Humans ; Mandibular Diseases ; prevention & control ; Osteoradionecrosis ; prevention & control ; Radiotherapy ; adverse effects ; Tooth Extraction

This paper reports a case of melanotic neuroectodermal tumor of infancy (MNTI)arising in the maxilla of a 3-month-old male infant.The treatment included surgical excision of the lesion with safe margin,curettage of the maxilla and removal of associated developing tooth bud.Microscopically,it proved to be a dual tumor with small,neuroblastic-like cells and larger epithelial cells.Immunohistochemical staining demonstrated epitheloid cells HMB45(+),EMA(+),CK(+);neuroblast-like cells NSE(+),GFAP(+),S-100(+),but both cells Vim(+),CD45(-),Myogenin(-).The 18-mouth follow-up showed no recurrence or metastasis.The related literature was re-viewed.

OBJECTIVETo investigate the preventive effect of low-intensity ultrasound on osteoradionecrosis of jaws (ORNJ).

METHODSTwenty-five canines were randomly divided into experimental group (n=20) and control group (n=5). The canines in experimental group received radiation exposure, and then were randomly subdivided into group A (n=10) and group B (n=10). Control group did not undergo radiotherapy. One month after radiotherapy, the fourth mandibular premolars of all animals were extracted. Group B was immediately treated by low-intensity ultrasound for twenty days, group A and control group did not receive any treatment. Two months after tooth extraction, the formation of ORNJ was determined and the occurrence rate of ORNJ was compared between group A and B. The microstructure of the mandible and changes in microvascular density in group A and B were evaluated and compared with those of control group.

RESULTSAll animals in group B and group A developed ORNJ after prophylactic ultrasound was applied for twenty days. Although the imaging examination of bony density of group A and B were lower than normal animals in control group, bone density in group B was significantly better than group A. Micro-CT showed that the trabecular bone volume fraction, trabecular thickness, bone surface/bone volume and trabecular number in group B were respectively (0.187±0.029)%, (0.160±0.039) µm, (12.536±2.558)/mm, (1.227±0.192)/mm, which were all greater than group A [(0.103±0.014)%, (0.069±0.013) µm, (5.598±0.731)/mm, (0.522±0.064)/mm)] (P<0.05).

CONCLUSIONSAlthough the preventive application of low intensity ultrasound can not prevent the formation of ORNJ, but can significantly improve the symptoms of ORNJ.

Animals ; Bone Density ; radiation effects ; Dogs ; Jaw Diseases ; etiology ; prevention & control ; Mandible ; Osteoradionecrosis ; prevention & control ; Radiation Injuries, Experimental ; Random Allocation ; Tooth Extraction ; Ultrasonic Therapy ; methods ; X-Ray Microtomography

OBJECTIVETo investigate the influence of zoledronic acid on vascular endothelial cells.

METHODSThe influence of zoledronic acid on proliferation, migration and adhesion of vascular endothelial cells were tested with 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), cell migration assay and cell adhesion assay. The results of each experimental group were compared with the control group and the data statistically analyzed.

RESULTSIn a concentration of 0-0.5 mmol/L, the absorbance value decreased from 0.09 to 0.34 as the drug concentration increased. Scratch test showed that the change of width of scratch before and after 24 hours in control, low, medium and high concentration groups were (38.7 ± 0.42), (35.8 ± 4.17), (19.9 ± 0.57) mm (P < 0.001), (12.5 ± 3.89) mm (P < 0.05). Adhesion test showed that the absorbance value in control, low, medium and high concentration groups were 1.14 ± 0.18, 0.95 ± 0.13, 0.81 ± 0.11 (P < 0.01), 0.67 ± 0.19 (P < 0.001). Comparisons between control and experimental groups were analyzed by t-test and P values < 0.05 were considered statistically significant.

CONCLUSIONSZoledronic acid inhibits the proliferation, migration and adhesion of vascular endothelial cells.

Cell Adhesion ; drug effects ; physiology ; Cell Movement ; drug effects ; physiology ; Cell Proliferation ; drug effects ; Diphosphonates ; pharmacokinetics ; pharmacology ; Endothelial Cells ; cytology ; drug effects ; Imidazoles ; pharmacokinetics ; pharmacology

Objective: To examine the proliferating cell nuclear antigen (PCNA) expression in submandibular gland of diabetic mice and to investigate the influence of fibroblast growth factor 1 (FGF-1) on PCNA expression and its possible mechanism. Methods: Sixteen db/db diabetic male mice were randomly divided into diabetic group and diabetic-FGF-1 group (n=8). Eight age-matched db/m mice served as a control group. After FGF-1 was administered intraperitoneally to diabetic-FGF-1 group continuously for 16 weeks, blood glucose and body weight of each mouse in the three groups were detected at 0, 4, 8, 12, 16 weeks. Then the flow rate of saliva in three groups was compared at 0, 8, 16 weeks. At 16 week, bilateral submandibular glands were resected. Then HE staining was performed to observe the histological morphology of submandibular gland and PCNA expression was examined by immunohistochemical staining. Results: Four weeks after administration, the blood glucose in diabetic-FGF-1 group decreased markedly, close to the control group (P>0.05). Weight loss in diabetic-FGF-1 group was noticeable at 8 weeks after administration, but still higher than that in the control group (P<0.05). The flow rate of saliva in diabetic-FGF-1 group increased gradually after administration, which was higher at 8, 16 weeks ([260.1±43.3], [308.5±34.0] mg·min^-1·kg^-1) respectively than that in the diabetic group at the same time point ([181.8±37.5], [194.9±49.8] mg·min^-1·kg^-1) (P<0.05). Compared with the control group, submandibular glands in diabetic group significantly atrophied and the glandular atrophy in diabetic-FGF-1 group was alleviated. The submandibular gland index in the control group, diabetic group and diabetic-FGF-1 group were (7.45±0.63), (2.23±0.26), (3.97±0.15) mg/g, respectively (P<0.05). HE staining showed that the histological morphology of submandibular gland in diabetic-FGF-1 group was clearer, and acinar and ductal atrophy were less significant than diabetic group. Immunohistochemistry showed that the rate of PCNA-positive cells in the control group, diabetic group and diabetic-FGF-1 group were (45.23±7.78)%, (11.50±1.69)%, (36.98±6.53)% respectively (P<0.05). Conclusions FGF-1 can up-regulate the expression of PCNA in submandibular gland of diabetic mice. This effect may be one of the important mechanisms of FGF-1 reversing the structural atrophy and dysfunction of submandibular gland caused by diabetes mellitus.