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Pathogenesis: Molecular mechanisms of osteoporosis
Published in Peter V. Giannoudis, Thomas A. Einhorn, Surgical and Medical Treatment of Osteoporosis, 2020
Anastasia E. Markatseli, Theodora E. Markatseli, Alexandros A. Drosos
The association of OPG with the markers of bone metabolism is surrounded by controversy. There are reports in the literature in which the concentration of OPG in serum was associated weakly with the markers of bone metabolism (173,174). However, other studies showed a positive association of OPG with these markers (175), while in other studies no correlation was detected (183). In another study, serum OPG levels were associated negatively with serum osteocalcin in elderly women (182). A study performed in women immediately after menopause showed a negative correlation between RANKL and 17β-estradiol in serum. RANKL levels were positively correlated with type I collagen N-terminal telopeptide (NTX-I) in urine and type I collagen C-terminal telopeptide (CTX-I) in serum in that study (186).
Metabolic and endocrine bone disorders
Published in Ashley W. Blom, David Warwick, Michael R. Whitehouse, Apley and Solomon’s System of Orthopaedics and Trauma, 2017
Whereas osteoid is rapidly mineralized following its synthesis, a process of secondary mineralization takes place after bone formation is complete. The latter process is time-dependent, and its extent depends on skeletal maturity. Skeletal maturity also influences the degree of collagen cross-link formation, a process whereby adjacent type I collagen fibrils undergo further protein binding to enhance tensile strength. The amino acid sequence where these cross-links occur, termed N-terminal telopeptide, are largely specific to bone, and their level in plasma following release into the circulation following bone resorption forms the basis of clinical measurement of bone turnover.
Calcium, phosphate and magnesium
Published in Martin Andrew Crook, Clinical Biochemistry & Metabolic Medicine, 2013
Concentrations of new bone markers, such as bone-specific alkaline phosphatase (bone formation), plasma osteocalcin (bone formation), type 1 procollagen peptides (bone formation), urinary deoxypyridinoline and cross-linked N-terminal telopeptide and C-terminal telopeptide of type 1 collagen (bone resorption), urinary hydroxyproline (bone resorption) and bone-resistant or tartrate-resistant acid phosphatase (bone resorption) are raised in osteoporosis and may be useful markers of the disease process. However, these bone markers do not give information about exact bone anatomy, for which imaging studies are necessary.
Osteoporosis in hemophilia: what is its importance in clinical practice?
Published in Expert Review of Hematology, 2022
Dagli et al. assessed BMD, PTH, 25-hydroxy vitamin D (vitamin D), and a bone creattion and resorption marker, procollagen type I N-terminal propeptide (PINP) and urinary N-terminal telopeptide (uNTX), respectively, in PWH and healthy controls [39]. Laboratory parameters related to the pathogenesis of bone loss such as neutrophil-lymphocyte ratio (NLR) and platelet-lymphocyte ratio (PLR) were also assessed. Thirty-five men over 18 years of age, with severe hemophilia (A and B) and experiencing secondary prophylaxis, were included in the study. The BMD was low in 34% of hemophilic patients. Vitamin D, calcium, and free testosterone levels were significantly lower, while PTH, PINP, and activated partial thromboplastin time (aPTT) levels were significantly higher, in hemophilic patients compared to controls. There was no significant difference between the two groups in NLR, PLR, phosphorus, thyroid-stimulating hormone, and uNTX level. Therefore, it seems that the reduction of bone mass in hemophilic patients may be assessed utilizing the markers of bone creation and resorption, enabling early detection and timely management [39].
Treatment of fibrous dysplasia: focus on denosumab
Published in Expert Opinion on Biological Therapy, 2022
Bogdan Huzum, Sabina Antoniu, Raluca Dragomir
Pharmacodynamics data have been provided by a phase I placebo controlled, single dose, dose escalation study performed in 49 postmenopausal women who were followed up from 6 to 9 months following their dose, depending on how high the dose was. Doses of 0.01, 0.03, 0.1, 0.3, 1, and 3 mg/body weight were administered, and bone turnover markers that included urinary N-terminal telopeptide of type 1 collagen (NTX), serum NTX, and serum bone-specific alkaline phosphatase (ALP) were assessed at 12 h after dosing. Compared to placebo, a dose-dependent decrease in bone turnover was characterized by urinary NTX (77% with denosumab (3 mg) versus 46% with placebo, p < 0.05). Urinary NTX constantly decreased in the denosumab (3 mg) dosing arm compared to placebo after 24 h (73% versus 10%). The maximal inhibitory effect on this biomarker depended on the dose and ranged from 2 weeks with 0.01 mg, to 1 month with 0.1 mg, to 3 months with 3 mg. The therapeutic effect of denosumab was reversed approximately 2 months after dosing in the 0.01 mg group, 4 months in the 0.1 mg group, and 9 months in the 3 mg group. These time intervals were all longer than those reported with bisphosphonates [28].
Clinical heterogeneity of SAPHO syndrome: Challenge of diagnosis
Published in Modern Rheumatology, 2018
The pathogenesis of SAPHO syndrome remains a mystery. Inflammation in crosstalk with bone destruction may play a central role. Anić et al. [30] proposed two patterns of the disease – the inflammatory pattern, suggesting the use of tumor necrosis factor-α (TNF-α) inhibitors, and the bone remodeling pattern, for which bisphosphonates seems to be effective. On one hand, in the study by Okuno [26], a series of inflammatory markers (e.g. CRP, ESR, CH50 and MMP-3) were determined to help quantify the status of inflammation. Our study also found that CRP may be a good parameter to monitor disease activity [11]. On the other hand, it is also of high interest to investigate into markers of bone metabolism to help determine the status of bone disease, including bone formation markers [e.g. bone-specific alkaline phosphatase (BSAP), N-terminal propeptide of type I procollagen (PINP), and osteocalcin] and bone resorption markers [e.g. N-terminal telopeptide crosslink (NTX), and C-telopeptide crosslink (CTX)]. Further translational study is urgent need to improve stratified management. As the authors stated in the article by Okuno [26], we call on better awareness of this under-recognized disease to facilitate patient recruitment and further characterizing of this highly heterogeneous syndrome.