Osteoporosis and inflammation: Cause to effect or comorbidity?
Michael O Khoury
Abstract
Osteoporosis (OP) was long viewed as an inevitable process of aging, due to an imbalance between osteoclast bone resorbing and osteoblast bone formation function, leading to a negative balance in bone remodeling. This leads to low bone mass and increased bone fragility putting the patient at risk for fracture. While this view still holds, a better understanding disclosed that OP can occur at any age, as a comorbidity or a complication of many diseases and treatments. Differentiation, maturation, and function of osteoclasts and osteoblasts are affected by many factors from different morbidities: endocrine, metabolic, mechanical and inflammatory. Inflammatory diseases are often complicated by a generalized bone loss that subsequently leads to OP. Factors such as glucocorticoid treatment, immobilization, malnutrition, and insufficient intake of vitamin D play a role. However, the inflammatory process itself is involved and the resulting bone loss is termed immune-mediated bone loss. Experiments on animals and on humans, in addition to clinical studies, shed light on the role of inflammation in OP.