Jacek Kobak, Karolina Chmielnicka, Paulina Komorowska, Daniela Alterio, Luca Bergamaschi, Barbara A Jereczek-Fossa, Mateusz Szczupak, Bogusław Mikaszewski
The available evidence supports clinically relevant overlap between OSA, frailty, and sarcopenia-related phenotypes, and a parallel association of sarcopenia and frailty with adverse HNC outcomes. However, the proposed triad should be interpreted as a hypothesis-generating framework rather than an established clinical entity. Future prospective studies should integrate objective OSA assessment, frailty evaluation, and radiological muscle measurements in HNC populations.
BACKGROUND: Sarcopenia, frailty syndrome, and obstructive sleep apnea (OSA) are increasingly recognized as age-related conditions with overlapping biological pathways. Their coexistence may be relevant in head and neck cancer and upper airway disorders, but direct evidence integrating OSA with head and neck cancer (HNC) and geriatric vulnerability remains limited.
OBJECTIVE: This scoping review aimed to map the evidence on the relationships among sarcopenia, frailty, and OSA in the context of head and neck cancer and upper airway disorders, and to determine whether the available literature supports an integrated clinical model linking OSA-related vulnerability with HNC outcomes.
METHODS: The review was conducted in accordance with PRISMA ScR guidelines. A literature search was performed in PubMed, EBSCO, and Google Scholar for studies published between January 2015 and December 2025. Eligible studies included adult populations and addressed sarcopenia, frailty, OSA, or their clinically relevant relationships in head and neck cancer and upper airway disorders.
RESULTS: Twelve studies met the inclusion criteria. Evidence clustered into two main streams. First, OSA was associated with frailty and sarcopenia-related phenotypes through mechanisms including intermittent hypoxia, systemic inflammation, sleep fragmentation, and neuroendocrine dysregulation. Second, in HNC, sarcopenia and frailty were associated with worse clinical outcomes, greater treatment burden, postoperative complications, treatment toxicity, and mortality. Direct evidence linking OSA with HNC within the included studies was limited. Therefore, the available evidence does not yet establish a fully demonstrated three-way clinical relationship among sarcopenia, frailty, and OSA in HNC.
CONCLUSION: The available evidence supports clinically relevant overlap between OSA, frailty, and sarcopenia-related phenotypes, and a parallel association of sarcopenia and frailty with adverse HNC outcomes. However, the proposed triad should be interpreted as a hypothesis-generating framework rather than an established clinical entity. Future prospective studies should integrate objective OSA assessment, frailty evaluation, and radiological muscle measurements in HNC populations.