, associated with clinical and esthetic problems. It differs in etiology, appearance, composition, location, severity, and firmness in adherence to the tooth surface. Basically, there are two types of tooth discolorations: those caused by extrinsic factors and those caused by intrinsic congenital or systemic influence. The intensity of stains may be worsened if there are enamel defects. Tooth discoloration presents two major challenges to the dental team. The first challenge is to ascertain the cause of the stain; the second is its management.
CLINICAL SIGNIFICANCEThis article reviews the etiology and clinical presentation of dental stains and outlines treatment options.
This study was performed to identify cephalometric and facial features of patients with beta-thalassaemia major. A total of 54 thalassaemic subjects were examined for craniofacial deformities, including 37 patients (24 males and 13 females, aged 5-16 years) who had lateral cephalometric radiographs. The thalassaemic groups were compared with a normal control group matched for sex and dental age, using a t-test. All thalassaemic patients had a Class II skeletal base relationship. The average ANB angle was significantly larger than the controls in dental stages 2 and 3 (P < 0.05). Mandibular base length (Ar-Gn) was significantly less in thalassaemic patients than in controls, with the greatest differences (P < 0.001) found in the younger age group. The maxilla was of normal length (PNS-ANS, Ptm'-ANS') and appeared prominent (3.3 mm in males and 5.1 mm in females) due to a reduced cranial base length (Ar'-S') and a short mandible (Ar'-P'). Vertically, thalassaemic patients showed a significantly increased maxillary/mandibular planes angle in all groups, with differences ranging between 6.19 and 12.55 degrees (P < 0.001). Thalassaemic patients also showed a reduced posterior facial height (S-Go, Ar-Go) and increased anterior facial proportions. Of the 54 thalassaemic patients examined, 17 per cent had severe facial disfigurements (grade 3).
We have previously reported that loss-of-function mutations in the cathepsin C gene (CTSC) result in Papillon-Lefèvre syndrome, an autosomal recessive condition characterized by palmoplantar keratosis and early-onset, severe periodontitis. Others have also reported CTSC mutations in patients with severe prepubertal periodontitis, but without any skin manifestations. The possible role of CTSC variants in more common types of non-mendelian, early-onset, severe periodontitis ("aggressive periodontitis") has not been investigated. In this study, we have investigated the role of CTSC in all three conditions. We demonstrate that PLS is genetically homogeneous and the mutation spectrum that includes three novel mutations (c.386T>A/p.V129E, c.935A>G/p.Q312R, and c.1235A>G/p.Y412C) in 21 PLS families (including eight from our previous study) provides an insight into structure-function relationships of CTSC. Our data also suggest that a complete loss-of-function appears to be necessary for the manifestation of the phenotype, making it unlikely that weak CTSC mutations are a cause of aggressive periodontitis. This was confirmed by analyses of the CTSC activity in 30 subjects with aggressive periodontitis and age-sex matched controls, which demonstrated that there was no significant difference between these two groups (1,728.7 +/- SD 576.8 micro moles/mg/min vs. 1,678.7 +/- SD 527.2 micro moles/mg/min, respectively, p = 0.73). CTSC mutations were detected in only one of two families with prepubertal periodontitis; these did not form a separate functional class with respect to those observed in classical PLS. The affected individuals in the other prepubertal periodontitis family not only lacked CTSC mutations, but in addition did not share the haplotypes at the CTSC locus. These data suggest that prepubertal periodontitis is a genetically heterogeneous disease that, in some families, just represents a partially penetrant PLS.
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