Figure 4.

Schematic diagram illustrating the relationship between critical illness and bone dysfunction. Many pathological conditions such as inflammation, endocrine and metabolic disturbances, electrolyte and acid-base imbalance or vitamin D deficiency, as well as other causes such as long-term bed-rest or glucocorticoid therapies in critical illness could result in impaired osteoblast function and increased osteoclast activity, ultimately leading to acute bone loss and even bone fracture. Furthermore, the impaired osteoblast function and enhanced bone resorption could also cause increased secretion of proinflammatory factors, which might exacerbate the systemic inflammatory response. The changes of some BDFs secreted by osteoblasts such as the decreased serum levels of OC, IL-7 and CXCL12 or increased FGF23 level in critical illness may also worsen metabolic or hematopoietic disorders. We define these damages or changes in the structure and functions of bone as bone dysfunction in critical illness.