Opportune Time of Tooth Extraction in Individuals Requiring Ventricular Assist Device Implantation: A Retrospective Cohort Study.

PURPOSE: Individuals with implantable ventricular assist devices (VADs) are at extremely high risk of bleeding, thromboembolism, and infection after undergoing invasive dental procedures. This study aimed to investigate the systemic and local complications of tooth extraction before and after VAD implantation. PATIENTS AND METHODS: This retrospective cohort study was conducted at a single center. Oral surgical procedures were performed in patients before and/or after left VAD implantation for bridge-to-heart transplantation between April 2013 and December 2017. In this study, the medical charts of the patients were retrospectively reviewed. Data about pre-extraction complete blood count, coagulation profile, biochemical profile, and incidence of local and systemic complications were compared in patients undergoing tooth extraction before VAD implantation (b-VAD group) versus after VAD implantation (a-VAD group). RESULTS: In total, 28 inpatients underwent 36 oral surgical procedures before and/or after VAD implantation. Moreover, 24 tooth extractions were performed in the b-VAD group, and 12 were performed in the a-VAD group. The incidence of post-extraction bleeding was higher in the a-VAD group (P = .001, Mann-Whitney U test), and a significant difference was observed in terms of activated partial thromboplastin time (P = .010, Mann-Whitney U test). Systemic complications associated with VADs included cerebral infarction (n = 2) and driveline infection (n = 1). Post-extraction bleeding was observed within 90 days after VAD implantation in all patients who underwent tooth extraction. CONCLUSIONS: The risk of bleeding after tooth extraction was higher in the a-VAD group (67%) than in the b-VAD group (13%). In 3 cases, VAD-related systemic complications developed within a short period after tooth extraction. The extraction management in the b-VAD group could be controlled without causing any problem. Hence, the opportune time of tooth extraction is before VAD implantation.

Applying orthodontic tooth extrusion in a patient treated with bisphosphonate and irradiation: a case report.

Bisphosphonates and irradiation are useful medical treatments, but can often cause oral complications such as medication-related oral necrosis of the jaw (MRONJ) and osteoradionecrosis (ORN) during oral surgery, including tooth extraction. Therefore, we should take all risks into consideration carefully before choosing dental treatment for patients with a medical history of such therapies. A 55-year-old woman who underwent cord blood transplantation to treat extranodal natural killer T (NK/T) cell lymphoma (nasal type IVB) had a medical history of bisphosphonate and irradiation treatments. We treated her residual tooth root by applying orthodontic extrusion to avoid extraction and successfully restored the tooth. Application of an orthodontic tooth extrusion technique for conservative treatment of a residual tooth is a useful means of avoiding MRONJ or ORN in patients who have a medical history of bisphosphonate and irradiation treatments.

Surface vacuolar ATPase in ameloblastoma contributes to tumor invasion of the jaw bone.

Ameloblastoma is the most common benign odontogenic tumor in Japan. It is believed that it expands in the jaw bone through peritumoral activation of osteoclasts by receptor activator of nuclear factor kappa-B ligand (RANKL) released from the ameloblastoma, as in bone metastases of cancer cells. However, the clinical features of ameloblastoma, including its growth rate and patterns of invasion, are quite different from those of bone metastasis of cancer cells, suggesting that different underlying mechanisms are involved. Therefore, in the present study, we examined the possible mechanisms underlying the invasive expansion of ameloblastoma in the jaw bone. Expression levels of RANKL assessed by western blotting were markedly lower in ameloblastoma (AM-1) cells than in highly metastatic oral squamous cell carcinoma (HSC-3) cells. Experiments coculturing mouse macrophages (RAW264.7) with AM-1 demonstrated low osteoclastogenic activity, as assessed by tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cell formation, probably because of low release of RANKL, whereas cocultures of RAW264.7 with HSC-3 cells exhibited very high osteoclastogenic activity. Thus, RANKL release from AM-1 appeared to be too low to generate osteoclasts. However, AM-1 cultured directly on calcium phosphate-coated plates formed resorption pits, and this was inhibited by application of bafilomycin A1. Furthermore, vacuolar-type H+-ATPase (V-ATPase) and H+/Cl- exchange transporter 7 (CLC-7) were detected on the surface of AM-1 cells by plasma membrane biotinylation and immunofluorescence analysis. Immunohistochemical analysis of clinical samples of ameloblastoma also showed plasma membrane-localized V-ATPase and CLC-7 in the epithelium of plexiform, follicular and basal cell types. The demineralization activity of AM-1 was only 1.7% of osteoclasts demineralization activity, and the growth rate was 20% of human normal skin keratinocytes and HSC-3 cells. These results suggest that the slow expansion of several typical types of ameloblastomas in jaw bone is attributable to its slow growth and low demineralization ability.

Targeted sonography using an image fusion technique for evaluation of incidentally detected breast lesions on chest CT: a pilot study.

BACKGROUND: With increasing use of computed tomography (CT), incidentally detected breast lesions are being encountered more frequently. The aim of our study was to verify the utility of targeted sonography using an image fusion technique, real-time virtual sonography (RVS) that coordinates real-time sonography images with previously obtained CT images using a magnetic position tracking system, for evaluation of incidentally detected breast lesions on chest CT. METHODS: Eleven lesions in 11 women with no history of breast cancer who were referred to our unit for assessment of breast lesions incidentally detected on CT were enrolled in this study. To assess the efficacy of targeted sonography using RVS, we analyzed the frequency of sonographic detection of incidentally detected breast lesions and the difference between sonography- and CT-determined diameters. RESULTS: Using RVS guidance, all 11 lesions were sonographically detected. Ten (91 %) of 11 lesions underwent sonography-guided biopsy, yielding a success rate of 90 % (9/10). The remaining sonography-guided biopsy failure lesion required surgical biopsy for definitive diagnosis; this was performed after RVS was used to mark CT imaging information onto the breast surface. Four (36 %) lesions subsequently proved to be malignant. The mean diameters provided by RVS were 14.9 ± 6.7 mm for sonography and 16.8 ± 7.5 mm for CT (p = 0.538). CONCLUSION: Using RVS, a sonographic probe was precisely guided to the lesions. Our results suggest that targeted sonography using RVS is a useful technique for identifying incidentally detected breast lesions on chest CT.

Cylindrical corrective osteotomy for Madelung deformity using a computer simulation: case report.

We report an adolescent patient with Madelung deformity that we successfully treated by cylindrical corrective osteotomy of the distal radius. We used customized surgical guides, which were designed based on preoperative 3-dimensional computer simulation.

Voltage-sensing phosphatase reveals temporal regulation of TRPC3/C6/C7 channels by membrane phosphoinositides.

TRPC3/C6/C7 channels, a subgroup of classical/canonical TRP channels, are activated by diacylglycerol produced via activation of phospholipase C (PLC)-coupled receptors. Recognition of the physiological importance of these channels has been steadily growing, but the mechanism by which they are regulated remains largely unknown. We recently used a membrane-resident danio rerio voltage-sensing phosphatase (DrVSP) to study TRPC3/C6/C7 regulation and found that the channel activity was controlled by PtdIns(4,5)P(2)-DAG signaling in a self-limiting manner (Imai Y et al., the Journal of Physiology, 2012). In this addendum, we present the advantages of using DrVSP as a molecular tool to study PtdIns(4,5)P(2) regulation. DrVSP should be readily applicable for studying phosphoinositide metabolism-linked channel regulation as well as lipid dynamics. Furthermore, in comparison to other modes of self-limiting ion channel regulation, the regulation of TRPC3/C6/C7 channels seems highly susceptible to activation signal strength, which could potentially affect both open duration and the time to peak activation and inactivation. Dysfunction of such self-limiting regulation may contribute to the pathology of the cardiovascular system, gastrointestinal tract and brain, as these channels are broadly distributed and affected by numerous neurohormonal agonists.

Counteracting effect of TRPC1-associated Ca2+ influx on TNF-α-induced COX-2-dependent prostaglandin E2 production in human colonic myofibroblasts.

TNF-α-NF-κB signaling plays a central role in inflammation, apoptosis, and neoplasia. One major consequence of this signaling in the gut is increased production of prostaglandin E(2) (PGE(2)) via cyclooxygenase-2 (COX-2) induction in myofibroblasts, which has been reported to be dependent on Ca(2+). In this study, we explored a potential role of canonical transient receptor potential (TRPC) proteins in this Ca(2+)-mediated signaling using a human colonic myofibroblast cell line CCD-18Co. In CCD-18Co cell, treatment with TNF-α greatly enhanced Ca(2+) influx induced by store depletion along with increased cell-surface expression of TRPC1 protein (but not of the other TRPC isoforms) and induction of a Gd(3+)-sensitive nonselective cationic conductance. Selective inhibition of TRPC1 expression by small interfering RNA (siRNA) or functionally effective TRPC1 antibody targeting the near-pore region of TRPC1 (T1E3) antagonized the enhancement of store-dependent Ca(2+) influx by TNF-α, whereas potentiated TNF-α induced PGE(2) production. Overexpression of TRPC1 in CCD-18Co produced opposite consequences. Inhibitors of NF-κB (curcumin, SN-50) attenuated TNF-α-induced enhancement of TRPC1 expression, store-dependent Ca(2+) influx, and COX-2-dependent PGE(2) production. In contrast, inhibition of calcineurin-nuclear factor of activated T-cell proteins (NFAT) signaling by FK506 or NFAT Activation Inhibitor III enhanced the PGE(2) production without affecting TRPC1 expression and the Ca(2+) influx. Finally, the suppression of store-dependent Ca(2+) influx by T1E3 antibody or siRNA knockdown significantly facilitated TNF-α-induced NF-κB nuclear translocation. In aggregate, these results strongly suggest that, in colonic myofibroblasts, NF-κB and NFAT serve as important positive and negative transcriptional regulators of TNF-α-induced COX-2-dependent PGE(2) production, respectively, at the downstream of TRPC1-associated Ca(2+) influx.