Pulp revascularization for immature replanted teeth: a case report

Immature avulsed teeth are not usually treated with pulp revascularization because of the possibility of complications. However, this therapy has shown success in the treatment of immature teeth with periapical lesions. This report describes the case of an immature replanted tooth that was successfully treated by pulp revascularization. An 8‐year‐old boy suffered avulsion on his maxillary left lateral incisor. The tooth showed incomplete root development and was replanted after 30 minutes. After diagnosis, revascularization therapy was performed by irrigating the root canal and applying a calcium hydroxide paste and 2% chlorhexidine gel for 21 days. In the second session, the intracanal dressing was removed and a blood clot was stimulated up to the cervical third of the root canal. Mineral trioxide aggregate was placed as a cervical barrier at the entrance of the root canal and the crown was restored. During the follow‐up period, periapical repair, apical closure and calcification in the apical 4 mm of the root canal was observed. An avulsed immature tooth replanted after a brief extra‐alveolar period and maintained in a viable storage medium may be treated with revascularization.     

Novel and recurrent germline LEMD3 mutations causing Buschke–Ollendorff syndrome and osteopoikilosis but not isolated melorheostosis

Mutations in the LEMD3 gene were recently incriminated in Buschke–Ollendorff syndrome (BOS) and osteopoikilosis, with or without melorheostosis. The relationship of this gene with isolated sporadic melorheostosis is less clear. We investigated LEMD3 in a two-generation BOS family showing an extremely variable expression of the disease, in a sporadic patient with skin features of BOS, and in an additional subject with isolated melorheostosis. We identified two different mutations, both resulting in a premature stop codon, in the two cases of BOS. The mutation (c.2564G>A) reported in the familial case is novel, while that observed in the sporadic case (c.1963C>T) has been previously reported in an American woman with osteopoikilosis and melorheostosis who had a family history of isolated osteopoikilosis. The search for mutations in DNA extracted from the peripheral blood, as well as skin and bone biopsies of the patient with melorheostosis failed to identify any pathogenic change. Our results further expand the LEMD3 mutation repertoire, corroborate the extreme interfamilial and intrafamilial clinical variability of LEMD3 mutations, and underline the lack of a clear phenotype–genotype correlation in BOS. The present study supports the general conclusion that LEMD3 mutations do not contribute to isolated sporadic melorheostosis. The genetic or epigenetic influences that are responsible for the development of melorheostosis require further investigation.     

Heat shock protein expression in cerebral vessels after subarachnoid hemorrhage

OBJECTIVE: The mechanisms of cerebral vasospasm after subarachnoid hemorrhage (SAH) remain controversial. Recent data have implicated two small heat shock proteins (HSPs), namely HSP20 and HSP27, in the regulation of vascular tone. Increases in the phosphorylation of HSP20 are associated with vasorelaxation, and increases in the phosphorylation of HSP27 are associated with impaired vasorelaxation. Therefore, we hypothesized that alterations in the expression and/or phosphorylation of these two small HSPs might play a role in cerebral vasospasm after SAH. METHODS: A rat model of endovascular perforation was used to induce SAH. Middle cerebral arteries were harvested from control animals, sham-treated animals, and animals with SAH, 48 hours after SAH induction. Dose-response curves for endothelium-independent (sodium nitroprusside, 10(-8) to 10(-4) mol/L) and endothelium-dependent (bradykinin, 10(-10) to 10(-5) mol/L) relaxing agents were recorded ex vivo. Physiological responses were correlated with the expression and phosphorylation of HSP20 and HSP27 by using one- and two-dimensional immunoblots. RESULTS: There was impaired endothelium-independent and endothelium-dependent relaxation in cerebral vessels after SAH. These changes were associated with decreased expression of both total and phosphorylated HSP20 and increases in the amount of phosphorylated HSP27. CONCLUSION: In this model, impaired relaxation of cerebral vessels after SAH was associated with increases in the amount of phosphorylated HSP27 and decreases in the expression and phosphorylation of HSP20. These data are consistent with alterations in the expression and phosphorylation of these small HSPs in other models of vasospasm.     

Identification of major loci controlling clinical manifestations of ankylosing spondylitis

OBJECTIVE: To identify genomic regions linked with determinants of age at symptom onset, disease activity, and functional impairment in ankylosing spondylitis (AS). METHODS: A whole genome linkage scan was performed in 188 affected sibling pair families with 454 affected individuals. Traits assessed were age at symptom onset, disease activity assessed by the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), and functional impairment assessed by the Bath Ankylosing Spondylitis Functional Index (BASFI). Parametric and nonparametric quantitative linkage analysis was performed using parameters defined in a previous segregation study. RESULTS: Heritabilities of the traits studied in this data set were as follows: BASDAI 0.49 (P = 0.0001, 95% confidence interval [95% CI] 0.23-0.75), BASFI 0.76 (P = 10(-7), 95% CI 0.49-1.0), and age at symptom onset 0.33 (P = 0.005, 95% CI 0.04-0.62). No linkage was observed between the major histocompatibility complex (MHC) and any of the traits studied (logarithm of odds [LOD] score <1.0). "Significant" linkage (LOD score 4.0) was observed between a region on chromosome 18p and the BASDAI. Age at symptom onset showed "suggestive" linkage to chromosome 11p (LOD score 3.3). Maximum linkage with the BASFI was seen at chromosome 2q (LOD score 2.9). CONCLUSION: In contrast to the genetic determinants of susceptibility to AS, clinical manifestations of the disease measured by the BASDAI, BASFI, and age at symptom onset are largely determined by a small number of genes not encoded within the MHC.     

Definition of disease flare in ankylosing spondylitis: the patients' perspective

OBJECTIVE: Ankylosing spondylitis (AS) is a systemic disorder occurring in genetically predisposed individuals. The disease course appears to be characterized by bouts of partial remission and flares. However, we have little understanding of what is a flare, why they occur, and what lasting effects they have on the patient. We examine the patient's perception of the factors important in defining flare. METHODS: Twenty group meetings of 7-12 participants were held over a one year period. A summary statement was written at the end of each discussion and patients were asked to sign the statement if they considered it to be an accurate summary of their answers, or to amend the statement where they disagreed. RESULTS: There were 214 patients questioned (169 men, 45 women; average disease duration 25 years; age of disease onset 22 years). Data show that the main symptoms of flare are pain (100% of groups), immobility (90%), fatigue (80%), and emotional symptoms (depression, withdrawal, anger) (75%). There are 2 types of flare: (1) localized: during which the symptoms affect one area; and (2) generalized: this is a severe event including all the above symptoms and a flu-like illness (fever, sweating) with hot, burning joints, muscle spasm, and increased sensitivity. All patients experience between one and 5 localized flares per year. Fifty-five percent of groups contained patients (n = 85) who experienced a generalized flare. The main perceived triggers of flare were stress (80%) and "overdoing it" (50%). Patients reported that a flare may last anywhere from a few days to a few weeks and relief from flare can be gained by analgesic injections (including opiates) from a doctor, relaxation, sleep, and cannabis (3 individuals). Three-quarters of the groups agreed that there was no longterm effect on the AS following a flare. CONCLUSION: There are 2 forms of flare: (1) localized to one area or (2) throughout the entire body. Examining the differences between these types of flares may aid our understanding of the biological mechanism of the disease process of AS and allow us to help relieve the symptoms of flare, a highly painful and often depressing phenomenon.     

The natural history of ankylosing spondylitis as defined by radiological progression

OBJECTIVE: Radiological status is an important objective endpoint in the assessment of ankylosing spondylitis (AS). We investigated the disease development of AS using radiological change. METHODS: The existing radiographs (n = 2,284) of 571 AS patients attending the Royal National Hospital for Rheumatic Diseases were scored retrospectively using the Bath Ankylosing Spondylitis Radiology Index. (1) Progression of disease was initially examined cross sectionally. Univariate analysis was used to examine factors associated with joint involvement. (2) Progression of disease was then examined longitudinally for patients with films at time of symptom onset. (3) Rate of progression of radiological change was calculated using longitudinal data of 2 sets of radiographs taken 10 years apart (patient number = 54). The results from this were used to extrapolate backwards to age at first radiological change. RESULTS: (1) Progression to cervical spine disease was a function of: disease duration, severity of hip and lumbar involvement, and a history of iritis (p < 0.001). Lumbar involvement was associated with disease duration, age now, and severity of cervical and hip involvement (p < 0.001). Hip involvement was a marker for cervical disease and associated with disease duration (p < 0.001). (2) Longitudinal analysis revealed marked variation among patients with a slow general rate of progression. (3) The progression of AS over any 10 year period is linear [first 10 years = 30% (SD 0.3) of potential change, 10-20 yrs = 40% (SD 0.3) change, 20-30 yrs = 35% (SD 0.4) change (p = 0.5)]. Backward extrapolation suggests that the approximate time of first radiological change is at the age of 8 years. CONCLUSION. (1) AS is a linearly progressive disease with about 35% change every 10 years. Spinal involvement is largely an expression of disease duration while the hips become involved in about 25% of individuals and may predict a more severe outcome for the cervical spine. (2) Backward extrapolation shows that the disease process may start as young as 8 years of age. However, the time interval between the disease trigger and radiological change remains unknown.     

Iatrogenic femoral pseudoaneurysms: thrombin injection after failed US-guided compression

Fifteen iatrogenic femoral pseudoaneurysms failed ultrasonography (US)-guided compression treatments. Despite concomitant antiplatelet or anticoagulation treatment, the 15 pseudoaneurysms were successfully and definitively treated without complication with US-guided thrombin injection. Results in this preliminary study suggest US-guided thrombin injection is a safe, expeditious, low-cost, and comfortable definitive treatment for femoral pseudoaneurysms that has advantages over both US-guided compression and open surgical repair.     

Acoustic neuroma--surgery or radiosurgery?

This paper discusses surgery and radiosurgery from the author's personal experience with both techniques. Multi-discipline assessment will allow the patient to make an informed decision regarding preferred management.