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Objective External apical root resorption ( EARR) is a frequent iatrogenic effect of orthodontic treatment. Substantial variability in responses to postorthodontic EARR has been observed among patients even when similar treatment protocols were used. This observation suggests that environmental and/or genetic variations between individuals may confer susceptibility or resistance to developing EARR. The objective of this study is to determine whether variants in the osteopontin gene, an essential mediator in the odontoclast fusion and attachment process, are positively/negatively associated with postorthodontic EARR. Materials and Methods Genetic screening of eighty-seven orthodontic patients was performed for two polymorphisms in the osteopontin gene cluster (rs9138 and rs11730582). Subjects were divided into groups, according to the presence or absence of EARR (>2 mm). Genotype distributions and allelic frequencies were calculated using the chi-square test. Logistic regression analysis was used to assess the extent to which clinical-related parameters interfered with the EARR. Odds ratios ( OR) and 95% confidence intervals were also calculated. Results Data from this study show that subjects heterozygous and homozygous for the most frequent allele of the osteopontin gene at position 89261521 [ OR: 0.035 ( P = 0.035*) (allele A)] and 89253600 [ OR: 0.20 ( P = 0.025*) (allele T)], respectively, are protected against postorthodontic EARR. Nevertheless, a highly significant association was found in the comparative analysis of homozygous subjects [2/2 ( CC)] for the osteopontin gene (rs9138), resulting in an increased risk of suffering postorthodontic EARR[ OR: 4.10; P = 0.045*; CI: 95%]. Subjects who were homozygous [2/2 ( CC)] for the osteopontin gene (rs11730582) were more likely, and to a greater extent, to be affected with EARR [ OR: 11.68; P < 0.039*; CI: 95%] compared with other genotypes. Conclusion Variations in the osteopontin gene (rs9138 and rs11730582) are determinants of a genetic predisposition to suffer EARR secondary to orthodontic treatment. [ABSTRACT FROM AUTHOR]

Background and Aims: Vascular calcification (VC) and atherosclerosis are associated with an increased cardiovascular morbimortality in chronic kidney disease (CKD). Osteoprotegerin (OPG) and osteopontin (OPN) are involved in both VC and CKD. Soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) has been related to cardiovascular disease. We hypothesized that OPG, OPN and sTWEAK levels may be associated with a higher prevalence of cardiovascular outcomes in patients with CKD., Methods: The presence of calcified or non-calcified atherosclerotic plaques was assessed in 1043 stage 3 to 5D CKD patients from The NEFRONA Study. Biochemical measurements and OPG, OPN and sTWEAK serum levels were analyzed. Patients were followed for cardiovascular outcomes (41 ± 16 months)., Results: At recruitment, 26% of CKD patients had VC. The adjusted odds ratios for having VC were 2.22 (1.32-3.75); p=.003 for OPG, and 0.45 (0.24-0.84); p=.01 for sTWEAK concentrations. After follow-up, 95 CV events occurred. In a Cox model, patients with OPG or OPN above and sTWEAK below their optimal cut-off points had an adjusted higher risk of cardiovascular events [HR: 2.10 (1.49-3.90); p=.02; 1.65 (1.02-2.65); p=.04; 2.05 (1.28-3.29), p=.003; respectively]. When CKD patients were grouped according to the number of biomarkers above (OPG and OPN) or below (sTWEAK) their cut-off points, the combination of these biomarkers showed the highest risk for cardiovascular events [HR: 9.46 (3.80-23.5) p < .001]. A composite score of these three biomarkers increased the C-statistic and net reclassification index beyond conventional risk factors and VC., Conclusions: The combination of OPG, OPN and sTWEAK increased the predictability of cardiovascular outcomes., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Objective: Rheumatoid arthritis (RA) is an autoimmune disease of unknown etiology characterized by cartilage and bone destruction. The main genetic determinant to RA, the shared epitope, maps to the HLA-DR locus, although this is not the only risk factor. The osteopontin (OPN) gene, with pleiotropic functions in inflammatory and immune responses, has been implicated in the pathogenesis of RA. We studied the association of polymorphisms in the OPN gene and predisposition to RA., Methods: Analysis was performed in a case-control study with 263 patients and 478 controls. Four single nucleotide polymorphisms (SNP), 327T/C, 795C/T, 1128A/G, and 1284A/C, of the OPN gene were genotyped by primer-specific amplification in the presence of SYBR Green., Results: Distorted transmission of these polymorphisms was studied in 58 RA trios and 61 affected sibling pairs. These SNP demonstrated strong linkage disequilibrium. No statistically significant association was observed (80% power to exclude a genotypic relative risk of 1.49 at the 5% significance level, with minor allele frequencies of 28%). This lack of association with RA was found after stratification for the shared epitope as well., Conclusion: Our data suggest that, unlike the reported effect of the OPN SNP conferring predisposition to common diseases such as multiple sclerosis or systemic lupus erythematosus, these OPN gene polymorphisms do not contribute to RA susceptibility in the Spanish population we studied.