Volume 11 · Number 2 · June 2019
- The Wnt/β-catenin pathway decreases the amount of osteoclasts in the bone and promotes its apoptosis [39-45]
- A novel therapeutic target for osteoarthritis: control of cellular plasticity and senescence using connexin43 [46-54]
- Qualitative and quantitative status of general bone in osteonecrosis of the jaws. Effect of bisphosphonates [55-63]
- Osteogenic cells affected by soluble tumor factors contribute to bone pre-metastatic niche formation [64-71]
Raised levels of air pollution have recently been been linked to the induction of inflammatory phenomena at both systemic and tissue levels. Chronic inflammatory diseases, such as rheumatoid arthritis or chronic obstructive pulmonary disease, reduce bone mineral density (BMD), which leads to an increase in the release of immune cells from the bone marrow. Particulate matter is associated with oxidative damage and inflammation, which can accelerate bone loss and increase the risk of fractures in older adults. However, the association between air pollution and osteoporosis is not yet well defined in the literature.
It seems that there are other indirect routes, such as vitamin D and PTH, which may also be altered by contamination and are involved in bone remodeling [1-8]. In the first place, air pollution (microparticles and ozone) presents a physical barrier to ultraviolet B solar radiation, thus contributing to a lower cutaneous production of vitamin D [2,4,5]. Similarly, a study conducted in the United States  indicated the relationship between low levels of PTH in blood and elevated levels of microparticles and carbon in the air, causing indirect harmful effects on bone mass.
( PDF ) Rev Osteoporos Metab Miner. 2019; 11 (4): 87-91 DOI: 10.4321/S1889-836X2019000400002 Ormeño Illanes JC1, Quevedo Langenegger EI2 1 Faculty of Medicine. University of Concepción. Concepción (Chile) 2 Endocrinology Section. Department of Internal Medicine....
Long-term efficacy and safety of polymethylmethacrylate (PMMA) in osteoporotic patients treated by percutaneous vertebroplasty
Without a doubt, vertebral fracture (VF) is the most prevalent type of bone rupture in patients with low bone mass . The most recent epidemiological data in the Spanish population indicate about 35% VF prevalence in women over 45 years of age . In men, the prevalence at 50 years is estimated 5 times lower than that of the female population, although this increases beyond 70 years of age .
Osteoporotic VFs (OVF) are conservatively treated, usually including rest, analgesia (in combination with muscle relaxants), orthotics and rehabilitation. This treatment is crucial in the first weeks post-fracture, so that proper follow-up usually resolves OVFs effectively. However, in 10-35% of patients, complications may arise from the fracture itself, such as delayed bone union, increased kyphosis, appearance of neurological disorders or the appearance of pseudo-arthrosis (Kümmell’s disease). In these cases, patients frequently do not respond well to conservative treatment, complicating the management of their symptoms. This tends to worsen over time .
Genome-wide association studies (GWAS) and candidate gene studies have found some single nucleotide polymorphisms (SNPs) in the SOST gene, which encodes sclerostin, associated with bone mineral density (BMD) and predisposition to fractures [1-4]. However, the mechanism responsible for this association is unknown. Among the general mechanisms by which genetic variants predispose to complex diseases are epigenetic mechanisms, such as DNA methylation, that modulate gene transcription directly (locally) or indirectly (remotely) . In this sense, it should be noted that the DNA methylation of the SOST promoter is inversely related to the gene expression levels of the gene .
DNA methylation is an epigenetic mark that consists in the addition of a methyl group at the 5 ’position of the cytosine ring, usually in cytosines that precede guanine, forming the so-called CpG sites. They are distributed throughout the genome and abundant in some specific regions, such as promoters, called CpG islands. Methylation levels of CpG sites and/or islands have specific profiles according to the tissue of origin and modulate gene expression in many tissues, including bone [7-10].
Factors that influence the results of bone ultra-microindentation tests. An experimental study in rats
Fragility fractures are the relevant hallmark of osteoporosis . The risk of fracture is closely related to bone strength, which, in turn, depends on bone mass, geometry and material quality [2-6]. Bone mass and geometry can be evaluated clinically using bone densitometry and high resolution imaging techniques. However, the mechanical properties of bone tissue are more difficult to explore. These properties determine bone quality, a concept that represents the intrinsic capacity of tissue to resist tension states, regardless of the amount of material (bone density) or its spatial distribution (bone architecture). Bone quality depends on the chemical composition and organization of the bone matrix .
In an indentation or hardness test, a sample is subjected to quasi-static loading by means of a small indenter, recording the size of the resulting footprint; Sometimes the curve that relates the applied load and the displacement experienced by the indenter during the test is also determined. Hardness is defined as the maximum force applied divided by the area of the footprint that remains in the material after the test. Hardness is the property of the material that characterizes its resistance to permanent/plastic deformation .
How to merge Orthogeriatrics Units with Fracture Coordination Units (FCU). Experience in the Joan XXIII Health Complex of Tarragona
Current scientific evidence and practical clinical guidelines recommend primary and secondary prevention of fragility fractures in geriatric patients [1,2]. A personal history of fragility fractures significantly increases the risk of new fractures. Up to 33% of patients with a femur fracture had suffered a previous fracture. Among the various fractures due to fragility, the femur is the most prevalent and presents the most repercussions (clinical, functional and social) in patients over 65 years of age, with the resulting depletion of health resources . The worldwide trend is estimated to rise from 1.7 million femoral fractures in 1990 to 6 million in 2050 .
In 2011, the Fractures Working Group of the Scientific Advisory Committee of the International Osteoporosis Foundation stressed the importance of coordination between orthopedics, osteoporosis services, fall units, patient, family, geriatrician and Primary Care physician. This multidisciplinary action was consolidated in the so-called “coordinated services for the treatment of fractures” or Fracture Liaison Services (FLS) that were initially implemented in the United Kingdom, Europe, Australia, Canada and the USA , with very good results.
In recent years there has been an impressive increase in the number of scientific articles related to the metabolism of calcium and vitamin D. We have gained a much deeper knowledge of many patho-physiological aspects. However, and in spite of this, a series of fraudulence, myths and legends have been developed in parallel on both calcium and vitamin D, many of them absolutely unjustified, and others derived from a misunderstanding of some scientific articles. Since this can lead to the abandonment of treatments or taking them in the wrong way, we have developed this article in order to clarify, with scientific evidence, some of these aspects.
Review of the physiology of calcium and vitamin D.
Calcium absorption depends on vitamin D and is a saturable mechanism. From a certain amount and reach the optimum level of absorption, all calcium that is ingested is not absorbed and is eliminated by feces.
Between 100 and 200 mg of calcium are removed by the kidney on a daily basis under normal conditions. Also, between 800 to 900 mg of calcium is lost by stool, as a result of the secretion of bile salts and pancreatic juices. These are known as “mandatory calcium losses” and together they constitute about 1,000 mg (Figure 1). Calcium cannot be synthesized by any metabolic route and, therefore, must be taken by diet .