Technetium-99m(V)-dimercaptosuccinic acid osteotropism in Staphylococcus aureus-induced arthritis regulated by glucose-mediated acidification.

OBJECTIVES

To study the possible mechanism of the technetium-99m complex of dimercaptosuccinic acid 99mTc(V)-DMSA accumulation in a model of Staphylococcus aureus-induced bacterial arthritis regulated by glucose.

MATERIALS AND

METHODS

After making the S. aureus-induced bacterial arthritis model, 14 rabbits were divided into two groups randomly, with one group receiving 6 g/kg 30% glucose administration. Then all the rabbits were injected with 74 MBq 99mTc(V)-DMSA. Whole-body single photon emission computed tomography was applied at different time points. The change of blood pH after blood glucose was also assayed. The percentage of residual activity was evaluated over time in multiple regions of interest, including the inflammatory joint lesions and the contralateral normal joints. Regional joint tissue pH was measured with a needle probe at different times after injecting glucose solution. Forty-two rabbits were divided into six groups to assay the percentage injected dose.

RESULTS

99mTc(V)-DMSA showed a noticeable osteotropic character in bone pathologies. There was no influence of biodistribution of 99mTc(V)-DMSA by glucose loading, but the glucose loading remarkably increased the uptake levels of 99mTc(V)-DMSA in inflammatory joint lesions. A peak difference in glucose-loaded lesion/normal uptake was observed after 6 h. The pH values of the inflammatory joints were noticeably lower than those of the normal joints of the contralateral legs.

CONCLUSION

The increased lesion uptake and tissue acidification in the glucose-loaded group supports the hypothesis that glucose acidosis increases DMSA uptake in bacterial arthritis, as has been observed in tumors.