High Circulating Sclerostin is Present in Patients with Thalassemia-associated Osteoporosis and Correlates with Bone Mineral Density

Voskaridou, Ersi; Christoulas, Dimitrios; Plata, Eleni; Bratengeier, Cornelia; Anastasilakis, Athanasios D.; Komninaka, Veroniki; Kaliontzi, D; Γκοτζαμανίδου, Μαρία; Polyzos, Stergios A.; Dimopoulou, Maria; Terpos, Evangelos

doi:10.1055/s-0032-1312618

Cited by 54 publications

(35 citation statements)

References 14 publications

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“…These findings give the rationale for the use of novel drugs targeting sclerostin and Dkk-1 in patients with thalassemia-induced osteoporosis. (45) [ …”

Section: Acquired Factorsmentioning

confidence: 99%

Bone Disease in Haemoglobin Disorders

Voskaridou

Terpos

2013

Thalassemia Reports

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Bone disease represents a prominent cause of morbidity in patients with thalassaemia and other haemoglobin disorders. The delay in sexual maturation, the presence of diabetes and hypothyroidism, the parathyroid gland dysfunction, the haemolytic anaemia, the progressive marrow expansion, the iron toxicity on osteoblasts, the iron chelators, and the deficiency of growth hormone or insulin growth factors have been identified as major causes of osteoporosis in thalassaemia. Adequate hormonal replacement, effective iron chelation, improvement of hemoglobin levels, calcium and vitamin D administration, physical activity, and smoking cessation are the main to-date measures for the management of the disease. During the last decade, novel pathogenetic data suggest that the reduced osteoblastic activity, which is believed to be the basic mechanism of bone loss in thalassemia, is accompanied by a comparable or even greater increase in bone resorption. Therefore, potent inhibitors of osteoclast activation, such as the aminobisphosphonates, arise as key drugs for the management of osteoporosis in thalassaemia patients and other haemoglobin disorders.

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“…These findings give the rationale for the use of novel drugs targeting sclerostin and Dkk-1 in patients with thalassemia-induced osteoporosis. (45) [ …”

Section: Acquired Factorsmentioning

confidence: 99%

Bone Disease in Haemoglobin Disorders

Voskaridou

Terpos

2013

Thalassemia Reports

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“…Additionally, sclerostin expression is regulated by mechanical strain in adult bone, and plasma sclerostin levels increase after WBV (17)(18)(19)(20). High plasma sclerostin levels were reported to indicate an increase in osteocyte activity (21). These reports constituted a basis for the second assumption of our study.…”

Section: Limitations Of This Studymentioning

confidence: 59%

“…WBV can cause changes in plasma sclerostin levels in adult women (20). Plasma sclerostin levels indicate osteocyte activity (21). Osteocytes, the primary mechanosensors in bone, are the 'receptors' of BMR (15).…”

Section: Methodsmentioning

confidence: 99%

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A Randomized Trial on the Effect of Bone Tissue on Vibration-induced Muscle Strength Gain and Vibration-induced Reflex Muscle Activity

Çidem¹,

Karacan²,

Dıraçoğlu³

et al. 2014

Balkan Med J

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Whole-body vibration (WBV), as a method of exercise training, is becoming increasingly popular in physical therapy, rehabilitation, and professional sports, and is increasingly used in beauty and wellness applications due to its beneficial effects on the neuromusculoskeletal system. These benefits include improved strength, power, flexibility, jump height, and balance (1-4).However, little is known about the physiological mechanisms underlying the effects of WBV on muscular performance, although the presence of reflex muscle activity during WBV has been shown (4, 5). Tonic vibration reflex (TVR) is the most commonly cited mechanism to explain the effects of WBV on muscular performance, although there is no conclusive evidence that tonic vibration reflex (TVR) occurs (4-6). Studies have reported that direct vibration applied to a muscle or tendon stimulates muscle spindles, thereby causing a TVR to occur. As highlighted by these studies, muscle spindle Background: Whole-body vibration (WBV) induces reflex muscle activity and leads to increased muscle strength. However, little is known about the physiological mechanisms underlying the effects of whole-body vibration on muscular performance. Tonic vibration reflex is the most commonly cited mechanism to explain the effects of whole-body vibration on muscular performance, although there is no conclusive evidence that tonic vibration reflex occurs. The bone myoregulation reflex is another neurological mechanism used to explain the effects of vibration on muscular performance. Bone myoregulation reflex is defined as a reflex mechanism in which osteocytes exposed to cyclic mechanical loading induce muscle activity. Aims: The aim of this study was to assess whether bone tissue affected vibration-induced reflex muscle activity and vibration-induced muscle strength gain. Study Design: A prospective, randomised, controlled, double-blind, parallel-group clinical trial. Methods: Thirty-four participants were randomised into two groups. High-magnitude whole-body vibration was applied in the exercise group, whereas low-magnitude whole-body vibration exercises were applied in the control group throughout 20 sessions. Hip bone mineral density, isokinetic muscle strength, and plasma sclerostin levels were measured. The surface electromyography data were processed to obtain the Root Mean Squares, which were normalised by maximal voluntarily contraction. Results: In the exercise group, muscle strength increased in the right and left knee flexors (23.9%, p=0.004 and 27.5%, p<0.0001, respectively). However, no significant change was observed in the knee extensor muscle strength. There was no significant change in the knee muscle strength in the control group. The vibration-induced corrected Root Mean Squares of the semitendinosus muscle was decreased by 2.8 times (p=0.005) in the exercise group, whereas there was no change in the control group. Sclerostin index was decreased by 15.2% (p=0.031) in the exercise group and increased by 20.8% (p=0.028) in the control group. A change in th...

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“…This pathway has been proposed to participate in the pathogenesis of osteoporosis in TM, and negative modulators of this signalling system (e.g. Dickkopf-1 (DKK-1) and sclerostin) have been also associated with BMD in TM patients (48)(49).…”

Section: Cytokines Networkmentioning

confidence: 99%

Pathogenesis of Thalassemia Major–Associated Osteoporosis: Review of the Literature and Our Experience

Gaudio¹,

Morabito²,

Catalano³

et al. 2018

Jcrpe

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Due to increasing life expectancy in thalassemia major (TM), osteoporosis is emerging as a significant problem. Its aetiology is multifactorial, culminating in increased bone resorption and remodelling. Hypogonadism and marrow expansion seem to play an important role, but iron overload, deferoxamine toxicity, a defective GH-IGF-1 axis and multiple endocrinopathies may represent additional causes of bone damage. Many of these patients, though under appropriate treatment programs, do not achieve normal peak bone mass. The RANK/RANKL/OPG and the Wnt/βCatenin systems work as major mediators of imbalanced bone turnover and bone loss. Additional genetic factors, such as collagen type I alpha 1 and vitamin D receptor gene polymorphisms, may exert some influence on the enhanced fracture risk observed in TM. To date, in spite of adequate hormone replacement, chelating therapy, and acceptable haemoglobin levels, subjects with TM display impaired bone density and imbalanced bone turnover, so the puzzle of the pathogenesis of thalassemia major-induced osteoporosis remains far from being solved.

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High Circulating Sclerostin is Present in Patients with Thalassemia-associated Osteoporosis and Correlates with Bone Mineral Density

Cited by 54 publications

References 14 publications

Bone Disease in Haemoglobin Disorders

Bone Disease in Haemoglobin Disorders

A Randomized Trial on the Effect of Bone Tissue on Vibration-induced Muscle Strength Gain and Vibration-induced Reflex Muscle Activity

Pathogenesis of Thalassemia Major–Associated Osteoporosis: Review of the Literature and Our Experience

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