Natalya G. Pravdyuk

Generalized osteoarthritis (GOA) is a clinical variant of osteoarthritis characterized by multiple joint involvement, including the joints of the hands, knees, hips, and the spinal joints. This article presents the evolution of the knowledge about GOA from the classic works of J.H. Kellgren and R. Moore (1952) to modern approaches addressing multi-joint osteoarthritis. Various definitions of multi-joint osteoarthritis are analyzed, demonstrating their dependence on the number of involved joint groups and their impact on the assessment of disease prevalence. Special attention is paid to the axial component of GOA: involvement of intervertebral discs and facet joints is considered as a single clinical and morphological phenotype with common pathophysiological mechanisms (inflammation, angiogenesis, extracellular matrix remodeling). Current diagnostic approaches are presented, including clinical assessment, instrumental methods, and promising biomarkers. A phenotype-oriented approach to the treatment of GOA is substantiated.

Aim. To demonstrate a multidisciplinary approach in management of a patient with generalized sarcoidosis, heart disease and a life-threatening complication in the form of cerebral infarction which required selection of treatment tactics. Material and methods. Patient A., 41, presented with sarcoidosis and Löfgren’s syndrome onset at the age of 23 and developed clinically manifested cardiac disease over the next three years. Cardiac sarcoidosis was characterized by complex life-threatening arrhythmias, progression of chronic heart failure, and infarction-like changes in electrocardiograms and echocardiograms necessitating differential diagnosis. Results. Uncontrolled intermittent use of prednisolone, lack of regular standard therapy for sarcoidosis, and lack of antiarrhythmic therapy largely predetermined the unfavorable course of events, including development of an ischemic stroke at a young age. The development of the cerebral infarction was due to a combination of factors: arrhythmia, newly diagnosed congenital heart defect (patent foramen ovale), hyperhomocysteinemia, and the presence of polymorphisms in the folate cycle genes (MTHFR, MTR). Conclusion. The diversity of clinical manifestations often leads to diagnostic difficulties and errors. In the absence of adequate therapy, the disease progresses and has an unfavorable prognosis. This article presents a clinical observation of a young patient with generalized sarcoidosis with progressive heart disease, hereditary thrombophilia, patent foramen ovale complicated by the development of a stroke.

BACKGROUND. The reduction in mass and function of paraspinal muscles and its contribution to axial instability and the development of back pain has become an active area of research. However, current diagnostic criteria for sarcopenia have limitations when applied to spinal sarcopenia. The condition of the spinal muscular system in patients with chronic back pain and degenerative spine disorders is of interest not only for treatment but also for disease prevention. OBJECTIVE. To assess the paraspinal muscle mass in patients with low back pain across different age groups using magnetic resonance imaging (MRI). MATERIALS AND METHODS. A total of 93 patients with low back pain were included in the study: young adults (n = 35, Me: 36.00 [30.00–42.00]), middle-aged (n = 30, Me: 50.00 [46.50–56.25]), and elderly patients (n = 28, Me: 66.00 [62.50–71.00]). Back pain intensity was measured using a Visual Analogue Scale (VAS, mm), and spinal function was assessed using the Backache Index (BAI). Intervertebral disc (IVD) degeneration was evaluated via MRI according to the Pfirrmann classification (2001). The cross-sectional areas of paraspinal muscles (psoas major, erector spinae, quadratus lumborum) were measured on axial MRI slices at the level of the third lumbar vertebra (L3). The muscle-to-vertebral index (MVI) was calculated by dividing the total cross-sectional area of the three paired muscles (Sm, cm2) by the crosssectional area of the L3 vertebral body at its superior endplate (Sv, cm ² ): MVI = (Smdextra + sinistra) / Sv. The anterior-posterior body dimension was also measured on sagittal slices at the upper edge of L3. RESULTS. Chronic back pain was reported in 80%, 83.3%, and 86.7% of the young, middle-aged, and elderly groups, respectively. The BAI scores indicating significant spinal dysfunction (0.80 [0.47–0.90], 0.67 [0.50–0.77], and 0.80 [0.65–1.00] respectively) positively correlated with VAS pain intensity across all subjects (r = 0.55, p < 0.0001). Obesity was twice as prevalent among elderly patients compared to younger and middle-aged individuals (30.0% vs. 14.3% and 16.7%, respectively). The mass of the paraspinal muscles according to the average MVI values in the groups was statistically lower in middleaged (p = 0.025) and elderly (p = 0.0001) individuals. Asymmetry of the quadratus lumborum muscle (right side larger than left) was identified in all patients (p < 0.05). An age-related increase in the cross-sectional area of the L3 vertebral body endplate was also found (p = 0.0003). A positive correlation was observed between the anterior-posterior torso dimension and the stage of IVD degeneration at L5–S1 (р = 0.054; r = 0.29). CONCLUSION. Paraspinal muscle mass in patients with back pain and degenerative spine disease decreases with age (p < 0.05), as reflected by reduced MVI values on MRI. The MVI is an effective tool for evaluating paraspinal muscle loss. Altered motor patterns lead to chronic imbalance and asymmetry of the quadratus lumborum muscle in all age groups studied. The increase in the vertebral body’s endplate area may reflect adaptive changes aimed at maintaining axial spinal stability. The positive correlation between the anterior-posterior body dimension and IVD degeneration suggests a contribution of the musculoskeletal-visceral component to the condition of the lumbar spinal motion segment.

Degenerative disc disease (DDD) is a major cause of chronic low back pain (LBP), yet the molecular mechanisms driving disc degeneration and pain remain poorly understood. This study analyzed intervertebral disc (IVD) tissue from 36 young patients (median age = 36.00 [31.00, 42.50] years) with herniated discs and LBP, alongside healthy controls, to investigate changes in the extracellular matrix (ECM) and neurochemical alterations. Disc degeneration was assessed using MRI (Pfirrmann grading) and histology (Sive’s criteria). Histochemical and immunohistochemical methods were used to evaluate aggrecan content, calcification, and the expression of nerve growth factor (NGF), substance P (SP), and S-100 protein. MRI findings included Pfirrmann grades V (30.55%), IV (61.11%), III (5.56%), and II (2.78%). Severe histological degeneration (10–12 points) was observed in three patients. Aggrecan depletion correlated with longer pain duration (r = 0.449, p = 0.031). NGF expression was significantly elevated in degenerated discs (p = 0.0287) and strongly correlated with SP (r = 0.785, p = 5.268 × 10⁻⁹). Free nerve endings were identified in 5 cases. ECM calcification, present in 36.1% of patients, was significantly associated with radiculopathy (r = 0.664, p = 0.005). The observed co-localization of NGF and SP suggests a synergistic role in pain development. These results indicate that in young individuals, aggrecan loss, neurochemical imbalance, and ECM calcification are key contributors to DDD and chronic LBP.

Introduction: Degenerative disc disease (DDD) is a major cause of lower back pain (LBP). Key pathological processes of intervertebral disc (IVD) degeneration include extracellular matrix (ECM) degradation (including aggrecan loss), cartilage dehydration, and pathological ingrowth of blood vessels and nerve fibers. Neurotrophins and neuropeptides, such as nerve growth factor (NGF) and substance P (SP), play an essential role in LBP pathogenesis, neoinnervation, inflammation, and the maintenance of chronic pain. Materials and Methods: Thirty-six young patients (mean age 36.00 [31.00, 42.50] years) with LBP associated with herniated discs and five healthy individuals were enrolled. IVD samples were collected during microdiscectomy. MRI-based Pfirrmann classification (2001) was used to assess the stages of disc degeneration. Histological grading was performed according to Sive’s criteria (2002). Histochemical staining (hematoxylin-eosin, Alizarin Red, Safranin O/Fast Green FCF) was conducted to evaluate ECM status, including aggrecan content. Immunohistochemical analysis was performed to assess NGF, S-100 protein, and SP expression. Results: All patients experienced chronic LBP. According to MRI, Pfirrmann grade V degeneration was found in 30.55% of patients, grade IV in 61.11%, grade III in 5.56%, and grade II in 2.78%. Histologically confirmed degeneration was observed in 23 cases (63.88%), with 3 patients showing severe degeneration (10-12 points). In patients with longer pain episodes (average duration 11.29 weeks), aggrecan loss was observed in 19.4% of cases (r=0.449; P=0.031). NGF expression was significantly higher in degenerated discs (P=0.0287) and positively correlated with SP levels (r=0.785; P=5.268 × 10 ⁻⁹ ). Increased NGF and SP expression were noted in patients with osteophytes, with levels correlating with both the histological degeneration score and MRI grading. Isolated free nerve endings were detected in the nucleus pulposus of 5 patients. Calcification was observed in 36.1% of cases, predominantly around hypertrophic chondrocytes and their clusters, and its severity correlated with radiculopathy (r=0.664; P=0.005). Conclusion: In young individuals, aggrecan loss, increased expression of NGF, SP, S-100 protein, and ECM calcification are key pathological features of IVD degeneration contributing to chronic LBP. The colocalization of NGF and SP suggests a synergistic role in the development of chronic pain. These findings highlight new therapeutic targets aimed at inhibiting pathological neoinnervation and ECM degradation.

Introduction: Sarcopenia of the spinal stabilizing muscles is one of the components of age-related sarcopenia and often associated with chronic back pain (CBP), including spinal osteoarthritis (OA). The age dynamics of paraspinal muscle mass in spinal OA is not sufficiently studied to date, although it is key in developing rehabilitation and prevention strategies. The aim of study: is to identify spinal sarcopenia in individuals with spinal OA by assessing paraspinal muscles mass and analyzing its relationship to degenerative spinal changes in different age groups using magnetic resonance imaging (MRI). Materials and methods: The study included 90 patients with spinal OA classified as stages 4 and 5 of degenerative disc disease according to the Pfirrmann grading system. Participants were evenly distributed across three age groups: young adults (Me: 36.00 [30.00-42.00]), middle age (Me: 50.00 [46.50-56.25]), and elderly (Me: 66.00 [62.50-71.00]). All participants underwent lumbar spine MRI in two sections – sagittal and axial – in T1- and T2-weighted images. Clinical assessments included evaluating the functional status of the lumbar spine using the Backache Index (BAI). Paraspinal muscle mass analysis was performed on axial sections at the level of the third lumbar vertebra (L3) for the following muscles: musculus psoas major, musculus erector spinae, and musculus quadratus lumborum. To comparatively assess spinal muscle mass, the musculovertebral index (MVI) was calculated by dividing the total cross-sectional area of the three pair muscles (Sm, cm²) by the cross-sectional area of the third lumbar vertebra (Sv, cm²) at the upper endplate level: MVI = (Sm dextra + Sm sinistra) / Sv. To identify the asymmetries of the paraspinal muscles, the ratio of the cross-sectional areas of the three muscles on the left and right sides was calculated. Additionally, the transverse torso thickness at L3 level was measured on sagittal sections. Results: The mean MVI values demonstrated that paraspinal muscle mass was significantly lower in elderly (p = 0.0001) and middle-aged (p = 0.025) groups compared to the young group, which indicates its decrease with age in patients. Statistically significant increase in the lumbar vertebra area with age (p=0.0003 young vs elderly) is explained by the spondylosis development and age-related marginal osteophyte growth as manifestations of spinal OA. The reduction in muscle cross-sectional area was evident for three right paraspinal muscle groups with age (p = 0.0252). Asymmetry for each pair of muscles was observed across all age groups, the right side always being larger than the left, particularly in the quadratus lumborum, where it was most pronounced in middle-aged (p = 2.762 × 10 ⁻⁶ ) and young individuals (p = 0.0009). The elderly persons demonstrated a tendency toward higher body mass index, a higher percentage of obese individuals, and increased torso thickness compared to the middle-aged and young groups (p = 0.067), suggesting a possible decline in abdominal muscle tone with age alongside body weight gain. Conclusions: MRI findings reveal an age-related decline in paraspinal muscle mass among patients with CBP, indicating the development of spinal sarcopenia, which likely contributes to the clinical course of spinal OA in the elderly. All three groups of muscles show asymmetry in all age groups, with the right side always being larger than the left. Torso thickness and body weight increase with age in patients with spinal OA potentially exacerbate the disease’s clinical progression. These findings highlight the need to include exercises targeting paraspinal and abdominal muscles in rehabilitation programs for patients with spinal OA in all age groups. Preventing spinal spinal sarcopenia by maintaining axial muscle stability is essential for preserving the spinal muscle framework and is an integral component of managing patients with CBP.

Osteoarthritis (OA) is increasingly recognized as a complex degenerative joint disease that develops under the influence of mechanical, biochemical and genetic factors. The pathogenesis of OA includes a complex of interactions at both cellular and molecular levels, leading to progressive damage to joint tissues – cartilage degeneration, synovial inflammation, remodeling of the subchondral bone, and periarticular changes. In the last decade, the term “early osteoarthritis” has been increasingly mentioned in the scientific literature. The concept of early OA was largely determined by the experience of rheumatoid arthritis treatment. Given the heterogeneity of OA, pathological processes at the cellular and molecular levels, reflecting the early stage of the disease, are diverse and depend on the factors that induce the disease. Symptoms of early OA of the knee joint can be suspected with the appearance of intermittent pain or discomfort in the joint, short-term “initial” stiffness and functional limitations. Clinical examination in most cases reveals pain on palpation of the joint, crepitation or moderate articular effusion. X-ray data are of limited importance at an early stage of the disease, since one of the typical signs of OA – narrowing of the articular gap – may not appear for many years. Quantitative, contrast-enhanced magnetic resonance imaging methods, as well as hybrid methods are used to visualize OA at an early stage. The final goals of developing classification criteria for early OA and early diagnosis of the disease in real clinical practice differ. Early OA represents a “window of opportunity” to prevent disease progression before OA becomes clinically apparent. It is necessary to continue research on the definition and classification of early OA of other localizations. Pharmacological innovations, regenerative methods, and gene therapy represent the future of OA treatment, including at an early stage of the disease. One of the modern drugs that modify the course of OA is Elmosa, a unique combination of glucosamine sulfate, boswellic acids combined with acetyl-L-carnitine and B vitamins.

Osteoporotic vertebral fractures (OVF) are a severe complication of osteoporosis associated adverse outcomes, acute and chronic pain syndrome. If vertebral fractures (deformities) are detected, osteoporosis is diagnosed regardless of bone mineral density and the 10-year absolute fracture risk scale of the Fracture Risk Assessment Tool, but subject to the exclusion of other metabolic osteopathies. The article presents differential diagnosis of OVF with osteopathies such as osteomalacia, tumors or metastatic lesions of the spine, Paget»s disease, myeloma, hyper parathyroid osteodystrophy, post-traumatic vertebral deformities, Scheuermann-Mau disease. Differential diagnosis between different types of osteopathies is based on features of the clinical picture, history, changes in laboratory parameters (calcium, phosphorus, alkaline phosphatase, parathyroid hormone, vitamin D3 and on data from X-ray of the skeleton examination. It is necessary to take into account conditions under which the vertebral fracture occurred, its localization, prevalence, peculiarities of changes in bone structures, presence or absence of osteoporotic background, degenerative-dystrophic changes in the spine. The tactics of managing the patients with OVF is determined by the time after the fracture, its severity, nature of the pain syndrome and includes non-drug and medical measures. Among non-pharmaceutical measures in the acute period of OVF, there are unloading of the spinal column, use of a corset, and physical therapy. Medical measures are aimed at pain relief using injectable and oral forms of nonsteroidal anti-inflammatory drugs, central acting muscle relaxants and anti-osteoporotic therapy. Dexketoprofen (Dexalgin) is the first-line drug for relief of acute pain in OVF which has a rapid and pronounced analgesic effect. For the anti-osteoporotic therapy, the drugs of choice are parenteral bisphosphonates, denosumab and teriparatide.

Back pain is a common reason for seeking primary care from older and younger people. Early spinal imaging by a therapist is indicated to eliminate potentially dangerous causes of pain. Independent magnetic resonance imaging or computed tomography examination at the patient’s initiative in the absence of “red flags” back pain in most cases does not come close to identifying the obvious cause of pain syndrome, and it creates the preconditions for the formation of an exaggerated picture of the disease in the patient himself, driving him into the “trap” of chronic pain. Attention of the polyclinic doctor to the clinical symptoms detailed in the article, following the standard algorithms of diagnosis will allow timely suspicion of “red flags” back pain, avoid hyperdiagnosis of the cause, and minimize the risk of its chronization. The algorithm for treatment of acute and chronic episodes of pain should include informing the patient about the favorable outcome in the vast majority of cases, optimizing the physical activity of the patient, the use of complex drug therapy, the basis of which are nonsteroidal anti-inflammatory drugs (predominantly selective), muscle relaxants and other pathogenetically based medicines.

Back pain in young people (14–35 years old) may have causes rooted in adolescence or even earlier childhood. Diagnosis in this case can present considerable difficulties for a therapist and general practitioner, since “nonspecific back pain” may hide pathological conditions inherent in childhood. The degree of compensation for scoliosis, hereditary abnormalities in the development of the spine, the severity of early degenerative processes, and metabolic diseases of the skeleton that were not identified during school years determine a non-standard scope of diagnostic and therapeutic measures for the doctor. These include collecting a family history and screening the patient for the presence of inflammatory back pain according to the 2009 ASAS criteria, a survey on the hospital anxiety and depression scale, a morphometric assessment of the stigma of dysembryogenesis and an assessment of hypermobility syndrome, advanced laboratory diagnostics with determination of indicators of mineral-calcium metabolism, X-ray diagnostics with functional tests, the use of magnetic resonance imaging or computed tomography of the spine in the absence of radicular symptoms. The patient’s active involvement in non-drug restorative treatment significantly improves his prognosis, and pharmacological support should have a health-saving direction and consider the presence of low-intensity inflammation in the pathogenesis of the disease. The choice of therapy for a reproductively active cohort of patients is made in favor of drugs with the maximum safety profile, which include, among others, selective non-steroidal anti-inflammatory drugs.