Disease relevance of Bone Diseases, Metabolic

• Plasma BGP was increased in patients with Paget's disease of bone, bone metastases, primary hyperparathyroidism, renal osteodystrophy, and osteopenia [1].
• Bone histology, bone mineral content, and calcium absorption were evaluated in 10 patients with primary biliary cirrhosis and osteopenia, before and after 1 yr of treatment with oral 25-hydroxycholecalciferol [2].
• Thus, patients receiving total parenteral nutrition may develop metabolic bone disease characterized by osteomalacia, hypercalcemia, hypercalciuria, and a negative calcium balance [3].
• Cortical osteopenia was significantly related to the duration of hyperprolactinemia (p less than 0.01) but not to the absolute levels of prolactin or androgens [4].
• The absence of SPARC in mice gives rise to aberrations in the structure and composition of the ECM that result in generation of cataracts, development of severe osteopenia, and accelerated closure of dermal wounds [5].

Psychiatry related information on Bone Diseases, Metabolic

• It is concluded that: 1) estrogen replacement cannot prevent progressive osteopenia in young women with anorexia nervosa; 2) a subset of patients may have improved BD with estrogen and progestin administration depending on initial body weight; and 3) recovery from anorexia nervosa is associated with significantly improved BD [6].
• Whether relative androgen deficiency results in a clinical syndrome similar to that reported in men, including osteopenia, increased fat mass, decreased libido, and diminished quality of life, has not been definitively established [7].
• Adult-onset alcohol consumption induces osteopenia in female rats [8].
• We conclude that, although alcoholism is a factor in the development of osteopenia, in males the ABO blood group status plays a significant role in the maximal mineralization of the skeleton and the amount of bone resorption during ageing, independent of alcohol abuse [9].
• These include stress and coping behaviors, and osteopenia associated with estrogen deficiency [10].

High impact information on Bone Diseases, Metabolic

• Osteopenia associated with renal transplantation remains a problem in the cyclosporine era [11].
• The importance of this regulatory mechanism for bone homeostasis is emphasized by the observation that mice deficient in IFN-beta signalling exhibit severe osteopenia (loss of bone mass) accompanied by enhanced osteoclastogenesis [12].
• It appears that at present, serum BGP is the one bone protein that has the most promise for assisting in the diagnosis and management of high turnover metabolic bone disease states [13].
• These results identify Fos as a key regulator of osteoclast-macrophage lineage determination in vivo and provide insights into the molecular mechanisms underlying metabolic bone diseases [14].
• CONCLUSIONS--Long-term thyroid hormone use at thyroxine-equivalent doses of 1.6 micrograms/kg or greater was associated with significant osteopenia at the ultradistal radius, midshaft radius, hip, and lumbar spine [15].

Chemical compound and disease context of Bone Diseases, Metabolic

• Immunosuppressive regimens including cyclosporine, which permit the use of lower doses of glucocorticoids, may reduce glucocorticoid-induced osteopenia [11].
• DESIGN--A survey of men and women from an established epidemiologic cohort who were separately screened for diabetes by oral glucose tolerance test between 1984 and 1987 and for osteopenia by BMD measured in 1988-1989 [16].
• We have reported previously that combined treatment with PTH and estrogen in estrogen-deficient rats was beneficial in correcting established osteopenia [17].
• Altered mineral metabolism in glucocorticoid-induced osteopenia. Effect of 25-hydroxyvitamin D administration [18].
• Thus, ritonavir may represent a bone-sparing PI capable of preventing development of osteopenia in patients currently on HAART [19].
• Administration of celecoxib resulted in further deterioration of osteopenia where bone formation was markedly suppressed, whereas bone resorption remained unchanged [20].

Biological context of Bone Diseases, Metabolic

• Interleukin 10-deficient mice develop osteopenia, decreased bone formation, and mechanical fragility of long bones [21].
• Defective bone mineralization and osteopenia in young adult FGFR3-/- mice [22].
• In the present study, we sought to clarify the relationship between periarticular osteopenia and osteoblast replicative senescence in RA [23].
• Reduced expression of interleukin-11 in bone marrow stromal cells of senescence-accelerated mice (SAMP6): relationship to osteopenia with enhanced adipogenesis [24].
• The osteopenia of Smad3 null mice is attributed to a decreased rate of bone formation associated with increased osteocyte number and apoptosis [25].

Anatomical context of Bone Diseases, Metabolic

• We conclude that IRS-1 deficiency in osteoblasts impairs osteoblast proliferation, differentiation, and support of osteoclastogenesis, resulting in low-turnover osteopenia [26].
• Pax5-deficient mice exhibit early onset osteopenia with increased osteoclast progenitors [27].
• Alendronate has a positive effect on secondary osteopenia/osteoporosis in children with connective tissue diseases [28].
• Our laboratory has previously demonstrated that the T-lymphocyte is critical in the development of cyclosporin A-induced osteopenia in the rat model [29].
• All four cases of aromatase-deficient men reported to date showed an identical skeletal phenotype, characterized by tall stature due to continued longitudinal growth, unfused epiphyses, high bone turnover, and osteopenia [30].

Gene context of Bone Diseases, Metabolic

• By generating CD44(-/-) human TNF-transgenic (hTNFtg) mice, we show that destruction of joints and progressive crippling is far more severe in hTNFtg mice lacking CD44, which also develop severe generalized osteopenia [31].
• Mice lacking the IRS-1 gene IRS-1(-/-) showed severe osteopenia with low bone turnover [26].
• RESULTS: Eight- and 12-week-old IL-10-/- mice developed osteopenia of both cancellous and cortical bone, evidenced by lower femoral ash weight, cancellous bone area and surface, trabecular number, and decreased cortical bone area and width [21].
• Unexpectedly, Cbfa1 transgenic mice showed osteopenia with multiple fractures [32].
• In summary, we present Fhl2-deficient mice as a unique model for osteopenia due to decreased osteoblast activity [33].

Analytical, diagnostic and therapeutic context of Bone Diseases, Metabolic

• The presence of osteopenia in persons with mild primary hyperparathyroidism is considered an indication for parathyroidectomy [34].
• When dosed orally at 30 mg/kg twice a day (b.i.d.) in the chronic ovariectomy (OVX)-induced rat model of osteopenia, compound 1 also prevented bone loss [35].
• CONCLUSIONS: Zoledronic acid administration led to significantly greater bone area, mineral content, strength, and trabecular number with reduced stress-shielding osteopenia in this model of distraction osteogenesis [36].
• We have measured the free and peptide-bound type I collagen cross-link excretions in normal women and in patients with metabolic bone disease using the HPLC technique and immunoassays recognizing specifically the free or peptide-bound forms of pyridinoline (Pyr) [37].
• Increased catabolism of 25-hydroxyvitamin D in patients with partial gastrectomy and elevated 1,25-dihydroxyvitamin D levels. Implications for metabolic bone disease [38].

References