Differences in morphology of temporomandibular joint ankylosis of traumatic and infective origin.

The aim of this study was to determine whether there are any differences in morphology between temporomandibular joint ankylosis (TMJA) of traumatic and infective origin. Cone beam computed tomography (CBCT) scans of 25 patients (28 joints) with TMJA of traumatic origin (trauma group) and 15 patients (15 joints) with TMJA of infectious origin (infection group) were included. The following morphological parameters were evaluated on multiple sections of the CBCT scans: lateral juxta-articular bone growth, residual condyle, residual glenoid fossa, ramus thickening, ankylotic mass fusion line, sclerosis of the ankylosed condyle and spongiosa of the glenoid fossa, and mastoid and glenoid fossa air cell obliteration. Lateral juxta-articular bone growth, juxta-articular extension of fusion, and the presence of normal medial residual condyle and residual glenoid fossa were exclusively found in post-traumatic TMJA. There were differences in ramus thickening (82.1% in trauma vs 53.3% in infection), sclerosis of the ankylosed condyle (100% in trauma vs 60% in infection), and sclerosis of the spongiosa of the glenoid fossa (100% in trauma vs 46.7% in infection) between the trauma and infection groups. Mastoid and glenoid fossa air cell obliteration was found more frequently in the infection group (mastoid obliteration: 23.1% in infection vs 4% in trauma; glenoid obliteration: 66.7% in infection vs 55.6% in trauma ). CBCT imaging can be helpful in differentiating between TMJA of traumatic and infectious origin.

Nutritional intervention during maxillomandibular fixation of jaw fractures prevents weight loss and improves quality of life.

Maxillomandibular fixation (MMF) for the management of jaw fractures leads to compromised nutritional intake and consequent weight loss and poor quality of life (QoL). The present study aimed to evaluate the effectiveness of a home-based dietary plan to prevent weight loss, and its effect on the QoL of patients who underwent four weeks of MMF for the treatment of maxillofacial fractures. A total of 50 patients were randomised into nutritional intervention (Group1) and non-intervention groups (Group 2). Patients in Group1 were counselled by a dietitian and given a diet plan. Patients in Group 2 were advised to take a liquid diet of their own choice in the form of shakes, juices, and milk, along with protein supplements. Patients in Group1 lost significantly less weight than those in Group 2 (p=0.001) at week four of follow up. Group1 patients had significantly better oral health-related QoL in the 'physical pain' domain during the two weeks of MMF, and in the 'physical discomfort' and 'psychological disability' domains two weeks after the release of MMF. They had significantly better nutrition-related QoL in all the domains during the two weeks of MMF and, except for the 'physical' domain, also during the two weeks after its release. Individual home-based diet plans effectively helped the patients maintain their weight and improved QoL.

Assessment of paediatric quality of life in temporomandibular joint ankylosis patients after interpositional arthroplasty: a pilot study.

A comprehensive evaluation of treatment outcomes in paediatric temporomandibular joint (TMJ) ankylosis patients should include the assessment of quality of life (QoL) along with the traditional clinical indicators. This longitudinal retrospective descriptive study evaluated the impact on QoL of interpositional arthroplasty for the treatment of TMJ ankylosis in 18 patients between 8 and 10 years of age. The subjects completed the Child Perceptions Questionnaire (CPQ 8-10) while their parents/primary caregivers completed the Parental/Caregiver Perceptions Questionnaire (PCPQ), once before and then at 3 months after the surgery. There was a significant improvement in mean cumulative scores for both questionnaires. Significant improvements were seen in the oral symptoms, functional limitation (P<0.02), and social wellbeing domains (P<0.05) of the CPQ, and in the oral symptoms and functional limitation (P<0.05) domains of the PCPQ. The improvements in the physical domains were considered important for treatment success by both groups. The psychosocial domains were observed to be largely unaffected by the condition. The level of agreement between the two groups was higher for physical domains as compared to psychosocial domains. This study indicates that QoL outcomes in paediatric TMJ ankylosis patients are largely influenced by the physical factors, while the psychosocial factors play a secondary role.

Quality of life assessment in temporomandibular joint ankylosis patients after interpositional arthroplasty: a prospective study.

Temporomandibular joint (TMJ) ankylosis significantly impacts both physical and psychosocial patient wellbeing. A complete evaluation of treatment outcomes necessitates knowing the extent to which a patient's quality of life (QoL) is impacted. This study was performed to evaluate the impact of TMJ ankylosis on QoL in 25 TMJ ankylosis patients treated by interpositional arthroplasty. The patients completed OHIP-14 and UWQoL questionnaires once before and then at 3 months after the surgery. There was a significant improvement in mean cumulative scores for both questionnaires. With the exception of functional limitation, all OHIP domains showed significant improvement. Preoperatively, the worst scores were found in the psychological distress domain, followed by the social handicap, physical pain and physical disability domains. More than half of the subjects (56%) reported having suicidal thoughts. Amongst the individual UWQoL domains, appearance, chewing, anxiety (P < 0.01), recreation and mood (P < 0.05) showed improved scores. Appearance and chewing were the top ranked priority domains before and after surgery. No significant change was found in speech, taste, sleep, or breathing. Psychosocial factors were found to play a much bigger role than previously thought. The physical, psychological, and social factors were intricately related and dynamically interacted with each other. Surgical treatment produced a definitive QoL improvement in the patients.

Assessment of the effectiveness of peripheral administration of fentanyl with lidocaine in inflamed dentoalveolar tissues.

Peripheral action of opioids for pain control, for which local inflammation has been shown to be crucial, is being increasingly used in clinical practice. The aim of this study was to evaluate the hypothesis that addition of fentanyl to lidocaine, when injected into inflamed dentoalveolar tissues, can improve the quality of analgesia during surgery. Seventy-one patients reporting with pain and tenderness in the maxillary tooth were assigned into the experimental (LAF) or control (LA) group in a prospective, randomized double-blind trial. The LAF group (n = 36) was injected submucosally with a mixture of 40 microg of fentanyl (0.8 ml) and 2% lidocaine hydrochloride with 1:200000 adrenaline (2 ml). In the LA group (n = 35) 0.9% of saline (0.8 ml) was added instead of fentanyl. The pain scores were recorded before injecting, 5 min after injection, and immediately after surgery using a visual analogue scale. The mean pain scores were not significantly different at all time intervals. Twelve patients in the LAF group (2.75+/-0.72 ml) and ten patients in the LA (2.90+/-0.70 ml) group required additional local anaesthetic to achieve pain control. In conclusion, there was no improvement in quality of intraoperative analgesia on addition of fentanyl to lidocaine in inflamed dentoalveolar tissues.

Aneurysmal bone cyst of the coronoid process of the mandible.

A rare case of aneurysmal bone cyst (ABC) located in the coronoid process of the mandible in a 12-year-old girl is presented. Treatment consisted of excision of the lesion through preauricular, submandibular and intraoral approach. An access osteotomy distal to second molar region was required to gain access to medial side of the coronoid process. To our knowledge, this is the third case of an aneurysmal bone cyst of the coronoid process of mandible. While examining a patient with a large expansile intrabony jaw cavity with thin peripheral bone, which is filled with blood without presence of bruit, thrills and pulse pressure, the diagnosis of aneurysmal bone cyst should be on top of the differential diagnosis list. Seventy-four to eighty-five percent of aneurysmal bone cysts of jaws occur in 10-20 years age group. Therefore, a pediatric dentist may be the first person to see such a lesion.

Desmoplastic ameloblastoma: a case report with fine-needle aspiration cytologic findings.

A case of desmoplastic ameloblastoma of the maxilla in a 25-yr-old woman is presented. Smears prepared from fine-needle aspiration cytology showed two populations of cellular elements: cohesive epithelial clusters with basaloid morphology present, mostly in bidimensional, irregularly outlined clusters with ill-formed palisading of nuclei at the periphery in some, and a mesenchymal component represented by 1) a sparse chunk of moderate-sized tissue fragments made up of spindle- or ovoid-shaped nuclei entrapped in mesenchymal matrix, and 2) many dissociated naked oval-to-spindle-shaped nuclei. The presence of epithelial and mesenchymal components and their benign nature lead us to consider the possibility of benign odontogenic tumors 1) of epithelial origin, such as ameloblastma with a stromal component, e.g., desmoplastic ameloblastoma; 2) of mesenchymal origin, such as odontogenic fibroma; and 3) of mixed epithelial and mesenchymal origin, such as ameloblastic fibroma. Excision and histopathological examination of this lesion confirmed the diagnosis of desmoplastic ameloblastoma. In the given clinical setting and radiological examination, the above cytological features suggest a benign odontogenic tumor, rather than precisely diagnosing any of the entities mentioned above. However, it is important to distinguish between these, since the treatment varies accordingly. The differential diagnosis is discussed.

Peripheral osteoma of mandible arising from anterior lingual alveolar plate--a case report.

Peripheral osteomas of the mandible are uncommon bony tumours. Of those that have been described, the location is normally posterior to the premolars on the lingual surface of the mandible or in the condylar area. This article presents a case of an atypical presentation of an osteoma arising from the anterior lingual alveolar cortical plate of the mandible.

Interaction of sickle erythrocytes with endothelial cells in the presence of endothelial cell conditioned medium induces oxidant stress leading to transendothelial migration of monocytes.

The abnormal adherence of sickle red blood cells (SS RBC) to endothelial cells has been thought to contribute to vascular occlusion, a major cause of morbidity in sickle cell disease (SCD). We determined whether the interaction of SS RBC with cultured endothelial cells induced cellular oxidant stress that would culminate in expression of cell adhesion molecules (CAMs) involved in the adhesion and diapedesis of monocytes and the adherence of SS reticulocytes. We showed that the interaction of SS RBC at 2% concentration in the presence of multimers of von Willebrand factor (vWf), derived from endothelial cell-derived conditioned medium (E-CM) with cultured human umbilical vein endothelial cells (HUVEC), resulted in a fivefold increased formation of thiobarbituric acid-reactive substances (TBARS) and activation of the transcription factor NF-kB, both indicators of cellular oxidant stress. Normal RBC show none of these phenomena. The oxidant stress-induced signaling resulted in an increased surface expression of a subset of CAMs, ICAM-1, E-selectin, and VCAM-1 in HUVEC. The addition of oxygen radical scavenger enzymes (catalase, superoxide dismutase) and antioxidant (probucol) inhibited these events. Additionally, preincubation of HUVEC with a synthetic peptide Arg-Gly-Asp (RGD) that prevents vWf-mediated adhesion of SS RBC reduced the surface expression of VCAM-1 and NF-kB activation. Furthermore, SS RBC-induced oxidant stress resulted in a twofold increase in the transendothelial migration of both monocyte-like HL-60 cells and human peripheral blood monocytes, and approximately a sixfold increase in platelet-endothelial cell adhesion molecule-1 (PECAM-1) phosphorylation, each of which was blocked by protein kinase C inhibitor and antioxidants. These results suggest that the adherence/contact of SS RBC to endothelial cells in large vessel can generate enhanced oxidant stress leading to increased adhesion and diapedesis of monocytes, as well as heightened adherence of SS reticulocytes, indicating that injury/activation of endothelium can contribute to vaso-occlusion in SCD.

Cysticercosis of the oral cavity: report of five cases and a review of literature.

This paper reports on five cases of cysticercosis of tongue and buccal mucosa, diagnosed on fine-needle aspiration cytology (FNAC), affecting child patients who presented between January 1994 and October 1997. Four cases presented with gradually increasing nodular swelling of the dorsum of tongue and in the fifth case the swelling was situated on the buccal mucosa of the left side. A clinical diagnosis of cysticercosis was not entertained in any of these patients, who each presented with a solitary lesion; instead, it was considered to be a benign cyst or benign tumour of salivary gland or mesenchymal tissue, before FNAC diagnosis. These lesions of the oral cavity may present first to a dentist and, in endemic areas, cysticercosis should be included in the differential diagnosis of solitary nodular lesions of the oral cavity, particularly in young individuals.

Oxidant stress-induced transendothelial migration of monocytes is linked to phosphorylation of PECAM-1.

Reactive oxygen species (ROS) are believed to cause vascular injury in the pathophysiology of atherosclerosis, diabetes, and vasoocclusion in sickle cell disease. Studies have shown that ROS causes increased adhesion of monocytes and neutrophils to the endothelium. We investigated the effects of tert-butylhydroperoxide (t-BuOOH), an inducer of oxidant stress, to determine the cellular signaling pathway leading to the transendothelial migration of polymorphonuclear leukocytes. Our studies revealed that signaling by t-BuOOH in human umbilical vein endothelial cells (HUVECs) causes a twofold increase in the transendothelial migration of monocyte-like HL-60 cells and a fivefold increase in platelet endothelial cell adhesion molecule-1 (PECAM-1) phosphorylation. The transmigration induced by t-BuOOH was inhibited by an antibody to PECAM-1. These events were inhibited by antioxidants and inhibitors of protein kinase C, p21ras and glutathione synthesis. However, treatment of HUVECs with the phosphatase inhibitor calyculin A augmented the t-BuOOH-mediated transendothelial migration of monocytes and PECAM-1 phosphorylation. Our results suggest that oxidative stress can induce the transendothelial migration of monocytes as a result of phosphorylation of PECAM-1, a crucial event in the diapedesis of leukocytes during pathophysiology of vascular diseases.

Diabetic RBC-induced oxidant stress leads to transendothelial migration of monocyte-like HL-60 cells.

Red blood cells (RBC) from patients with diabetes mellitus exhibit an increased propensity to adhere to cultured human umbilical vein endothelial cells (HUVEC) as a result of interaction of advanced glycation end products with their counter receptors, contributing to the pathogenesis of vascular complications. We determined whether the interaction of diabetic RBC with HUVEC induced cellular oxidant stress that would culminate in adherence and diapedesis of monocytes, these being initiating events in endothelial injury and atherogenesis. We show that the adherence of diabetic RBC (2% hematocrit), but not normal RBC, to HUVEC results in a fourfold increase in the production of lipid peroxides. Furthermore, diabetic RBC-induced oxidant stress causes a sixfold increase in platelet endothelial cell adhesion molecule-1 (PECAM-1) phosphorylation and doubles transendothelial migration of monocyte-like HL-60 cells; both are blocked by antioxidants and protein kinase C (PKC) inhibitors. Our results show that the adherence of diabetic RBC to endothelial cells initiates a cascade of cellular events resulting in PKC activation, causing PECAM-1 phosphorylation and concomitant transendothelial migration of monocytes. The increased diapedesis of monocytes, brought about by the interaction of diabetic RBC across vascular endothelium, may play an important role in accelerated atherosclerosis and cardiovascular disease in diabetics.

Non-familial cherubism--a case report.

A case of cherubism in a 9 year old boy with no familial history is presented. Clinical features, histologic appearance, radiographic findings, differential diagnosis and rationale for treatment is discussed.

Hypoxia induces PECAM-1 phosphorylation and transendothelial migration of monocytes.

Polymorphonuclear neutrophils (PMN) adhere to the vascular endothelium under hypoxic conditions, causing microvascular injury. The molecular mechanism of hypoxia-induced adhesion of PMN to and diapedesis through the vascular endothelium is poorly understood. We examined the effects of hypoxia on the transendothelial migration of monocytes. Exposure of human umbilical vein endothelial cells (HUVEC) cultured in Transwell chambers under low oxygen tension (3% O2 compared with 21% O2) resulted in an increased rate of migration of both monocyte-like HL-60 cells and human peripheral blood monocytes. Migration was inhibited by addition of an antibody to platelet endothelial cell adhesion molecule-1 (PECAM-1), a protein kinase C (PKC) inhibitor, or a platelet-activating factor (PAF)-receptor antagonist. In HUVEC, hypoxic conditions (1, 3, 5, and 14% O2) increased the phosphorylation of PECAM-1. The extent of phosphorylation of PECAM-1 was inversely related to the concentration of oxygen to which HUVEC were exposed. Hypoxia-induced phosphorylation of PECAM-1 was inhibited by either a PKC inhibitor or a PAF-receptor antagonist, indicating the involvement of hypoxia-induced release of PAF in both PKC activation and the concomitant phosphorylation of PECAM-1. These results were substantiated by the findings that treatment of HUVEC with 100 nM PAF under normoxic conditions augmented 11.8-fold the phosphorylation of PECAM-1 and twofold increase in the transendothelial migration of monocyte-like HL-60 cells. We conclude that PAF, produced by cultured endothelial cells in response to hypoxia, acts in an autocrine fashion to activate PKC, causing PECAM-1 phosphorylation and thus the transendothelial migration of monocytes.

Glucose-induced transmigration of monocytes is linked to phosphorylation of PECAM-1 in cultured endothelial cells.

The adherence of circulating monocytes to the endothelium, their migration into the subendothelium, and the subsequent formation of foam cells are initial events in the pathogenesis of atherosclerosis. However, the effect of hyperglycemia on the transendothelial migration of monocytes is not known. Exposure of human umbilical vein endothelial cells (HUVEC) cultured in a Transwell chamber to 25 mM D-glucose (a concentration representing a hyperglycemic state) for 2 h resulted in a twofold increase in the migration of vitamin D3-differentiated monocyte-like HL-60 cells. The migration was inhibited by addition of either an antibody to platelet-endothelial cell adhesion molecule-1 (PECAM-1) or a protein kinase C inhibitor, GF-109203X. In HUVEC, high concentrations of D-glucose (25 mM), but not of other sugars such as L-glucose, 2-deoxyglucose, D-galactose, or D-mannitol, caused a sevenfold increase in the phosphorylation of PECAM-1 as a result of activation of protein kinase C. The 25 mM D-glucose-induced PECAM-1 phosphorylation and transmigration of monocyte-like HL-60 cells were further increased by treatment of HUVEC with the phosphatase inhibitor calyculin A. These results suggest that direct phosphorylation of PECAM-1 in response to elevated glucose promotes transendothelial migration of monocytes, contributing to accelerated atherogenesis in diabetics.

Lipoxygenase metabolites induced expression of adhesion molecules and transendothelial migration of monocyte-like HL-60 cells is linked to protein kinase C activation.

Studies have shown that, among lipoxygenase metabolites examined, 15(S)-hydroperoxy-5,8,11,13-eicosa-tetraenoic acid (15[S]-HPETE), at micromolar concentrations, selectively causes injury to cultured endothelial cells. We investigated whether physiologically relevant concentrations of lipoxygenase metabolites affected the expression of cell adhesion molecules (CAMs) involved in the adhesion of leukocytes and/or the accumulation of leukocytes in the vascular endothelium, these being the initial events in endothelial cell injury. Among lipoxygenase metabolites, 15(S)-HPETE and 12(S)-HETE, at nanomolar concentrations, induced surface expression of a subset of cell adhesion molecules (CAM), ICAM-1, ELAM-1, and VCAM-1, in human umbilical vein endothelial cells (HUVEC), which is associated with an increased binding activity of the transcription factor, NF-kappa B, to the consensus motif common to the CAM genes in the HUVEC nuclear extracts. Furthermore, 15(S)-HPETE (1 nM) caused a threefold increase in the rate of transendothelial migration of vitamin D3-differentiated HL-60 monocyte-like cells and showed a thirtyfold increase in the phosphorylation of PECAM-1, an adhesion molecule involved in endothelial cell-cell adhesion. Both an antibody to PECAM-1 and the protein kinase C inhibitor, GF 109203X, reduced 15(S)-HPETE-induced transmigration of monocyte-like HL-60 cells by approximately 75% and 85%, respectively. Treatment of HUVEC with a phosphatase inhibitor, calyculin A, augmented both the phosphorylation of PECAM-1 and transmigration of monocyte-like HL-60 cells induced by 15(S)-HPETE. Our results show that 15(S)-HPETE, at physiological concentrations, induced activation of protein kinase C in HUVEC and leads to the phosphorylation of PECAM-1, thus facilitating the migration of monocyte-like HL-60 cells across the endothelial cell monolayer. It is suggested that phosphorylation/dephosphorylation events in PECAM-1 are important in regulating the trafficking of monocytes across the endothelial cell monolayer.

Cigarette smoke condensate-induced adhesion molecule expression and transendothelial migration of monocytes.

Cigarette smoking is clearly linked with increased incidence of atherosclerosis and cardiovascular disease. The adherence of blood monocytes to the endothelium, followed by their migration beneath the endothelium, are initiating events in the formation of foam cells, promoting atherogenesis. We show that cigarette smoke condensate (CSC)-induced surface expression of a subset of cell adhesion molecules (CAM) [intercellular adhesion molecule 1 (ICAM-1), endothelial leukocyte adhesion molecule 1 (ELAM-1), and vascular cell adhesion molecule 1 (VCAM-1)] in human umbilical vein endothelial cells (HUVEC) is associated with an increase in the binding activity of nuclear transcription factor NF-kappa B to the consensus motif common to the CAM genes. Furthermore, CSC (25 microgram/ml) both increases the rate of transendothelial migration of vitamin D3-differentiated monocyte-like cells across the HUVEC monolayer by 200% and causes an approximately 10-fold increases in the phosphorylation of platelet endothelial CAM (PECAM-1), an adhesion molecule located at intercellular junctions and involved in endothelial cell-cell adhesion. Our results show that CSC-induced activation of protein kinase C in endothelial cells initiates a signaling pathways, leading to heightened binding of NF-kappa B to specific DNA sequences, which in turn increases surface expression of the subset of CAMs. Furthermore, our studies demonstrate a link between the phosphorylation of PECAM-1 and the migration of blood monocytes across vascular endothelium.