# Osteosarcopenia: A Narrative Review on Clinical Studies

**Authors:** Angela Polito, Lorenzo Barnaba, Donatella Ciarapica, Elena Azzini

PMC · DOI: 10.3390/ijms23105591 · International Journal of Molecular Sciences · 2022-05-17

## TL;DR

Osteosarcopenia combines bone and muscle loss, and this review explores its causes, risks, and treatment strategies based on clinical studies.

## Contribution

This paper provides a comprehensive clinical review of osteosarcopenia, emphasizing its connection to NCDs and the need for combined interventions.

## Key findings

- Osteosarcopenia is linked to increased risks of frailty, falls, and fractures.
- Nutrition and physical exercise are key non-pharmacological strategies for managing osteosarcopenia.
- Pharmacological interventions may benefit muscle and bone health but require further RCTs.

## Abstract

Osteosarcopenia (OS) is defined by the concurrent presence of osteopenia/osteoporosis and sarcopenia. The pathogenesis and etiology of OS involve genetic, biochemical, mechanical, and lifestyle factors. Moreover, an inadequate nutritional status, such as low intake of protein, vitamin D, and calcium, and a reduction in physical activity are key risk factors for OS. This review aims to increase knowledge about diagnosis, incidence, etiology, and treatment of OS through clinical studies that treat OS as a single disease. Clinical studies show the relationship between OS and the risk of frailty, falls, and fractures and some association with Non-communicable diseases (NCDs) pathologies such as diabetes, obesity, and cardiovascular disease. In some cases, the importance of deepening the related mechanisms is emphasized. Physical exercise with adequate nutrition and nutritional supplementations such as proteins, Vitamin D, or calcium, represent a significant strategy for breaking OS. In addition, pharmacological interventions may confer benefits on muscle and bone health. Both non-pharmacological and pharmacological interventions require additional randomized controlled trials (RCT) in humans to deepen the synergistic effect of exercise, nutritional interventions, and drug compounds in osteosarcopenia.

## Linked entities

- **Diseases:** diabetes (MONDO:0005015), obesity (MONDO:0011122), cardiovascular disease (MONDO:0004995)

## Full-text entities

- **Genes:** PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, TNFSF11 (TNF superfamily member 11) [NCBI Gene 8600] {aka CD254, ODF, OPGL, OPTB2, RANKL, TNLG6B}, CYP27A1 (cytochrome P450 family 27 subfamily A member 1) [NCBI Gene 1593] {aka CP27, CTX, CYP27}, LMNA (lamin A/C) [NCBI Gene 4000] {aka CDCD1, CDDC, CMD1A, CMT2B1, EMD2, FPL}, SOST (sclerostin) [NCBI Gene 50964] {aka CDD, DAND6, SOST1, VBCH}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, SHBG (sex hormone binding globulin) [NCBI Gene 6462] {aka ABP, SBP, TEBG}, BGLAP (bone gamma-carboxyglutamate protein) [NCBI Gene 632] {aka BGP, OC, OCN}, AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}, MSTN (myostatin) [NCBI Gene 2660] {aka GDF8, MSLHP}
- **Diseases:** disabilities (MESH:D009069), endocrine disorder (MESH:D004700), dyslipidemia (MESH:D050171), NCDs (MESH:D000073296), Sarcopenia (MESH:D055948), loss of muscle mass, strength, and function (MESH:D009135), mobility limitations (MESH:D051346), Osteoporosis (MESH:D010024), Fractures (MESH:D050723), Falls (MESH:C537863), muscle wasting (MESH:D009133), adiposity (MESH:D018205), hip fracture (MESH:D006620), loss of self-sufficiency in daily activities (MESH:D020773), loss of independence (MESH:D064129), skeletal muscle (MESH:D005207), sex hormone abnormalities (MESH:D012729), T2DM (MESH:D003924), IR (MESH:D007333), malnutrition (MESH:D044342), Obesity (MESH:D009765), Osteoporosis and Frailty (MESH:D000073496), physical disability (MESH:D059445), fragility (MESH:D005600), chronic inflammation (MESH:D007249), CAD (MESH:D003324), Cardiovascular Diseases (MESH:D002318), HIT (MESH:D013921), death (MESH:D003643), hypertension (MESH:D006973), W (MESH:C538106), impaired musculoskeletal health (MESH:D009140), diabetes (MESH:D003920), disorientation (MESH:D003221), antioxidant vitamins (MESH:D014802), MCI (MESH:D060825), diabetes complications (MESH:D048909), osteoporotic (MESH:D058866), inflammatory cytokines (MESH:D000080424), postural instability (MESH:D054972), vertebral fracture (MESH:C535781), depression (MESH:D003866), atrophy (MESH:D001284), vascular calcifications (MESH:D061205), COVID-19 (MESH:D000086382), Osteopenia (MESH:D001851), overweight (MESH:D050177), bone fragility (MESH:C536063), PCOS (MESH:D011085), muscle strength (MESH:D019042), osteogenic (MESH:D012516), liver disease (MESH:D008107), osteopenic (MESH:C567172), bone loss (MESH:D001847), Anemia (MESH:D000740), cognitive impairment (MESH:D003072)
- **Chemicals:** Ins (MESH:D007204), cholecalciferol (MESH:D002762), W (MESH:D014414), Denosumab (MESH:D000069448), hydroxyapatite (MESH:D017886), bisphosphonates (MESH:D004164), calcium (MESH:D002118), phosphorus (MESH:D010758), lipid (MESH:D008055), Vitamin D (MESH:D014807), free fatty acids (MESH:D005230), glucose (MESH:D005947), Glu (MESH:D018698), romosozumab (MESH:C557282), A and E (-), teriparatide (MESH:D019379),  (MESH:D002136)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606]
- **Mutations:** M 154 W

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC9147376/full.md

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC9147376/full.md

## References

88 references — full list in the complete paper: https://tomesphere.com/paper/PMC9147376/full.md

---
Source: https://tomesphere.com/paper/PMC9147376