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The maintenance of endothelial integrity is of great importance in coping with age-related vascular alterations. Endothelium-derived nitric oxide is one of the various vasoactive substances able to regulate vascular tone and homeostasis, and whose decrease is known to be related with senescence in endothelial cells. There are reports on the efficacy of silicon, especially as silicic acid, in protecting vascular integrity during age-related vascular diseases. The aim of this study was to evaluate the ability of supplementation of silicic acid in drinking water in the maintenance of vascular health in a mouse model of early physiological aging. In particular, we evaluated the relationship between Si supplementation and endothelial nitric oxide synthase (eNOS) expression, taking into account also the aquaporin-1 (AQP-1) isoform that, as recently reported, seems to be involved in nitric oxide transport across cell membranes. Our results showed that silicic acid supplementation increased both eNOS and AQP-1 expression, suggesting that silicic acid modulation of endothelial nitric oxide synthase and aquaporin-1 could represent a potential strategy against age-related vascular senescence., (Copyright © 2012 Elsevier GmbH. All rights reserved.)

The trigeminal ganglia are involved in transmission of orofacial sensitivity. The free radical gas nitric oxide (NO) has recently been found to function as a messenger molecule in both central and peripheral trigeminal primary afferent neurons. NO is produced within neurons mainly by two enzymes: a constitutive (neuronal) form of NO synthase (nNOS) or an inducible form of NOS (iNOS). The aim of the study was to evaluate the distribution of trigeminal neurons according to size (small, medium and large neurons) and to correlate the percentage of NOS-immunopositive neurons with regard to neuronal size. The results showed a significant relationship between the percentage of nNOS-immunopositive neurons and the size of neurons. Evaluation of the percentage of nNOS-immunopositive neurons showed that they constitute about 50% of the total number of neurons and that they are represented mainly as large-sized neurons. The iNOS immunolabelling was very faint in all neuronal types. Since the nitroxidergic system is well represented in human trigeminal ganglia, this study indicates that it could play a relevant role in trigeminal neurotransmission., (2009 Elsevier GmbH. All rights reserved.)

It has been suggested that heat-shock proteins (HSPs) might be involved in autoimmune disease mechanisms in humans, considering the high degree of sequence homology between bacterial and human HSPs. Several authors have postulated that HSPs might be involved in periodontal disease processes, but not specifically in peri-implantitis. Consequently, using immunohistochemical techniques, we studied the distribution of HSP25, HSP32, HSP60 and HSP72 in three groups of patients: (1) subjects with natural teeth (healthy periodontal tissue), (2) subjects with normal peri-implant mucosa and (3) subjects with clinically evident peri-implantitis. The immunolabelling for HSP25 and HSP60 was increased in the peri-implantitis group HSP32 immunolabelling slightly decreased in peri-implant and peri-implantitis gingiva. Labelling for HSP72 was undetectable in all three groups. In conclusion, we observed in peri-implantitis a clearly enhanced immunolabelling of two specific HSPs, HSP25 and HSP60, restricted to gingival epithelium and this could indicate a signal of local altered homeostasis.

The extra-cellular matrix of the gingival tissue plays an important role in the homeostasis of dental implants. In this work we have studied immunohistochemically the distribution of collagen I-III-IV-V, tenascin, metalloproteinases (MMP) 1-3-8-13 and TIMP-1 in three groups of patients: (1) subjects with natural teeth (healthy periodontal tissue), (2) subjects with normal peri-implant mucosa and (3) subjects with clinically evident peri-implantitis. The immunolabelling for collagen I-III-IV showed a similar pattern in all three groups. The labelling for collagen V increased in lamina propria of healthy peri-implant tissue and peri-implantitis. Tenascin immunolabelling in healthy and peri-implant tissues was scattered in lamina propria. In peri-implantitis tenascin immunolabelling increased mainly near to the basal lamina. The MMP-1-3-8 and TIMP-1 immunolabelling were very faint and localized in the stroma in all three groups. In healthy and peri-implant tissues MMP-13 immunolabelling was found in the lamina propria whereas in peri-implantitis MMP-13 immunolabelling was also in epithelium. On the whole, these data suggest that in the extracellular matrix of peri-implantitis there are alterations of collagen V, tenascin and MMP-13 patterns.