ASBMR: American Society for Bone and Mineral Research

The National Bone Health Alliance working group expanded criteria for the clinical diagnosis of osteoporosis to include T-score < 2.5 at the spine or hip; low-trauma hip fracture; low-trauma vertebral, proximal humerus, pelvis or some distal forearm fractures in the setting of osteopenia; or FRAX score in a patient with osteopenia meeting or exceeding the National Osteoporosis Foundation Guidelines.

Osteogenesis imperfecta, a skeletal disorder caused by mutations in type I collagen, exhibits structural and functional differences on a genotypic level that contribute to diverse phenotypes.

Fracture Liaison Services (FLS) attempt to ensure that patients with potentially osteoporosis-associated fractures are followed appropriately with screening and intervention. In the United States, industry, non-profits, and governmental steering committees support FLS.

Autophagy functions in numerous critical ways, including in quality control, cell remodeling, and energy production. Understanding the molecular pathways of autophagy can result in understanding and treating neurodegenerative disorders, metabolic disorders, and physiologic changes associated with aging.

Cilia appear in a wide variety of cell types, including osteoclasts and osteoblasts, where they function as physiologic and biochemical sensors.

By studying dense connective tissue, scientists are discovering ways that the cell nucleus adapts and changes in response to the administration of force, time, and differentiation.

Current novel therapeutics for the prevention and treatment of bone loss in patients with inflammatory joint disease target cytokines and other inflammatory mediators. Mesenchymal stem cell therapy is a compelling new treatment currently being studied in clinical trials.

Bone erosion, a common side-effect of rheumatoid arthritis, can be prevented by using a combination of close patient monitoring and individualized therapeutic regimens that include agents to block cytokines, block osteoclasts, or target abnormal cellular reactions.

Inflammatory bone loss is caused by a complex pathway that begins with inflammatory cell production of cytokines, progresses to abnormal bone absorption, and culminates in the destruction of joints, bone fractures, and patient debility.