Plasma cell gingivitis apparently related to the use of khat: report of a case.

Plasma cell gingivitis (PCG) is characterized by massive infiltration of plasma cells into the subepithelial tissue. It is a rare condition; the cause of which is still not fully understood. A case of PCG is reported in the mandibular gingiva probably caused by chewing khat. This report is the first, as far as we know, that relates PCG to the use of khat. The histological examination revealed infiltration of polyclonal plasma cells without signs of fungus, tuberculosis or malignancy. It is concluded that the changes were compatible with an allergic-like reaction. The patient, a 30-year-old immigrant from Somalia, revealed in a subsequent consultation that he regularly used khat. The leaves are placed in the buccal sulcus. The PCG disappeared within two weeks of the use of khat being discontinued. Dental surgeons (periodontists) in Europe and the New World will, due to increasing immigration from Africa and the Arabian Peninsula, meet more patients who regularly use khat. This means that PCG and other khat related intraoral changes will become more common in the future.

The BMP family member Gdf7 is required for seminal vesicle growth, branching morphogenesis, and cytodifferentiation.

Epithelial-mesenchymal interactions play an important role in the development of many different organs and tissues. The secretory glands of the male reproductive system, including the prostate and seminal vesicles, are derived from epithelial precursors. Signals from the underlying mesenchyme are required for normal growth, branching, and differentiation of the seminal vesicle epithelium. Here, we show that a member of the BMP family, Gdf7, is required for normal seminal vesicle development. Expression and tissue recombination experiments suggest that Gdf7 is a mesenchymal signal that acts in a paracrine fashion to control the differentiation of the seminal vesicle epithelium.

fucosyltransferase1 and H-type complex carbohydrates modulate epithelial cell proliferation during prostatic branching morphogenesis.

The prostate undergoes branching morphogenesis dependent on paracrine interactions between the prostatic epithelium and the urogenital mesenchyme. To identify cell-surface molecules that function in this process, monoclonal antibodies raised against epithelial cell-surface antigens were screened for antigen expression in the developing prostate and for their ability to alter development of prostates grown in serum-free organ culture. One antibody defined a unique expression pattern in the developing prostate and inhibited growth and ductal branching of cultured prostates by inhibiting epithelial cell proliferation. Expression cloning showed that this antibody binds fucosyltransferase1, an alpha-(1,2)-fucosyltransferase that synthesizes H-type structures on the complex carbohydrate modifications of some proteins and lipids. The lectin UEA I that binds H-type 2 carbohydrates also inhibited development of cultured prostates. These data demonstrate a previously unrecognized role for fucosyltransferase1 and H-type carbohydrates in controlling the spatial distribution of epithelial cell proliferation during prostatic branching morphogenesis. We also show that fucosyltransferase1 is expressed by epithelial cells derived from benign prostatic hyperplasia or prostate cancer; thus, fucosyltransferase1 may also contribute to pathological prostatic growth. These data further suggest that rare individuals who lack fucosyltransferase1 (Bombay phenotype) should be investigated for altered reproductive function and/or altered susceptibility to benign prostatic hyperplasia and prostate cancer.

Cytomegalovirus inhibits p53 nuclear localization signal function.

Endothelial cells (EC) infected with the VHL strain of cytomegalovirus (CMV) are resistant to p53-mediated apoptosis, which may be relevant to EC dysfunction and atherogenesis. This resistance to apoptosis may be mediated by cytoplasmic sequestration of p53, which functions only in the nucleus. We explored the hypothesis that CMV sequesters p53 in the cytoplasm by blocking p53 nuclear localization signal (NLS) function. We transfected VHL CMV infected EC with recombinant p53 NLSI conjugated with chicken muscle pyruvate kinase (PK) plasmid. NLSI is responsible for 90% of p53 nuclear localization, and PK is not normally translocated to the nucleus after cytoplasmic production. Thus it cannot be localized in the nucleus without the assistance of the artificial NLSI. A double-labeling immunofluorescence staining method was used to identify the localization of p53 NLSI-conjugated PK in CMV-infected EC. We found that CMV infection sequesters PK and p53 in the cytoplasm by blocking NLSI function. This inactivation of NLSI function is dependent upon infection stage; it occurs only in the early and late phases and not the immediate early phase of infection. These findings may be relevant to endothelial dysfunction and initiation of atherogenesis. Our study also suggests a novel mechanism of the p53 inactivation by virus, which may be important for atherogenesis and tumorgenesis.

Activated monocytes in sickle cell disease: potential role in the activation of vascular endothelium and vaso-occlusion.

Sickle cell anemia is characterized by painful vaso-occlusive crises. It is hypothesized that monocytes are activated in sickle cell disease and can enhance vaso-occlusion by activating endothelium. To test this hypothesis, human umbilical vein endothelial cells (HUVEC) and human microvascular endothelial cells (MVEC) with sickle and normal mononuclear leukocytes were incubated, and endothelial activation was measured. Endothelial cells incubated with sickle mononuclear leukocytes were more activated than those incubated with normal mononuclear leukocytes, as judged by the increased endothelial expression of adhesion molecules and tissue factor and the adhesion of polymorphonuclear leukocytes (PMNL). Monocytes, not lymphocytes or platelets, were the mononuclear cells responsible for activating endothelial cells. Sickle monocytes triggered endothelial nuclear factor-kappa B (NF-kappaB) nuclear translocation. Cell-to-cell contact of monocytes and endothelium enhanced, but was not required for, activation. Antibodies to tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1beta) blocked activation of the endothelium by monocytes. Peripheral blood monocytes from patients with sickle cell disease had 34% more IL-1beta (P =.002) and 139% more TNF-alpha (P =.002) per cell than normal monocytes. Sixty percent of sickle monocytes expressed the adhesion molecule ligand CD11b on their surfaces compared with only 20% of normal monocytes (P =.002). Serum C-reactive protein, a marker of systemic inflammation, was increased 12-fold in sickle serum than in normal serum (P =.003). These results demonstrate that sickle monocytes are activated and can, in turn, activate endothelial cells. It is speculated that vascular inflammation, marked by activated monocytes and endothelium, plays a significant role in the pathophysiology of vaso-occlusion in sickle cell anemia.

Fractures of the mandibular condyle. Part 1: patterns of distribution of types and causes of fractures in 348 patients.

This prospective study was designed to record relevant characteristics of mandibular condyle fractures and to evaluate the relationship between these. Data were recorded on sex, age, cause of trauma, level of fracture, dislocation of the mandibular head, dental state and associated fractures of all patients diagnosed in our hospital during the period 1984-1996 with mandibular condyle fractures. Data were analysed in our Computer Department. The sample comprised 348 patients with 444 fractures, and a male:female ratio of 2:1. Traffic accidents were the most common cause: 103 (41%) of the unilateral and 54 (56%) of the bilateral fractures, followed by alleged assault and falls. Low fractures were the most common -n = 314 of 444 (71%). The causes that involved considerable force (traffic accidents and falls) resulted in more dislocations of the mandibular head, more bilateral fractures, a tendency to fractures higher on the condyle and significantly more intracapsular fractures. Absence of molar occlusion also gave more high and fewer low fractures, but played no part in dislocation of the mandibular head from the glenoid fossa.

Fractures of the mandibular condyle. Part 2: results of treatment of 348 patients.

This study was designed to record the results of conservative treatment of condylar fractures and to find out if there were any variables that were predictive of complications. Data were analysed in our computer department. During the period 1984-1996, all patients who presented with a fracture of the mandibular condyle and who attended for control examination one year after treatment were recorded at the end of treatment and one year later. The ability to open the mouth, deviation and occlusion were recorded. After one year 45 of the 348 patients (13%) had minor physical complaints such as reduced ability to open the mouth, deviation, or dysfunction. Ten of them (3%) had pain in the joint or muscles or both. Eight patients (2%) had malocclusion, which in seven could be related to dislocation of the condylar head out of the fossa. Five of the eight patients had had bilateral fractures. We conclude that conservative treatment of condylar fractures is non-traumatic, safe, and reliable and in only a few cases may cause disturbances of function and malocclusion. The risk associated with the latter is greatest with bilateral fractures and dislocation of the condylar head from the fossa.

Human cytomegalovirus immediate early proteins upregulate endothelial p53 function.

Infected endothelial cells are found to be resistant to apoptosis possibly mediated by p53 cytoplasmic sequestration. We explored whether the immediate early 84 kDa protein (IE84) of cytomegalovirus (CMV) is responsible for p53 cytoplasmic sequestration. The endothelial cells were transfected with plasmids containing IE1 and 2 coding regions which are known to synthesize IE84 and 72 proteins. Our study found that p53 expression was significantly elevated in endothelial cells transfected with IE1 and 2 plasmids. However, p53 was only found in the nucleus rather than sequestered in the cytoplasm. We have demonstrated that IE84 and 72 are not responsible for p53 dysfunction caused by CMV infection, rather they upregulate p53 function and promote endothelial apoptosis.

Cancer of the nasal cavity and paranasal sinuses: a series of 115 patients.

A total of 115 patients with sinonasal cancer was assessed during the period 1978-1995. Ninety-one patients received treatment with curative intent. A combination of irradiation and operation was used. The 5-year crude survival for patients, who were treated with curative intent, was 41%; the disease-specific survival throughout the period was 48%. Primary irradiation followed by maxillectomy was widely used in the first half of the period. Treatment in the last part was changed to primary lateral rhinotomy with post-operative irradiation whenever possible. Twelve maxillectomies were performed during the first half of the period, and during the last part, only two. Disease-specific survival was equal in the first and the second halves of the period.

Spectrum of Bmp5 mutations from germline mutagenesis experiments in mice.

Over 40 years of mutagenesis experiments using the mouse specific-locus test have produced a large number of induced germline mutations at seven loci, among them the short ear locus. We have previously shown that the short ear locus encodes bone morphogenetic protein 5 (BMP5), a member of a large family of secreted signaling molecules that play key roles in axis formation, tissue differentiation, mesenchymalepithelial interactions, and skeletal development. Here we examine 24 chemical- and radiation-induced mutations at the short ear locus. Sequence changes in the Bmp5 open reading frame confirm the importance of cysteine residues in the function of TGF beta superfamily members. The spectrum of N-ethyl-N-nitrosourea-induced mutations also provides new information about the basepair, sequence context, and strand specificity of germline mutations in mammals.

Osseointegrated implants for prosthetic rehabilitation after treatment of cancer of the oral cavity.

The treatment of oral cancer usually involves extensive resection of the mandible, excision of oro-facial soft tissue and often radiotherapy. This causes difficulty in the subsequent oral rehabilitation. The present paper reports our experience with implant treatment of this patient group. The material comprises 38 implants in 12 patients. Four patients died during follow-up, two before loading the implants. The observation time after implantation was 7 to 47 months with a median of 14 months. Six of the patients had been subjected to preoperative radiation therapy. All 38 implants osseointegrated without complications. It is concluded that healing after implantation in irradiated mandibles can be achieved without hyperbaric oxygen. Provided certain guidelines are complied with i.e. careful surgical technique, use of antibiotics and prolonged period of healing prior to loading of the implants, a radiation dosage of up to 50 Gy appears to be of little significance.

Immediate obturation of the surgical defect after partial maxillectomy in the endentulous patient.

Closure of the surgical defect immediately after partial maxillectomy is the treatment of choice. The advantages are: maintaining facial contour, rapid re-establishment of speech, swallowing and mastication. A number of methods for the fixation of the immediate obturator in patients without teeth have been described. A new technique is reported where a transnasal wire holds the existing denture in position after partial maxillectomy. The method has been carried out on 7 patients with sino-nasal cancer during the period 1978-1994. The advantages of the technique are that the wire acts as an axis of rotation which together with the sponge in the cavity provide good stability of the denture. There is minimal preoperative laboratory work and simplification in replacing the surgical dressing.

Iron and atherosclerosis: inhibition by the iron chelator deferiprone (L1).

BACKGROUND: Accumulating evidence suggests that oxidative modification of lipoproteins may play a significant role in atherogenesis. In this study, we hypothesized that the iron chelator deferiprone (L1) would function as an antioxidant and decrease atherosclerosis progression. MATERIALS AND METHODS: For the in vitro studies, human low-density lipoprotein (LDL) was collected and then subjected to oxidation by either hemin/H2O2 or copper sulfate in the presence of various concentrations of L1. Lag time to oxidation was measured to assess antioxidant activity of L1. In addition, human umbilical vein endothelial cells (HUVEC) were subjected to oxidized LDL in the presence of varying concentrations of L1 to assess the antioxidant cytoprotective ability of L1. For the in vivo studies, rabbits (n = 21) were maintained on a 0.25% by weight cholesterol diet for 10 weeks; 9 rabbits also received twice daily L1 by gavage (total dose = 100 mg/kg/day). Lipid profiles were measured during the study. At 10 weeks, rabbits were sacrificed, and thoracic aorta cholesterol content (TACC) and planimetry were determined to assess atherosclerosis severity. RESULTS: In vitro, L1 prevented oxidation of LDL and protected HUVEC from the cytotoxic effects of oxidized LDL in a concentration-dependent manner. In vivo, L1 reduced TACC (P = 0.001), while also significantly decreasing total plasma cholesterol (P = 0.003), very-low-density lipoprotein cholesterol (P = 0.01), and LDL cholesterol (P = 0.002) compared to control animals. However, no significant differences between L1-treated animals and controls were evident for the surface area of plaque involvement by planimetry (P = 0.3) or in the serum iron levels (P = 0.3). CONCLUSIONS: These results confirm that L1 possesses antioxidant activity in vitro and may reduce atherogenesis in vivo.

Treatment of large odontogenic keratocysts by decompression and later cystectomy: a long-term follow-up and a histologic study of 23 cases.

OBJECTIVE: The purpose of this study was to determine the course of healing, the frequency of recurrence, and the changes in the epithelium of keratocysts after decompression treatment. STUDY DESIGN: The treatment of 23 keratocysts, which had been divided into two groups (12 and 11 patients, respectively), was carried out in two phases: (1) insertion of a polyethylene drain and removal of a biopsy specimen from the cyst wall, and (2) cystectomy and removal of the drain approximately 1 year later. Histologic examination of the biopsy material from the two phases was carried out, and the material classified according to Forssell. RESULTS: Reduction in cyst volume together with bone healing occurred in all cases, although there was recurrence in two patients. Decompression resulted in substantial histologic changes in the epithelium in 19 cases (83%). CONCLUSIONS: (1) Decompression results in new bone formation and thickening of the cyst wall. (2) This treatment conserves bone and anatomic structures. (3) The frequency of recurrence is low. (4) The keratocyst epithelium is modulated histologically to nonkeratocyst after decompression.

Incompletely erupted third molars in the line of mandibular fractures. A retrospective analysis of 57 cases.

A retrospective investigation was carried out of 57 cases of mandibular angle fractures, where a completely or partially impacted third molar was present in the line of fracture. Closed reduction was used in all of the cases, using intermaxillary fixation over a period of 42 days. Antibiotics were given to all patients for a period of 1 week. Thirty-one patients (55%) were treated within the first 24 hours and 43 (75%) within 48 hours. Infection at the fracture site occurred in two patients (3.5%). Both of these patients had been treated within the first 24 hours. It is concluded that closed reduction with retention of the mandibular third molar within the line of a mandibular angle fracture can be carried out with less morbidity compared with cases in which rigid fixation is used and movement of the jaws permitted immediately. Because of the size of the study group, no relationship could be demonstrated between cases with infection and the time from trauma to fixation.

[Lymphangioma of the tongue: case report and review of the literature]. / Lymfangiom i tungen: en oversigt og praesentation af et tilfaelde.

A case of lymphangioma in the tongue is discussed with special reference to diagnosis, treatment and prognosis. The patient is a boy, aged 13, with a congenital malformation in the right half of the tongue. The lesion was removed by surgery. Histologic examination showed lymphangioma. In cases of minor, localized lymphangiomas the clinical diagnosis may be difficult. A past history information of recurring swellings can be regarded as almost diagnostic. The treatment of choice is surgery, if necessary in several settings. Recurrences are often seen.

Metastases to the mouth and jaws from hepatocellular carcinomas. A case report.

Hepatocellular carcinoma metastasis to the jaw and soft tissue of the oral cavity is a rare phenomenon. A case of metastatic hepatocellular carcinoma to the mandible is described. A review of the literature showed that only 19 such cases have been reported so far. As severe haemorrhage may occur during surgical removal of these metastases, it is advisable to carry out fine needle aspiration biopsy when metastasis from a hepatocellular carcinoma is suspected.

A case of benign lymphoepithelial lesion of the hard palate.

The benign lymphoepithelial lesion is a rare condition, most frequently affecting the parotid gland. A review of the literature brought to light 4 earlier cases with localization in the accessory salivary glands in the oral cavity. The present report presents a 5th case arising from the accessory salivary glands on the left side of the hard palate. Destruction of the underlying bone was demonstrated radiologically; the latter has not previously been described. The present report contains a survey of the literature, as well as a review of the pathogenesis, clinical aspects and treatment of the disease.