UDC 611-018.4:616-085

Introduction. Osteopenia is a multifactorial condition that develops under estrogen deficiency and reduced mechanical loading. Experimental models of postmenopausal osteoporosis enable investigation of bone remodeling mechanisms and evaluation of corrective interventions. Aim. To experimentally evaluate the effect of low-intensity whole-body vibration on bone remodeling, mineral component, and nanocomposite structural organization in ovariectomized rats. Materials and Methods. The study was performed on Wistar rats divided into three groups: SHAM-operated, ovariectomized (OVE), and ovariectomized treated with whole-body vibration (OVE+WBV; 50 Hz, 0.3 g, 30 min/ day, 5 days/week) over 24 weeks. Bone remodeling markers (osteocalcin, alkaline phosphatase, TRAP-5b) were assessed, and the structural characteristics of the mineral phase were analyzed using X-ray diffraction. Results. Ovariectomy resulted in a significant decrease in the bone mineral component as early as week 8, which persisted throughout the study. Whole-body vibration prevented early bone loss during weeks 8–16, as evidenced by higher crystalline phase fraction and increased crystallite size compared to the OVE group. Biochemical markers confirmed increased bone remodeling after ovariectomy, while vibration partially modulated these changes. At week 24, the effect of vibration was no longer statistically significant. Conclusions. Low-intensity whole-body vibration attenuates early post-ovariectomy bone loss and modulates bone remodeling processes, reflected by changes in biochemical markers and mineral phase structure. The effect is most pronounced during the early post-ovariectomy period.

Abstract. Long-term glucocorticoid therapy, commonly used because of its potent anti-inflammatory effects, frequently leads to glucocorticoid-induced osteoporosis (GIOP), causing severe bone loss and increased fracture risk. Given the limited effectiveness of current therapies in addressing both bone structural deterioration and impaired bone innervation, we evaluated whether low-dose zoledronic acid (ZOL) could alleviate these detrimental effects on bone architecture and neural integrity in a rat model of GIOP. Thirty-six male Wistar rats were divided into three groups: control (saline), glucocorticoid-treated (methylprednisolone, 3 mg/kg every other day) and glucocorticoid-ZOL-treated (0.025 mg/kg monthly). After 8 and 16 weeks, comprehensive histological and immunohistochemical analyses were performed to assess bone morphology, the expression of osteocalcin (OC), osteoprotegerin (OPG) and receptor activator of nuclear factor kappa-B ligand (RANKL), as well as neural integrity using markers vasoactive intestinal polypeptide (VIP) and protein gene product 9.5 (PGP9.5). Glucocorticoid treatment significantly increased cytokine responses at trabecular bone surfaces, indicating accelerated remodelling and structural deterioration. It also adversely affected the neuronal morphology and distribution within the femoral bone. ZOL partially mitigated glucocorticoidinduced bone structural impairments, significantly reducing trabecular bone loss and remodelling disturbances. Importantly, ZOL did not exacerbate the glucocorticoid-induced neuronal alterations. We conclude that low-dose periodic administration of ZOL effectively reduces glucocorticoid-induced structural deterioration of the femoral bone without negatively influencing neuronal integrity. These findings support ZOL as a potential therapeutic strategy for simultaneously preserving bone health and neural function in glucocorticoid-induced osteoporosis.