Frailty and pain, human studies and animal models

The hypothesis that pain can predispose to frailty development has been recently investigated in several clinical studies suggesting that frailty and pain may share some mechanisms. Both pain and frailty represent important clinical and social problems and both lack a successful treatment. This circumstance is mainly due to the absence of in-depth knowledge of their pathological mechanisms. Evidence of shared pathways between frailty and pain are preliminary. Indeed, many clinical studies are observational and the impact of pain treatment, and relative pain-relief, on frailty onset and progression has never been investigated. Furthermore, preclinical research on this topic has yet to be performed. Specific researches on the pain-frailty relation are needed. In this narrative review, we will attempt to point out the most relevant findings present in both clinical and preclinical literature on the topic, with particular attention to genetics, epigenetics and inflammation, in order to underline the existing gaps and the potential future interventional strategies. The use of pain and frailty animal models discussed in this review might contribute to research in this area.

Automated summary

The hypothesis that pain may contribute to the development of frailty has been investigated in recent clinical studies, but further research is needed to understand the shared mechanisms between pain and frailty, particularly in genetics, epigenetics, and inflammation. Current evidence is preliminary, with observational clinical studies and a lack of investigation into the impact of pain treatment on frailty progression. Specific research on the pain-frailty relationship is necessary to uncover potential intervention strategies.