Although chronological changes in functional cup position do occur after THA, their magnitude is relatively low. However, posterior impingement is likely to occur, which may cause edge loading, wear of the polyethylene liner, and anterior dislocation of the hip. We believe that, for the combined anteversion technique, the safe zone should probably be 5°-10° narrower in patients predicted to show considerable changes in functional cup position compared with standard cases.

No abstract

Purpose Clinically, arthrogenic muscle inhibition (AMI) has a negative impact on functional recovery in musculoskeletal disorders. One possible technique to relieve AMI is motor imagery, which is widely used in neurological rehabilitation to enhance motor neuron excitability. The purpose of this study was to verify the efficacy of visually-assisted motor imagery against AMI using a human experimental pain model. Methods Ten healthy volunteers were included. Experimental ankle pain was induced by hypertonic saline infusion into unilateral Kager’s fat pad. Isotonic saline was used as control. Subjects were instructed to imagine while watching a movie in which repetitive motion of their own ankle or fingers was shown. H-reflex normalized by the motor response (H/M ratio) on soleus muscle, maximal voluntary contraction (MVC) force of ankle flexion, and contractile activities of the calf muscles during MVC were recorded at baseline, pre-intervention, post-intervention, and 10 minutes after the pain had subsided. Results Hypertonic saline produced continuous and constant peri-ankle pain (VAS peak [median]= 6.7 [2.1–8.4] cm) compared to isotonic saline (0 [0–0.8] cm). In response to pain, there were significant decreases in the H/M ratio, MVC and contractile activities (P<0.01), all of which were successfully reversed after the ankle motion imagery. In contrast, no significant changes were observed with the finger motion imagery. Conclusion Visually-assisted motor imagery improved the pain-induced AMI. Motor imagery of the painful joint itself would efficiently work for relieving AMI. This investigation possibly shows the potential of a novel and versatile approach against AMI for patients with musculoskeletal pain.

Purpose Mast cells are multifunctional in osteoarthritis (OA), and infiltration of activated mast cells likely contributes to disease severity and progression. However, the detailed mechanisms of action are unclear. The purpose of this study was to elucidate the role of mast cell infiltration in OA at histological level using a new mice model and to investigate pharmacological inhibitory effects of existing mast cell stabilizers in this model. Methods Mice were injected intra-articularly with monosodium iodoacetate (MIA 0.5 mg) or PBS on day 0, and PBS, with or without mast cells (MC: 1 × 106 cells) on day 14. They were divided into four groups: OA flare (MIA + MC), OA (MIA + PBS), MC non-OA (PBS + MC), and PBS non-OA (PBS + PBS). In OA flare, the MC stabilizer drug (tranilast: 400 mg/kg/day) or PBS was administered intraperitoneally from days 15 to 21. Results Histologically, modified Mankin score of the OA flare was significantly higher than that of OA (7.0 [1.8] vs. 3.3 [1.3], P < 0.05), and a larger number of mast cells was observed in OA flare than in OA (34.5 [6.3]/mm2 vs. 27.2 [2.3]/mm2, P < 0.05) on day 22. OA flare also showed acute exacerbation of pain and increased gene expression of pro-inflammatory cytokines and aggrecanase compared with OA. Administration of tranilast to OA flare-up provoked significant improvements in term of histological changes, pain, and gene expression at day 22. Conclusion Our novel model possibly mimics OA flare conditions, which may open a new strategy of disease-modifying treatment for OA, focused on controlling the multiple functions of mast cells.

This study reports on a 70-year-old man with recurrent cervical myelopathy 20 years after anterior decompression and fusion of C4–7 using a free vascularised strut graft. The recurrent myelopathy was secondary to a kyphotic deformity of a fractured graft and residual ossification of the posterior longitudinal ligament with stenosis at C3/4. Intra-operative spinal cord–evoked potentials indicated that spinal cord traction secondary to progressive kyphosis of the cervical spine after the graft fracture was the cause. The patient underwent laminoplasty at C3 and laminectomy at C4 to decompress the stenosis at C3/4 as well as posterior cervical spinal fusion at C3–7 with pedicle screws and a lateral mass screw and a bone graft to prevent further progression of the kyphosis. At postoperative 18 months, the patient's Japanese Orthopaedic Association score had improved to 14 from 8, and he could walk without support.