Details

Autor(en) / Beteiligte

• Gielen, Evelien
• Dupont, Jolan
• Dejaeger, Marian
• Laurent, Michaël R.

Titel

Sarcopenia, osteoporosis and frailty

Ist Teil von

• Metabolism, clinical and experimental, 2023-08, Vol.145, p.155638-155638, Article 155638

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2023

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Muscles and bones are intricately connected tissues displaying marked co-variation during development, growth, aging, and in many diseases. While the diagnosis and treatment of osteoporosis are well established in clinical practice, sarcopenia has only been classified internationally as a disease in 2016. Both conditions are associated with an increased risk of adverse health outcomes such as fractures, dysmobility and mortality. Rather than focusing on one dimension of bone or muscle mass or weakness, the concept of musculoskeletal frailty captures the overall loss of physiological reserves in the locomotor system with age. The term osteosarcopenia in particular refers to the double jeopardy of osteoporosis and sarcopenia. Muscle-bone interactions at the biomechanical, cellular, paracrine, endocrine, neuronal or nutritional level may contribute to the pathophysiology of osteosarcopenia. The paradigm wherein muscle force controls bone strength is increasingly facing competition from a model centering on the exchange of myokines, osteokines and adipokines. The most promising results have been obtained in preclinical models where common drug targets have been identified to treat these conditions simultaneously. In this narrative review, we critically summarize the current understanding of the definitions, epidemiology, pathophysiology, and treatment of osteosarcopenia as part of an integrative approach to musculoskeletal frailty. [Display omitted] •Osteosarcopenia refers to the synergy of osteopenia and sarcopenia.•Muscle and bone are co-regulated by exercise, nutrition and endocrine signals.•Muscle-bone interactions also invoke myokines, osteokines and adipokines.•The activin receptor pathway restrains muscle hypertrophy and bone formation.•Regulation involves mesenchymal stem cell differentiation and cellular senescence.