Oral manifestations of plummer-vinson syndrome: a classic report with literature review.

Plummer-Vinson syndrome (PVS) is a triad of microcytic hypochromic anemia, atrophic glossitis, and esophageal webs or strictures. It is one of the syndromes associated with iron deficiency anemia. Symptoms resulting from anemia predominates the clinical picture, apart from the additional features such as glossitis, angular cheilitis, and dysphagia. Dysphagia is main clinical feature of PVS. PVS carries an increased risk of development of squamous cell carcinoma of esophagus and pharynx. A classic case report of PVS with clinical features, oral manifestations, malignant potential, differential diagnosis, investigation, dental implication, and treatment is discussed here with the literature review from the dentist's point of view. The article carries a message that dental surgeons have to be familiar with the oral manifestations of anemia and be able to suspect PVS to aid in early diagnosis and prompt treatment.

Concentrations of extracellular free zinc (pZn)e in the central nervous system during simple anesthetization, ischemia and reperfusion.

"Free Zn2+" (rapidly exchangeable Zn2+) is stored along with glutamate in the presynaptic terminals of specific specialized (gluzinergic) cerebrocortical neurons. This synaptically releasable Zn2+ has been recognized as a potent modulator of glutamatergic transmission and as a key toxin in excitotoxic neuronal injury. Surprisingly (despite abundant work on bound zinc), neither the baseline concentration of free Zn2+ in the brain nor the presumed co-release of free Zn2+ and glutamate has ever been directly observed in the intact brain in vivo. Here, we show for the first time in dialysates of rat and rabbit brain and human CSF samples from lumbar punctures that: (i) the resting or "tonic" level of free Zn2+ signal in the extracellular fluid of the rat, rabbit and human being is approximately 19 nM (95% range: 5-25 nM). This concentration is 15,000-fold lower than the "300 microM" concentration which is often used as the "physiological" concentration of free zinc for stimulating neural tissue. (ii) During ischemia and reperfusion in the rabbit, free zinc and glutamate are (as has often been presumed) released together into the extracellular fluid. (iii) Unexpectedly, Zn2+ is also released alone (without glutamate) at a variable concentration for several hours during the reperfusion aftermath following ischemia. The source(s) of this latter prolonged release of Zn2+ is/are presumed to be non-synaptic and is/are now under investigation. We conclude that both Zn2+ and glutamate signaling occur in excitotoxicity, perhaps by two (or more) different release mechanisms.