Knee osteoarthritis (KOA) is characterized by low-grade inflammation, loss of articular cartilage, subchondral bone remodeling, synovitis, osteophyte formation, and pain. Strong, continuous pain may indicate the need for joint replacement in patients with end-stage OA, although postoperative pain (POP) of at least a two-month duration persists in 10–40% of patients with OA. Study purpose: The inflammation observed in joint tissues is linked to pain caused by the production of proinflammatory cytokines. Since the biosynthesis of cytokines requires energy, their production is supported by extensive metabolic conversions of carbohydrates and fatty acids, which could lead to a disruption in cellular homeostasis. Therefore, this study aimed to investigate the association between POP development and disturbances in energy metabolic conversions, focusing on carbohydrate and fatty acid metabolism. Methods: Peripheral blood samples were collected from 26 healthy subjects and 50 patients with end-stage OA before joint replacement surgery. All implants were validated by orthopedic surgeons, and patients with OA demonstrated no inherent abnormalities to cause pain from other reasons than OA disease, such as malalignment, aseptic loosening, or excessive bleeding. Pain levels were assessed before surgery using the visual analogue scale (VAS) and neuropathic pain questionnaires, DN4 and PainDETECT. Functional activity was evaluated using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). Three and six months after surgery, pain indices according to a VAS of 30 mm or higher were considered. Total RNA isolated from whole blood was analyzed using quantitative real-time RT-PCR (qRT-PCR) for the expression of genes related to carbohydrate and fatty acid metabolism. Protein levels of the examined genes were measured using an ELISA in the peripheral blood mononuclear cells (PBMCs). We used qRT-PCR because it is the most sensitive and reliable method for gene expression analysis, while an ELISA was used to confirm our qRT-PCR results. Key findings: Among the study cohort, 17 patients who reported POP demonstrated significantly higher (p < 0.05) expressions of the genes PKM2, LDH, SDH, UCP2, CPT1A, and ACLY compared to pain-free patients with KOA. Receiver-operating characteristic (ROC) curve analyses confirmed the association between these gene expressions and pain development post-arthroplasty. A principle component analysis identified the prognostic values of ACLY, CPT1A, AMPK, SDHB, Caspase 3, and IL-1β gene expressions for POP development in the examined subjects. Conclusion: These findings suggest that the disturbances in energy metabolism, as observed in the PBMCs of patients with end-stage KOA before arthroplasty, may contribute to POP development. An understanding of these metabolic processes could provide insights into the pathogenesis of KOA. Additionally, our findings can be used in a clinical setting to predict POP development in end-stage patients with KOA before arthroplasty.

Лечение асептического некроза головки бедренной кости. Клинические рекомендации

Osteoarthritis (OA) pain implies an indication for joint replacement in patients with end-stage OA. However, chronic postoperative pain is observed in 10–40% of patients with OA. Here, we identified genes whose expression in the peripheral blood before surgery could denote the risk of postoperative pain development. We examined the peripheral blood of 26 healthy subjects and 50 patients with end-stage OA prior to joint replacement surgery. Pain was evaluated before surgery using the visual analog scale (VAS) index and neuropathic pain questionnaires, Douleur Neuropathique 4 Questions (DN4) and PainDETECT questionnaires. Functional activity was assessed using the Western Ontario and McMaster Universities osteoarthritis index (WOMAC). Three and six months after surgery, pain indices according to VAS of 30% and higher were considered. Metalloproteinase (MMP)-9 and tissue inhibitor of metalloproteinase (TIMP)1 protein levels were measured using ELISA in the peripheral blood mononuclear cells (PBMCs). Total RNA isolated from whole blood was analysed using quantitative real-time RT-PCR for caspase-3, MMP-9, TIMP1, cathepsins K and S, tumour necrosis factor (TNF)α, interleukin (IL)-1β, and cyclooxygenase (COX)-2 gene expression. Seventeen patients reported post-surgical pain. Expression of cathepsins K and S, caspase-3, TIMP1, IL-1β, and TNFα genes before surgery was significantly higher in these patients compared to pain-free patients with OA. Receiver-operating characteristic (ROC) curve analyses confirmed significant associations between these gene expressions and the likelihood of pain development after arthroplasty. High baseline expression of genes associated with extracellular matrix destruction (cathepsins S and K, TIMP1), inflammation (IL-1β, TNFα), and apoptosis (caspase-3) measured in the peripheral blood of patients with end-stage OA before knee arthroplasty might serve as an important biomarker of postoperative pain development.

Chronic shoulder pain (CSP) is a clinical syndrome associated with inflammatory and degenerative musculoskeletal changes, characterized by pain in the shoulder that persists for at least 3 months, arising or aggravated by functional activity in this area. The frequency of CSP in the modern population reaches 20–33%, it is one of the leading causes of severe suffering, disability and seeking for medical attention. The main causes of CSP are shoulder rotator impingement syndrome (subacromial impingement syndrome), calcific tendinitis, adhesive capsulitis, shoulder and acromioclavicular joint osteoarthritis. Accurate diagnosis of these diseases is necessary for the correct choice of treatment. Differential diagnosis is carried out using tests that evaluate the function of the shoulder joint and the rotator cuff muscles (Neer, Speed, Hawkins tests, etc.), as well as using instrumental methods (ultrasound, magnetic resonance tomography, X-ray). In CSP, it is necessary to exclude septic, oncological, visceral, systemic rheumatic and other diseases, as well as musculoskeletal pathology of the cervical spine, upper chest and back, which can cause pain in the shoulder region.Therapy for diseases that cause CSP should be personalized and complex, aimed at maximum pain control and restoration of function. For this purpose, non-steroidal anti-inflammatory drugs, local injection therapy with glucocorticoids, hyaluronic acid, and platelet-rich plasma are used. In some cases, muscle relaxants, antidepressants, anticonvulsants, local injections of botulinum toxin type A are indicated. Physiotherapy and medical rehabilitation methods play a fundamental role in the treatment of CSP.

Transient MHD activity in the multiple-mirror trap GOL-3 at the stage of plasma cooling after decay of the net current was studied. Such events are diagnosed as short bursts (generally shorter than 5 cycles) of oscillations of azimuthal magnetic field with the frequency within 0.1 ÷ 1 MHz. Earlier transient events at the plasma decay stage were also observed. At that time an existence of long-lived internal current structures in the GOL-3 plasma was supposed. The paper presents new results from the magnetic diagnostics. Azimuthal and longitudinal mode localization agrees with the assumption that the magnetic field is generated by filaments with the current in the range of 1 ÷ 50 A in nearly uniform azimuthal distribution. Statistical analysis shows that the main oscillation frequencies are grouped near the inversed time of the Alfven wave propagation along the trap. Power dependence of the pulse probability on its amplitude with the index α = -1.87 was found. Relationships of MHD activity on the regime of plasma heating and on a degree of the beam stabilization at the exit receiver are discussed.

Trauma causes a complex local and systemic reaction of the macroorganism, the consequences of which can be various functional, neurological and psychoemotional disorders. One of the most painful complications of injuries of the musculoskeletal system is chronic post-traumatic pain (CPTP), which occurs, depending on the severity of the damage, in 10–50% of cases. The pathogenesis of this syndrome is multifactorial and includes the development of chronic inflammation, degenerative changes (fibrosis, angiogenesis, heterotopic ossification), pathology of the muscular and nervous systems, neuroplastic changes leading to the development of central sensitization, as well as depression, anxiety and catastrophization. Risk factors for CPTP should be considered the severity of injury, comorbid diseases and conditions (in particular, obesity), stress and serious trauma-related experiences (within the framework of post-traumatic stress disorder), the development of post-traumatic osteoarthritis and chronic tendopathy, genetic predisposition, deficiencies in treatment and rehabilitation in the early period after injury. To date, there is no clear system of prevention and treatment of CPTP. Considering the pathogenesis of this suffering, adequate anesthesia after injury, active anti–inflammatory therapy (including local injections of glucocorticoids), the use of hyaluronic acid, slow-acting symptomatic agents and autologous cellular preparations – platelet-riched plasma, mesenchymal stem cells, etc. are of fundamental importance. However, therapeutic and surgical methods of CPTP control require further study