Examination of the relationship between masseter muscle activity during sleep and wakefulness measured by using a wearable electromyographic device.

Purpose This study aimed to measure masseter muscle activity throughout the day in outpatients suspected of having awake bruxism (AB) and/or sleep bruxism (SB) and examine the relationship between AB and SB by comparing muscle activity during daytime wakefulness and nighttime sleep.Methods Fifty outpatients with suspected SB and/or AB participated in this study. A single-channel wearable electromyogram (EMG) device was used for EMG recording. The selected EMG bursts were divided into bursts during sleep (S-bursts) and bursts during awake state (A-bursts). The number of bursts per hour, average burst duration, and ratio of burst peak value to maximum voluntary contraction were calculated for both the S- and A-bursts. These values of the S- and A-bursts were then compared, and the correlations between them were analyzed. Additionally, the ratios of phasic and tonic bursts in the S- and A-bursts were compared.Results The number of bursts per hour was significantly higher for A-bursts than for S-bursts. No significant correlation was found between the numbers of S- and A-bursts. The ratio of phasic bursts was large and that of tonic bursts was small in both the S- and A-bursts. A comparison of the S- and A-bursts showed that the S-bursts had a significantly lower ratio of phasic bursts and higher ratio of tonic bursts than the A-bursts.Conclusions The number of masseteric EMG bursts during wakefulness did not show any association with that during sleep. It became clear that sustained muscle activity was not dominant in AB.

Frequency distribution of the number and amplitude of electromyographic waveforms of the masseter muscle during sleep in patients with a clinical diagnosis of sleep bruxism.

OBJECTIVE: This study aimed to clarify frequency distribution of number and peak amplitude of electromyographic (EMG) waveforms of sleep bruxism (SB) in outpatients with clinical diagnosis of SB (probable bruxer: P-bruxer). METHODS: Subjects were 40 P-bruxers. Masseteric EMG during sleep was measured at home using a wearable EMG system. EMG waveforms with amplitude of more than two times the baseline and with duration of 0.25 s were extracted as SB bursts. Clusters of bursts, i.e. SB episodes, were also scored. RESULTS: There were large variations among the subjects in numbers of SB bursts and episodes and in burst peak amplitude. As for burst peak amplitude within a subject, a wide right-tailed frequency distribution was shown with the highest frequency at the class of 5-10% maximum voluntary contraction. CONCLUSION: The number and amplitude of SB waveforms for P-bruxers were distributed over a wide range, indicating the existence of large individual differences.

[Satisfaction and Difficulties in the Daily Life of Patients with Breast Cancer Who Received Chemotherapy through a Central Venous Port System-A Questionnaire Survey].

We conducted a questionnaire survey of patients with breast cancer who underwent implantation of a subcutaneous central venous port system for chemotherapy; we aimed to evaluate their satisfaction with the port and difficulties in daily life. Overall, 130 patients with breast cancer who underwent port implantation for chemotherapy between 2016 and 2018 responded to our survey. Although the overall satisfaction was high(78.5%), 82(63.1%)patients reported difficulties in daily life, such as"pain or discomfort,""irritation over the implanted area while wearing a seat belt,"and"unable to wear a bag across their bodies."Some patients(10.8%)responded that these negative factors were associated with difficulties in carrying out social roles. The proportion of patients who understood the explanation provided before port implantation was 80.0%, and the satisfaction of these patients tended to be high(85.6%).

Chronological immunolocalization of sclerostin and FGF23 in the mouse metaphyseal trabecular and cortical bone.

To assess the chronological participation of sclerostin and FGF23 in bone metabolism, this study tracked the immunolocalization of sclerostin and FGF23 in the metaphyses of murine long bones from embryonic day 18 (E18) through 1 day after birth, 1 week, 2 weeks, 4 weeks, 8 weeks, and 20 weeks of age. We have selected two regions in the metaphyseal trabeculae for assessing sclerostin and FGF23 localization: close to the chondro-osseous junction, i.e., bone modeling site even in the adult animals, and the trabecular region distant from the growth plate, where bone remodeling takes place. As a consequence, sclerostin-immunopositive osteocytes could not be observed in both close and distant trabecular regions early at the embryonic and young adult stages. However, osteocytes gradually started to express sclerostin in the distant region earlier than in the close region of the trabeculae. Immunoreactivity for FGF23 was observed mainly in osteoblasts in the early stages, but detectable in osteocytes in the later stages of growth in trabecular and cortical bones. Fgf23 was weakly expressed in the embryonic and neonatal stages, while the receptors, Fgfr1c and αKlotho were strongly expressed in femora. At the adult stages, Fgf23 expression became more intense while Fgfr1c and aKlotho were weakly expressed. These findings suggest that sclerostin is secreted by osteocytes in mature bone undergoing remodeling while FGF23 is synthesized by osteoblasts and osteocytes depending on the developmental/growth stage. In addition, it appears that FGF23 acts in an autocrine and paracrine fashion in fetal and neonatal bones.

Ultrastructural and biochemical aspects of matrix vesicle-mediated mineralization.

Matrix vesicle-mediated mineralization is an orchestrated sequence of ultrastructural and biochemical events that lead to crystal nucleation and growth. The influx of phosphate ions into the matrix vesicle is mediated by several proteins such as TNAP, ENPP1, Pit1, annexin and so forth. The catalytic activity of ENPP1 generates pyrophosphate (PPi) using extracellular ATPs as a substrate, and the resultant PPi prevents crystal overgrowth. However, TNAP hydrolyzes PPi into phosphate ion monomers, which are then transported into the matrix vesicle through Pit1. Accumulation of Ca2+ and PO43- inside matrix vesicles then induces crystalline nucleation, with calcium phosphate crystals budding off radially, puncturing the matrix vesicle's membrane and finally growing out of it to form mineralized nodules.

Histochemical assessment for osteoblastic activity coupled with dysfunctional osteoclasts in c-src deficient mice.

Since osteoblastic activities are believed to be coupled with osteoclasts, we have attempted to histologically verify which of the distinct cellular circumstances, the presence of osteoclasts themselves or bone resorption by osteoclasts, is essential for coupled osteoblastic activity, by examining c-fos-/- or c-src-/- mice. Osteopetrotic c-fos deficient (c-fos-/-) mice have no osteoclasts, while c-src deficient (c-src-/-) mice, another osteopetrotic model, develop dysfunctional osteoclasts due to a lack of ruffled borders. c-fos-/- mice possessed no tartrate-resistant acid phosphatase (TRAPase)-reactive osteoclasts, and showed very weak tissue nonspecific alkaline phosphatase (TNALPase)-reactive mature osteoblasts. In contrast, c-src-/- mice had many TNALPase-positive osteoblasts and TRAPase-reactive osteoclasts. Interestingly, the parallel layers of TRAPase-reactive/osteopontin-positive cement lines were observed in the superficial region of c-src-/- bone matrix. This indicates the possibility that in c-src-/- mice, osteoblasts were activated to deposit new bone matrices on the surfaces that osteoclasts previously passed along, even without bone resorption. Transmission electron microscopy demonstrated cell-to-cell contacts between mature osteoblasts and neighboring ruffled border-less osteoclasts, and osteoid including many mineralized nodules in c-src-/- mice. Thus, it seems likely that osteoblastic activities would be maintained in the presence of osteoclasts, even if they are dysfunctional.

Histochemical Examination on Periodontal Tissues of Klotho-Deficient Mice Fed With Phosphate-Insufficient Diet.

To elucidate which of elevated serum concentration of inorganic phosphate (Pi) or disrupted signaling linked to αklotho/fibroblast growth factor 23 (FGF23) is a predominant regulator for senescence-related degeneration seen in αKlotho-deficient mice, we have examined histological alteration of the periodontal tissues in the mandibular interalveolar septum of αKlotho-deficient mice fed with Pi-insufficient diet. We prepared six groups of mice: wild-type, kl/kl, and αKlotho-/- mice with normal diet or low-Pi diet. As a consequence, kl/klnorPi and αKlotho-/-norPi mice showed the same abnormalities in periodontal tissues: intensely stained areas with hematoxylin in the interalveolar septum, dispersed localization of alkaline phosphatase-positive osteoblasts and tartrate-resistant acid phosphatase-reactive osteoclasts, and accumulation of dentin matrix protein 1 in the osteocytic lacunae. Although kl/kllowPi mice improved these histological abnormalities, αKlotho-/- lowPi mice failed to normalize those. Gene expression of αKlotho was shown to be increased in kl/kl lowPi specimens. It seems likely that histological abnormalities of kl/kl mice have been improved by the rescued expression of αKlotho, rather than low concentration of serum Pi. Thus, the histological malformation in periodontal tissues in αKlotho-deficient mice appears to be due to not only increased concentration of Pi but also disrupted αklotho/FGF23 signaling.

Localization of Minodronate in Mouse Femora Through Isotope Microscopy.

Minodronate is highlighted for its marked and sustained effects on osteoporotic bones. To determine the duration of minodronate's effects, we have assessed the localization of the drug in mouse bones through isotope microscopy, after labeling it with a stable nitrogen isotope ([(15)N]-minodronate). In addition, minodronate-treated bones were assessed by histochemistry and transmission electron microscopy (TEM). Eight-week-old male ICR mice received [(15)N]-minodronate (1 mg/kg) intravenously and were sacrificed after 3 hr, 24 hr, 1 week, and 1 month. Isotope microscopy showed that [(15)N]-minodronate was present mainly beneath osteoblasts rather than nearby osteoclasts. At 3 hr after minodronate administration, histochemistry and TEM showed osteoclasts with well-developed ruffled borders. However, osteoclasts were roughly attached to the bone surfaces and did not feature ruffled borders at 24 hr after minodronate administration. The numbers of tartrate-resistant acid phosphatase-positive osteoclasts and alkaline phosphatase-reactive osteoblastic area were not reduced suddenly, and apoptotic osteoclasts appeared in 1 week and 1 month after the injections. Von Kossa staining demonstrated that osteoclasts treated with minodronate did not incorporate mineralized bone matrix. Taken together, minodronate accumulates in bone underneath osteoblasts rather than under bone-resorbing osteoclasts; therefore, it is likely that the minodronate-coated bone matrix is resistant to osteoclastic resorption, which results in a long-lasting and bone-preserving effect.