Excessive sliding occurs in surgical treatment for pertrochanteric fractures with posterior displacement of the head and neck fragment. In such cases, we recommend appropriate reduction prior to internal fixation.

Background and aim The pathophysiology of rheumatoid arthritis (RA) is characterized by excess production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) by neutrophils and macrophages in synovium. Additionally, these cytokines promote the production of reactive oxygen species (ROS), and increased production of matrix metalloproteinases (MMPs), including MMP-3, in synoviocytes that result in joint destruction. There is limited information on how proteolytic enzymes such as MMP-3 can be regulated. We evaluated the effect of the antioxidant N -acetylcysteine (NAC) on RA and identified the relationship between the c-Jun N terminal kinase (JNK) pathway and MMP-3. We hypothesized that elucidating this relationship would lead to novel therapeutic approaches to RA treatment and management. Methods We investigated the effect of administering a low dose (1000 μM or less) of an antioxidant (NAC) to human rheumatoid fibroblast-like synoviocytes (MH7A cells). We also investigated the response of antioxidant genes such as nuclear factor erythroid -derived 2-related factor 2 (Nrf2) and Sequestosome 1 (p62). The influence of MMP-3 expression on the JNK pathway leading to joint destruction and the mechanisms underlying this relationship were investigated through primary dispersion culture cells collected from the synovial membranes of RA patients, consisting of rheumatoid arthritis-fibroblast-like synoviocytes (RA-FLS). Results Low-dose NAC (1000 μM) increased the expression of Nrf2 and phospho-p62 in MH7A cells, activating antioxidant genes, suppressing the expression of MMP-3, and inhibiting the phosphorylation of JNK. ROS, MMP-3 expression, and IL-6 was suppressed by administering 30 μM of SP600125 (a JNK inhibitor) in MH7A cells. Furthermore, the administration of SP600125 (30 μM) to RA-FLS suppressed MMP-3. Conclusions We demonstrated the existence of an MMP-3 suppression mechanism that utilizes the JNK pathway in RA-FLS. We consider that the JNK pathway could be a target for future RA therapies.

Porphyromonas gingivalis infection can lead to periodontitis and dysbiosis, which are known risk factors for rheumatoid arthritis (RA). We investigated whether P. gingivalis administration affected bone regeneration in mice with or without arthritis. We administered P. gingivalis to male DBA/1 J mice that were or were not sensitised to type II collagen-induced arthritis (CIA). All mice underwent drilling of bilateral femurs. We histologically evaluated new bone regeneration (bone volume of the defect [BVd]/tissue volume of the defect [TVd]) using micro-computed tomography (micro-CT), osteoclast number/bone area, and active osteoblast surface/bone surface (Ob.S/BS). We measured serum cytokine levels and bone mineral density of the proximal tibia using micro-CT. CIA resulted in significantly reduced bone regeneration (BVd/TVd) at all time-points, whereas P. gingivalis administration showed similar effects at 2 weeks postoperatively. CIA resulted in higher osteoclast number/bone area and lower Ob.S/BS at 2 and 3 weeks postoperatively, respectively. However, P. gingivalis administration resulted in lower Ob.S/BS only at 2 weeks postoperatively. During later-stage bone regeneration, CIA and P. gingivalis administration synergistically decreased BVd/TVd, increased serum tumour necrosis factor-α, and resulted in the lowest bone mineral density. Therefore, RA and dysbiosis could be risk factors for prolonged fracture healing.

The characteristics of biogas-oxygen diffusion flames were experimentally investigated using small counterflow burners, where the apparent equivalence ratio was set to unity. The flame thickness and flame diameter were determined as functions of the inner diameter of burners, the distance between burners and the flow rate of gases. When burners with large inner diameter were used, diffusion flames were observed in small burner distance. The flame thickness and flame diameter decreased as the burner distance became smaller, and they increased as the flow rate became larger. The flame stretch had a great influence on the flame thickness, i.e. the flame thickness decreased monotonously as the flame stretch rate became larger. In addition, the relation between flame thickness and flame stretch depended strongly on the inner diameter of burners and the flow rate of gases.

To determine the effect of tocilizumab (TCZ) on reactive oxygen species (ROS) in 11 patients with rheumatoid arthritis (RA), reactive oxygen metabolites (d-ROM) were measured using a Free Radical Elective Evaluator. The Disease Activity Score (DAS28) and matrix metalloproteinase-3 (MMP-3) level were also evaluated. d-ROM measured 392 ± 110 Carratelli units [U. CARR] on initiation of TCZ, and significantly decreased to 237 ± 82, 248 ± 88, and 226 ± 91 U.CARR after 3, 6, and 12 months, respectively (p < 0.05). The DAS28-4-ESR was 4.77 ± 1.0 on initiation of TCZ, and significantly decreased to 2.19 ± 1.23, 1.51 ± 0.71, and 1.48 ± 0.48 after 3, 6, and 12 months, respectively (p < 0.05). Serum MMP-3 level was 197 ± 150 ng/ml on initiation of TCZ, and was significantly decreased to 92 ± 56, 73 ± 53, and 69 ± 41 ng/ml after 3, 6, and 12 months, respectively (p < 0.05). Pearson analysis showed that d-ROM value was significantly correlated with DAS28 (r = 0.543, p < 0.05), but not with MMP-3 (r = 0.174, p = 0.29). TCZ was found to rapidly and significantly decrease ROS in patients with RA, and d-ROM value may be useful as a marker of disease activity of RA.