Inflammaging: The driving force in osteoporosis?

Abstract

With advancing age, the balance between the amounts of old bone removed and new bone formed during the remodelling process becomes negative. In the past, it was commonly thought that skeletal involution was the result of age-related changes in other organs, and in particular from the decline in ovarian function in women at menopause. Nonetheless, with regard to emerging epidemiologic studies, the hypothesis suggesting that age-related changes such as inflammatory modifications importantly account for age-related bone loss is gaining increasing interest. Aging is indeed associated with immune dysfunction that coexists with a chronic subclinical inflammatory status. The latter is illustrated by a 2–4-fold increase in the levels C-reactive protein (CRP) or interleukin (IL)-6. This inflammatory status, which has been referred to by the neologism “inflammaging”, is of sufficient magnitude to impact health and survival time, and correlates with age-related diseases such as atherosclerosis, insulin resistance and Alzheimer’s disease. In this article, we first present the factors that condition inflammaging, and propose the hypothesis that inflammaging may be the driving force in age-related bone loss and may even be responsible for osteoporosis due to estrogen deficiency. Finally, we discuss the possibility that pro-inflammatory biomarkers may be used to provide clinical information for identifying patients at risk for osteoporosis, and the possibility that inflammatory cytokines may be targeted to improve bone formation in aged patients undergoing orthopaedic surgery.