[Mechanisms of development of osteoporosis in patients with chronic obstructive pulmonary disease]

Chronic obstructive pulmonary disease (COPD) is the leading chronic pulmonary pathology and its systemic manifestations, such as the loss of muscular mass, connective tissue dysplasia, and osteoporosis (OP), have recently drawn increasingly more attention. The inflammatory process during COPD is underlain by disbalance between pro- and anti-inflammatory cytokines. As a rule, cytokines act as local regulators but become systemic agents when their production and concentration in blood increase during intense and long-standing inflammatory processes. Proinflammatory cytokines induce OP while anti-inflammatory ones prevent its development. As known, there are many modifiable and non-modifiable (e.g. iatrogenic) risk factors influencing OP pathogenesis. Both iatrogenic and primary pathophysiological mechanisms are responsible for the development of osteopenic syndrome during COPD. The leading cause in pathogenesis of reduced mineral bone density (MBD) and disturbed osseous metabolism is disbalanced cytokine production resulting from chronic inflannation, oxidative stress, and increasing tissue hypoxia and hypercapnia. An additional contribution to the development of pulmogenic osteopenia comes from the body mass deficit, myopathy, organic physical activity, and smoking. A wealth of current publications suggest the importance of body mass loss during COPD. Domestic and especially foreign authors emphasize that pathogenesis of OP in patients with COPD remains poorly known. Long-term studies and methods for early diagnostics of this condition are needed to resolve the problem.