Impaired Bone Metabolism Research Articles

Sodium butyrate protect bone mass in lipopolysaccharide-treated rats by reducing oxidative stress and inflammatory

ABSTRACT Objective The study will be to observe the effect of Sodium butyrate (NaB) on bone loss in lipopolysaccharide (LPS)-treated rats. Methods In the rat model, we observed that changes in the expression of oxidative stress regulators, inflammatory markers and target genes were measured by immunofluorescence and RT–PCR after treatment. Changes in viability and osteogenesis of MC3T3-E1, osteoclast differentiation in RAW264.7 cells in the presence of LPS were evaluated using CCK-8, ALP staining, RES staining, and TRAP staining. Results In vitro experiments have shown that LPS-induced inhibition of JC-1, SIRT1, GPX1 and SOD2 is associated with increased levels of inflammation and oxidative stress. In addition, NaB has been found to suppress oxidative stress, inflammation and Mito SOX, promote osteogenic differentiation, and inhibit osteoclast differentiation. In addition, NaB significantly promoted SITR1 expression, repaired impaired bone metabolism, and improved bone strength and bone mineral density. Conclusion Given all this experimental evidence, the results strongly suggest that NaB can restore osteogenic activity in the presence of LPS by reducing intracellular ROS, inhibiting osteoclast differentiation and reducing bone loss in LPS-treated rat models.

Kurarinone, a flavonoid from Radix Sophorae Flavescentis, inhibits RANKL-induced osteoclastogenesis in mouse bone marrow-derived monocyte/macrophages.

Inflammation-induced osteoclast proliferation is a crucial contributor to impaired bone metabolism. Kurarinone (KR), a flavonoid extracted from the Radix Sophorae Flavescentis, exhibits notable anti-inflammatory properties. Nevertheless, the precise influence of KR on osteoclast formation remains unclear. This study's objective was to assess the impact of KR on osteoclast activity in vitro and unravel its underlying mechanism. Initially, a target network for KR-osteoclastogenesis-osteoporosis was constructed using network pharmacology. Subsequently, the intersecting targets were identified through the Venny platform and a PPI network was created using Cytoscape 3.9.1. Key targets within the network were identified employing topological algorithms. GO enrichment and KEGG pathway analysis were then performed on these targets to explore their specific functions and pathways. Additionally, molecular docking of potential core targets of KR was conducted, and the results were validated through cell experiments. A total of 83 target genes overlapped between KR and osteoclastogenesis-osteoporosis targets. Enrichment analysis revealed their role in inflammatory response, protein tyrosine kinase activity, osteoclast differentiation, and MAPK and NF-κB signaling pathways. PPI analysis and molecular docking demonstrate that key targets MAPK14 and MAPK8 exhibit more stable binding with KR compared to other proteins. In vitro experiments demonstrate that KR effectively inhibits osteoclast differentiation and bone resorption without cellular toxicity. It suppresses key osteoclast genes (NFATc1, c-Fos, TRAP, MMP9, Ctsk, Atp6v2), hinders IκB-α degradation, and inhibits ERK and JNK phosphorylation, while not affecting p38 phosphorylation. The results indicate that KR may inhibit osteoclast maturation and bone resorption by blocking NF-κB and MAPK signaling pathways, suggesting its potential as a natural therapeutic agent for osteoporosis.

Melatonin prevents bone loss in osteoporotic rats with valproic acid treatment by anti-inflammatory and anti-oxidative stress

Melatonin (MEL) has shown positive effects in anti-inflammatory and anti-oxidative stress research. This study investigates whether MEL can positively impact bone loss induced by valproic acid (VPA) in rats. The study examines changes in MC3T3-E1 cell viability and osteogenic potential, along with osteoclast differentiation in RAW264.7 cells in the presence of VPA using CCK-8, ALP staining, AR staining, and TRAP staining. In vitro experiments reveal that VPA-induced inhibition of osteogenic differentiation and promotion of osteoclastic differentiation are linked to increased inflammation and oxidative stress. Furthermore, MEL has demonstrated the ability to reduce oxidative stress and inflammation, boost osteogenic differentiation, and inhibit osteoclast differentiation. Animal experiments confirm that MEL significantly increases SOD2 expression and decreases TNF-α expression, leading to the restoration of impaired bone metabolism, enhanced bone strength, and higher bone mineral density. The combined experimental results strongly suggest that MEL can enhance osteogenic activity in the presence of VPA by reducing inflammation and oxidative stress, impeding osteoclast differentiation, and alleviating bone loss in VPA-treated rat models.

Ganoderic Acid A prevents bone loss in lipopolysaccharide-treated male rats by reducing oxidative stress and inflammatory

Ganoderic Acid A (GAA) has demonstrated beneficial effects in anti-inflammatory and anti-oxidative stress studies. However, it remains unknown whether GAA exerts positive impacts on bone loss induced by lipopolysaccharide (LPS). This study aims to investigate the influence of GAA on bone loss in LPS-treated rats. The study assesses changes in the viability and osteogenic potential of MC3T3-E1 cells, as well as osteoclast differentiation in RAW264.7 cells in the presence of LPS using CCK-8, ALP staining, AR staining, and Tartrate-resistant acid phosphatase (TRAP) staining. In vitro experiments indicate that LPS-induced inhibition of osteoclasts (OC) and Superoxide Dismutase 2 (SOD2) correlates with heightened levels of inflammation and oxidative stress. Furthermore, GAA has displayed the ability to alleviate oxidative stress and inflammation, enhance osteogenic differentiation, and suppress osteoclast differentiation. Animal experiment also proves that GAA notably upregulates SOD2 expression and downregulates TNF-α expression, leading to the restoration of impaired bone metabolism, improved bone strength, and increased bone mineral density. The collective experimental findings strongly suggest that GAA can enhance osteogenic activity in the presence of LPS by reducing inflammation and oxidative stress, hindering osteoclast differentiation, and mitigating bone loss in LPS-treated rat models.

Comparative Analysis of Myokines and Bone Metabolism Markers in Prepubertal Vegetarian and Omnivorous Children.

The role of bone and muscle as endocrine organs may be important contributing factors for children's growth and development. Myokines, secreted by muscle cells, play a role in regulating bone metabolism, either directly or indirectly. Conversely, markers of bone metabolism, reflecting the balance between bone formation and bone resorption, can also influence myokine secretion. This study investigated a panel of serum myokines and their relationships with bone metabolism markers in children following vegetarian and omnivorous diets. A cohort of sixty-eight healthy prepubertal children, comprising 44 vegetarians and 24 omnivores, participated in this study. Anthropometric measurements, dietary assessments, and biochemical analyses were conducted. To evaluate the serum concentrations of bone markers and myokines, an enzyme-linked immunosorbent assay (ELISA) was used. The studied children did not differ regarding their serum myokine levels, except for a higher concentration of decorin in the vegetarian group (p = 0.020). The vegetarians demonstrated distinct pattern of bone metabolism markers compared to the omnivores, with lower levels of N-terminal propeptide of type I procollagen (P1NP) (p = 0.001) and elevated levels of C-terminal telopeptide of type I collagen (CTX-I) (p = 0.018). Consequently, the P1NP/CTX-I ratio was significantly decreased in the vegetarians. The children following a vegetarian diet showed impaired bone metabolism with reduced bone formation and increased bone resorption. Higher levels of decorin, a myokine involved in collagen fibrillogenesis and essential for tissue structure and function, may suggest a potential compensatory mechanism contributing to maintaining bone homeostasis in vegetarians. The observed significant positive correlations between myostatin and bone metabolism markers, including P1NP and soluble receptor activator of nuclear factor kappa-B ligand (sRANKL), suggest an interplay between muscle and bone metabolism, potentially through the RANK/RANKL/OPG signaling pathway.

Pathophysiology and Therapeutic Management of Bone Loss in Patients with Critical Illness.

Patients with critical illnesses are at higher risk of comorbidities, which can include bone mineral density loss, bone turnover marker increase, and fragility fractures. Patients admitted to intensive care units (ICUs) have a higher risk of bone fractures. Since hypermetabolism is a characteristic of ICU patients, such patients are often rapidly affected by systemic deterioration, which often results in systemic wasting disease. Major risk factors for ICU-related bone loss include physical restraint, inflammation, neuroendocrine stress, malnutrition, and medications. A medical history of critical illness should be acknowledged as a risk factor for impaired bone metabolism. Bone loss associated with ICU admission should be recognized as a key component of post-intensive care syndrome, and further research that focuses on treatment protocols and prevention strategies is required. Studies aimed at maintaining gut integrity have emphasized protein administration and nutrition, while research is ongoing to evaluate the therapeutic benefits of anti-resorptive agents and physical therapy. This review examines both current and innovative clinical strategies that are used for identifying risk factors of bone loss. It provides an overview of perioperative outcomes and discusses the emerging novel treatment modalities. Furthermore, the review presents future directions in the treatment of ICU-related bone loss.

Emerging factors affecting peri-implant bone metabolism.

Implant dentistry has evolved to the point that standard implant osseointegration is predictable. This is attributed in part to the advancements in material sciences that have led toward improvements in implant surface technology and characteristics. Nonetheless, there remain several cases where implant therapy fails (specifically at early time points), most commonly attributed to factors affecting bone metabolism. Among these patients, smokers are known to have impaired bone metabolism and thus be subject to higher risks of early implant failure and/or late complications related to the stability of the peri-implant bone and mucosal tissues. Notably, however, emerging data have unveiled other critical factors affecting osseointegration, namely, those related to the metabolism of bone tissues. The aim of this review is to shed light on the effects of implant-related factors, like implant surface or titanium particle release; surgical-related factors, like osseodensification or implanted biomaterials; various drugs, like selective serotonin reuptake inhibitors, proton pump inhibitors, anti-hypertensives, nonsteroidal anti-inflammatory medication, and statins, and host-related factors, like smoking, diet, and metabolic syndrome on bone metabolism, and aseptic peri-implant bone loss. Despite the infectious nature of peri-implant biological complications, these factors must be surveyed for the effective prevention and management of peri-implantitis.

Bone Microarchitecture and Volumetric Mineral Density Assessed by HR-pQCT in Patients with 21- and 17α-Hydroxylase Deficiency.

Due to disturbances in hormones and long-term glucocorticoid replacement therapy (GRT), congenital adrenocortical hyperplasia (CAH) patients are at risk of impaired bone structure and metabolism. This cross-sectional, case-control study aims to investigate for the first time bone microarchitecture features in 21-hydroxylase deficiency (21OHD; N = 38) and 17α-hydroxylase deficiency (17OHD; N = 16) patients using high-resolution peripheral quantitative computed tomography (HR-pQCT) by matching the same sex and similar age [21OHD vs. control: 29.5 (24.0-34.3) vs. 29.6 (25.9-35.2) years; 17OHD vs. controls: 29.0 (21.5-35.0) vs. 29.7 (24.6-35.3) years] with healthy controls (1:3). All patients underwent HR-pQCT scans of the nondominant radius and tibia, and had received GRT. Compared with corresponding controls, 17OHD cases had higher height (P < 0.001), weight (P = 0.013) and similar body mass index (BMI), while 21OHD had lower height (P < 0.001), similar weight and higher BMI (P < 0.001). 17OHD and 21OHD patients demonstrated various significant bone differences in most HR-pQCT indices, suggesting abnormalities in bone microarchitectures from healthy people. Further correlation analyses revealed that some characteristics, such as height and hormones, may contribute to the bone differences in HR-pQCT indices between two diseases. However, treatment dosage and time were not correlated, indicating that the current glucocorticoid doses may be within safety limits for bone impairment. Overall, our study for the first time revealed changes of bone microarchitecture in CAH patients and their potential relations with clinical characteristics. Further longitudinal researches are required to confirm these findings.

THU605 Impact Of Abnormal Circadian Cortisol Secretion On Bone Metabolism In Patients With Mild Autonomous Cortisol Secretion

Abstract Disclosure: J. Saini: None. R. Nathani: None. S. Singh: None. V. Fell: None. E. Atkinson: None. S. Achenbach: None. S. Khosla: None. I. Bancos: None. Background: Previous studies reported that both cortisol secretion and bone metabolism biomarkers follow a circadian pattern of secretion. Patients with mild autonomous cortisol secretion (MACS) demonstrate an increased risk of fractures. As most patients with MACS do not have increased cortisol production, we hypothesized that abnormal circadian cortisol secretion is associated with impaired bone metabolism. Objective: To compare the circadian secretory pattern of bone metabolism biomarkers in relation to cortisol circadian secretion in patients with MACS versus referent subjects. Methods: We conducted a pilot cross-sectional study of patients with MACS and referent subjects. MACS was diagnosed in patients with adrenal adenomas based on an abnormal 1 mg dexamethasone suppression test (cortisol &amp;gt;1.8 mcg/dL). Referent subjects with available abdominal imaging within 5 years and adrenal disorder were recruited from the community. Participants were admitted to the clinical research unit for blood sampling every 2 hours over 24h period. Measurements included total and free cortisol, calcium, parathyroid hormone (PTH), osteocalcin, amino-terminal propeptide type 1 collagen (PINP), and carboxy-terminal telopeptide of type 1 collagen (CTX). Subjects with disorders or medication affecting bone metabolism were excluded. Time periods of blood draw were categorized into the morning (6 to 12 hours), afternoon (14-18 hours) and night (20-2 hours). Delta (morning measurements/afternoon measurements) was calculated. Results: Subjects included 12 patients with MACS (median age 57, IQR 48-67, 83% women) and 10 referent subjects (median age 57, IQR 50-63, 80% women). The 24-hour area under the curve for total (10342 vs 9090 mcg/dL, p=0.468) and free cortisol (437 vs 329 mcg/dL, p=0.086) was no different between patients with MACS and referent subjects. However, the mean night total (6.7 vs 4.3 mcg/dL, p=0.056) and free cortisol (0.2 vs 0.1 mcg/dL, p=0.035) was higher in MACS vs referent subjects. The area under the curve for calcium, phosphorus, CTX, osteocalcin and PINP were similar between patients and referent subjects, however, the area under the curve for PTH was higher in patients vs referent subjects (mean 64179 vs 42602 pg/mL, p=0.021). Both delta total cortisol (mean 8.6 vs 5.5, p=0.01) and delta PTH (mean -1.5 vs 4.2, p=0.051) was higher in referent subjects vs patients with MACS. Conclusion: When compared to referent subjects, patients with MACS have similar 24-hour cortisol production but demonstrate an increase in night-time cortisol secretion and a blunting of diurnal cortisol (lower morning/afternoon cortisol). Patients with MACS have higher PTH production overall, as well as an abnormal diurnal PTH secretion. Noted abnormalities in PTH may contribute to the MACS-associated impairment in bone health. Presentation: Thursday, June 15, 2023

Key Trace Elements Zinc and Magnesium Levels Decline After Fracture in a Rat Model

Category: Basic Sciences/Biologics; Basic Sciences/Biologics Introduction/Purpose: Zinc and magnesium are crucial for bone health, and their deficiencies can lead to impaired bone metabolism and repair. Although enhancing their bioavailability has been linked to better fracture healing, their levels during healing have not been studied. We hypothesized that zinc and magnesium levels transiently decrease at the fracture site compared to intact bone. This study is the first to explore temporal trace element levels during the initial stages of fracture healing. The findings will reveal when each element changes its concentration at the fracture site, which is associated with specific functions necessary for appropriate healing. Understanding the connection between trace element concentration and repair processes could lead to more effective treatment or supplementation during fracture healing. Methods: Following induction of a femur fracture in male BB Wistar rats, injured and intact contralateral femurs were harvested at 1- (n=3), 3- (n=4), and 7-days (n=3) after fracture. Fracture segments 10mm in length were resected 5mm from the center of the callus in either direction. Contralateral non-fractured femur segments were resected from the same region within the femoral diaphysis. Samples were analyzed via inductively coupled mass spectrometry using an Agilent ICP-MS 7900 (Agilent Technologies, Santa Clara, CA). Data was converted from ppb to percent weight zinc and magnesium per weight of bone (w/w%). The difference between zinc and magnesium in contralateral intact bone vs. fractured bone was calculated and averaged (∆) for each group. The average % change were also determined. An independent sample two-tailed t-test was performed comparing average w/w% of zinc and magnesium between fracture and contralateral samples. A p-value of &lt; 0.05 was considered significant. Results: After 1-day post-fracture, there was a -29.09 average % change in zinc levels (∆ 6.90x10^-03 ± 5.05x10^-03) (p = 0.033) and a -25.76 average % change in magnesium levels (∆ 1.21x10^-01 ± 7.36x10^-02 w/w%) (p = 0.241) between fractured and non- fractured femurs. After 3-days post-fracture, there was a -22.51 average % change in zinc levels (∆ 5.45x10^-03 ± 3.95x10^-03 w/w%) (p = 0.022) and a -33.07 average % change in magnesium levels (∆ 1.84x10^-01 ± 1.05x10^-01 w/w%) (p = 0.025). After 7- days post-fracture, there was a -9.40 average % change in zinc levels (∆ 1.90x10^-03 ± 3.98x10^-03) (p = 0.377) and a -17.88 average % change in magnesium levels (∆ 9.04x10^-02 ± 1.24x10^-01 w/w%) (p = 0.159) between fractured and non-fractured femurs. Conclusion: Previous research has established the significance of trace elements, namely zinc and magnesium, in the process of fracture healing. Zinc has been shown to improve fracture healing, while magnesium has been found to play a role regulating inflammation during early fracture healing. The findings of this study corroborate our hypothesis that levels of these elements transiently decline following fracture. By evaluating these changes in trace element levels, we can gain a better understanding of their function in the fracture healing process. These observations may offer insight into potential therapeutic approaches utilizing zinc and magnesium for fracture healing in the future.

E05 Is subchondral bone marrow edema predictive of bone mineral density loss in juvenile idiopathic arthritis?

Abstract Introduction Inflammation plays a crucial role in impaired bone metabolism [1]. Subchondral bone marrow oedema (BME) in Magnetic Resonance Imaging (MRI) was associated to bone mineral density (BMD) loss in adult spondyloarthritis [1]. BME was less studied in juvenile idiopathic arthritis (JIA). Objectives We aimed to study the link between MRI BME and BMD in JIA patients. Methods We conducted a retrospective study of 44 patients with JIA who fulfilled the International League of Associations for Rheumatology (ILAR) 2001 criteria. For each patient we collected the following data: age, age at the onset of JIA, JIA subtype, disease duration, C-reactive protein (CRP) and Erythrocyte sedimentation rate (ERS) levels, BMD assessed using bone densitometry and MRI. Disease activity was assessed using the JADAS score. Statistical analysis was performed using SPSS software. Results We included 28 boys and 16 girls. The mean age was 13.65 ± 4.62 years. The mean age at the onset of the disease 9.57 ± 3.97 years. The mean disease duration was 4.34 ± 3.09 years. There was enthesitis-related arthritis in 61% of the cases (n = 27), oligoarticular JIA in 14% of the cases (n = 6), polyarticular JIA in 11% of the cases (n = 5), and psoriatic arthritis in 7% of the cases (n = 3). JIA was undifferentiated in 7% of the cases (n = 3). The mean CRP and ESR were 14.42 ± 19.67 mg/l and 26.56 ± 20.87 mm, respectively. The mean JADAS was 6.6 ± 4.7. Bone densitometry was performed in 17 patients. The mean BMD and the mean Z-score were 0.961 ± 0.128 g/cm2 and -0.4 ± 1.16 standard deviation, respectively. Magnetic resonance imaging (MRI) showed BME in 52% of the patients (n = 23). Bone marrow oedema was present in the sacroiliac joints in 43% of the cases (n = 19), in the coxofemoral joints in 27% of the cases (n = 12), and in the spine in 9% of the cases (n = 4). The presence of BME was associated with a higher ESR (32.71 ± 25.71 vs 18.94 ± 10.72 mm, P = 0.032), higher JADAS (8.01 ± 5.36 vs 4.75 ± 3.29, P = 0.023), and a lower Z-score (-1.3 ± 0.77 vs 0.4 ± 0.8 standard deviation, P = 0.001). Conclusion Our study showed that MRI BME was associated with high disease activity and BMD loss in JIA patients. This result is consistent with those of Akgöl et al. [2]. Bone marrow oedema seems to predict BMD loss in JIA and should lead to optimizing the treatment.

The Inflammatory Contribution of B-Lymphocytes and Neutrophils in Progression to Osteoporosis.

Osteoporosis is a bone disease characterized by structural deterioration and low bone mass, leading to fractures and significant health complications. In this review, we summarize the mechanisms by which B-lymphocytes and neutrophils contribute to the development of osteoporosis and potential therapeutics targeting these immune mediators to reduce the proinflammatory milieu. B-lymphocytes-typically appreciated for their canonical role in adaptive, humoral immunity-have emerged as critical regulators of bone remodeling. B-lymphocytes communicate with osteoclasts and osteoblasts through various cytokines, including IL-7, RANK, and OPG. In inflammatory conditions, B-lymphocytes promote osteoclast activation and differentiation. However, B-lymphocytes also possess immunomodulatory properties, with regulatory B-lymphocytes (Bregs) secreting TGF-β1 to restrain pathogenic osteoclastogenesis. Neutrophils, the body's most prevalent leukocyte, also contribute to the proinflammatory environment that leads to osteoporotic bone remodeling. In aged individuals, neutrophils display reduced chemotaxis, phagocytosis, and apoptosis. Understanding the delicate interplay between B-lymphocytes and neutrophils in the context of impaired bone metabolism is crucial for targeted therapies for osteoporosis.

Is it possible to stop the osteolysis of the periprosthetic bone during re-endoprosthetics of the hip joint against the background of osteoporosis?

Revision interventions due to aseptic instability show a marked upward trend, and one of the reasons is an increase in the number of people with osteoporosis in the population. The impaired bone metabolism in these cases persist even after re-endoprosthetics. The authors aim to draw attention of trauma orthopaedists to the need to treat osteoporosis either before or immediately after the re-endoprosthetic surgery. A clinical case is presented. A 65-year-old patient T., 5 months after surgery, complained of persistent pain in the left hip joint radiating to the left knee joint, which intensified when walking, lameness, inability to move without additional support (two crutches), limited range of motion within the left hip joint that had undergone surgery (endoprosthesis). The patient had a history of femoral neck fracture associated with a low energy fall. The left hip joint re-endoprosthetics was performed due to aseptic instability of the femoral and acetabular components of the prosthetic implant. The diagnosed diseases included secondary osteoporosis, D-deficiency, hypocalcemia, and periprosthetic osteolysis. Given the increased intensity of resorption and the fact that the femoral neck fracture occurred with underlying secondary osteoporosis, it was decided to prescribe antiresorptive therapy with denosumab 60 mg once every 6 months combined with alfacalcidol and calcium supplement. Despite an objective 3-month delay in antiresorptive therapy initiation, the treatment result was achieved in the observed patient. In summary, denosumab 60 mg increases the effectiveness of re-endoprosthetics with underlying osteoporosis by reducing activity of the periprosthetic bone osteolysis.

Artificial neural networks in predicting impaired bone metabolism in diabetes mellitus

Growing incidence of diabetes mellitus (DM), given significant socioeconomic consequences that low-trauma fractures entail, determines a need to improve diagnostic standards and minimize the risk of medical errors, which will reduce costs and contribute to better treatment outcomes in this category of patients.Aim. To assess diagnostic capabilities of the method based on the use of an artificial neural network (ANN) for predicting changes in reparative osteogenesis in diabetes mellitus.Materials and methods. A single-center, one-stage, cross-sectional study included 235 patients with type 1 and type 2 diabetes mellitus and 82 persons of the control group (the total of 317 patients). Further, the obtained data were processed using the MATLAB software to develop an ANN with a training (80%) and test (20%) set. The ANN model was trained by optimizing the relationship between a set of input data (a number of clinical and laboratory parameters: gender, age, body mass index, duration of diabetes mellitus, etc.) and a set of corresponding output data (variables reflecting the state of bone metabolism: bone mineral density, markers of bone remodeling).Results. The ANN-based algorithm predicted estimated values of bone metabolism parameters in the examined individuals by generating output data using deep learning. Machine learning was repeated until the error was minimized for all variables. The accuracy of the validation test to predict changes in bone metabolism based on patient data was 92.86%.Conclusion. The developed ANN-based method made it possible to design an auxiliary tool for stratification of patients with changes in bone metabolism in diabetes mellitus, which will help reduce healthcare costs, speed up the diagnosis due to fast data processing, and customize treatment for this category of patients.

«Синдромокомплекс» идиопатического сколиоза

Introduction Multifactoriality in the etiology of idiopathic scoliosis (IS) requires an integrated approach to diagnosis, while the regular examination of patients is limited to radiography, computed tomography without a detailed analysis of the data obtained on the state of the musculoskeletal system. The problem of complex diagnosis of IS is practically not covered by the literature including the syndromic approach to the rationale for the method of treatment and rehabilitation. Purpose of the study To define the concept of "syndromocomplex" of idiopathic scoliosis based on the study of the state of the spine, muscles, proximal femur, bone mineral density (BMD), mineral metabolism and bone metabolism using current diagnostic methods. Materials and methods The state of the spine (300 patients), proximal femur (57 patients), paravertebral (40 patients) and gluteal muscles (60 patients of the main group and 40 of the control group) were studied using the method of multislice computed tomography (MSCT) and magnetic resonance imaging (MRI), densitometry – BMD (40 patients of the main and 40 of control one), mineral metabolism and bone metabolism were studied by biochemical methods in 55 patients with IS. Results and discussion The study of patients with idiopathic scoliosis at different ages and with different grades of deformities in various parts of the musculoskeletal system revealed pronounced disorders in the shape of the vertebrae, including an increase in the frontal diameter, wedge shape with a significant difference in density along the convex and concave sides, structural changes in the vertebrae, manifested in a decrease in density, the presence of rarefaction zones, areas of maximum density at the top of the deformity, malnutrition and fatty degeneration of the paravertebral and gluteal muscles, a decrease in BMD, a decrease in the density of the femoral head, impaired mineral metabolism and bone metabolism. Conclusion Severe disorders in the shape, X-ray morphological changes in the vertebrae, malnutrition and fatty degeneration of the paravertebral and gluteal muscles, concomitant changes in BMD, hip joint, mineral metabolism and bone metabolism, are included in the concept of "syndromocomplex” of idiopathic scoliosis, underlie the tactical concept for diagnosis, treatment and further rehabilitation measures for patients with severe forms of scoliosis.

Pathogenetic and diagnostic role of osteoprotegerin in the combined course of osteoarthritis and obesity

In recent years, it has been proven that the formation of OA can occur against the background of impaired bone metabolism.&#x0D; Bone remodeling is considered as a continuous complex process aimed at eliminating microdamages and updating the bone matrix. A key link in the regulation of this process is the system RANK / RANKL / OPG (osteoprotegerin), which provides a balance of activity of osteoblasts and osteoclasts. It blocks the interaction between RANK and RANKL by intercepting the RANKL ligand, which inhibits osteoclast development and reduces bone resorption.&#x0D; Thus, these properties of OPG can be considered as one of the pathogenetic factors in patients with dystrophic joint lesions.&#x0D; Objective: to investigate the content and role of osteoprotegerin in young patients with osteoarthritis, which occurs against the background of changes in body weight.&#x0D; Materials and methods. The study involved 75 young patients (mean age - 30.92 ± 0.546 years) with overweight or obesity, who in the previous stages of the study was diagnosed with osteoarthritis (main group). The comparison group was represented by 50 patients with osteoarthritis and normal body weight. The age of patients was 30.95 ± 0.545 years; as in the previous group, men predominated - 64% and 36% respectively.&#x0D; Benchmarks of osteoprotegerin were obtained in a study of 37 relatively healthy individuals of the same age and sex.&#x0D; The level of osteoprotegerin was determined by enzyme-linked immunosorbent assay using the FineTest EH0247 reagent kit, China.&#x0D; The outcomes were processed by the methods of variation statistics using the computer program STATISTICA.Results and discussion. When determining the content of OPG in the serum of patients of the main group was found to increase to 124.03 pg / ml, against control - 65.64 pg / ml. In the group of patients with isolated OA, this value was 92.29 pg / ml. Meaning that, in OA, running on the background of altered BMI, the content of OPG is likely to increase, both in relation to the norm and the results of the comparison group (p &lt;0,001).&#x0D; The formation and course of osteoarthritis is accompanied by an increase in osteoprotegerin, the content of which depends on the degree of obesity and the radiological stage of the process.&#x0D; Conclusions: The course of osteoarthritis is accompanied by an increase in osteoprotegerin, which is considered a negative regulator of bone resorption.&#x0D; In osteoarthritis, which occurs against the background of changes in body mass index, a direct correlation with the degree of obesity.&#x0D; Changes in osteoprotegerin in patients with osteoarthritis depend on the radiological stage of joint damage and are most pronounced in individuals with stage 2 obesity and stage 2 radiological changes

Usefulness of the trabecular bone score in maintenance dialysis patients : A single center observational study.

BackgroundThe number of dialysis patients is steadily increasing. Associated comorbidities include impaired bone and mineral metabolism, termed chronic kidney disease-mineral and bone disorder (CKD-MBD), leading to a high fracture risk, increased morbidity and mortality and impaired quality of life. While the bone density is assessed with dual-energy X‑ray absorptiometry (DXA), the trabecular bone score (TBS) captures the image texture as a potential index of skeletal microarchitecture. The aim of this study was to evaluate the clinical relevance of DXA and TBS in dialysis patients with and without prevalent fractures.MethodsBone disorders were evaluated in 82 dialysis patients (37% female) at the University Hospital of Graz, Austria, by DXA including the assessment of the TBS based on a patient interview and the local routine patient database software. The patient cohort was stratified by having sustained a fragility fracture in the past or not. Descriptive statistics, t‑tests for continuous variables and χ2-tests for nominal variables including results of DXA and TBS were performed to compare these groups considering the dialysis modality and duration as well as the number of kidney transplantations.ResultsOf the 82 patients, 32 (39%) had a positive history of fractures. There was a significant association between dialysis duration and fracture prevalence (p < 0.05) as well as musculoskeletal pain (p < 0.01). No significant correlation between DXA/TBS parameters and musculoskeletal pain could be established. The DXA scores did not correlate with fracture prevalence with the exception of DXA radius measurements; however, fracture prevalence significantly correlated inversely with TBS (p < 0.001).ConclusionThe use of DXA has a limited role in fracture prediction in dialysis patients; however, the TBS seems to add information as an additional tool for fracture risk estimation in this patient population.

DENYING TOTAL HIP ARTHROPLASTY IN SMOKERS, PATIENTS WITH ALCOHOL ABUSE OR IN PATIENTS WITH HUMAN IMMUNODEFICIENCY VIRUSES. WHY?

Nowadays total hip arthroplasty (THA) is one of the most successful surgical procedures in the world and the number of procedures performed is growing every year. However, its success largely depends on the absence of postoperative complications. Among the risk factors affecting the occurrence of postoperative complications are smoking, alcohol abuse, drug abuse, human immunodeficiency viruses (HIV), obesity, anemia, diabetes mellitus, malnutrition, rheumatoid arthritis, cardiovascular diseases, renal failure and dialysis, depression and anxiety. In the presented manuscript, such factors as HIV, smoking and alcohol abuse were considered. In smokers, bone regeneration slows down due to impaired bone metabolism and a slowdown in vascular recovery. Alcohol abuse affects human immunity, inhibiting T-helper cells, and also causing blood coagulation disorders. Alcohol abuse increases the risk of hospital complications, surgery related complications and general medical complications. Smoking can increase the risk of septiccomplications (lower respiratory tract infection, sepsis, urinary tract infection), myocardial infarction, risk of aseptic loosening of implants. Mortality was also higher in smokers compared to nonsmokers. HIV increases bone fragility, debilitation, rate of cardiovascular diseases and decreases the number of CD4+ cells in the blood, which directly affects the risk of periprosthetic joint infections and revision. All three factors increase the patient's lengthof stay in the hospital after THA. Currently, recommendations have been developed for preventive measures that need to be taken to reduce the risk of postoperative complications by performing primary THA. According to the recommendations, quitting smoking and drinking alcohol 4 weeks before THA will significantly reduce the risk of postoperative complications. For HIV-positive patients, antiretroviral therapy and subsequent assessing the viral load arerequired prior to THA. Preoperative care in this category of patients, undergoing primary THA, can reduce the risk of complications.

Increased Medical and Implant-Related Complications in Total Hip Arthroplasty Patients With Underlying Chronic Obstructive Pulmonary Disease

BackgroundChronic obstructive pulmonary disease (COPD) has been associated with impaired bone metabolism. The purpose of this study is to investigate rates of readmission, respiratory complications, implant-related complications, and revision after total hip arthroplasty (THA) in patients with and without underlying COPD. MethodsThe PearlDiver Mariners database was used to divide patients undergoing primary THA (CPT-27130) into two cohorts: 1) THA with COPD (including asthma) or 2) THA without COPD. The incidence of 30-day readmission, COPD exacerbation, pneumonia, other respiratory complications as well as dislocations, mechanical loosening, and joint prosthetic infection was calculated through logistic regression. The risk of THA revision was also assessed through Cox-proportional hazards regression. All regression controlled for age, gender, and medical comorbidities found to be associated with COPD. ResultsBetween 2010 and 2018, 97,784 THA patients with COPD and 338,243 THA patient without COPD were studied. THA patients with COPD had higher risk of 30-day readmission (aOR = 1.17, 95% CI 1.11-1.23, P < .0001). There was higher risk of 30-day pneumonia (aOR = 2.07, 95% CI 1.76-2.44, P < .0001). THA patients with COPD also faced higher risk of 30-day dislocations (aOR = 1.31, 95% CI 1.19-1.45, P < .0001), joint prosthetic infections (aOR = 1.25, 95% CI 1.14-1.37, P < .0001), and periprosthetic fracture (aOR = 1.19, 95% CI 1.07-1.32, P = .0015). Regarding revisions, 3.3% of THA patients with COPD underwent THA revision at 1 year, a higher risk than THA patients without COPD (aOR = 1.11, 95% CI 1.06-1.16, P < .0001). ConclusionPatients undergoing THA with underlying COPD face a higher rate of comorbidities, respiratory complications, implant complications, and revision surgeries, than patients without COPD. Level of EvidenceIII.

Correlation between Serum Bone Turnover Markers and Estimated Glomerular Filtration Rate in Chinese Patients with Diabetes.

Objective Diabetes is a growing global public health concern with many significant disease complications. Multiple studies show that bone turnover markers (BTMs) are decreased in diabetes patients, indicating impaired bone metabolism in diabetes patients. A recent study also showed that in diabetes patients, BTMs are correlated with urine albumin to creatinine ratio, an indicator of nephropathy. However, whether BTMs are correlated with estimated glomerular filtration rate (eGFR) in diabetes remains unknown. This retrospective study accessed correlations between serum BTMs and eGFR in Chinese patients with diabetes and compare levels of BTMs and eGFR between diabetic patients and healthy individuals. Methods This study analyzed data from 221 diabetic patients (include type1 and type 2 diabetes) and 155 healthy individuals. Serum BTM levels and eGFR were compared between diabetic patients and healthy individuals. Pearson correlation analysis was used to assess correlations between BTMs and eGFR. Multiple logistic regression analysis adjusted for gender and age was performed to measure odd ratio (OR) and 95% confidence interval (95% CI) of BTMs on diabetes. Results Patients with diabetes had significant lower 25-hydroxyvitamin D (25(OH)D) levels (15.07 ± 6.20 ng/mL) than healthy group (17.89 ± 6.41 ng/mL) (P < 0.05). For patients with diabetes, eGFR was negatively correlated with osteocalcin (OC) (r = −0.434, P < 0.05), procollagen type 1 intact N-terminal propeptide (P1NP) (r = −0.350, P < 0.05), and β-carboxy-terminal cross-linking telopeptide of type I collagen (β-CTX) (r = −0.179, P < 0.05) levels. For healthy people, eGFR was negatively correlated with 25(OH)D (r = −0.290, P < 0.05) levels. Multiple logistic regression analysis adjusted for age and gender (mean age of diabetes was 64.9 years and the percentage of female was 66.9%, mean age of healthy people was 48.4 years and the percentage of female was 37.4%) showed that 25(OH)D (OR = 0.909, 95%CI = 0.862 − 0.959, P < 0.05) was protective factors for diabetes. Conclusions In the stage of diabetic nephropathy, bone turnover may accelerate. It is important to detect BTMs in the stage of diabetic nephropathy.