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Migration of a mandibular canine across the midline (transmigration) is a rare condition. Bilateral transmigration is extremely rare, there being only two published accounts. Of the five cases of transmigration described in this report, one involved bilateral transmigration. Treatment options are discussed.
Six young adults were found to have transmigrated mandibular canines. One patient presented with two transmigrated canines. Of the seven impacted teeth, the left mandibular canines was involved in five instances and the right two. In all patients, the primary canine was present in the dental arch. A supernumerary tooth was disclosed on the panoramic radiograph of two patients. Five patients underwent surgical removal of the transmigrated tooth from an intraoral approach. One patient experienced transient postoperative paresthesia in the zone innervated by the mental nerve. When the transmigrated canine is accessible, and especially if it is symptomatic, removal of unerupted tooth is recommended. Otherwise, it should be left alone and kept under observation.
OBJECTIVES: To test the hypothesis that loss of polymorphonuclear neutrophil tumor necrosis factor alpha (TNF-alpha) receptors during transmigration renders the exudate neutrophil refractory to TNF-alpha-mediated stimulation of apoptosis; and to investigate the surface expression of Fas on both circulating and exudate neutrophils. DESIGN: A prospective cohort study. SETTING: Surgical laboratory of a tertiary care hospital. PARTICIPANTS: Twenty-one healthy human volunteers. INTERVENTIONS: All subjects had circulating neutrophils and exudate neutrophils collected by venipuncture and skin window methods, respectively. MAIN OUTCOME MEASURES: Circulating and exudate neutrophils were incubated in culture medium (1.0x10(6) neutrophils per milliliter) alone or with TNF-alpha (100 ng/mL). Apoptosis was evaluated by flow cytometry (annexin V-fluorescein isothiocyanate and propidium iodide). Tumor necrosis factor alpha-phycoerythrin and anti-human Fas-fluorescein isothiocyanate were used to evaluate neutrophil TNF-alpha receptors and surface expression of Fas. RESULTS: Exudate neutrophils had a significant delay in apoptosis rates when compared with circulating neutrophils. The percentage of neutrophils expressing TNF-alpha receptors was significantly diminished after exudation (80%+/-15% vs 33%+/-9%; P<.001), as was the median channel number of TNF-alpha phycoerythrin fluorescence (8.1+/-1.6 vs 5.2+/-0.5; P=.001). However, the expression of Fas was unchanged after transmigration (percentage positive for Fas: 98.7%+/-0.7% vs 92.8%+/-3.4%, P=.89; Fas antibody-fluorescein isothiocyanate median channel fluorescence: 12.2+/-1.1 vs 13.1+/-1.2; P=.80). Exposure of exudate neutrophils to TNF-alpha failed to increase their rate of apoptosis. CONCLUSIONS: Exudate polymorphonuclear neutrophils are confirmed to have delayed apoptosis. Loss of TNF-alpha receptors during transmigration is necessary for neutrophil survival in the extravascular inflammatory milieu.
Mucosal tissues, such as the lung and intestine, are primary targets for ischemic damage. Under these conditions, neutrophil (polymorphonuclear leukocyte; PMN) infiltration into the protective epithelium has been implicated as a pathophysiologic mediator. Because PMN transepithelial migration results in increased paracellular permeability, and because our previous data revealed that epithelial hypoxia enhances PMN transmigration, we hypothesized that macromolecular permeability may be altered in epithelium exposed to hypoxia and reoxygenation (H/R) in the presence of PMNs. Human intestinal epithelia (T84) were grown on permeable supports, exposed to cellular hypoxia (pO2 20 torr) for 0-72 hr, and examined for increases in PMN-evoked permeability by using standard flux assays. Increasing epithelial hypoxia potentiated PMN-induced permeability of labeled paracellular tracers (size range 3-500 kD). Such increases were blocked by monoclonal antibody (mAb) to the PMN integrin CD11b (82 +/- 1% decreased compared with control mAb) and were partially blocked by anti-CD47 mAb (51 +/- 1%). Assessment of barrier recovery revealed that monolayers exposed to H/R were significantly diminished in their ability to reseal following PMN transmigration (recovery of 36 +/- 6% in H/R vs. 94 +/- 2% in normoxic controls). Because intracellular cyclic AMP (cAMP) has been demonstrated to regulate epithelial permeability, and because PMN-derived compound(s), (i.e., 5'-adenosine monophosphate; AMP) elevate epithelial cAMP, we examined the impact of hypoxia on epithelial cAMP responses. These experiments revealed that hypoxic epithelia were diminished in their ability to generate cAMP, and pharmacologic elevation (8-bromo-cAMP) of intracellular cAMP in hypoxic cells normalized both PMN-induced permeability changes and restoration of barrier function. These results support a role for PMN in increased intestinal permeability associated with reperfusion injury and imply a substantial role for cAMP signaling in maintenance of permeability during PMN transmigration.
Accumulating evidence support a role of neutrophils in coronary artery disease (CAD). However little is known about the action of neutrophils at a local inflammatory site represented by an atherosclerotic plaque. To gain insight into these issues, we applied a skin blister model that permits analyses of in vivo transmigrated neutrophils. We hypothesised that the chronic inflammation in stable CAD mediates priming of neutrophils that impacts the out-come of neutrophil action at an inflammatory site. Thirteen patients with angiographically verified CAD were eligible for study entry together with 13 age and sex matched controls. Markers of inflammation (IL-6 and CRP), neutrophil activation (IL-8 and MMP-9/NGAL), and functional aspects (CD11b up-regulation and intracellular H(2)O(2) production) of peripheral and in vivo transmigrated neutrophils were studied. Systemic IL-8 and MMP-9/NGAL concentrations were significantly increased in patients indicating a primed state in circulating neutrophils. In vivo transmigrated neutrophils in stable CAD patients had an increased propensity to release MMP-9/NGAL and a reduced capacity to up-regulate CD11b and to produce hydrogen peroxide. These aberrations at the inflammatory site may be a consequence of a primed state of circulating neutrophils and point towards potential mechanisms whereby neutrophils at a local inflammatory site may contribute to the pathogenesis of CAD.
Cannabinoids are known to possess both anti-inflammatory and neuroprotective effects. In the present study, we have investigated the ability of cannabinoids to inhibit the transmigration of neutrophils in response to chemotaxic stimuli. The cannabinoid receptor agonist WIN 55,212-2 ((R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)-pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-naphthalenylmethanone mesylate) significantly decreased the number of migrating neutrophils across a monolayer of tumour necrosis factor alpha (TNF-alpha) activated ECV304 cells at concentrations >or=1 microM. In contrast, the agonists HU210 and CP 55,940 (0.01-1 microM) and the endocannabinoid anandamide (0.1-10 microM) were without significant effect on the response to TNF-alpha. The ability of WIN 55,212-2 to reduce the neutrophil transmigration was still seen in the presence of the cannabinoid CB(1) receptor antagonist/inverse agonist AM251 (0.1-1 microM) and the cannabinoid CB(2) receptor antagonist/inverse agonist AM630 (0.1-1 microM). TNF-alpha treatment of ECV304 cells caused release of interleukin-8 (IL-8), but WIN 55,212-2 did not affect either the ability of neutrophils to migrate across chemotaxis plates in response to an IL-8 stimulus, or to change the percentage of CXC 1 and CXC 2 receptors expressed by the neutrophils. WIN 55,212-2 at a concentration of 1 microM, but not at lower concentrations, produced a significant inhibition of IL-8 release from ECV304 cells in response to TNF-alpha-stimulation. Thus WIN 55,212-2 reduces the transmigration of neutrophils across a monolayer of TNF-alpha-activated ECV304 cells by an indirect action upon the release of IL-8 and/or other chemokine release from the ECV304 cells, and that this effect is brought about mainly by a cannabinoid CB receptor-independent mechanism.
OBJECTIVE: Although several methods for the generation of dendritic cells (DCs) exist, little is known about the transmigration capacities of the cells developed. Their ability to migrate to the adjacent lymphatic system is relevant since their efficacy does also rely on their potential to interact with lymphocytes. METHODS: We studied the transmigration of DCs derived from hematopoietic progenitor cells (HPC), from peripheral blood monocytes, and from leukemic cells. DCs from monocytes and leukemic cells could be generated within 1 week, whereas DCs from HPC needed 2 weeks for maturation. RESULTS: While DCs from all sources showed similar morphologic features and allostimulatory capacities, their transmigration capacities varied: HPC-derived DCs showed the highest migratory response to macrophage inflammatory protein (MIP)-3alpha and beta. Monocyte-derived DCs were equally attracted to MIP-3beta and stroma-derived factor (SDF)-1alpha. Only few leukemic DCs migrated in response to SDF-1. Other chemoattractants tested included MIP-1alpha and RANTES. Replacement of fetal bovine by human serum did not change the DC's overall migratory capacities. It did, however, influence the responsiveness to certain chemokines. CONCLUSION: Although DCs from all three sources are immunocompetent antigen-presenting cells, our findings suggest that HPC and monocyte-derived DCs can be administered subcutaneously and intravenously, but that leukemic DCs should be injected into the lymph node.
The manifestations of Lyme disease, caused by Ixodes spp. tick-transmitted Borrelia burgdorferi, range from skin infection to bloodstream invasion into the heart, joints and nervous system. The febrile infection human granulocytic anaplasmosis is caused by a neutrophilic rickettsia called Anaplasma phagocytophilum, also transmitted by Ixodes ticks. Previous studies suggest that co-infection with A. phagocytophilum contributes to increased spirochetal loads and severity of Lyme disease. However, a common link between these tick-transmitted pathogens is dissemination into blood or tissues through blood vessels. Preliminary studies show that B. burgdorferi binds and passes through endothelial barriers in part mediated by host matrix metalloproteases. Since neutrophils infected by A. phagocytophilum are activated to release bioactive metalloproteases and chemokines, we examined the enhanced B. burgdorferi transmigration through vascular barriers with co-infection in vitro. To test whether endothelial transmigration is enhanced with co-infection, B. burgdorferi and A. phagocytophilum-infected neutrophils were co-incubated with EA.hy926 cells (HUVEC-derived) and human brain microvascular endothelial cells in Transwell cultures. Transmigration of B. burgdorferi through endothelial cell barriers was determined and endothelial barrier integrity was measured by transendothelial electrical resistivity. More B. burgdorferi crossed both human BMEC and EA.hy926 cells in the presence of A. phagocytophilum-infected neutrophils than with uninfected neutrophils without affecting endothelial cell integrity. Such a mechanism may contribute to increased blood and tissue spirochete loads.
This study evaluated whether glutamine (GLN) concentration was related to endothelial surface molecule expression and the migration of polymorphonuclear neutrophils (PMNs) through endothelial cells (ECs) stimulated by arsenic. Human umbilical vein endothelial cells (HUVECs) and PMNs were treated with different GLN concentrations (0, 300, 600 and 1000 microM) for 24 h. After that, we stimulated HUVECs for 3 h with 0.5 microM arsenic, and PMNs were allowed to transmigrate to ECs for 2 h. HUVEC surface expressions of cell adhesion molecules and integrin (CD11b) and interleukin (IL)-8 receptor expressions on PMNs were measured. The transendothelial migration of PMNs was also analyzed. The results showed that cell adhesion molecule (CAM) and integrin expressions in arsenic groups were higher than in those without arsenic. Among the arsenic groups, the expression of CAMs on ECs and CD11b, and IL-8 receptor on PMNs was lowest with 0 microM compared with the other GLN concentrations. Vascular CAM-1 on ECs and CD11b on PMN expression were higher with 300 microM than with 600 and 1000 microM GLN. IL-8 secretions from ECs and PMNs were higher with 300 muM than with 600 and 1000 microM GLN, and this was consistent with the expression of the IL-8 receptor on PMNs. Polymorphonuclear neutrophil transmigration was significantly higher with 300 muM GLN than with other GLN concentrations. These results suggest that ECs and PMNs were activated after arsenic stimulation. Cell adhesion molecule expressions on ECs and PMNs were suppressed in the absence of GLN. A low GLN concentration comparable to catabolic conditions resulted in higher adhesion molecule expression and greater transendothelial migration of neutrophils. Glutamine administration at levels similar to or higher than physiological concentrations reduced IL-8 and adhesion molecule expression; PMN transmigration was also decreased after stimulation with arsenic.
OBJECTIVES: Herniation of the fundoplication wrap through the esophageal hiatus is a common reason for surgical failure in children who have undergone laparoscopic Nissen fundoplication. Extensive mobilization of the gastroesophageal junction in combination with decreased adhesions after laparoscopy may contribute to the development of this complication. In an attempt to decrease the incidence of wrap migration, we changed our technique to minimal mobilization of the intraabdominal esophagus and to placement of esophageal-crural sutures. In this study, we investigate the impact of these modifications on outcome. METHODS: A retrospective analysis was performed on all patients undergoing laparoscopic fundoplication by the senior author (GWH) from January 2000 through December 2004. Those undergoing operation with extensive esophageal mobilization and without esophagocrural sutures (January 2000 to March 2002) (group I) were compared with those in whom there was minimal esophageal dissection with placement of these esophagocrural sutures (April 2002 to December 2004) (group II). RESULTS: Two hundred forty-nine patients underwent laparoscopic Nissen fundoplication during the study period. One hundred thirty patients were in group I, and 119 patients were in group II. The rate of transmigration decreased from 12% in group I to 5% in group II (P = .072). The relative risk of transmigration with extensive esophageal mobilization and without the esophagocrural sutures was 2.29. CONCLUSIONS: This retrospective study has shown that placement of esophagocrural sutures and minimization of the dissection around the esophagus results in a more than 2-fold reduction in the risk of wrap transmigration after laparoscopic Nissen fundoplication.
Mycoplasma bovis can cause arthritis or mastitis following pneumonia and mycoplasmemia in cattle. Interactions with pulmonary vascular endothelium have been recorded as localized vasculitis, perivascular mononuclear cell infiltrations, and accumulation of inflammatory cells in lesions. We compared adhesion mediators and cytokine gene expression as well as cytotoxicity of cultured primary bovine aortic and bovine pulmonary microvascular endothelial cells (BPMEC) challenged with M. bovis. We also tested if abscess-forming ability of strains of M. bovis is associated with changes on endothelial cells. Increased VCAM-1 surface expression was found in both cell types, while only infected BPMEC increased MCP-1 transcription, both mediators specific for mononuclear cell transmigration. Given no induction of ICAM-1 mRNA in either cell type, induction of IL-8 mRNA by BPMEC suggested that neutrophil transmigration was signaled in microvascular areas. Infected BPMEC showed early induction of IL-1beta and IL-6 mRNA. Excepting VCAM-1, differential strain effects were limited to BPMEC and not correlated with their abscess-forming capability. In addition, only strain DSA16 had minor cytotoxic effect on both cell types. We thus show that BPMEC are more susceptible than aortic cells to M. bovis-induced activation. Activation preferentially yielded signals for mononuclear cell transmigration, correlating well with in vivo observations of infiltrating cells at pulmonary sites.
OBJECTIVE: This study analyzed plasma glutamine (GLN) concentrations in women with preeclampsia. Also, in an in vitro study we evaluated whether GLN concentration was related to surface molecule expressions on endothelial cells (ECs) and polymorphonuclear neutrophils (PMNs) and the transendothelial migration of PMNs through ECs stimulated by preeclamptic plasma. METHODS: Blood samples were collected from 20 women with preeclampsia and 15 normal pregnant women for plasma GLN analysis. In the in vitro study, human umbilical vein endothelial cells and PMNs were treated with different concentrations (0, 300, 500, and 1000 microM) of GLN for 24 h. After that, we stimulated human umbilical vein endothelial cells for 3 h with plasma from patients with preeclampsia, and PMNs were allowed to transmigrate through ECs for 2 h. EC surface expressions of cellular adhesion molecules (CAMs) and integrin (CD11b) interleukin-8 (IL-8) receptor expressions on PMNs were measured by flow cytometry. The transendothelial migration of PMNs through ECs was also analyzed. RESULTS: Women with preeclampsia exhibited significantly lower plasma GLN concentrations than did normal pregnant women. The in vitro study showed that, compared with normal plasma, CAM expressions on human umbilical vein endothelial cells and PMNs were increased when preeclamptic plasma was stimulated. Among the groups with preeclamptic plasma stimulation, intracellular CAM-1 expression on ECs and CD11b and IL-8 receptor expressions on PMNs were lower with 500 and 1000 microM than with 300 microM of GLN. IL-8 production from ECs and PMNs was also lower with 500 and 1000 microM than with 300 microM of GLN. PMN transmigration was significantly higher with 300 microM of GLN than with the other GLN concentrations. CONCLUSIONS: Plasma GLN is depleted in women with preeclampsia. The result of this in vitro study showed that ECs and PMNs were activated after preeclamptic plasma stimulation. A low GLN concentration resulted in greater CAM expression and greater transendothelial migration of neutrophils. GLN administration at levels similar to or higher than physiologic concentrations decreased IL-8 and CAM expressions, and PMN transmigration decreased after stimulation with preeclamptic plasma.
Inflammatory bowel disease (IBD) consisting of ulcerative colitis (UC) and Crohn's (CD) typically displays a waxing and waning course punctuated by disease flares that are characterized by transepithelial migration of neutrophils (PMN) and altered barrier function. Since epithelial barrier function is primarily regulated by the apical most intercellular junction referred to as the tight junction (TJ), our aim was to examine expression of TJ and adherens junction (AJ) proteins in relation to PMN infiltration in mucosal tissue samples from patients with active IBD. Expression of epithelial intercellular TJ proteins (occludin, ZO-1, claudin-1, and JAM) and subjacent AJ (beta-catenin and E-cadherin) proteins were examined by immunoflourescence/confocal microscopy, immunohistochemistry, and Western blotting. Colonic mucosa from patients with UC revealed dramatic, global down-regulation of the key TJ transmembrane protein occludin in regions of actively transmigrating PMN and in quiescent areas in the biopsy samples. Significant decreases in occludin expression were observed at the protein and mRNA levels by Western and Northern blotting. In contrast, expression of other TJ and AJ proteins such as ZO-1, claudin-1, JAM, beta-catenin, and E-cadherin were down-regulated only in epithelial cells immediately adjacent to transmigrating PMN. Analysis of inflamed mucosa from Crohn's disease patients mirrored the results obtained with UC patients. No change in TJ and AJ protein expression was observed in colonic epithelium from patients with collagenous colitis or lymphocytic colitis that are respectively characterized by a thickened subepithelial collagen plate and increased intraepithelial lymphocytes. These results suggest that occludin expression is diminished in IBD by mechanisms distinct from those regulating expression of other intercellular junction proteins. We speculate that down-regulation of epithelial occludin may play a role in enhanced paracellular permeability and PMN transmigration that is observed in active inflammatory bowel disease.
This study describes an in vitro investigation on the role of Pasteurella multocida cells and its isolated protein H and LPS on neutrophil adhesion and migration through bovine endothelial cell monolayers. P. multicoda cells, protein H and LPS increased the adhesion and transmigration of neutrophils through BAEC. The bacteria/cell ratio of 100 for P. multocida, protein H concentration 0.05-0.2 microM and LPS concentration 0.5-1.0 microM respectively, induced the maximum adhesion and transmigration of neutrophils through BAEC. The optimal time of incubation with bacteria or bacterial products was 4-6 h. Our results confirm the role of Gram-negative bacteria and of components of the outer membrane such as protein H or LPS in activating the neutrophils and in promoting the adhesion and cells transmigration from the vessels to the site of inflammation.
Transmigration of impacted mandibular cuspid is a rare finding. A cuspid is classified as "transmigrated" when more than half of its length has passed the mid-line. 13 cases of transmigration of impacted mandibular cuspids are presented, 3 of which occurred in pairs, raising the total number of teeth to 16. Radiographs showed positions ranging from a vertical impaction, to a cuspid having crossed the mid-line completely, reaching the first molar area of the opposite side.
Transmigration is a rare occurrence relating to the movement of a mandibular canine across the mid-line of the mandible. Two cases are presented where patients referred for assessment of third molar problems subsequently revealed on radiological examination the asymptomatic phenomenon of transmigration. With dental panoramic radiography becoming more widespread among dental practitioners it is possible that more cases of transmigration will be observed.
During inflammatory bowel diseases, commitment of extravased polymorphonuclear leucocytes (PMN) to apoptosis is required for the resolution of inflammation. To investigate the effect of transepithelial migration on PMN apoptotic rates, PMN transepithelial migration was reproduced in vitro using T84 intestinal monolayers. Transepithelial migration was found to delay neutrophil apoptosis, and this survival effect correlated with a downregulation of the surface expression of Fas ligand (FasL) and with a decrease in both procaspases-3, and -8 mRNA and procaspases-3, -6, -7 and -8 protein levels. Moreover, neutrophil survival and FasL shedding mediated by transepithelial migration were abrogated by a broad-spectrum metalloproteinase inhibitor, BB-94. Although Erk1/2 and p38 MAPK were activated in transmigrated PMN, inhibition of these MAP kinases did not impair transmigration-induced PMN survival. Taken together, our results show that trans-epithelial migration induces the downregulation of proapoptotic proteins expression in transmigrated PMN, which results in their increased lifespan.
Very few people have seen transmigrant mandibular canines and little has been presented in the literature about this rare phenomenon. In this case report, identification techniques and treatment options are presented along with the treatment results of a patient diagnosed with a transmigrant mandibular canine. This rare condition usually requires extraction of the involved tooth because orthodontic forces are seldom successful at erupting these teeth into their proper location. The treatment protocol for this patient involved a combination of orthodontic procedures, surgical extractions, gingivectomy and frenectomy, and implant replacement of the impacted transmigrant tooth. Through a collaborative effort of a team made up of an orthodontist, periodontist, prosthodontist, and oral surgeon, these techniques were used to achieve an excellent esthetic and functional outcome.