Bone Fragility in Gastrointestinal Disorders

Abstract

Osteoporosis is a common systemic disease of the skeleton, characterized by compromised bone mass and strength, consequently leading to an increased risk of fragility fractures. In women, the disease mainly occurs due to the menopausal fall in estrogen levels, leading to an imbalance between bone resorption and bone formation and, consequently, to bone loss and bone fragility. Moreover, osteoporosis may affect men and may occur as a sequela to different diseases or even to their treatments. Despite their wide prevalence in the general population, the skeletal implications of many gastrointestinal diseases have been poorly investigated and their potential contribution to bone fragility is often underestimated in clinical practice. However, proper functioning of the gastrointestinal system appears essential for the skeleton, allowing correct absorption of calcium, vitamins, or other nutrients relevant to bone, preserving the gastrointestinal barrier function, and maintaining an optimal endocrine-metabolic balance, so that it is very likely that most chronic diseases of the gastrointestinal tract, and even gastrointestinal dysbiosis, may have profound implications for bone health. In this manuscript, we provide an updated and critical revision of the role of major gastrointestinal disorders in the pathogenesis of osteoporosis and fragility fractures.

Keywords: Helicobacter pylori; celiac disease; chronic gastritis and peptic ulcer disease; dysbiosis; gastric cancer and gastrectomy; inflammatory bowel disease; osteoporosis.

Figure 1

Pathophysiology bone fragility induced by Inflammatory Bowel Disease (IBD). (HyperPTH: hyperparathyroidism).

Figure 2

Effects of a gluten-free diet (GFD) on the spinal bone mineral content (BMC) (a) as assessed by the dual X-ray absorptiometry (DXA) technique and annual BMC increment and (b) in children with celiac disease (n = 22) as compared with 428 healthy, age-matched controls (derived from Barera G et al. [81]). Bas: baseline.

Figure 3

Trabecular (a) and cortical (b) volumetric BMD changes at the distal radius or tibia and variation of cortical thickness (c) assessed with high-resolution peripheral quantitative computed tomography (HRpQCT), before and after 1 year on a gluten-free diet (GFD) in a cohort of premenopausal women with newly diagnosed celiac disease (CD), as compared with healthy females (CTs) of similar age and BMI (derived from Zanchetta MB et al. [86]).

Figure 4

Pathophysiology of bone fragility induced by Helicobacter Pylori infection.