Pathomorphological Features of Diabetic Myopathy in Comorbid Conditions

Background/Objectives: Despite advances in diagnostic, preventive, and therapeutic strategies, diabetes mellitus remains a major global medico-social challenge with a high rate of complications, including diabetic myopathy. However, structural and functional changes in the masticatory muscles and disturbances of myodynamic balance in diabetes under stress remain insufficiently studied. This research aimed to clarify the pathomorphological patterns of diabetic myopathy development under chronic immobilization stress. Methods: Twenty-eight six-month-old male albino rats were equally divided into four groups: Group 1—streptozotocin-induced diabetes mellitus (SIDM) combined with chronic immobilization stress (CIS); Group 2—SIDM; Group 3—CIS; Group 4—control. Samples were collected on day 56. Histological, electron microscopy, biochemical, and statistical methods were applied. Results: Myopathy in experimental conditions was characterized by aseptic myositis, focal fibrosis of the masticatory muscle, muscle fiber atrophy, and peripheral neuropathy. These changes developed on the background of pronounced diabetic microangiopathy, manifested by hemorheological disturbances, reduced vascular capacity of the haemomicrocirculatory bed (confirmed by an increased Vogenvort index), thickening and proliferation of the capillary basement membrane, and decreased capillary density. Degenerative muscle fiber alterations included vacuolar dystrophy, necrosis, ferroptosis, necroptosis, and autolysis. Neuropathic changes involved segmental demyelination, axonal atrophy, decreased sprouting, and extensive neuromuscular junction destruction, possibly leading to impaired neuromuscular transmission. Conclusions: Chronic immobilization stress acts as a trigger that aggravates diabetic myopathy progression by impairing microcirculation and inducing neuromuscular junction damage, resulting in subsequent muscle atrophy.