The pediatric AIDS epidemic began in the U.S.A. between 1983 and 1985. Hemophilia patients were among the first victims of this disease with the majority of these patients infected prior to 1984. At the South Texas Hemophilia Center 69 of 108 patients less than 21 years of age demonstrated serologic evidence of infection. Of these patients, 6 subsequently developed malignancies between 1987 and 1994. Between 1992 and 1996 data was subsequently accumulated on the development of malignancy in HIV positive patients through the Pediatric Oncology Group, which to date has enrolled 24 HIV positive children with malignancy. In these studies the majority of patients had B cell, non-Hodgkin's lymphomas, however approximately 20% of the patients were identified with leiomyosarcomas. Histologic studies of tumors of 6 children with AIDS and leiomyosarcomas or leiomyoma identified the EBV receptor or CD 21 in the tumor using immunoperoxidase techniques, whereas similar staining was not seen in smooth muscle tumors from HIV negative children. In situ hybridization techniques identified EBV-EBER probe in the tumors from HIV positive patients. In 2 patients with adequate tumor tissue EBV genome was present in high concentration using PCR techniques and Southern blot studies showed a monoclonal and biclonal proliferation. Other laboratories have reported similar EBV findings in lymphomas from AIDS patients. Thus EBV appears to be an important cofactor in development of malignancy in pediatric AIDS patients.
An attempt was made to explore the myeloperoxidase (MPO) activity in medium used for incubation of peripheral venous blood (PVB) leukocytes from patients with gingivitis and periodontitis and to compare it with that of periodontally healthy subjects. The study population included 54 gingivitis patients (G), 52 periodontitis patients (P) and 52 control subjects (C). All these groups were assessed by clinical, laboratory and statistical methods. The leukocytes were incubated with opsonized zymosan, Escherichia coli ATCC25922, nonopsonized E.coli or Staphylococcus aureus 256. The respective levels of MPO activity in incubation media of PVB leukocytes taken from group G patients were 598.0±29.2 conventional units (c. u.), 640.0±26.3 c. u., 662.0±37.6 c. u. and 750.0±40.8 c. u. (control incubation medium : 564.0±25.1 c. u.); those for group P patients were 672.0±34.3 c. u., 678.0±43.1 c. u., 692.0±47.9 c. u. and 762.0±34.7 c. u. (control : 612.0±35.2 c. u.); those for group C subjects were 556.0±30.2 c. u., 714.0±28.2 c. u., 1 276.0±69.0 c. u. and 794.0±47.1 c. u. (control : 534.0±29.0 c. u.). MPO activity was increased most significantly when nonopsonized E.coli was added to the incubation medium of PVB leukocytes taken from subjects with intact periodontium. MPO activity was unchanged when the leukocytes were taken from periodontitis patients.
A study was conducted in rats and rabbits to histologically evaluate the effect of acute and late interruption of blood supply on the myenteric plexus located between the circular and longitudinal layers of the muscularis externa (Auerbach's plexus). An intestinal segment measuring 2 cm in rats and approximately 8cm in rabbits was sectioned and isolated on a mesenteric vascular pedicle. Animals in Group underwent clamping of the vascular pedicle for 1, 2, 3, 4, 5 or 6 h. There were 5 animals in each of these subgroups. Group : Intestinal segments with intact vascular pedicles were transferred from the abdominal cavity into the subcutaneous space. Groups with 5 animals in each underwent pedicle ligation immediately and at 1, 2, 3 or 4 weeks after the first operation. Three days later, histological studies were carried out. Injury to the myenteric plexus and the longitudinal muscle was observed in the viable intestinal segments when the mesenteric vascular pedicle was clamped for 4 to 5 h. Similar findings were observed when the pedicle was ligated within 1 to 2 weeks after grafting. The present results show that ischemia can cause injury to the myenteric plexus in the surviving intestine.
Ten patients with skeletal and dental Class III malocclusion with mandibular prognathism were treated ortho-dontically and surgically and the effects of the ramus sagittal split osteotomy technique on facial morphology and the dentofacial complex were investigated.
Seven dental cyst epithelia were cultured in vitro and the conditioned media were analyzed for periodontal ligament fibroblast collagenase production. All the cyst epithelium-conditioned media stimulated fibroblast collagenase production, indicating that dental cyst epithelium, which is considered to be identical to the cell rests of Malassez, might play a role in periodontal pocket formation.
A case of peripheral ameloblastoma in a 57-years-old woman is presented, along with a discussion of the clinical and histological characteristics of the lesion. After clinical and radiographic examinations, and with a differential diagnosis of pyogenic granuloma, an excisional biopsy was performed and the material collected was sent for histological examination. On the basis of the histopathological diagnosis, a second operation was performed with a wide safety margin, including bone tissue, which did not show any involvement with the odontogenic neoplasm.
Mouth-rinsing with oxydized water which contains electrolytically generated chlorine is known to hinder dental plaque formation and growth, but it also accelerates the deterioration of metallic restorations in the mouth. The present work consists of an in vitro study to elucidate the electrochemical reactions involved in the reduction of oxydized water on dental alloys through a systematic investigation of the potentiostatic polarization behavior of dental alloy electrodes. The five dental alloys selected for investigation were gold alloy, gold alloy containingplatinum, silver-palladium-gold alloy, conventionalamalgam and high copper amalgam. The corrosion potentials of all dental alloy electrodes were shown to be more noble in oxydized water than in0.1N sodium chloride solution. The potential differences between the corrosion potentials were relatively small in the case of amalgam electrodes. The polarization curves for all of the dental alloy electrodes in oxydized water revealed reduction currents of chlorine, hypochlorous acid, dissolved oxygen and oxonium ion. The reduction of chlorine and hypochlorous acid started at a more noble potential than that of dissolved oxygen. The dental alloys studied, except the amalgams, did not dissolve excessively at the corrosion potentials in oxydized water.