A New Way to Model Periodontitis in Laboratory Animals.

The prevalence of periodontal diseases is increasing, tends to increase with age and is considered as one of the main causes of tooth loss. To assess the effectiveness of new methods of treatment of periodontal diseases, studies on laboratory animals can be promising. THE AIM OF THE STUDY: to develop a new method of accelerated modeling of experimental periodontitis on laboratory animals. MATERIAL AND METHODS: The study was carried out on 22 female rats. A wire ligature was applied to the cervical area of the incisors of the animals in an eight-shaped manner. Plaque obtained from a patient with periodontitis was placed under the wire, and nicotine and ethyl alcohol solutions were injected under the gingival mucosa. A complex index has been proposed to assess inflammation. At the end of the experiment the animals were euthanized, their jaws were dissected into dentoalveolar blocks and further descriptive histologic analysis was performed. RESULTS: On the second day the gingiva of the rats acquired a cyanotic-pink color, on the fourth day the consistency of the gingiva became friable, mobility appeared in the lower incisors. Complex index of inflammation in animals of the main group: before the study-9, on the 7th day-195. Gingival preparations showed signs of exudative inflammation. In alveolar processes-irreversible resorption of bone structures. The difference of indicators in animals before and after the experiment was statistically significant (p < 0.05). CONCLUSION: The new experimental model of periodontitis is reproduced in a short period of time, provides intensive development of inflammation, leads to disruption of the integrity of epithelial and connective tissue attachment, destruction of alveolar bone.

Intermittent hypoxia stimulates formation of binuclear neurons in brain cortex- a role of cell fusion in neuroprotection?

Oligodendrocyte fusion with neurons in the brain cortex is a part of normal ontogenesis and is a possible means of neuroregeneration. Following such fusion, the oligodendrocyte nucleus undergoes neuron-specific reprogramming, resulting in the formation of binuclear neurons, which doubles the functional capability of the neuron. In this study, we tested the hypothesis that the formation of binuclear neurons is involved in long-term adaptation of the brain to intermittent hypobaric hypoxia, which is known to be neuroprotective. Rats were adapted to hypoxia in an altitude chamber at a simulated altitude of 4000 m above sea level for 14 days (30 min increasing to 4 h, daily). One micrometer sections of the left motor cortex were analyzed by light microscopy. Phases of the fusion and reprogramming process were recorded, and the number of binuclear neurons was counted for all section areas containing pyramidal neurons of layers III-V. For the control group subjected to sham hypoxia, the density of binuclear neurons was 4.49 ± 0.32 mm(2). In the hypoxia-adapted group, this density increased to 5.71 ± 0.39 mm(2) (P < 0.04). In a subgroup of rats exposed to only one hypoxia session, the number of binuclear neurons did not differ from the number observed in the control group. We suggest that the increased content of binuclear neurons may serve as a structural basis for the neuroprotective effects of the adaptation to hypoxia.

Increased cell fusion in cerebral cortex may contribute to poststroke regeneration.

In this study, we used a model of a hemorrhagic stroke in a motor zone of the cortex in rats at the age of 3 months The report shows that cortical neurons can fuse with oligodendrocytes. In formed binuclear cells, the nucleus of an oligodendrocyte undergoes neuron specific reprogramming. It can be confirmed by changes in chromatin structure and in size of the second nucleus, by expression of specific neuronal markers and increasing total transcription rate. The nucleus of an oligodendrocyte likely transforms into a second neuronal nucleus. The number of binuclear neurons was validated with quantitative analysis. Fusion of neurons with oligodendrocytes might be a regenerative process in general and specifically following a stroke. The appearance of additional neuronal nuclei increases the functional outcome of the population of neurons. Participation of a certain number of binuclear cells in neuronal function might compensate for a functional deficit that arises from the death of a subset of neurons. After a stroke, the number of binuclear neurons increased in cortex around the lesion zone. In this case, the rate of recovery of stroke-damaged locomotor behavior also increased, which indicates the regenerative role of fusion.