The biology of osteocytes

Kogianni, Giolanta; Noble, Brendon

doi:10.1007/s11914-007-0007-z

Cited by 58 publications

(63 citation statements)

References 61 publications

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“…Numerous studies in mammals have demonstrated that osteocytes are highly active cells and that mature osteocytes are capable of resorbing mineral substance as well as organic matrix from their surrounding bone under physiological and pathological conditions (for reviews: Kogianni & Noble 2007). In humans, osteoporosis caused by long-term GC treatment is accompanied by a significant enlargement of the periosteocytic lacunar surface area (Baud & Boivin 1978, Wright et al 1978.…”

Section: Cortisol-induced Osteocytic Osteolysismentioning

confidence: 99%

Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?

Sbaihi

Rousseau

Baloche

et al. 2009

Journal of Endocrinology

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Endogenous excess cortisol and glucocorticoid (GC) therapy are a major cause of secondary osteoporosis in humans. Intense bone resorption can also be observed in other vertebrates such as migratory teleost fish at the time of reproductive migration and during fasting when large amounts of calcium and phosphate are required. Using a primitive teleost, the European eel, as a model, we investigated whether cortisol could play an ancestral role in the induction of vertebral skeleton demineralization. Different histological and histomorphometric methods were performed on vertebral samples of control and cortisoltreated eels. We demonstrated that cortisol induced a significant bone demineralization of eel vertebrae, as shown by significant decreases of the mineral ratio measured by incineration, and the degree of mineralization measured by quantitative microradiography of vertebral sections. Histology and image analysis of ultrathin microradiographs showed the induction by cortisol of different mechanisms of bone resorption, including periosteocytic osteolysis and osteoclastic resorption. Specificity of cortisol action was investigated by comparison with the effects of sex steroids. Whereas, testosterone had no effect, estradiol induced vertebral skeleton demineralization, an effect related to the stimulated synthesis of vitellogenin (Vg), an oviparous specific phospho-calciolipoprotein. By contrast, the cortisol demineralization effect was not related to any stimulation of Vg. This study demonstrates GC-induced bone demineralization in an adult non-mammalian vertebrate, which undergoes natural bone resorption during its life cycle. Our data suggest that the stimulatory action of cortisol on bone loss may represent an ancestral and conserved endocrine regulation in vertebrates.

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Section: Cortisol-induced Osteocytic Osteolysismentioning

confidence: 99%

Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?

Sbaihi

Rousseau

Baloche

et al. 2009

Journal of Endocrinology

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“…It is also supported by other studies which mentioned that; bone tissue responds to repeated mechanical deformation and muscular contractions, which lead to an increase in electric pulsed currents in bone via piezoelectric effects. When mechanical forces through mechanical loads during exercise are converted into electrical stimuli, specific bone tissue cells can begin the osteogenesis process resulting in an increase in BMD (23,24) . From the gained results it could be concluded that; weight bearing exercises had significant improvements of bone mineral density in cases of osteoporosis following thyroidectomy.…”

Section: Discussionmentioning

confidence: 99%

Response of Bone Mineral Density to Physical Exercises after Thyroidectomy

Mohamady¹

2015

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Introduction: Thyroidectomy could be associated with bone loss because of an endogenous excess of thyroxin, over enthusiastic thyroid replacement therapy following surgery, deregulation of bone resorption as consequence of calcitonin deficiency or some combination of these factors. The aim was to investigate the effect of weight bearing exercises on Improving bone mineral density in post thyroidectomy patients suffering from osteoporosis. Subjects and methods: Thirty osteoporotic patients were assigned randomly into two equal groups; their ages ranged from 20-45 years. The study group received weight bearing exercises program in addition to routine medical treatment. Control group received medical treatment only. Study group received two sessions per week for two successful months. The data were collected before and after the same period of treatment for both groups. Evaluation procedures were carried out to evaluate the bone mineral density using Dual Energy X-ray Absorptiometry. Results: Post treatment both groups showed a variant improvement in bone mineral density, but a significant improvement difference was recorded between the two groups in favor of the study group. Percentage of improvement of bone mineral density in the study group was 10.69%, while it was 2.8% in the control group. Conclusion: Weight bearing exercises were considered to be an effective modality for improving bone mineral density in subjects suffering from osteoporosis following thyroidectomy.

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“…Bone resorption is followed by activation of osteoblasts and formation of osteoid. During this latter period of formation of about 3 months, resorption cavities are filled (13).…”

Section: Bone Biologymentioning

confidence: 99%

Osteoporozda Yeni Tedavi Ajanları

Güven¹,

Çeliker²,

Atalay³

et al. 2011

Tftr

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Sum maryPostmenopausal osteoporosis is characterized by an increase in resorption and inadequate bone formation. Alteration in bone remodeling is associated with an accelerated risk of fracture. Pharmacological agents that increase bone mass, reduce bone loss or decrease fracture risk have become available in the last few decades. Current compounds used for the treatment of osteoporosis mostly inhibit osteoclast-mediated bone resorption, while few others have an anabolic effect. Inhibition of bone resorption by currently available agents does not restore bone structure or bone that has already been lost and it is coupled with inhibition of bone formation. The identification of new pathways involved in bone turnover, will accelerate clinical research to develop new formation-stimulating and resorption-inhibiting agents with improved safety profile and efficacy in fracture prevention in osteoporosis. In the light of new data, it is estimated that novel antiosteoporotic compounds will increase considerably in the coming years. Turk J Phys Med Re hab 2011;57:165-71.

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The biology of osteocytes

Cited by 58 publications

References 61 publications

Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?

Cortisol mobilizes mineral stores from vertebral skeleton in the European eel: an ancestral origin for glucocorticoid-induced osteoporosis?

Response of Bone Mineral Density to Physical Exercises after Thyroidectomy

Osteoporozda Yeni Tedavi Ajanları

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