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Osteoprotegerin (OPG), a member of the tumour necrosis factor receptor (TNFR) superfamily of proteins known to be involved in a large number of biological systems, plays a pivotal role in bone remodelling. In addition to the roles of OPG in bone metabolism, it has been reported to be associated with a high cardiovascular risk in patients with metabolic syndrome. In most cases, the exact functions of OPG remain to be established; however, the widespread expression of OPG suggests that this molecule may have multiple biological activities, mainly in the cardiometabolic environment. The aim of this study was to evaluate the value of OPG as a predictive marker for cardiovascular and metabolic risk in osteoporotic patients. The study group comprised patients with osteoporosis, in order to evaluate the association between OPG serum levels and cardiovascular pathology. Our results revealed significant correlations between classical biochemical bone and metabolic parameters, such as osteocalcin and parathyroid hormone with lipid and glucose biomarkers, sustaining the crosstalk between calcium and bone parameters and cardiovascular risk. The OPG serum level proved to have a significant and independent predictive value for metabolic syndrome (MetS) as a cardiovascular risk standard in osteoporotic patients. The OPG serum levels were increased in patients with MetS as a protective response against the atherosclerotic lesions. The serum levels of 25-hydroxy vitamin D had significant and independent predictive value for cardiovascular and metabolic risk in our subjects, sustaining the active role of vitamin D beyond the area of bone metabolism.

A drug administered in the same dosage, under similar conditions, to adult individuals from a population homogeneous in race, gender and age, triggers different pharmacological effects. This phenomenon represents the pharmacological variability in a relatively homoge‐ neous population, as a natural expression of the biological variability of the response to any stimulus. The cause of the pharmacological variability to a drug is often considerably differ‐ ent between the individuals of the same population. The pharmacology variability (pharma‐ cokinetics, pharmaco-dynamics and pharmaco-toxicological) is therefore of two types: interindividual (on population level) and, respectively, intra-individual (on individual level).

The neurons represent unique anatomical fractions, with the ability to forward the information in a network system, which justifies the experience-dependent mechanisms such as memorization, learning or consciousness. In order to fulfill these functions, the neurons are, structurally and functionally polarized. This aspect is obvious in their tripartite composition: cell body, axon and dendrites. While the body comprises the biosynthesis structure (nucleus, ribosomes, endoplasmic reticulum, Golgi apparatus and mitochondria for energy storage), the axon is equipped with molecular and under-cellular components for the propagation of the action potential from the cell body to distant targets, the dendrites represent a set of branched endings which prolong from the cell body and have as result an increase of it, in order to receive the signal. The structural connections for the signal transmission are the basis of the neural architecture. Inside the mature nervous system, normally, the neural circuit (neuroarchitecture) supports adaptive changes. Inside an old synapses neural cells can involute (until their disappearance), with simultaneous formation of new branches (new neuritis) which will establish new synapses. These changes in the neurotic and synaptic architecture prove the great plasticity (capacity) of the nervous system to adapt to the environmental conditions. Today we consider that there are two major intracellular classes of factors (signals) which adjust the neuronal development and adaptation: growth factors (the growth factor fibroblasts, the ciliary neutrophil factor, etc.) and the neurotransmitters factors (dopamine, serotonin, acetylcholine, glutamate, etc.). The loss of balance between the two systems of factors leads to the development of the pathological states.

The effect of smoking is in our days a serious global public health problem of major concern. Incidence of oral squamous cell carcinoma (SCC) in cigarette smokers is four to seven times higher than in nonsmokers. There is a constant and direct attack of various cigarette smoke constituents on the oral epithelial cells, which gradually accumulate and cause malignant transformation. Saliva is the first biological fluid that encounters inhaled cigarette smoke (CS). We have studied the influence of CS on salivary antioxidant capacity, uric acid, amylase and LDH (lactate dehydrogenase). In our study both, gas and particulate phase of CS were tested separately, and possible antioxidant effect of pyridoxine on salivary components was examined. Our results indicate that exposure to both, gas and particulate phase of CS caused a statistically significant decrease in salivary uric acid, LDH and amylase activity. We have also studied the effect of vitamin C (10 mg/dl) and vitamin B6 (1 mM) during incubation of saliva in the presence of CS. The addition of vitamin C had a significant (p0.05) protective effect on salivary uric acid level (0.25 +/- 0.12 for saliva incubated with gas phase of CS vs. 0.65 +/- 0.12 for saliva incubated with gas phase of CS in the presence of vitamin C). Vitamin C was not able to maintain/restore the original uric acid level. In the presence of the gas phase, pyridoxine had no protective effect, neither on salivary uric acid level nor on the FRAP activity of saliva. The purpose of our study was to discover a connection between the level of antioxidants in saliva in the presence of the two components of CS. Our results show that salivary antioxidant system is significantly and distinctly affected by both gas and particulate phase of CS and suggest that an adequate intake of antioxidants may help smokers to avoid CS-induced oxidative damage and to prevent degenerative diseases.