The aim of this survey was to determine the prevalence of oral mucosa lesions in children aged 4-13 yr from two schools, one (S1) having a higher socioeconomic status than the other (S2). In all, 846 children were examined, 463 from S1 and 383 from S2, of whom 555 were boys and 291 were girls. There were 359 boys and 104 girls in S1; 196 boys and 187 girls in S2. Fifteen different lesion types were discerned. The most frequent ones were recurrent aphthous ulceration (RAU) (92 cases); fissured cheilitis (54); herpes labialis (44); angular cheilitis (30); geographic tongue (25); smooth tongue (22); and plicated tongue (17). An outstanding finding was the contrasting distribution of certain lesion types in the two schools. RAU was observed in 19% of the children from S1, making up 50% of all lesions detected. However, in S2 only 2% exhibited RAU, making up less than 4% of observed lesions. On the other hand, herpes labialis was seen in 1% of S1 and 10% of S2 children, regardless of age or sex. Plicated tongue was found in 3.2% in S1 and 0.5% in S2; fissured cheilitis in 2.9% in S1 and 12.8% in S2; and angular cheilitis in 1.1% in S1 and 6.5% in S2. Therefore, there were no statistical differences between the schools in the ratio of total lesions observed to children examined, but a significant difference was apparent when individual lesions were taken into account.

Along the last years it has been demonstrated that non-neural cells play a major role in the pathogenesis of the primary degenerative disorders (PDDs) of the human central nervous system. Among them, astrocytes coordinate and participate in many different and complex metabolic processes, in close interaction with neurons. Moreover, increasing experimental evidence hints an early astrocytic dysfunction in these diseases. In this mini review we summarize the astrocytic behavior in PDDs, with special consideration to the experimental observations where astrocytic pathology precedes the development of neuronal dysfunction. We also suggest a different approach that could be consider in human investigations in Alzheimer’s and Parkinson’s disease. We believe that the study of PDDs with human brain samples may hold the key of a paradigmatic physiopathological process in which astrocytes might be the main players.

Despite the fact that astrocytes are the most abundant glial cells, critical for brain function, few studies have dealt with their possible role in neurodegenerative diseases like Parkinson's disease (PD). This article explores relevant evidence on the involvement of astrocytes in experimental PD neurodegeneration from a molecular signaling perspective. For a long time, astrocytic proliferation was merely considered a byproduct of neuroinflammation, but by the time being, it is clear that astrocytic dysfunction plays a far more important role in PD pathophysiology. Indeed, ongoing experimental evidence suggests the importance of astrocytes and dopaminergic neurons' cross-linking signaling pathways. The Wnt-1 (wingless-type MMTV integration site family, member 1) pathway regulates several processes including neuron survival, synapse plasticity, and neurogenesis. In PD animal models, Frizzled (Fzd) neuronal receptors' activation by the Wnt-1 normally released by astrocytes following injuries leads to β-catenin-dependent gene expression, favoring neuron survival and viability. The transient receptor potential vanilloid 1 (TRPV1) capsaicin receptor also participates in experimental PD genesis. Activation of astrocyte TRPV1 receptors by noxious stimuli results in reduced inflammatory response and increased ciliary neurotrophic factor (CNTF) synthesis, which enhances neuronal survival and differentiation. Another major pathway involves IκB kinase (IKK) downregulation by ARL6ip5 (ADP-ribosylation-like factor 6 interacting protein 5, encoded by the cell differentiation-associated, JWA, gene). Typically, IKK releases the proinflammatory NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) molecule from its inhibitor. Therefore, by downregulating NF-κB inhibitor, ARL6ip5 promotes an anti-inflammatory response. The evidence provided by neurotoxin-induced PD animal models guarantees further research on the neuroprotective potential of normalizing astrocyte function in PD.

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