Introduction: Gingival overgrowth, with its potential cosmetic implications and for providing new niches for the growth of microorganisms, is a serious concern for both patients and clinicians. Amlodipine is a comparatively new calcium channel blocker and is being used with increasing frequency in the management of hypertension and angina. Although amlodipine is considered a safe drug, it may induce gingival overgrowth in some individuals.Case Presentation: A rare case of amlodipine‐induced gingival overgrowth in a 60‐year‐old Indian woman who was on amlodipine for 3 years and subsequent periodontal management of the overgrowth is reported here. The patient did not have any gingival overgrowth for 2 years despite the fact that she was taking amlodipine, but she developed the gingival overgrowth 9 months before her initial visit, coincident with uncontrolled diabetes mellitus and use of a cholesterol‐lowering drug. She was treated with drug substitution for the systemic condition and surgical treatment for the overgrowth. She was followed up for 1 year, regularly.Conclusion: We speculate that overgrowth could have been triggered by uncontrolled type 2 diabetes mellitus and by altered pharmacokinetics of amlodipine resulting from the drug interaction of amlodipine with a cholesterol‐lowering drug.
The title compound, C20H20N2O, was studied as a part of our work on pyrazoline derivatives. It represents a trans-isomer. The central pyrazoline ring adopts an envelope conformation with the asymmetric C atom having the largest deviation of 0.107 (1) Å from the mean plane. It forms dihedral angles of 6.2 (1) and 86.4 (1)° with the adjacent p-tolyl and styrene groups, respectively. In the crystal, C—H⋯O interactions link molecules into infinite chains along the c axis.
Congenital tooth agenesis (CTA) is one of the most common craniofacial anomalies. Its frequency varies among different population depending upon the genetic heterogeneity.CTA could be of familial or sporadic and syndromic or non-syndromic. Five major genes are found to be associated with non-syndromic CTA namely, PAX9, MSX1, EDA1, AXIN2 and WNT10A. In this study, an India family with CTA was investigated and a novel c.336C>G variation was identified in the exon 3 of PAX9, leading to substitution of evolutionary conserved Cys with Trp at 112 amino acid position located at the functionally significant DNA binding paired domain region. Functional analysis revealed that p.Cys112Trp mutation did not prevent the nuclear localization although mutant protein had higher cytoplasmic retention. EMSA using e5 probe revealed that mutant protein was unable to bind with the paired-domain binding site. Subsequently, GST pull-down assay revealed lower binding activity of the mutant protein with its known interactor MSX1. Further RNAsequencing of PAX9 over-expressed HEK293, identified two potential novel targets, WNT4 and WNT7b those are up-regulated by wild-type PAX9 but not by mutant. These in vitro results were consistent with the computational results. The in vitro and computational observations altogether suggest that c.336C>G (p.Cys112Trp) variation leads to loss-offunction of PAX9 leading to CTA in this family.
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