Gradual Correction of Valgus Deformities of the Tibia Using a Monolateral External Fixator.

Objective: To present a review of patients subjected to gradual correction of a valgus deformity of the tibia using a monolateral external fixator. Method: This retrospective review included patients from January 2012 to May 2022 who met the following inclusion criteria: deviation of mechanical axis of the limb due to valgus deformity of the tibia; tibial deformity in the coronal plane on radiographic examination; a documented outpatient pre-operative evaluation by an orthopaedic surgeon and age between 10 and 70 years. The following exclusion criteria were applied: the presence of another tibia deformity preventing gradual correction using the proposed assembly; skin conditions incompatible with the surgical procedure; inadequate pre- or post-operative radiological evaluation; and insufficient information in the medical records. Results: The mean age of patients with a valgus deformity of the tibia was 30.8 ± 15.9 years. These patients had a body mass index (BMI) of 26.1 ± 5.5 kg/m2. A congenital or developmental aetiology was attributed to 58.3% of the cases. Most commonly, the deformity was found in the middle third of the tibia with a mean deformity of 14.7 ± 6.6 degrees. The total external fixator time ranged from 73 to 229 days (average 149.7 ± 36.1 days). The mean medial proximal and lateral distal tibial angles differed significantly for pre- and post-operative measurements (p ≤ 0.05). There were complications in eight cases; five cases of pin site infections, two cases of medial cortical fracture and one case of peroneal nerve neuropraxia. Conclusion: The proposed correction technique produces a satisfactory angular correction and with similar outcomes as described in the literature. How to cite this article: Motta DP, Faria JLR, Couto A, et al. Gradual Correction of Valgus Deformities of the Tibia Using a Monolateral External Fixator. Strategies Trauma Limb Reconstr 2023;18(2):123-132.

Metabolomics as a promising tool for early osteoarthritis diagnosis.

Osteoarthritis (OA) is the main cause of disability worldwide, due to progressive articular cartilage loss and degeneration. According to recent research, OA is more than just a degenerative disease due to some metabolic components associated to its pathogenesis. However, no biomarker has been identified to detect this disease at early stages or to track its development. Metabolomics is an emerging field and has the potential to detect many metabolites in a single spectrum using high resolution nuclear magnetic resonance (NMR) techniques or mass spectrometry (MS). NMR is a reproducible and reliable non-destructive analytical method. On the other hand, MS has a lower detection limit and is more destructive, but it is more sensitive. NMR and MS are useful for biological fluids, such as urine, blood plasma, serum, or synovial fluid, and have been used for metabolic profiling in dogs, mice, sheep, and humans. Thus, many metabolites have been listed as possibly associated to OA pathogenesis. The goal of this review is to provide an overview of the studies in animal models and humans, regarding the use of metabolomics as a tool for early osteoarthritis diagnosis. The concept of osteoarthritis as a metabolic disease and the importance of detecting a biomarker for its early diagnosis are highlighted. Then, some studies in plasma and synovial tissues are shown, and finally the application of metabolomics in the evaluation of synovial fluid is described.

ESRRB polymorphisms are associated with comorbidity of temporomandibular disorders and rotator cuff disease.

Temporomandibular disorders (TMD) are associated with comorbidity. Shoulder pain is among the symptoms associated with TMD. The purpose of this study was to investigate the association between TMD and rotator cuff disease (RCD) and related genetic aspects. All subjects underwent orofacial and shoulder examinations. The control group comprised 30 subjects with no pain. Affected subjects were divided into three groups: RCD (TMD-free, n=16), TMD (RCD-free, n=13), and TMD/RCD (patients with both RCD and TMD, n=49). A total of eight single nucleotide polymorphisms in the ESRRB gene were investigated. A chemiluminescent immunoassay was used to measure estradiol levels. Surface electromyography recorded head and cervical muscle activity. The χ(2) test and Student t-test/Mann-Whitney test were used to assess the significance of nominal and continuous variables. A P-value of <0.05 was considered significant. TMD subjects were seven times more susceptible to RCD than controls. The rs1676303 TT (P=0.02) and rs6574293 GG (P=0.04) genotypes were associated with RCD and TMD, respectively. TMD/RCD subjects showed associations with rs4903399 (P=0.02), rs10132091 (P=0.02), and CTTCTTAG/CCTCTCAG (P=0.01) haplotypes and lower muscle activity. Estradiol levels were similar among groups. This study supports TMD as a risk factor for RCD. ESRRB haplotypes and low muscle activity are common biomechanical characteristics in subjects with both diseases.

CCN2/CTGF silencing blocks cell aggregation in embryonal carcinoma P19 cell

Connective tissue growth factor (CCN2/CTGF) is a matricellular-secreted protein involved in extracellular matrix remodeling. The P19 cell line is an embryonic carcinoma line widely used as a cellular model for differentiation and migration studies. In the present study, we employed an exogenous source of CCN2 and small interference RNA to address the role of CCN2 in the P19 cell aggregation phenomenon. Our data showed that increasing CCN2 protein concentrations from 0.1 to 20 nM decreased the number of cell clusters and dramatically increased cluster size without changing proliferation or cell survival, suggesting that CCN2 induced aggregation. In addition, CCN2 specific silencing inhibited typical P19 cell aggregation, which could be partially rescued by 20 nM CCN2. The present study demonstrates that CCN2 is a key molecule for cell aggregation of embryonic P19 cells.

CCN2/CTGF silencing blocks cell aggregation in embryonal carcinoma P19 cell.

Connective tissue growth factor (CCN2/CTGF) is a matricellular-secreted protein involved in extracellular matrix remodeling. The P19 cell line is an embryonic carcinoma line widely used as a cellular model for differentiation and migration studies. In the present study, we employed an exogenous source of CCN2 and small interference RNA to address the role of CCN2 in the P19 cell aggregation phenomenon. Our data showed that increasing CCN2 protein concentrations from 0.1 to 20 nM decreased the number of cell clusters and dramatically increased cluster size without changing proliferation or cell survival, suggesting that CCN2 induced aggregation. In addition, CCN2 specific silencing inhibited typical P19 cell aggregation, which could be partially rescued by 20 nM CCN2. The present study demonstrates that CCN2 is a key molecule for cell aggregation of embryonic P19 cells.