This work is devoted to the chemical synthesis of sulfated chitosan and its experimental verification in an animal model of early atherosclerosis. The method of chitosan quaternization with sulfate-containing ingredients resulted in a product with a high content of sulfate groups. Implantation of this product into the fascial-muscular sheath of the main limb artery along the leg and thigh in rabbits led to the extraction of cholesterol from the subintimal region. Simplified methods for the chemical synthesis of quaternized sulfated chitosan and the use of these products in a model of experimental atherosclerosis made it possible to perform a comparative morphological analysis of the vascular walls of the experimental and control limbs under conditions of a long-term high-cholesterol diet. The sulfated chitosan samples after implantation were shown to change the morphological pattern of the intimal and middle membranes of the experimental limb artery. The implantation led to the degradation of soft plaques within 30 days after surgical intervention, which significantly increased collateral blood flow. The implantation of sulfated chitosan into the local area of the atherosclerotic lesions in the artery can regulate the cholesterol content in the vascular wall and destroy soft plaques in the subintimal region.

It is known that complexes based on natural polysaccharides are able to eliminate bone defects. Prolonged hyperglycemia leads to low bone regeneration and a chronic inflammatory response. The purpose of this study was to increase the efficiency of early bone formation in a cavity of critical size in diabetes mellitus in the experiment. The polyelectrolyte complex contains high-molecular ascorbate of chitosan, chondroitin sulfate, sodium hyaluronate, heparin, adgelon serum growth factor, sodium alginate and amorphous nanohydroxyapatite (CH–SA–HA). Studies were conducted on five groups of white female Wistar rats: group 1—regeneration of a bone defect in healthy animals under a blood clot; group 2—regeneration of a bone defect under a blood clot in animals with diabetes mellitus; group 3—bone regeneration in animals with diabetes mellitus after filling the bone cavity with a collagen sponge; group 4—filling of a bone defect with a CH–SA–HA construct in healthy animals; group 5—filling of a bone defect with a CH–SA–HA construct in animals with diabetes mellitus. Implantation of the CH–SA–HA construct into bone cavities in type I diabetic rats can accelerate the rate of bone tissue repair. The inclusion of modifying polysaccharides and apatite agents in the construction may be a prospect for further improvement of the properties of implants.

The chapter is devoted to the research of experimental complete mechanical spinal injury in adult rats and attempts at bioengineering restoration of the structure and function of the spinal cord using a protein-polysaccharide construct that includes bovine collagen, highly purified crab chitosan ascorbate, nanostructuring additives in the form of sodium chondroitin sulfate, sodium hyaluronate, heparin sulfate in the presence of complete nutrient medium DMEM, neural supplement N2, conditioned nutrient medium, obtained about brain cell mouse embryos and mouse embryonic stem cells, retinoic acid, and mouse neural progenitor cells derived from embryonic stem cells. After a complete intersection of the spinal cord at the level of the ninth thoracic vertebra, the authors directly implanted a collagen-chitosan construct into the gap between the ends of the spinal cord. Analysis of the recovery of motor and sensory and vegetative functions of the spinal cord for 20 weeks after surgery using the cytological immune-fluorescent method showed a high viability of the transplanted neural cell precursors during the entire observation period and the early emergence of activity of mediators of nerve signal transmission in the implantation zone of the structure with accompaniment active dynamics of reducing neurodeficiency.

A biomaterial is proposed for closing extensive bone defects in the maxillofacial region. The composition of the biomaterial includes high-molecular chitosan, chondroitin sulfate, hyaluronate, heparin, alginate, and inorganic nanostructured hydroxyapatite. The purpose of this study is to demonstrate morphological and histological early signs of reconstruction of a bone cavity of critical size. The studies were carried out on 84 white female rats weighing 200–250 g. The study group consisted of 84 animals in total, 40 in the experimental group and 44 in the control group. In all animals, three-walled bone defects measuring 0.5 × 0.4 × 0.5 cm³ were applied subperiosteally in the region of the angle of the lower jaw and filled in the experimental group using lyophilized gel mass of chitosan–alginate–hydroxyapatite (CH–SA–HA). In control animals, the bone cavities were filled with their own blood clots after bone trepanation and bleeding. The periods for monitoring bone regeneration were 3, 5, and 7 days and 2, 3, 4, 6, 8, and 10 weeks. The control of bone regeneration was carried out using multiple morphological and histological analyses. Results showed that the following process is an obligatory process and is accompanied by the binding and release of angiogenic implantation: the chitosan construct actively replaced early-stage defects with the formation of full-fledged new bone tissue compared to the control group. By the 7th day, morphological analysis showed that the formation of spongy bone tissue could be seen. After 2 weeks, there was a pronounced increase in bone volume (p < 0.01), and at 6 weeks after surgical intervention, the closure of the defect was 70–80%; after 8 weeks, it was 100% without violation of bone morphology with a high degree of mineralization. Thus, the use of modified chitosan after filling eliminates bone defects of critical size in the maxillofacial region, revealing early signs of bone regeneration, and serves as a promising material in reconstructive dentistry.

Damage to peripheral arteries by the atherosclerotic process accounts for about 3% of the world's population, which puts this problem in the category of major social problems. Modified lipoproteins and cholesterol crystals are known to accumulate in the arterial intima and cause the formation of proatherogenic macrophages, foam cells, and inflammation. Defective efferocytosis of apoptotic foam cells leads to the formation of a necrotic core, a sign of failure to resolve inflammation. Resolution of inflammation is mediated by specialized pro-resorption lipid mediators, proteins and signaling gases. Improving the balance between pro-inflammatory and anti-inflammatory factors contributes to the reverse development of local atherogenesis. Active direct intervention in the reconstruction of the adventitial layer of the arterial wall using cholesterol-affinity polysaccharide hydrogels containing a cocktail of growth factors creates conditions for the formation of additional extracellular matrix and reversal of cholesterol mass from the subintimal zone. Creating concentration and electrostatic gradients in the adventitia zone using a hydrogel may be one of the effective ways to degrade early soft atherogenic plaques and locally restore the damaged structure of the vessel wall. Growing scientific interest in the previously insufficiently studied adventitia indicates its important role in angionesis and atherogenesis.