Periodontitis is an oral chronic infection/inflammatory condition, identified as a source of mediators of inflammation into the blood circulation, which may contribute to exacerbate several diseases. There is increasing evidence that inflammation plays a key role in the pathophysiology of Alzheimer’s disease (AD). Although inflammation is present in both diseases, the exact mechanisms and crosslinks between periodontitis and AD are poorly understood. Therefore, this article aims to review possible comorbidity between periodontitis and AD. Here, the authors discuss the inflammatory aspects of periodontitis, how this oral condition produces a systemic inflammation and, finally, the contribution of this systemic inflammation for worsening neuroinflammation in the progression of AD.

Tissue engineering is an emerging field of science that focuses on creating suitable conditions for the regeneration of tissues. The basic components for tissue engineering involve an interactive triad of scaffolds, signaling molecules, and cells. In this context,

Massive infantile spasms (MIS), a seizure disorder unique to infants, is considered an agedependent response of the immature brain to various insults and stressors. The seizures improve with ACTH and glucocorticoids, both major components of the brain-adrenal axis. We hypothesized that CNS levels of these hormones are abnormal in infants with MIS and studied CSF from 14 infants with MIS and 13 age-matched controls by analysis for corticotropin-releasing hormone (CRH), ACTH, cortisol, and interleukin-1-beta. ACTH levels in CSF of patients were significantly lower than those of controls, but differences in cortisol levels between patients and controls were not statistically significant. CRH levels in both groups were similar and fluctuated diurnally. These results indicate an alteration of specific CNS components of the brain-adrenal axis in MIS.Massive infantile spasms (MIS), or West syndrome, consists of myoclonic seizures, hypsarrhythmic EEG, and subsequent mental retardation. 1-4 MIS is age-specific: onset of spasms is usually between the third and ninth postnatal month, and rarely after the first year. [1][2][3] Since MIS occurs in one of 2,400 to 4,000 live births and the majority of patients have long-term cognitive sequelae, the entity is an important cause of mental retardation. 1,5 MIS has been associated with structural abnormalities, neurocutaneous syndromes, intrauterine infections, metabolic aberrations, meningitis, encephalitis, and cerebral infarcts. [1][2][3][4] Infants with MIS and other neurologic abnormalities (symptomatic) are distinguished from those with no known etiology for the seizures (cryptogenic). The cryptogenic group is further subdivided by the neurologic examination (normal or delayed).The pathophysiology of MIS is unclear. The common denominator of infants with symptomatic MIS is the past occurrence of a major CNS insult or stress. 6 Thus, MIS has been considered a unique, age-dependent manifestation of stress or injury to the immature brain. 6,7 The therapy of MIS remains unsatisfactory. Conventional anticonvulsants, with the possible exception of benzodiazepines, are generally ineffective. [1][2][3][4] Benzodiazepines, including nitrazepam, may be less effective than corticotropin (ACTH) and glucocorticoids (GC). 1,8 Since the original administration of ACTH by Sorel in the late 1950s, ACTH and steroids have been the mainstay of therapy. 1,9 Numerous uncontrolled studies, as well as a doubleblinded and controlled one, 10 have shown their efficacy to be 60 to 70%. Control of the spasms themselves, moreover, may not affect the overall outcome: mental retardation occurs We hypothesize that ACTH and GC are efficacious in MIS because they counteract an abnormality of the brain-adrenal axis. Such abnormalities might include increased abundance of corticotropin-releasing hormone (CRH) or a reduction of ACTH. Methods Patient populationInfants presenting to the neurology service of Childrens Hospital of Los Angeles (CHLA) between July 1988 and March 1991 with a clinical diagnosis...

The aim of this study was to assess the performance of glass ionomer cement (GIC) added with TiO2 nanotubes. TiO2 nanotubes [3%, 5%, and 7% (w/w)] were incorporated into GIC's (Ketac Molar EasyMix™) powder component, whereas unblended powder was used as control. Physical-chemical-biological analysis included energy dispersive spectroscopy (EDS), surface roughness (SR), Knoop hardness (SH), fluoride-releasing analysis, cytotoxicity, cell morphology, and extracellular matrix (ECM) composition. Parametric or nonparametric ANOVA were used for statistical comparisons (α ≤ 0.05). Data analysis revealed that EDS only detected Ti at the 5% and 7% groups and that GIC's physical-chemical properties were significantly improved by the addition of 5% TiO2 as compared to 3% and GIC alone. Furthermore, regardless of TiO2 concentration, no significant effect was found on SR, whereas GIC-containing 7% TiO2 presented decreased SH values. Fluoride release lasted longer for the 5% and 7% TiO2 groups, and cell morphology/spreading and ECM composition were found to be positively affected by TiO2 at 5%. In conclusion, in the current study, nanotechnology incorporated in GIC affected ECM composition and was important for the superior microhardness and fluoride release, suggesting its potential for higher stress-bearing site restorations.

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