ミニープレートの破折

Mini-plate fracture was found in a case of the bone grafting after the segmental mandibular excision, and a case of osteomyelitis in the radiographic follow-up examinations. It was emphasized that usefulness of mini-plate would be evaluated by modification in shape and number of mini-plate used for fixation or reconstruction

Acute inflammation at a mandibular solitary horizontal incompletely impacted molar

Acute inflammation is frequently seen in the elderly around incompletely impacted molars located apart from molars or premolars. To identify the factors causing acute inflammation in the solitary molars without second molars or without second and first molars, ages of patients and rates of acute inflammation in 75 horizontal incompletely impacted mandibular molars in contact or not in contact with molars in subjects 41 years old or older were studied using orthopantomographs. Acute inflammation was seen in nine third molars out of 48 third molars in contact with second molars (18.8%), whereas acute inflammation was seen in 11 molars out of 19 solitary molars without second molars or without first and second molars (57.9%) (p < 0.01). The mean age of 48 subjects with third molars in contact with the second molar was 50.42 ± 7.62 years, and the mean age of 19 subjects with isolated molars was 65.16 ± 10.41 years (p < 0.0001). These indicate that a solitary horizontal incompletely impacted molar leads more frequently to acute inflammation along with aging due to possible bone resorption resulting from teeth loss

ステロイド使用による下顎頭骨坏死の1例

Avascular necrosis or osteonecrosis has been discussed as a possible cause of condylar degeneration and pain. Avascular necrosis is a degenerative disease originates from diminished blood flow in the bone marrow. Avascular necrosis is seen in relationship with idiopathic, corticosteroids, alcoholism, sickle cell disease, pregnancy, and Caisson\u27s disease. Corticosteroid has been suggested to be an etiologic factor affecting bone organization, fat metabolism, and blood vessel. Indeed, corticosteroid can affect the bilateral joints of the shoulder, hip, and knee. However, the occurrence of the avascular necrosis of in the temporomandibular joint alone has not been reported. The clinical, laboratory, radiographic, and imagings features of a case of the condylar process of the mandible are presented

顎舌骨筋運動ニューロンと一次求心線維のシナプス接合について

Horseradish peroxidase conjugated with wheat germ agglutinin (HRP-WGA) was injected into the muscle branch of the mylohyoid nerve in rats. HRP-labeled neuronal cell bodies were observed ipsilaterally in the caudal portion of the trigeminal mesencephalic nucleus and the ventromedial division of the trigeminal motor nucleus (Vmo.vm). Electron microscope observations were carried out on sections through Vmo.vm containing HRP-labeled cell bodies. Synaptic contacts were found between HRP-labeled axon terminals and HRP-labeled nerve cells. The results suggested that mylohyoid muscle spindle afferents are synaptic contacts on the mylohyoid motoneurons

Serum Antibody Against NY-ESO-1 and XAGE1 Antigens Potentially Predicts Clinical Responses to Anti–Programmed Cell Death-1 Therapy in NSCLC

Introduction: Programmed cell death-1 (PD-1) inhibitors effectively treat NSCLC and prolong survival. Robust biomarkers for predicting clinical benefits of good response and long survival with anti-PD-1 therapy have yet to be identified; therefore, predictive biomarkers are needed to select patients with benefits. Methods: We conducted a prospective study to explore whether serum antibody against NY-ESO-1 and/or XAGE1 cancer-testis antigens predicted primarily good clinical response and secondarily long survival with anti-PD-1 therapy for NSCLC. The serum antibody was detected by enzyme-linked immunosorbent assay, and tumor immune microenvironment and mutation burden were analyzed by immunohistochemistry and next-generation sequencing. Results: In the discovery cohort (n = 13), six antibody-positive NSCLC cases responded to anti-PD-1 therapy (two complete and four partial responses), whereas seven antibody-negative NSCLC cases did not. Antibody positivity was associated with good response and survival, regardless of tumor programmed death ligand 1 (PD-L1) expression, mutation burden, and CD8+ T-cell infiltration. In the validation cohort (n = 75), 17 antibody-positive NSCLC cases responded well to anti-PD-1 therapy as compared with 58 negative NSCLC cases (objective response rate 65% versus 19%, p = 0.0006) and showed significantly prolonged progression-free survival and overall survival. Antibody titers highly correlated with tumor reduction rates. In the multivariate analysis, response biomarkers were tumor programmed death ligand 1 expression and antibody positivity, and only antibody positivity was a significantly better predictive biomarker of progression-free survival (hazard ratio = 0.4, p = 0.01) and overall survival (hazard ratio = 0.2, p = 0.004). Conclusions: Our results suggest that NY-ESO-1 and/or XAGE1 serum antibodies are useful biomarkers for predicting clinical benefits in anti-PD-1 therapy for NSCLC and probably for other cancers

Low zone tolerance requires ICAM-1 expression to limit contact hypersensitivity elicitation.

Painting subsensitizing doses of contact sensitizers on skin (low-dose tolerization) induces antigen (Ag)-specific tolerance, known as low zone tolerance (LZT), which has been experimentally demonstrated by the inhibition of contact hypersensitivity (CHS). Although LZT resulted from the inhibition of the sensitization phase, the effects on the effector/elicitation phase remain unknown. L-selectin and ICAM-1 regulate leukocyte influx into inflamed tissues during the elicitation phase of CHS. LZT was investigated in mice lacking either L-selectin or ICAM-1 to evaluate the roles these leukocyte receptors play in LZT during the elicitation phase. Low-dose tolerization effectively suppressed CHS in wild-type and L-selectin-deficient mice, but not in ICAM-1-deficient mice. Low-dose-tolerized ICAM-1-deficient splenocytes effectively suppressed the elicitation phase in naive wild-type recipients. Sensitized ICAM-1-deficient splenocytes showed normal proliferative responses to the sensitizing Ag and generated normal CHS in wild-type recipients. Thus, ICAM-1 deficiency did not affect sensitization. LZT was associated with a lack of ICAM-1 upregulation after elicitation, suggesting a potentially mechanistic role for ICAM-1. The blockade of IL-10, a possible mediator of LZT, produced by hapten-specific suppressor cells, abrogated LZT and restored ICAM-1 upregulation. These results indicate that low-dose tolerization controls CHS by abrogating ICAM-1 upregulation during the elicitation phase