Lymphatic architecture of the human gingival interdental papilla.

Many studies have investigated the lymphatic architecture of head and neck using experimental animals, confirming the existence of lymphatic networks beneath the epithelium in gingival tissue. In this study, we investigated the use of these lymphatics as a drug delivery route by studying the architecture of lymphatic vessels in human interdental papilla. Serial cryosections were cut using the film-transfer method. To identify lymphatics, the sections were stained using enzyme histochemical and immunohistochemical techniques and three-dimensional images of lymphatics were reconstructed using 3D visualization software. Capillary lymphatic networks were observed in the lamina propria beneath the epithelium in human interdental papilla, and they joined with lymphatic networks beneath the epithelium in free gingiva. The networks consisted of a single layer of large irregular, hexagonal meshes and precollecting lymphatic vessels heading toward collecting lymphatic vessels that exited on the periosteum of the alveolar crest. These findings suggest that lymphatic flow from the interdental papilla drains into collecting lymphatic vessels running buccolingually on the alveolar crest of the interdental papilla. This may be an important anatomical feature during inflammation throughout the oral cavity in that the drainage function is maintained by part of lymphatic flow that is not impaired during the healing process.

[Acute myeloblastic leukemia showing pronounced skin infiltration during administration of low-dose cytarabine and etoposide with granulocyte colony-stimulating factor].

A 26-year-old woman was admitted to our hospital for lumbago on November 29, 1995. The white blood cell count was 6,500/microliter with 26.5% myeloblasts and the bone marrow was hyperplastic due to myeloblasts. Myeloblasts were negative for myeloperoxidase and positive for alpha-naphthyl butylate esterase, CD11a (89%), CD11b (38%), CD11c (92%), CD33 (91%) and HLA-DR (58%). Chromosomal abnormalities were recognized: 46, XX, t(9;11) (p22;q23), 45, XX, -7, t(9;11) (p22;q23) and 47, XX, +19, t(9;11) (p22;q23). Acute myeloblastic leukemia (M5a) was diagnosed. Disseminated intravascular coagulation was also present. The patient received induction therapy and achieved remission on January 9, 1996, but myeloblasts increased to 3.6% in bone marrow despite consolidation therapy. Low doses of cytarabine (AraC) and etoposide were instituted on March 7, granulocyte colony-stimulating factor (G-CSF) was started on March 15, and pronounced skin infiltration developed on March 18. The patient received reinduction therapy from April 16 and administration of G-CSF was combined for 2 days, and a marked increment of myeloblasts in the peripheral blood was observed. After discontinuation of G-CSF, myeloblasts decreased and skin infiltration disappeared. However, the patient died of cerebral infiltration on June 30. The response of myeloblasts to G-CSF by in vitro liquid culture was noteworthy. The present case stresses the requirement for great caution to be exercised in the use of G-CSF in patients receiving low dose AraC.