Sociedad Española de Investigacion Ósea y Metabolismo Mineral

Revista de Osteoporosis y Metabolismo Mineral

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Volume 14 · Number 4 · December 2022


Mesoporous silica nanoparticles and osteoporosis

Nanomedicine: The application of nanotechnology in medicine has given rise to a new discipline: nanomedicine, which, as we can imagine, is a multidisciplinary field where many main actors take part: engineers, physicists, chemists, biologists, doctors and even legislators [1]. Nanomedicines are so popular today among the scientific community due to a series of factors, among which we would highlight the control over the pharmacokinetic profile, the protection of transported therapeutic agents against possible degradation within the organism, the possibility of developing targeted therapies towards specific tissues, the possibility of including different therapeutic agents in the same transporter and even the possible inclusion of contrast agents to have a biomedical image for diagnosis. In this sense, among the possible systems of drug release, nanoparticles have acquired great prominence since they present great versatility from the point of view of their composition, shape, size, and external surface [2].

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Low-density granulocytes: A new marker of bone deterioration in patients on peritoneal dialysis

The concept of metabolic bone disease associated with chronic kidney disease (CKD-MBD, Chronic Kidney Disease-Mineral and Bone Disorder) to refer to bone abnormalities (osteodystrophy), laboratory (calcium, P, vitamin D, parathyroid hormone –PTH–, fibroblast growth factor 23 –FGF23– and Klotho) and vascular (VC) or soft tissue calcification that occur in kidney patients has been established since 2007 and converge in an increase in cardiovascular risk (CVR), risk of fracture and, in short, an excess of morbidity and mortality [1,2].
Chronic inflammation plays a very important role in the development of vascular disorders in kidney patients and previous studies identified the importance of low-density granulocytes (LDG) in vascular calcification in dialysis patients compared to the control population [3], as well as in CVR of patients with lupus [4].

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Delphi Consensus on Therapeutic Strategies and Health Prevention of hypovitaminosis D

Vitamin D is an essential hormone for skeletal metabolism, since it regulates the absorption of calcium and phosphorus at the intestinal level and bone remodeling [1,2]. In addition, some studies suggest that vitamin D performs other multiple functions at the extraskeletal level, acting as a protector against diseases such as cancer, inflammatory and autoimmune diseases, diabetes and cardiovascular diseases [1-4].
The main source of vitamin D is synthesis at the skin level by the action of ultraviolet B rays (UVB) on its precursor [2], giving rise to cholecalciferol or vitamin D3. Another less important source of cholecalciferol is found in food, mainly fish, eggs and dairy products. Regardless of its origin, cholecalciferol must be hydroxylated in the liver, becoming 25-hydroxyvitamin D3 [25(OH)D] or calcifediol and, subsequently in a highly regulated manner, in the kidney to give rise to the active metabolite, 1, 25-dihydroxyvitamin D3 [1,25(OH)2D] or calcitriol [1].

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Usefulness of the trabecular bone score in adult subjects with osteogenesis imperfecta

Osteogenesis imperfecta (OI) is a congenital disease that comprises a heterogeneous group of clinical and genetic disorders of connective tissue, mainly caused by mutations in the COL1A1 and COL1A2 genes of type I collagen. It has been estimated that the incidence of OI is approximately 1:10-20.000 [1-4] and the clinical manifestations can vary from almost asymptomatic forms to very severe cases. The main characteristic of this entity is bone fragility, due to a decrease in bone mass, cortical thickness and an alteration in the trabecular architecture which, together with defects in the bone matrix, affect its quality and resistance, and lead to to a marked increase in the risk of fracture, evident from childhood [1-3,5]. Classically, OI was considered an autosomal dominant genetic disorder and patients were classified into four subtypes based on clinical severity (classification by Sillence et al. [6]: type I being the mildest, followed by types IV, III and type II, the most severe that confers perinatal mortality). Over the years new genes and pathogenic variants have been identified, adding new groups to the classification (OI type V – type XX) [1,2,4,5]. However, this classification is no longer practical and some authors prefer to classify patients according to the degree of clinical involvement of the OI (mild, moderate, severe, lethal), including the genetic defect they present [4].

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Postoperative hypocalcaemia predictors after total thyroidectomy

Total thyroidectomy is one of the most frequent cervical surgeries, with a growing incidence in recent decades due to the increase in diagnoses of thyroid disease [1-3]. One of the thyroid surgery complications is hypocalcaemia due to iatrogenic hypoparathyroidism [1,2,4-11]. This hypo-function may be due to direct mechanical or thermal damage, inadvertent devascularization or removal of the parathyroid glands, post-surgical edema or hemorrhagic complications [1-4,8,9,12]. Both the direct damage, as well as the edema and devascularization, can be reversed over time. This explains why hypoparathyroidism is usually transient in most cases [3,8,12].

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