The articular cartilage was studied under conditions of experimental osteoarthrosis with tunnelization of the subchondral zone and injection of autologous bone marrow into the channels. Histomorphological studies showed that tunnelization of the subchondral zone with injection of autologous bone marrow into the channels stimulated reparative regeneration of the chondral tissue by inhibiting destruction of the joints.

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The role of subchondral bone in the restoration of the articular cartilage was determined in experiments on mongrel dogs subjected to gonarthrosis modeling followed by subchondral zone tunneling and introduction of bone marrow suspension into the canal. Light microscopy, computer histomorphometry, and electron probe microanalysis showed that stimulation of functional activity of chondrocytes was achieved via correction of homeostasis of the cartilage and subchondral bone and improvement of tissue trophic. Restoration of the microarchitecture of the subchondral bone and improving its vascularization after tunneling with the introduction of bone marrow suspension into the drill holes enhances chondrocyte metabolism and recovers their functionality.

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Reactive and adaptive changes in mechanically uninjured nerves during fracture healing have not been studied previously although the status of innervation is important for bone union and functional recovery. This study explores whether subclinical nerve fibre degeneration occurs in mechanically uninjured nerves in an animal fracture model and to quantify its extent and functional significance. Twenty-four dogs were deeply anaesthetized and subjected to experimental tibial shaft fracture and Ilizarov osteosynthesis. Before fracture and during the experiment, electromyography was performed. In 7, 14, 20, 35–37 and 50 days of fixation and 30, 60–90 and 120 days after fixator removal, the dogs were euthanized. Samples from sciatic, peroneal and tibial nerves were processed for semithin section histology and morphometry. On the 37th postoperative day, M-response amplitudes in leg muscles were 70 % lower than preoperative ones. After fixator removal, these increased but were not restored to normal values. There were no signs of nerve injuries from bone fragments or wires from the fixator. The incidence of degenerated myelin fibres (MFs) was less than 12 %. Reorganization of Remak bundles (Group C nerve fibres—principally sensory) led to a temporal increase in numerical nerve fibre densities. Besides axonal atrophy, the peroneal nerve was characterized with demyelination–remyelination, while tibial nerve with hypermyelination. There were changes in endoneural vessel densities. In spite of minor acute MF degeneration, sustained axonal atrophy, dismyelination and retrograde changes did not resolve until 120 days after fracture healing. Correlations of morphometric parameters of degenerated MF with M-response amplitudes from electromyography underlie the subclinical neurologic changes in functional outcomes after tibial fractures even when nerves are mechanically uninjured.