The central nervous system (CNS) is protected by a highly selective barrier, the blood-brain barrier (BBB), that regulates the exchange and homeostasis of bloodborne molecules, excluding xenobiotics. This barrier forms the first line of defense by prohibiting pathogens from crossing to the CNS. Aging and chronic exposure of the BBB to pathogens renders it permeable, and this may give rise to pathology in the CNS such as Alzheimer’s disease (AD). Researchers have linked pathogens associated with periodontitis to neuroinflammation and AD-like pathology in vivo and in vitro. Although the presence of periodontitis-associated bacteria has been linked to AD in several clinical studies as DNA and virulence factors were confirmed in brain samples of human AD subjects, the mechanism by which the bacteria traverse to the brain and potentially influences neuropathology is unknown. In this review, we present current knowledge about the association between periodontitis and AD, the mechanism whereby periodontal pathogens might provoke neuroinflammation and how periodontal pathogens could affect the BBB. We suggest future studies, with emphasis on the use of human in vitro models of cells associated with the BBB to unravel the pathway of entry for these bacteria to the CNS and to reveal the molecular and cellular pathways involved in initiating the AD-like pathology. In conclusion, evidence demonstrate that bacteria associated with periodontitis and their virulence factors are capable of inflecting damage to the BBB and have a role in giving rise to pathology similar to that found in AD.

Objective The aim of this experimental study was to test the possibility of applying internal sinus elevation techniques using controlled hydrodynamic or pneumatic pressure and evaluate their elevation effectiveness. Materials and methods A device was specially designed for this study and was used to elevate the sinus membrane internally in 12 halves of freshly slaughtered sheep heads. The sample was divided into two groups randomly according to the type of controlled pressure applied (hydrodynamic or pneumatic). The elevation height of the membrane was measured in addition to investigating the presence or absence of perforation. Results The maxillary sinus membranes started to be elevated at an average pressure value of 21.6 ± 7.5 millibars (mbar) when hydrodynamic pressure was applied, and at an average pressure value of 23.3 ± 8.1 mbar when pneumatic pressure was applied. The mean values ​​of elevation height after applying the controlled hydrodynamic and pneumatic pressure were 13.00 ± 2.76 and 10.33 ± 3.88 mm, respectively. No perforations occurred in either of the groups. Conclusions The use of a controlled hydrodynamic or pneumatic pressure, which is appropriate for the characteristics of the maxillary sinus membrane in the process of internal elevation, is effective, and it yielded an amount of lifting similar to that we get when using the external elevation.

The central nervous system (CNS) is protected by a highly selective barrier, the blood-brain barrier (BBB), that regulates the exchange and homeostasis of bloodborne molecules, excluding xenobiotics. This barrier forms the first line of defense by prohibiting pathogens from crossing to the CNS. Aging and chronic exposure of the BBB to pathogens renders it permeable, and this may give rise to pathology in the CNS such as Alzheimer’s disease (AD). Researchers have linked pathogens associated with periodontitis to neuroinflammation and AD-like pathology in vivo and in vitro. Although the presence of periodontitis-associated bacteria has been linked to AD in several clinical studies as DNA and virulence factors were confirmed in brain samples of human AD subjects, the mechanism by which the bacteria traverse to the brain and potentially influences neuropathology is unknown. In this review, we present current knowledge about the association between periodontitis and AD, the mechanism whereby periodontal pathogens might provoke neuroinflammation and how periodontal pathogens could affect the BBB. We suggest future studies, with emphasis on the use of human in vitro models of cells associated with the BBB to unravel the pathway of entry for these bacteria to the CNS and to reveal the molecular and cellular pathways involved in initiating the AD-like pathology. In conclusion, evidence demonstrates that bacteria associated with periodontitis and their virulence factors are capable of inflecting damage to the BBB and have a role in giving rise to pathology similar to that found in AD.

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