Balancing the role of the dental school in teaching, research and patient care; including care for underserved areas

Inequalities within dentistry are common and are reflected in wide differences in the levels of oral health and the standard of care available both within and between countries and communities. Furthermore there are patients, particularly those with special treatment needs, who do not have the same access to dental services as the general public. The dental school should aim to recruit students from varied backgrounds into all areas covered by the oral healthcare team and to train students to treat the full spectrum of patients including those with special needs. It is essential, however, that the dental student achieves a high standard of clinical competence and this cannot be gained by treating only those patients with low expectations for care. Balancing these aspects of clinical education is difficult. Research is an important stimulus to better teaching and better clinical care. It is recognized that dental school staff should be active in research, teaching, clinical work and frequently administration. Maintaining a balance between the commitments to clinical care, teaching and research while also taking account of underserved areas in each of these categories is a difficult challenge but one that has to be met to a high degree in a successful, modern dental school.

Cavernous sinus thrombosis in a patient with facial myiasis

Cavernous sinus thrombosis is a severe encephalic complication of the cervicofacial infections that can lead to death if not treated in adequate time. Among the several etiologies related to the development of this infection, myiasis has not been reported, enforcing the importance of the report of a case of thrombosis of the cavernous sinus developed from a facial myiasis. (Quintessence Int 2010;41:e72-e74)

Schilbach-Rott/blepharofacioskeletal syndrome in a Brazilian patient

We report on a 4-year-old girl with blepharophimosis, a typical facial gestalt and skeletal abnormalities seen in the blepharofacioskeletal syndrome (BFSS). A comparative review with previous cases provides further evidence that BFSS and Schilbach-Rott syndrome (SRS) are the same condition. (C) 2008 Wiley-Liss, Inc.

Iodide Transport Defect: Functional Characterization of a Novel Mutation in the Na(+)/I(-) Symporter 5 `-Untranslated Region in a Patient with Congenital Hypothyroidism

Context: Iodide transport defect (ITD) is an autosomal recessive disorder caused by impaired Na(+)/I(-) symporter (NIS)-mediated active iodide accumulation into thyroid follicular cells. Clinical manifestations comprise a variable degree of congenital hypothyroidism and goiter, and low to absent radioiodide uptake, as determined by thyroid scintigraphy. Hereditary molecular defects in NIS have been shown to cause ITD. Objective: Our objective was to perform molecular studies on NIS in a patient with congenital hypothyroidism presenting a clinical ITD phenotype. Design: The genomic DNA encoding NIS was sequenced, and an in vitro functional study of a newly identified NIS mutation was performed. Results: The analysis revealed the presence of an undescribed homozygous C to T transition at nucleotide -54 (-54C>T) located in the 5`-untranslated region in the NIS sequence. Functional studies in vitro demonstrated that the mutation was associated with a substantial decrease in iodide uptake when transfected into Cos-7 cells. The mutation severely impaired NIS protein expression, although NIS mRNA levels remained similar to those in cells transfected with wild-type NIS, suggesting a translational deficiency elicited by the mutation. Polysome profile analysis demonstrated reduced levels of polyribosomes-associated mutant NIS mRNA, consistent with reduced translation efficiency. Conclusions: We described a novel mutation in the 5`-untranslated region of the NIS gene in a newborn with congenital hypothyroidism bearing a clinical ITD phenotype. Functional evaluation of the molecular mechanism responsible for impaired NIS-mediated iodide concentration in thyroid cells indicated that the identified mutation reduces NIS translation efficiency with a subsequent decrease in protein expression and function. (J Clin Endocrinol Metab 96: E1100-E1107, 2011)