Basic and clinical aspects of osteoporosis in inflammatory bowel disease

Abstract

Lor e n a R o d r í g u e z -B o r e s , J o s u é B a r a h o n a G ar r ido, Jesús K Yamamoto-Furusho, IBD Clinic, Department of Gastroenterology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán. AbstractLow bone mineral density and the increased risk of fracture in gastrointestinal diseases have a multifactorial pathogenesis. Inflammatory bowel disease (IBD) has been associated with an increased risk of osteoporosis and osteopenia and epidemiologic studies have reported an increased prevalence of low bone mass in patients with IBD. Certainly, genetics play an important role, along with other factors such as systemic inflammation, malnutrition, hypogonadism, glucocorticoid therapy in IBD and other lifestyle factors. At a molecular level the proinflammatory cytokines that contribute to the intestinal immune response in IBD are known to enhance bone resorption. There are genes influencing osteoblast function and it is likely that LRP5 may be involved in the skeletal development. Also the identification of vitamin D receptors (VDRs) and some of its polymorphisms have led to consider the possible relationships between them and some autoimmune diseases and may be involved in the pathogenesis through the exertion of its immunomodulatory effects during inflammation. Trying to explain the physiopathology we have found that there is increasing evidence for the integration between systemic inflammation and bone loss likely mediated via receptor for activated nuclear factor kappa-B (RANK), RANK-ligand, and osteoprotegerin, proteins that can affect both osteoclastogenesis and T-cell activation. Although glucocorticoids can reduce mucosal and systemic inflammation, they have intrinsic qualities that negatively impact on bone mass. It is still controversial if all IBD patients should be screened, especially in patients with preexisting risk factors for bone disease. Available methods to measure BMD include single energy x-ray absorptiometry, DXA, quantitative computed tomography (QCT), radiographic absorptiometry, and ultrasound.DXA is the establish method to determine BMD, and routinely is measured in the hip and the lumbar spine. There are several treatments options that have proven their effectiveness, while new emergent therapies such as calcitonin and teriparatide among others remain to be assessed.

Low Body Mass Index Can Identify Majority of Osteoporotic Inflammatory Bowel Disease Patients Missed by Current Guidelines

“…The pathogenesis of low BMD in IBD is complex and considered to be multifactorial. Risk factors for the development of low BMD include the general risk factors for osteoporosis such as age, smoking as well as IBD-specific risk factors such as corticosteroid use, malnutrition, small bowel resection, vitamin D (25-hydroxyvitamin D [25-OHD]) deficiency, and proinflammatory cytokines [5, 6]. Recognizing the increased risk for fractures in patients with low BMD, American College of Gastroenterology (ACG) and American Gastroenterology Association (AGA) guidelines recommend screening IBD patients with Dual Energy X-ray Absorptiometry (DXA) if they have one of the following risk factors: postmenopausal state, ongoing corticosteroid treatment, cumulative prior use of corticosteroids exceeding 3 months, history of low-trauma fractures, or age over 60 [7–9].…”

Nutrient Intake and Bone Mineral Density by Nutritional Status in Patients with Inflammatory Bowel Disease

“…[20,27,28] However, more recommendations indicate that daily management is required to ensure adequate levels of calcium and vitamin D in the diet and to improve malnutrition to prevent osteoporosis. [1,29] Because of the limited number of subjects, this study was not able to represent all IBDs. Nonetheless, our results were useful in confirming the role of malnutrition, nutrient intake, and bone density in patients with chronic IBD.…”

Novel Biomarkers and the Future Potential of Biomarkers in Inflammatory Bowel Disease

“…The equilibrium of osteoclast and osteoblast activity is coordinated primarily by the receptor activator of nuclear factor- κ B (RANK) and its ligand (RANKL). OPG acts as a decoy receptor for RANK [16, 18, 20–22]. In this role as a decoy receptor, OPG inhibits the differentiation, survival, and function of osteoclasts by competitively blocking the interaction between RANK and RANKL [18] promoting bone formation as a counter regulatory response to factors such as inflammatory cytokines (IL-1, TNF α ) [23].…”

“…The OPG/RANKL/RANK triad may contribute to mucosal and systemic inflammation [17, 20, 22]. RANK, RANKL, and OPG decrease the functional capacity of dendritic cells (DC) and activated T cells but enhance B cell maturation [26–28].…”