Relationship among densitometry, bone histomorphometry, and histologic stage in idiopathic myelofibrosis

Mellibovsky, Leonardo; Mariñoso, M.L.; Cervantes, Francisco; Besses, Carlos; Nacher, Montserrat; Nogués, Xavier; Florensa, Lourdes; Munné, Assumpta; Díez-Pérez, Adolfo; Serrano, Sergi

doi:10.1016/j.bone.2003.10.010

Cited by 10 publications

(6 citation statements)

References 16 publications

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“…In a Swedish cross-sectional study including 16 patients with varying degrees of mastocytosis, vertebral fractures were found in 13 of 16 patients and observed different types of skeletal lesions, including both low bone mineral density (BMD) as well as increased BMD with Quantitative histomorphometry, assessment of number of osteoblasts and osteoclasts [12] Guillaume et al (2013) Cross-sectional study 45 Radiographic imaging, bone mineral density, bone turnover marker [13] Cundy et al (1987) Case report 1 Osteopenia and response to treatment with inhibition of bone resorption [14] Johansson et al (1996) Cross-sectional study 16 Bone density, bone markers and radiological features [15] Brockow et al (2005) Cross-sectional study 29 Level of interleukin-6 level reflects severity of disease [16] Theoharides et al (2002) Cross-sectional study 26 Level of interleukin-6 level reflects severity of disease and osteoporosis [17] Barete et al (2010) Cross-sectional study 75 Bone involvement assessed by X-ray and DXA [18] Rossini et al (2011) Cross-sectional study 82 Bone mineral density, bone turnover markers and fractures [19] Broesby-Olsen et al (2013) Cross-sectional study 48 KIT D816 mutation burden does not correlate to severity of bone loss in SM [20] Essential thrombocythemia and polycythemia vera Histomorphometry and micro-CT [26] Guermazi et al (1999) Review Images of radiological abnormalities in MF, incl. Osteosclerosis [27] Mellibovsky et al (2004) Case report 9 DXA, bone histomorphometry in MF [28] Diamond et al (2002) Case report and review 4 DXA, bone histomorphometry in MF [29] Farmer et al (2015) Cross-sectional study 18 Bone structure assesses by DXA, HR-pQCT, and bone turnover [30] Barosi et al (1989) Cross-sectional study 78 Markers of collagen in MF [31] Jensen et al ( sclerotic changes …”

Section: Resultsmentioning

confidence: 98%

“…Osteosclerosis usually affects the vertebral column, pelvis and proximal segment of long bones as seen by conventional x-ray [27]. Bone density assessed using DXA in MF patients has been found to be higher than the background population in two case reports including four and nine patients [28,29]. We have performed a study using noninvasive methods with DXA and HR-pQCT among 18 MF patients and 18 age-, sex-and height-matched healthy individuals [30].…”

Section: Myelofibrosismentioning

confidence: 96%

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Bone morbidity in chronic myeloproliferative neoplasms

Farmer

Ocias

Vestergaard

et al. 2015

Expert Review of Hematology

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Patients with the classical Philadelphia chromosome-negative chronic myeloproliferative neoplasms including essential thrombocythemia, polycythemia vera and primary myelofibrosis often suffer from comorbidities, in particular, cardiovascular diseases and thrombotic events. Apparently, there is also an increased risk of osteoporotic fractures among these patients. However, the true prevalence, mechanisms involved and therapeutic implications are not well described. In this review, we summarize what is currently known about possible associations between bone disease and chronic myeloproliferative neoplasms. Chronic inflammation has been suggested to explain the initiation of clonal development and progression in chronic myeloproliferative neoplasms. Decreased bone mineral density and enhanced fracture risk are well-known manifestations of many chronic systemic inflammatory diseases. As opposed to systemic mastocytosis (SM) where pathogenic mechanisms for bone manifestations probably involve effects of mast cell mediators on bone metabolism, the mechanisms responsible for increased fracture risk in other chronic myeloproliferative neoplasms are not known.

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Section: Resultsmentioning

confidence: 98%

Section: Myelofibrosismentioning

confidence: 96%

Bone morbidity in chronic myeloproliferative neoplasms

Farmer

Ocias

Vestergaard

et al. 2015

Expert Review of Hematology

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“…The electronic search for bone health in hematopoietic disorders identified 177 articles for BT, 89 for SCA; 39 for PV, 11 for ET, 63 for CML, 83 for MF; 87 for MC, 212 for LL, 683 for MM, and 43 for HC. After screening, we selected 5 articles for BT, 6 for SCA; 2 for PV, 2 for ET, 3 for CML, 5 for MF; 4 for MC, 4 for LL, 5 for MM, and 4 for HC (Fig. ).…”

Section: Resultsmentioning

confidence: 99%

Bone Health in Patients With Hematopoietic Disorders of Bone Marrow Origin: Systematic Review and Meta- Analysis

Steer

Stavnichuk

Morris

et al. 2016

Journal of Bone and Mineral Research

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Blood cell production and bone homeostasis are physically interlinked systems that exhibit active cross-talk. We examined how bone health is affected in patients with hematopoietic disorders due to abnormal proliferation of bone marrow cells. The electronic databases Medline, Embase, PubMed, BIOSIS Previews, Web of Science, and Cochrane were searched for studies presenting numerical values for trabecular bone volume or bone mineral density in control and patients with hematopoietic disorders. We identified 5 studies for beta-thalassemia, 6 for sickle cell anemia, 2 for polycythemia vera and essential thrombocythemia, 3 for chronic myelogenous leukemia, 6 for myelofibrosis, 5 for multiple myeloma, and 4 studies each for systemic mastocytosis, lymphocytic leukemia, and hemochromatosis. The effect of the disease state on bone density was significant and negative for beta-thalassemia (r = -2.00; 95% confidence interval [CI] -3.41, -0.58; p < 0.005), sickle cell anemia (-0.91; -1.36, -0.47; p < 0.00005), chronic myelogenous leukemia (-0.55; -0.88, -0.22; p < 0005), mastocytosis (-0.99; -1.16, -0.82; p < 0.00001), lymphoblastic leukemia (-0.69; -0.98, -0.40; p < 0.00001), multiple myeloma (-0.67; -0.99, -0.35; p < 0.00005), and hemochromatosis (-1.15; -1.64, -0.66; p < 0.00001). The changes were negative but not significant for polycythemia vera (-0.16; -0.38, 0.05; p = 0.069) and essential thrombocythemia (-0.33; -0.92, 0.26; p = 0.14). In myelofibrosis, disease state was associated with increased bone density (0.74; 0.12, 1.36; p < 0.05). Bone density change significantly and negatively correlated with the level of ferritin and bone marrow cellularity but not with hemoglobin or erythropoietin. Thus, independent of hematopoietic lineage, abnormal proliferation of bone marrow cells appears to be associated with bone loss. Iron metabolism may independently contribute to bone homeostasis. © 2016 American Society for Bone and Mineral Research.

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“…However, a complete inhibition of bone resorption is equally unfavorable, as the overactivation thereof. Osteopetrosis is another consequence of osteoclast dysfunction (Albers-Schönberg 1904, Mellibovsky et al 2004 mainly caused by the presence of mutations in the cells. The above-mentioned evidence points to a The process of cortical bone remodeling.…”

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confidence: 99%

Bone remodeling in the context of cellular and systemic regulation: the role of osteocytes and the nervous system

Niedźwiedzki¹,

Filipowska²

2015

Journal of Molecular Endocrinology

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Bone is a dynamic tissue that undergoes constant remodeling. The appropriate course of this process determines development and regeneration of the skeleton. Tight molecular control of bone remodeling is vital for the maintenance of appropriate physiology and microarchitecture of the bone, providing homeostasis, also at the systemic level. The process of remodeling is regulated by a rich innervation of the skeleton, being the source of various growth factors, neurotransmitters, and hormones regulating function of the bone. Although the course of bone remodeling at the cellular level is mainly associated with the activity of osteoclasts and osteoblasts, recently also osteocytes have gained a growing interest as the principal regulators of bone turnover. Osteocytes play a significant role in the regulation of osteogenesis, releasing sclerostin (SOST), an inhibitor of bone formation. The process of bone turnover, especially osteogenesis, is also modulated by extra-skeletal molecules. Proliferation and differentiation of osteoblasts are promoted by the brain-derived serotonin and hypothetically inhibited by its intestinal equivalent. The activity of SOST and serotonin is either directly or indirectly associated with the canonical Wnt/β-catenin signaling pathway, the main regulatory pathway of osteoblasts function. The impairment of bone remodeling may lead to many skeletal diseases, such as high bone mass syndrome or osteoporosis. In this paper, we review the most recent data on the cellular and molecular mechanisms of bone remodeling control, with particular emphasis on the role of osteocytes and the nervous system in this process.

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Relationship among densitometry, bone histomorphometry, and histologic stage in idiopathic myelofibrosis

Cited by 10 publications

References 16 publications

Bone morbidity in chronic myeloproliferative neoplasms

Bone morbidity in chronic myeloproliferative neoplasms

Bone Health in Patients With Hematopoietic Disorders of Bone Marrow Origin: Systematic Review and Meta- Analysis

Bone remodeling in the context of cellular and systemic regulation: the role of osteocytes and the nervous system

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