Bone remodeling, humoral networks and smart biomaterial technology for osteoporosis.
One of the unfortunate sequelae of increased life expectancy is a growing number of age-related degenerative diseases, a prime example being osteoporosis. This form of metabolic bone disease and related co-morbidities consume tremendous resources and costs from a nation's health care system. Osteoporosis results from genetic, age-related, and hormone-dependent causes as well as a compendium of secondary pathophysiological states. The presence of osteoporosis as a comorbidity confers a significant negative prognostic element following orthopedic procedures. In vitro and in vivo studies of osteoporotic bone implicate microarchitectural bone rarefaction, microenvironmental and functional disturbance of osteoblast-osteoclast coupling, and abnormal tissue and signalling molecule repertoires, each having detrimental effects on the regenerative and osteointegration processes. This review explores the pathophysiology of bone remodeling from a macro- and micro- systems biology standpoint with a focus on cytokine interactions. Furthermore, therapeutic interventions exploiting vulnerable nodes in these physiological networks will be posited. One exciting development in this area is the use of novel biomaterials.
Fini
Milena
M
Laboratory of Surgical and Preclinical Studies, Rizzoli Orthopaedic Institute, Bologna, Italy.
Carpi
Angelo
A
Borsari
Veronica
V
Tschon
Matilde
M
Nicolini
Andrea
A
Sartori
Maria
M
Mechanick
Jeffrey
J
Giardino
Roberto
R
D016723:Bone Remodeling / Q000502:physiology*; D018786:Bone Substitutes / Q000627:therapeutic use; D016207:Cytokines / Q000378:metabolism*; D006728:Hormones / Q000378:metabolism; D006801:Humans; D010006:Osteoblasts / Q000378:metabolism; D010010:Osteoclasts / Q000378:metabolism; D010024:Osteoporosis / Q000276:immunology* / Q000503:physiopathology* / Q000628:therapy*
D018786:Bone Substitutes; D016207:Cytokines; D006728:Hormones