Abstract: Objective: To identify the potential effects of low-frequency sin-wave alternating electromagnetic fields on bone turnover indices in ovariectomized rats and to provide important evidence for clarifying the potential regulatory mechanism of alternating electromagnetic fields on bone metabolism in ovariectomized rats. Methods: Four-month-old male SD rats (n=36) were randomly and equally assigned into the blank control (Control), ovariectomy (OVX) and ovariectomy with alternating electromagnetic fields stimulation (EMF) groups. The bilateral ovaries for the rats in the OVX and EMF groups were removed to establish the ovariectomized animal model. The rats in the blank control group were also subjected to the opening of the abdominal cavity, but the ovaries were not removed. The rats in the EMF group were exposed to whole-body sin-wave alternating electromagnetic magnetic fields at 15 Hz and 20 Gs with 2 hours per day. The rats in the Control and OVX groups were also placed into the coils which were not activated by the current. After 12 weeks, all rats were sacrificed and the blood samples were collected. The serum calcium and phosphorus concentrations were determined using automatic biochemistry analyzer. Serum OCN, P1NP, TRACP5b and CTX concentrations were measured using the commercial ELISA kits. Results: Alternating electromagnetic fields significantly up-regulated bone formation markers serum OCN and P1NP concentrations (P<0.05), and also significantly down-regulated serum TRACP5b and CTX concentrations (P<0.05). Moreover, alternating electromagnetic fields also exhibited significant effects on the increase of serum calcium and phosphorus concentrations in ovariectomized rats (P<0.05). Conclusion: Alternating electromagnetic fields is capable of increasing bone formation rate, inhibiting bone resorption rate, and enhancing serum calcium and serum phosphorus concentrations in ovariectomized rats. This study provides evidence for clarifying the mechanism by which alternating electromagnetic fields regulate estrogen deficiency-induced osteoporosis.