Objectives: Human T cell leukemia virus type-I (HTLV-I) is a causative agent of human T-cell leukemia and HTLV-I associated myelopathy (HAM/TSP). HTLV-I carriers are often infected vertically, especially via mother's milk. Since 1985, clinical measures have been adopted at a hospital in Okinawa to prevent vertical infections.
Methods: We examined HTLV-I antibodies in all of the women (total 11, 506) who gave birth after 24 gestational weeks at a hospital on the Okinawa main island from January 1985 to December 1999.
Results: The positive rate among all pregnant women was always higher than that among primipara alone. Both figures decreased over the period studied, but the primiparity rate (36-39%) did not change significantly. The percentage of HTLV-I positive primipara pregnant women among the HTLV-I positive total was close to the primiparity rate from 1985 to 1988, but it was considerably lower than the overall primiparity rate thereafter (22-26%).
Conclusions: Preventive measures against HTLV-I infection did not contribute to the decrease in HTLV-I positive mothers before 1999 because these measures were adopted from 1985, and so there must be other reasons for the decrease in HTLV-I positive rate. Further studies on social factors and by year of birth are needed to identify factors influencing HTLV-carrier ratios among pregnant women.

Osteoclasts are bone-specific multinucleated cells generated by the differentiation of monocyte/macrophage lineage precursors. Regulation of osteoclast differentiation is considered an effective therapeutic approach to the treatment of bone-lytic diseases. Periodontitis is an inflammatory disease characterized by extensive bone resorption. In this study, we investigated the effects of sodium fluoride (NaF) on osteoclastogenesis induced by Porphyromonas gingivalis, an important colonizer of the oral cavity that has been implicated in periodontitis. NaF strongly inhibited the P. gingivalis-induced alveolar bone loss. That effect was accompanied by decreased levels of cathepsin K, interleukin (IL)-1β, matrix metalloproteinase 9 (MMP9), and tartrate-resistant acid phosphatase, which were up-regulated during P. gingivalis-induced osteoclastogenesis. Consistent with the in vivo anti-osteoclastogenic effect, NaF inhibited osteoclast formation caused by the differentiation factor RANKL (receptor activator of nuclear factor κB ligand) and macrophage colony-stimulating factor (M-CSF). The RANKL-stimulated induction of the transcription factor nuclear factor of activated T cells (NFAT) c1 was also abrogated by NaF. Taken together, our data demonstrate that NaF inhibits RANKL-induced osteoclastogenesis by reducing the induction of NFATc1, ultimately leading to the suppressed expression of cathepsin K and MMP9. The in vivo effect of NaF on the inhibition of P. gingivalis-induced osteoclastogenesis strengthens the potential usefulness of NaF for treating periodontal diseases.
Acid Phosphatase ; drug effects ; Alveolar Bone Loss ; microbiology ; prevention & control ; Animals ; Anti-Bacterial Agents ; therapeutic use ; Anti-Inflammatory Agents ; therapeutic use ; Bacteroidaceae Infections ; microbiology ; prevention & control ; Bone Density Conservation Agents ; therapeutic use ; Cathepsin K ; drug effects ; Interleukin-1beta ; drug effects ; Interleukin-6 ; analysis ; Interleukin-8 ; drug effects ; Isoenzymes ; drug effects ; Macrophage Colony-Stimulating Factor ; drug effects ; Male ; Matrix Metalloproteinase 9 ; drug effects ; Osteoclasts ; drug effects ; Periodontitis ; microbiology ; prevention & control ; Porphyromonas gingivalis ; drug effects ; RANK Ligand ; drug effects ; Rats ; Rats, Sprague-Dawley ; Sodium Fluoride ; therapeutic use ; Tartrate-Resistant Acid Phosphatase ; Transcription Factors ; drug effects ; X-Ray Microtomography ; methods