Part of the book: Periodontal Diseases
Periodontal tissues exhibit important vascular, lymphatic, and nervous connections with the rest of the body. Thus, periodontal inflammation caused by the interaction between the subgingival bacterial biofilm and the host immune response has an impact reaching further than the oral cavity. The concept of “periodontal medicine” reunites the bidirectional relationships that exist between periodontal disease and systemic conditions such as diabetes mellitus or cardiovascular disease. The chronic inflammation of hepatic tissues during hepatitis C virus (HCV) infection causes changes in the general homeostasis that can reverberate at periodontal level and influence periodontal inflammation. Various mechanisms such as insulin resistance or pro-inflammatory cytokines production could be the link between the two conditions. In addition, periodontal inflammation could impact HCV transmission, as HCV RNA molecules and antibodies have been found in infected patients’ saliva and gingival fluid. During periodontal inflammation, gingival bleeding is frequent, and the viral molecules could enter oral fluids while being carried by peripheral blood cells. Clinical particularities that suggest the onset of periodontal disease have also been frequently observed in HCV-infected patients. The connections between periodontal disease and hepatitis C need to take into consideration by practitioners of both specialties due to their important implications on clinical manifestations and treatment strategies.
Part of the book: Hepatitis C
Due to brain plasticity, the nervous system is capable of manifesting behavioral variations, adapted to the influences from both external and internal environment. Multiple neurotransmitters are involved in the mediation of pathological processes at the molecular, cellular, regional, and interregional levels participating in cerebral plasticity, their intervention being responsible for various structural, functional, and behavioral disturbances. The current therapeutic strategies in neuroprotection aim at blocking on different levels, the molecular cascades of the pathophysiological mechanisms responsible for neuronal dysfunctions and ultimately for neuronal death. Different agents influencing these neurotransmitters have demonstrated beneficial effects in neurogenesis and neuroprotection, proved in experimental animal models of focal and global ischemic injuries. Serotonin, dopamine, glutamate, N-methyl-D-aspartate, and nitric oxide have been shown to play a significant role in modulating nervous system injuries. The imidazoline system is one of the important systems involved in human brain functioning. Experimental investigations have revealed the cytoprotective effects of imidazoline I2 receptor ligands against neuronal injury induced by hypoxia in experimental animals. The neuroprotective effects were also highlighted for kappa and delta receptors, whose agonists demonstrated the ability to reduce architectural lesions and to recover neuronal functions of animals with experimentally induced brain ischemia.
Part of the book: Neuroprotection
The bacterial challenge on the periodontal tissues triggers an inflammatory reaction, driven by pro-inflammatory cytokines, that eventually leads to the periodontal structures’ damage. The pathogenic mechanisms of this inflammatory reaction are complex and are influenced by the type of host-immune response and certain local and systemic factors. These factors can influence periodontal inflammation, through the action of the various pro-inflammatory cytokines. Periodontal disease and certain systemic conditions can have a mutual association, as the pathogenic mechanisms of these diseases can involve similar molecular and cellular elements. The concept of ‘periodontal medicine’ comprises these pathogenic connections, focusing on the key role that periodontal health has on the general homeostasis and well-being.
Part of the book: Cytokines