scholarly journals The Interplay between Immune System and Microbiota in Osteoporosis

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Pietro Locantore ◽  
Valeria Del Gatto ◽  
Silvia Gelli ◽  
Rosa Maria Paragliola ◽  
Alfredo Pontecorvi
Keyword(s):  
Immune System ◽  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Bone Cells ◽  
Bone Microarchitecture ◽  
Interleukin 17 ◽  
Mineral Density ◽  
Increased Risk ◽  
Long Term Treatment ◽  
Wide Range

Osteoporosis is a disease characterized by low bone mass and alterations of bone microarchitecture, with an increased risk of fractures. It is a multifactorial disorder that is more frequent in postmenopausal women but can be associated to other diseases (inflammatory and metabolic diseases). At present, several options are available to treat osteoporosis trying to block bone reabsorption and reduce the risk of fracture. Anyway, these drugs have safety and tolerance problems in long-term treatment. Recently, gut microbiota has been highlighted to have strong influence on bone metabolism, becoming a potential new target to modify bone mineral density. Such evidences are mainly based on mouse models, showing an involvement in modulating the interaction between the immune system and bone cells. Germ-free mice represent a basic model to understand the interaction between microbiota, immune system, and bone cells, even though data are controversial. Anyway, such models have unequivocally demonstrated a connection between such systems, even if the mechanism is unclear. Gut microbiota is a complex system that influences calcium and vitamin D absorption and modulates gut permeability, hormonal secretion, and immune response. A key role is played by the T helper 17 lymphocytes, TNF, interleukin 17, and RANK ligand system. Other important pathways include NOD1, NOD2, and Toll-like receptor 5. Prebiotics and probiotics are a wide range of substances and germs that can influence and modify microbiota. Several studies demonstrated actions by different prebiotics and probiotics in different animals, differing according to sex, age, and hormonal status. Data on the effects on humans are poor and controversial. Gut microbiota manipulation appears a possible strategy to prevent and treat osteopenia and/or osteoporosis as well as other possible bone alterations, even though further clinical studies are necessary to identify correct procedures in humans.

scholarly journals The use of an in-vitro batch fermentation (human colon) model for investigating mechanisms of TMA production from choline, l-carnitine and related precursors by the human gut microbiota

2021 ◽  
Author(s):  
Priscilla Day-Walsh ◽  
Emad Shehata ◽  
Shikha Saha ◽  
George M. Savva ◽  
Barbora Nemeckova ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Human Colon ◽  
Human Studies ◽  
Bacterial Strains ◽  
Increased Risk ◽  
Carnitine Metabolism ◽  
Registration Number ◽  
Vitro Model

Abstract Purpose Plasma trimethylamine-N-oxide (TMAO) levels have been shown to correlate with increased risk of metabolic diseases including cardiovascular diseases. TMAO exposure predominantly occurs as a consequence of gut microbiota-dependent trimethylamine (TMA) production from dietary substrates including choline, carnitine and betaine, which is then converted to TMAO in the liver. Reducing microbial TMA production is likely to be the most effective and sustainable approach to overcoming TMAO burden in humans. Current models for studying microbial TMA production have numerous weaknesses including the cost and length of human studies, differences in TMA(O) metabolism in animal models and the risk of failing to replicate multi-enzyme/multi-strain pathways when using isolated bacterial strains. The purpose of this research was to investigate TMA production from dietary precursors in an in-vitro model of the human colon. Methods TMA production from choline, l-carnitine, betaine and γ-butyrobetaine was studied over 24–48 h using an in-vitro human colon model with metabolite quantification performed using LC–MS. Results Choline was metabolised via the direct choline TMA-lyase route but not the indirect choline–betaine-TMA route, conversion of l-carnitine to TMA was slower than that of choline and involves the formation of the intermediate γ-BB, whereas the Rieske-type monooxygenase/reductase pathway for l-carnitine metabolism to TMA was negligible. The rate of TMA production from precursors was choline > carnitine > betaine > γ-BB. 3,3-Dimethyl-1-butanol (DMB) had no effect on the conversion of choline to TMA. Conclusion The metabolic routes for microbial TMA production in the colon model are consistent with observations from human studies. Thus, this model is suitable for studying gut microbiota metabolism of TMA and for screening potential therapeutic targets that aim to attenuate TMA production by the gut microbiota. Trial registration number NCT02653001 (http://www.clinicaltrials.gov), registered 12 Jan 2016.

scholarly journals DXA parameters, Trabecular Bone Score (TBS) and Bone Mineral Density (BMD), in fracture risk prediction in endocrine-mediated secondary osteoporosis

Endocrine ◽  
2021 ◽  
Author(s):  
Enisa Shevroja ◽  
Francesco Pio Cafarelli ◽  
Giuseppe Guglielmi ◽  
Didier Hans
Keyword(s):  
Bone Mineral Density ◽  
Trabecular Bone ◽  
Bone Mineral ◽  
Trabecular Bone Score ◽  
Bone Microarchitecture ◽  
Fragility Fractures ◽  
Endocrine Disorders ◽  
Mineral Density ◽  
Increased Risk

AbstractOsteoporosis, a disease characterized by low bone mass and alterations of bone microarchitecture, leading to an increased risk for fragility fractures and, eventually, to fracture; is associated with an excess of mortality, a decrease in quality of life, and co-morbidities. Bone mineral density (BMD), measured by dual X-ray absorptiometry (DXA), has been the gold standard for the diagnosis of osteoporosis. Trabecular bone score (TBS), a textural analysis of the lumbar spine DXA images, is an index of bone microarchitecture. TBS has been robustly shown to predict fractures independently of BMD. In this review, while reporting also results on BMD, we mainly focus on the TBS role in the assessment of bone health in endocrine disorders known to be reflected in bone.

scholarly journals TSH suppressive therapy and bone

2020 ◽  
Vol 9 (7) ◽  
pp. R158-R172 ◽  
Author(s):  
Alessandro Brancatella ◽  
Claudio Marcocci
Keyword(s):  
Bone Loss ◽  
Postmenopausal Women ◽  
Bone Cells ◽  
Trabecular Bone Score ◽  
Experimental Studies ◽  
Bone Architecture ◽  
Tsh Receptor ◽  
Suppressive Therapy ◽  
Mineral Density ◽  
Increased Risk

Thyroid hormones stimulate bone turnover in adults by increasing osteoclastic bone resorption. TSH suppressive therapy is usually applied in patients with differentiated thyroid cancer (DTC) to improve the disease outcome. Over the last decades several authors have closely monitored the potential harm suffered by the skeletal system. Several studies and meta-analyses have shown that chronic TSH suppressive therapy is safe in premenopausal women and men. Conversely, in postmenopausal women TSH suppressive therapy is associated with a decrease of bone mineral density, deterioration of bone architecture (quantitative CT, QCT; trabecular bone score, TBS), and, possibly, an increased risk of fractures. The TSH receptor is expressed in bone cells and the results of experimental studies in TSH receptor knockout mice and humans on whether low TSH levels, as opposed to solely high thyroid hormone levels, might contribute to bone loss in endogenous or exogenous thyrotoxicosis remain controversial. Recent guidelines on the use of TSH suppressive therapy in patients with DTC give value not only to its benefit on the outcome of the disease, but also to the risks associated with exogenous thyrotoxicosis, namely menopause, osteopenia or osteoporosis, age >60 years, and history of atrial fibrillation. Bone health (BMD and/or preferably TBS) should be evaluated in postmenopausal women under chronic TSH suppressive therapy or in those patients planning to be treated for several years. Antiresorptive therapy could also be considered in selected cases (increased risk of fracture or significant decline of BMD/TBS during therapy) to prevent bone loss.

Selenium: A Trace Element for a Healthy Skeleton - A Narrative Review

2020 ◽  
Vol 20 ◽  
Author(s):  
Fabio Vescini ◽  
Iacopo Chiodini ◽  
Andrea Palermo ◽  
Roberto Cesareo ◽  
Vincenzo De Geronimo ◽  
...  
Keyword(s):  
Bone Mass ◽  
Bone Metabolism ◽  
Bone Cells ◽  
Fragility Fractures ◽  
Serum Selenium ◽  
Mineral Density ◽  
Increased Risk ◽  
Serum Selenium Levels ◽  
Essential Nutrient ◽  
The Relationship

: Inadequate serum selenium levels may delay the growth and the physiological changes in bone metabolism. In humans, reduced serum selenium concentrations are associated with both increased bone turnover and reduced bone mineral density. Moreover, a reduced nutritional intake of selenium may lead to an increased risk of bone disease. Therefore, selenium is an essential nutrient playing a role in bone health, probably due to specific selenium-proteins. Some selenium-proteins have an anti-oxidation enzymatic activity and participate in maintaining the redox cellular balance, regulating inflammation and proliferation/differentiation of bone cells too. At least nine selenium-proteins are known to be expressed by fetal osteoblasts and appear to protect bone cells from oxidative stress at bone microenvironment. Mutations of selenium-proteins and reduced circulating levels of selenium are known to be associated with skeletal diseases such as the Kashin-Beck osteoarthropathy and postmenopausal osteoporosis. In addition, the intake of selenium appears to be inversely related to the risk of hip fragility fractures. Recent data suggest that an altered selenium state may affect bone mass even in males and seleniumproteins and selenium concentrations were positively associated with the bone mass at femoral, total and trochanteric site. However, selenium, but not selenium-proteins, seems to be associated with femoral neck bone mass after adjustment for many bone fracture risk factors. The present review summarizes the findings of observational and interventional studies, which have been designed for investigating the relationship between selenium and bone metabolism.

scholarly journals Bone mineral density and microarchitecture among Chinese patients with rheumatoid arthritis: a cross-sectional study with HRpQCT

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Shangyi Jin ◽  
Mengtao Li ◽  
Qian Wang ◽  
Xiaofeng Zeng ◽  
Weibo Xia ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Bone Mineral Density ◽  
Bone Mineral ◽  
Bone Microarchitecture ◽  
Fragility Fractures ◽  
Cross Sectional Study ◽  
Mineral Density ◽  
Cross Sectional ◽  
X Ray ◽  
Increased Risk

Abstract Background Patients with rheumatoid arthritis (RA) are at increased risk of fractures. Although their decline in bone mineral density (BMD) is well-established, data regarding the alterations in bone microarchitecture are limited. In this study, we aimed to evaluate bone microarchitecture, geometry, and volumetric BMD among patients with RA in mainland China using high-resolution peripheral quantitative computed tomography (HRpQCT). Methods In this cross-sectional study, patients with RA were recruited from the Peking Union Medical College Hospital site of the Chinese Registry of rhEumatoiD arthrITis (CREDIT). Each participant underwent HRpQCT scanning (Scanco XtremeCT II), thoracolumbar X-ray and dual-energy X-ray absorptiometry. The primary outcomes were HRpQCT-related measures at distal radius and tibia. Data regarding demographic features, RA-related characteristics, and history of fragility fractures were collected. Correlation between HRpQCT parameters and potentially related factors were analyzed using linear regression analysis. A group of age- and sex-matched healthy controls was included for comparison. Results A total of 81 patients with RA [69 women, aged 57.9 ± 8.7 years, disease duration 5.7 (IQR 1.4–11.2) years] and 81 matched healthy controls were included. Compared with controls, patients with RA had significantly larger bone area and lower total and trabecular vBMD at both the distal radius and tibia. Lower cortical bone thickness was also shown at the distal tibia. Among patients with RA, advanced age, low BMI, female sex, disease duration, and activity were associated with decreased vBMD and impaired bone microstructure. Female reproductive factors including menopause, late menarche, breast feeding, and early childbirth also showed negative correlation with these parameters. Compared to patients with RA without fractures, patients with fragility fractures (n = 11) showed lower trabecular and cortical vBMD, thinner cortical bone, impaired trabecular microstructure, and a trend of declined bone strength. Current glucocorticoid intake was related to decreased vBMD, trabecular number, increased trabecular separation, and inhomogeneity. Conclusions In this study, we observed alterations in bone mineral density, geometry, and microarchitecture among patients with RA compared to healthy individuals, which may impair bone strength and lead to increased risk of fractures. Both traditional risk factors for osteoporosis and RA-associated factors need to be considered in the assessment of the bone quality.

scholarly journals SAT0468 EFFECTS OF ANDROGEN DEPRIVATION THERAPY ON BONE QUALITY (TBS) IN PATIENTS WITH PROSTATE CANCER

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1191.2-1192
Author(s):  
S. Garcia-Cirera ◽  
E. Casado ◽  
J. Muñoz ◽  
L. Del Río ◽  
M. Arévalo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Lumbar Spine ◽  
Androgen Deprivation Therapy ◽  
Bone Quality ◽  
Bone Microarchitecture ◽  
Androgen Deprivation ◽  
Mineral Density ◽  
Increased Risk ◽  
One Year

Background:Androgen deprivation therapy (ADT), by inducing severe hypogonadism, leads to a loss of bone mineral density (BMD) and an increased risk of fragility fractures after 6 months of treatment in men with prostate cancer1. However, its effect on bone quality has not been described.Objectives:To evaluate the changes on bone microarchitecture (bone quality) assessed by TBS (trabecular Bone Score) in male patients with prostate cancer after one year of treatment with ADT.Methods:All patients diagnosed with prostate cancer candidates for long-term ADT admitted to Urology department of Hospital Universitari Parc Tauli (reference population of 450,000 inhabitants) between April 2017 and December 2019 were included. Patients who received chemotherapy, previous hormonal therapy or specific treatment for osteoporosis in the last year or those who had a very impaired functional capacity (Barthel index <30) were excluded.Demographic, clinical and analytical data (testosterone, calcium, phosphorous, alkaline phosphatase, 25-hidroxyvitamin D, PTH) were collected in all patients. A bone densitometry (GE-Lunar Prodigy) including the measurement of lumbar spine TBS (L1-L4) using Medimaps Software was performed at baseline and at 12 months of treatment with ADT.Results:78 patients were included. Mean age 77,9±8,3 years. The median Gleason score was 7,88±1,05. 3 patients had previous fragility fracture (one sacral fracture, one fibula and one multiple vertebral fracture). Baseline analytical values in patients were the following: testosterone11,6±74,9 nmol/L.; 25-hidroxyvitamin D 20,8±10,4 ng/ml; PTH 51,8±23,0 pg/ml; CTX 0,58±0,66. The daily calcium intake was 573±207 mg/day.According to BMD, 17 patients (21,8%) had osteoporosis before starting ADT, with the following average T-score values: lumbar spine +0,15±1,85, femoral neck -1,75±1,00, and total hip -1,19±1,16. Mean baseline TBS value of the entire cohort was 1,279±0,122. 30,5% of the patients showed very degraded microarchitecture (TBS<1,230), 28,8% had partially degraded microarchitecture (TBS 1,230-1,310) and in 40,7% showed normal microarchitecture (TBS >1,310).After one year of ADT treatment, TBS mildly worsened in this cohort, with a median value of 1,256±0,131 (p = NS). However up to 43% of patients reached highly degraded microarchitecture, 27% partially degraded and only 29,5% had a normal TBS (p = NS).Conclusion:Most patients with prostate cancer have an altered bone quality before starting ADT. After 12 months of treatment, the percentage of patients with highly degraded bone microarchitecture increases, although not significantly. More studies are needed to confirm this trend and to evaluate if these patients present more long-term fractures.References:[1]Lee R, et al. Bone 2011; 48 (1): 88-95Disclosure of Interests:Silvia Garcia-Cirera: None declared, Enrique Casado Speakers bureau: UCB, Lilly, Amgen, Theramex, Gebro, Gedeon-Richter, Stada, Jesús Muñoz: None declared, Luis Del Río: None declared, Marta Arévalo: None declared, Menna Rusiñol: None declared, Noemí Navarro: None declared, Víctor Parejo: None declared, Jordi Gratacos-Masmitja Grant/research support from: a grant from Pfizzer to study implementation of multidisciplinary units to manage PSA in SPAIN, Consultant of: Pfizzer, MSD, ABBVIE, Janssen, Amgen, BMS, Novartis, Lilly, Speakers bureau: Pfizzer, MSD, ABBVIE, Janssen, Amgen, BMS, Novartis, Lilly

scholarly journals Bone Microarchitectural Changes in Hyperthyroid Women Compared to a Normal Canadian Cohort

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A256-A257
Author(s):  
Terra G Arnason ◽  
David Cooper ◽  
Reza Behdani ◽  
Saija Kontulainen
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Fracture Risk ◽  
Trabecular Bone ◽  
Bone Microarchitecture ◽  
Critical Role ◽  
Primary Objective ◽  
Mineral Density ◽  
Tsh Suppression ◽  
Increased Risk

Abstract Thyroid hormones play a critical role in bone physiology during childhood, but also impacts adult bone metabolism. Hyperthyroidism promotes accelerated bone turnover and bone remodelling which is associated with net loss of bone mineral density over time (BMD) and these changes have been quantitated using the gold standard of measuring BMD, Dual Energy X-ray Absorptiometry (DEXA). Ordinarily, biochemical thyroid hormone normalization restores BMD towards normal, yet an increased risk of fractures remains lifelong. DEXA, therefore, cannot explain the underlying etiology for fracture risk which may be due to undetected changes in bone microarchitecture. Our primary objective was to utilize an investigational 3-dimensional bone imaging technology, High Resolution peripheral Quantitative Tomography (HR-pQCT), to study bone microarchitecture in actively hyperthyroid women to determine if there are changes in cortical and trabecular bone microarchitecture from that of age-matched controls. A subset of women were rescanned using HR-pCT after thyroid hormones had been normalized for at least 6 months to determine if there were cortical/trabecular architectural changes that reversed towards normal in these individual cases. We enrolled 20 hyperthyroid women (age 20–76) for this pilot study who had persistent TSH suppression for &gt;3 months (TSH&lt; 0.5, normal range: 0.5–4.49 mU/L) without secondary causes for bone loss. Their etiology was divided amongst TSH suppression for thyroid carcinoma, Grave’s disease and iatrogenic hyperthyroidism. HR-pQCT scans of the radius were compared to age-matched scans of normal females, available from the robust Canadian Multicentre Osteoporosis Study (CaMOS) control cohort. Four participants were re-scanned after 6 months of TSH normalization to assess reversibility. The observed data showed statistically significant differences in key parameters of bone microarchitecture in hyperthyroidism, independent of etiology. We observed decreased cortical thickness and increased failure load as statistically different from age-matched controls. Increases in cortical bone porosity and decreases in volumetric bone density (cortical, trabecular and total) were notable but did not reach significance in this small study. Repeat scans following normalization of thyroid hormone levels revealed consistent (partial, nonsignificant) normalization of multiple bone microarchitecture elements including increased trabecular number/thickness, and decreased cortical porosity. These findings suggest that there are changes in both cortical and trabecular bone during active hyperthyroidism that may contribute to increased lifelong fracture risk.

scholarly journals MICROSCOPIC STRUCTURE AND MORPHOMETRIC PARAMETRES OF LONG TUBULAR BONES OF SENILE RATS WITH INDUCED HYPERGLYCEMIA

2019 ◽  
Vol 19 (3) ◽  
pp. 151-155
Author(s):  
A.A. Ponyrko
Keyword(s):  
Structural Changes ◽  
Bone Growth ◽  
Growth Parameters ◽  
Cortical Layer ◽  
Pathological Changes ◽  
Mineral Density ◽  
Chronic Hyperglycemia ◽  
Increased Risk ◽  
Wide Range ◽  
Tubular Bones

Recent studies have shown that patients with diabetes mellitus are found very often to have pathological changes in the musculoskeletal system. Discussing the development of pathological changes in the bone tissue due to hyperglycemia, it should be noted that many aspects of this problem are still unexplained, and in particular the frequency of bone damage varying in a fairly wide range, the mechanism of reducing bone mineral density that leads to the occurrence of frequent fractures. This article discusses the effects of hyperglycemia on the state of long tubular bones. The goal of our experiment was to study the structural changes in the long tubular bones of senile rats of both sexes with induced hyperglycemia. The period the rats were included into the experiment ranged from 30 to 180 days. During the experiment, various research methods were applied. To perform the histological analysis, we took rat femurs and fixed them in 10% phosphate buffered formalin for 24 hours. Then samples were decalcified in 10% formic acid solution, the materials obtained were embedded in paraffin. The study revealed a gradual thinning of the cortical layer in senile rats that is of great importance due to the fact that there is clinically confirmed increased risk of femoral neck fracture in individuals with type II diabetes. The level of blood glucose throughout the experiment was rather high that indicates the development of chronic hyperglycemia. Having analyzed the data on the effect of hyperglycemia on bone growth parameters and comparing these indicators with the control, we can suggest a delay in longitudinal growth of bones. The results and timing of the experiment show that the degree of changes obtained depends on the duration of the experiment.

scholarly journals To Cull or Not To Cull? Considerations for Studies of Endocrine-Disrupting Chemicals

Endocrinology ◽  
2016 ◽  
Vol 157 (7) ◽  
pp. 2586-2594 ◽  
Author(s):  
Alexander Suvorov ◽  
Laura N. Vandenberg
Keyword(s):  
Laboratory Animal ◽  
Animal Studies ◽  
Metabolic Diseases ◽  
Endocrine Disrupting Chemicals ◽  
Animal Experiments ◽  
Postnatal Growth ◽  
Increased Risk ◽  
Wide Range ◽  
Endocrine Disrupting ◽  
Health Related

The power of animal models is derived from the ability to control experimental variables so that observed effects may be unequivocally attributed to the factor that was changed. One variable that is difficult to control in animal experiments is the number and composition of offspring in a litter. To account for this variability, artificial equalization of the number of offspring in a litter (culling) is often used. The rationale for culling, however, has always been controversial. The Developmental Origins of Health and Disease concept provides a new context to evaluate the pros and cons of culling in laboratory animal studies, especially in the context of endocrine-disrupting chemicals. Emerging evidence indicates that culling, especially of large litters, can drastically change the feeding status of a pup, which can result in compensatory growth with long-term consequences for the animal, including increased risk of cardio-metabolic diseases. Similarly, culling of litters to intentionally bias sex ratios can alter the animal's behavior and physiology, with effects observed on a wide range of outcomes. Thus, in an attempt to control for variability in developmental rates, culling introduces an uncontrolled or confounding variable, which itself may affect a broad spectrum of health-related consequences. Variabilities in culling protocols could be responsible for differences in responses to endocrine-disrupting chemicals reported across studies. Because litter sex composition and size are vectors that can influence both prenatal and postnatal growth, they are essential considerations for the interpretation of results from laboratory animal studies.

Trabecular Bone Score in Female Patients with Systemic Sclerosis: Comparison with Rheumatoid Arthritis and Influence of Glucocorticoid Exposure

2014 ◽  
Vol 42 (2) ◽  
pp. 228-235 ◽  
Author(s):  
Eugénie Koumakis ◽  
Jérôme Avouac ◽  
Renaud Winzenrieth ◽  
Emese Toth ◽  
Judith Payet ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Systemic Sclerosis ◽  
Trabecular Bone ◽  
Trabecular Bone Score ◽  
Bone Microarchitecture ◽  
Bone Involvement ◽  
High Risk Population ◽  
Mineral Density ◽  
Female Patients ◽  
Increased Risk

Objective.Systemic sclerosis (SSc) is associated with an increased risk of osteoporosis and fractures. To date, the etiology of bone loss in SSc is unclear. Trabecular bone score (TBS) provides an indirect measurement of bone microarchitecture, independent of areal bone mineral density (aBMD). The aims were to assess bone involvement in SSc using TBS in comparison with a “high-risk” population with rheumatoid arthritis (RA) and controls, and to investigate the determinants of a low TBS.Methods.This was a cross-sectional study of 65 women with SSc, 138 age-matched female patients with RA, and 227 age-matched female controls. Spine and hip aBMD were assessed using dual-energy X-ray absorptiometry. TBS was calculated from the anteroposterior image of the spine aBMD.Results.TBS was significantly lower in SSc compared to controls (p < 0.0001) and did not differ from RA (p = 0.128), despite lower cumulative and daily glucocorticoid (GC) dose (p < 0.0001). Further, patients with SSc receiving GC ≥ 5 mg/day had a significantly lower TBS than those receiving GC < 5 mg/day (p = 0.001). Multivariate analysis revealed that a low TBS was independently associated with daily GC dose (OR 5.6, 95% CI 1.7–19.2) and a T score ≤ −2.5 SD (OR 5.0, 95% CI 1.5–7.0) in SSc. No association between GC and TBS was found in RA.Conclusion.Our results support the development of a combined approach using both TBS and aBMD for the assessment of bone microarchitecture in inflammatory rheumatic diseases. Our study showed that SSc-related bone involvement is characterized by an impairment in bone quality in addition to reduced bone quantity, and highlights that TBS can identify the negative effect of GC on bone microarchitecture.

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