Adolescent idiopathic scoliosis correction by instrumented vertebral arthrodesis with autologous bone graft from local harvesting without bone substitute use: results with mean 3 year follow-up

Purpose

Bone substitutes’ advantage is enhancing arthrodesis biologic support without further autologous bone graft harvested from other skeleton sites, as from posterior iliac crests; however, in our experience, bone substitutes’ integration is often incomplete.

Methods

From 2012 to 2017, we operated 108 patients by posterior instrumented vertebral arthrodesis in adolescent idiopathic scoliosis (AIS) correction, mean main curve 80° Cobb, and mean age 12 years and 6 months, with all pedicle screws instrumentation in main curve/curves area and hooks at upper tip of implant; bone graft has been harvested only at vertebral level, without bone substitutes or autologous graft from other patient sites or allogenic bone graft. We matched this group with 98 patients previously operated in which we used calcium triphosphate.

Results

At 3 year mean follow-up, all patients in group treated with autologous bone graft only have complete and stable arthrodesis without loss of correction (mean curve 27° Cobb) or instrumentation failure. At 6 year mean follow-up in the group treated with autologous bone graft augmented by calcium triphosphate, 96 patients have stable arthrodesis without loss of correction (mean curve 24°), 1 case has implant break, and 1 case has 8° Cobb loss of correction.

Conclusion

Bone substitutes are a further cost in arthrodesis surgery and suboptimal integration leaves foreign bodies on vertebras. Our experience shows that all pedicle screw instrumentation and bracing after surgery obtain stable correction showing in time a solid arthrodesis with autologous bone only, harvested at local site, without bone substitutes or further bone graft.

Graphical abstract

Open image in new window

     

Comparative Motor Pre-clinical Assessment in Parkinson’s Disease Using Supervised Machine Learning Approaches

Millions of people worldwide are affected by Parkinson’s disease (PD), which significantly worsens their quality of life. Currently, the diagnosis is based on assessment of motor symptoms, but interest toward non-motor symptoms is increasing, as well. Among them, idiopathic hyposmia (IH) is associated with an increased risk of developing PD in healthy adults. In this work, a wearable inertial device, named SensFoot V2, was used to acquire motor data from 30 healthy subjects, 30 people with IH, and 30 PD patients while performing tasks from the MDS-UPDRS III for lower limb assessment. The most significant and non-correlated extracted parameters were selected in a feature array that can identify differences between the three groups of people. A comparative classification analysis was performed by applying three supervised machine learning algorithms. The system resulted able to distinguish between healthy and patients (specificity and recall equal to 0.967), and the people with IH can be identified as a separate class within a three-group classification (accuracy equal to 0.78). Thus, the system could support the clinician in objective assessment of PD. Further, identification of IH together with changes in motor parameters could be a non-invasive two-step approach to investigate the early onset of PD.     

Microparticles and autophagy: a new frontier in the understanding of atherosclerosis in rheumatoid arthritis

Microparticles (MPs) are small membrane vesicles released by many cell types under physiological and pathological conditions. In the last years, these particles were considered as inert cell debris, but recently many studies have demonstrated they could have a role in intercellular communication. Increased levels of MPs have been reported in various pathological conditions including infections, malignancies, and autoimmune diseases, such as rheumatoid arthritis (RA). RA is an autoimmune systemic inflammatory disease characterized by chronic synovial inflammation, resulting in cartilage and bone damage with accelerated atherosclerosis increasing mortality. According to the literature data, also MPs could have a role in endothelial dysfunction, contributing to atherosclerosis in RA patients. Moreover many researchers have shown that a dysregulated autophagy seems to be involved in endothelial dysfunction. Autophagy is a reparative process by which cytoplasmic components are sequestered in double-membrane vesicles and degraded on fusion with lysosomal compartments. It has been shown in many works that basal autophagy is essential to proper vascular function. Taking into account these considerations, we hypothesized that in RA patients MPs could contribute to atherosclerosis process by dysregulation of endothelial autophagy process.     

ZNF687 mutations are frequently found in pagetic patients from South Italy: implication in the pathogenesis of Paget's disease of bone

Paget's disease of bone (PDB) is a skeletal disorder whose molecular basis is not fully elucidated. However, 10% of patients show a familial PDB and 35% of them carry mutations in the SQSTM1 gene. We recently reported a founder mutation (p.Pro937Arg) in the ZNF687 gene, underlying PDB complicated by giant cell tumor (GCT/PDB) and rarely occurring in PDB patients without neoplastic degeneration. Since 80% of Italian GCT/PDB patients derive from Avellino, we hypothesized that ZNF687 mutation rate was higher in this region than elsewhere. Interestingly, our molecular analysis on 30 PDB patients showed that 33% hosted ZNF687 mutations, with the p.Pro937Arg identified in 8 familial cases. Two novel ZNF687 mutations (p.Pro665Leu and p.Gln784Glu) were detected in 2 sporadic patients. Only 2 subjects were positive for the p.Pro392Leu mutation in SQSTM1. ZNF687‐mutated patients showed a severe PDB, with a remarkable number of affected sites. in vitro studies revealed that the ZNF687‐mutant osteoclasts appeared as giant sized with up to 150 nuclei, never described in PDB. Finally, we also confirmed the causality of the p.Pro937Arg mutation in 4 additional GCT/PDB cases deriving from the same geographic area, indicating that PDB and GCT/PDB represent 2 sides of the same coin.     

The degree of HIV-1 amino acid variability is strictly related to different disease progression rates

The aim of this study is to evaluate the amino acid variability of HIV-1 Gp41, C2–V3, and Nef in a group of patients characterized by different disease progression rates. HIV-1 sequences were collected from 19 Long term non progressor patients (LTNPs), 9 slow progressors (SPs), and 11 rapid progressors (RPs). Phylogenetic trees were estimated by MEGA 6. Differences in amino acid variability among sequences belonging to the 3 groups have been evaluated by amino acid divergence, Shannon entropy analysis, and the number of amino acid mutations (defined as amino acid variations compared with HxB2). The involvement of amino acid mutations on epitope rich regions was also investigated. The population was mainly composed of males (74.3%) and HIV-1 subtype B strains (B: 92.32%, CRF_12BF, A1, C: 2.56% each). Viral load (log₁₀ copies/mL) and CD4⁺T cell count (cells/mm³) were 3.9 (3.5–4.2) and 618 (504–857) in LTNPs, 3.3 (2.8–4.7) and 463 (333–627) in SPs, and 4.6 (4.3–5.3) and 201 (110–254) in RPs. Gp41 and C2–V3 amino acid divergence was lower in LTNP and SP strains compared to RPs (median value: 0.085 and 0.091 vs. 0.114, p?=?0.005 and 0.042) and a trend of lower variability was observed for Nef (p?=?0.198). A lower entropy value was observed at 10, 3, and 7 positions of Gp41, C2–V3, and Nef belonging to LTNPs and at 7, 3, and 1 positions of Gp41, C2–V3, and Nef belonging to SPs compared with RPs (p?<?0.05). Focusing on epitope rich regions, again a higher degree of conservation was observed in Gp41 and C2–V3 sequences belonging to LTNPs and SPs compared to those belonging to RPs. This study shows that the extent of amino acid variability correlates with a different HIV-1 progression rate. This variability also involves CTL epitope rich regions, thus suggesting its involvement in the immune escape process modulation.