Type 1 diabetes mellitus (DM1) has been associated with lower bone mass for more than 30 years [1,2], although existing data in children and adolescents are contradictory [3-8]. Published results on bone mass development in the adult diabetic population show a lower BMD in type 1 diabetics that persists over time and a higher risk of fractures [9-11]. However, in the pediatric population with DM1, longitudinal studies are very limited and with discrepant results. Some authors report a reduction in BMD during follow-up [6,12,13], while others do not observe long-term changes [14,15]. These discrepant results may be due to multiple variables such as the length of follow-up, which is almost always too short; the different ages and anthropometric variables, or the different pubertal stages of the diabetic population included in the studies [11-14].

After a spinal cord injury (SCI) there is a marked loss of bone mass and an increase in remodeling that leads to the development of osteoporosis and skeletal fractures, especially below the level of the injury [1-3]. Thus, more than 50% of patients with complete SCI develop densitometric osteoporosis one year after SCI1, which can reach 81% of patients after more than 5 years of SCI [4]. However, despite the high incidence of osteoporosis and fractures, the therapeutic approach to these patients is clearly deficient, since less than 10-20% of them receive anti-osteoporotic treatment [2,5].

Worldwide, 1 in 3 women and 1 in 5 men will experience a fragility fracture in their lifetime. Every 3 seconds there is 1 fragility fracture in the world. The most frequent fractures associated with osteoporosis are located in the hip, spine and wrist [1,2].
Hip fracture has become an international barometer of osteoporosis, associated with low bone mineral density, high health care costs, and greater disability than other types of osteoporotic fracture [3]. Only 30% of people with a hip fracture regain their pre-fracture level of physical function, and many are left with reduced mobility, loss of functional independence, and requiring long-term care. For this reason, among other reasons, the International Osteoporosis Foundation (IOF) has developed the Capture the Fracture program, aimed at reducing secondary and posterior fractures by facilitating the implementation of Fracture Liaison Services (FLS) [1,2].

In January 2020, when a group of researchers from the Chinese province of Wuhan published the outbreak caused by a novel corona virus, few of us imagined the storm that was looming[1]. The experience of epidemic outbreaks due to emerging viral infections that have occurred worldwide in the past twenty years should have warned us that something like this could happen[2-4]. But even the very serious situation of the Ebola virus outbreak in West Africa in 2014 did not alert us, until just a few tragic cases spread across borders, set off alarm bells in Europe[5]. But it seems more incomprehensible that, with the appearance of new viruses of zoonotic origin, such as SARS-CoV-1, MERS, avian influenza viruses (H5N1 and H7N9), or the 2009-H1N1 influenza virus that caused the first pandemic of the XXI century, in the year 2020 we were still ignoring the impending dangers[6].

The vitamin D system has extraskeletal pleiotropic functions, including the modulation of the adaptive immune response and the enhancement of the innate response[1-3]. This explains why vitamin D influence on infections has been the subject of many analyses. The implication of vitamin D deficiency in tuberculosis has been known for decades. But it has also been associated with other infections, mainly respiratory tract infections and others such as the flu, exacerbations of chronic obstructive pulmonary disease or cystic fibrosis, sepsis or human immunodeficiency virus infection. More recently, there has been interest in knowing its influence on the pathogenesis and possible therapeutic use in SARS-CoV-2 infection[4]. In this article we will review the role of vitamin D in the immune system and its influence on infectious diseases.

Vitamin D is a fundamental hormone for the maintenance of musculoskeletal health and the proper functioning of the immune system[1]. The new coronavirus pandemic, SARS-CoV-2, which emerged in Wuhan at the end of 2019, has hit the world with extraordinary virulence[2]. Several lines of evidence support a potential role for vitamin D in COVID-19. First, a recent meta-analysis has shown a beneficial effect of vitamin D in preventing viral respiratory diseases, especially in those subjects with greater deficiency of this hormone[3]. In addition, vitamin D is crucial in modulating the innate immune system (production of antimicrobial peptides such as cathelicidin and activation of autophagy) and adaptive (inhibition of the activation of Th1 lymphocytes, activation of Th2 lymphocytes, decrease of cells Th17/Treg and inhibition of the proliferation and differentiation of B lymphocytes). Vitamin D deficiency is especially conspicuous in the elderly, in obese individuals and those with chronic diseases such as cancer, diabetes or cardiovascular diseases, which also represent the groups with the highest severity of COVID-19. Finally, vitamin D inhibits proinflammatory cytokine production and its deficiency can induce activation of the renin-angiotensin system (RAS), leading to the production of profibrotic factors and lung damage. This dysregulation of the RAS in COVID-19, mediated by the ACE2 receptor, through which SARS-CoV-2 penetrates the host cell, is responsible for the cytokine storm that precedes the characteristic acute respiratory distress syndrome. of the most serious form of infection by this coronavirus[4].

The intervention of vitamin D in our immune system activity led to the study of this hormone’s effect on SARS-CoV-2 infection from the start of the pandemic. Published studies have already been analyzed in other chapters of this special edition. Some societies and scientific and health institutions have considered this topic, and based on these reflections, offer recommendations to the health community. In this chapter, we present a brief overview.

Seven years have passed since the most recent version of the Osteoporosis Guidelines of the Spanish Society for Bone Research and Mineral Metabolism (SEIOMM) was drawn up, using the standard methodology of evidence‐based medicine [1]. This update incorporates information released since then. The full text is available in the Guide.

2. Methods
A group of experts (see annexe) reviewed each section to incorporate the new findings published in recent years. The new text was disseminated to other interested entities (including SEIOMM partners, patient associations, the Spanish Agency for Medicines and Health Products, and pharmaceutical industries) to provide input to the document, which was subsequently analysed by the group of experts. Osteoporosis in postmenopausal women was analysed first, followed by osteoporosis in men and glucocorticoid‐induced osteoporosis.

Seven years have passed since the publication of the previous version of the Osteoporosis Guidelines of the Spanish Society for Bone Research and Mineral Metabolism (SEIOMM) that was created in accordance with the standard methodology of evidence‐based medicine [1]. This update incorporates the most essential information that has appeared since the publication of the previous version, with particular reference to new diagnostic procedures and therapeutic options. Novel diagnostic modalities discussed in these guidelines include the Trabecular Bone Score (TBS) and the detection of vertebral fractures by densitometry. Among the therapeutic options, we discuss the use of novel anabolic drugs (abaloparatide and romosozumab). Studies that compare the efficacy of various drug regimens for the treatment of severe osteoporosis are also considered. Likewise, the guidelines for action after the withdrawal of antiresorptive drugs and other sequential and combined treatment schemes are assessed.

Diabetes mellitus (DM2) and osteoporosis are increasing prevalence diseases due to the aging of the population, and gender, genetic and environmental factors, such as an unbalanced diet, obesity and a sedentary life. DM2 increased alarmingly in 2014, affecting more than 420 million people worldwide [1]. Patients with DM2 present a higher risk of falls and increased prevalence and incidence of fragility fractures have been observed in these patients [2-5], causing significant mortality, morbidity and increased healthcare costs.
DM2 affects bone homeostasis [6,7], and is associated with a higher risk of fractures [8], despite the fact that patients exhibit higher bone mineral density (BMD) [4,9-12]. Furthermore, reduced circulating levels of bone turnover markers have been observed in DM2 [13], which should influence the high fracture risk in patients with DM2.

Obesity is a chronic metabolic disease with an increasing incidence that is associated with the development of multiple metabolic and mechanical comorbidities, it has also been associated with a higher incidence of tumors, a worse evolution of autoimmune diseases (SEEDO/WHO) [1,2] and a increase in all-cause mortality [3,4]. According to Spain’s Ministry of Health data, the prevalence of obesity in the adult population (25-65 years) is 14.5% (17.5% in women; 13.2% in men), with a parallel increase with people’s age (21.6% and 33.6% in women and men over 65 years of age, respectively). This situation is a public health challenge, not only because of its prevalence, but also due to the increase in morbidity and mortality, accelerated aging, the economic costs and associated social implications [5,6].
To date, intensive medical treatment and lifestyle modifications in obese patients have not shown a significant decrease in the development of complications during follow-up (10-20 years) [7-9]. In contrast, bariatric surgery (BS) is an intervention that entails significant weight loss (25-58% at 10 years), associated with a significant improvement in comorbidities directly and indirectly related to the disease [7,10]. Additionally, BS reduces the risk of mortality by 51% [10]. Different meta-analyzes suggest reductions in cardiovascular mortality (OR, 0.58, 95% CI, 0.46-0.73), all-cause mortality (OR: 0.70, 95% CI, 0.59-0 ,84) and increased life expectancy of up to 7 years in patients with underlying cardiovascular disease [11].