Pain, according to the recent definition of the International Association for the Study of Pain, is an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage 1. Many pathologies, which have pain as their primary clinical expression, contribute significantly to morbidity and mortality on a global scale.
Although there is growing evidence in the literature of a possible relationship between low levels of 25-hydroxy vitamin D [25(OH)D] and different types of acute or chronic pain and how adequate vitamin D supplementation, particularly in patients with a deficiency, can lead to an improvement in pain symptoms, clinical trials conducted for this purpose have provided inconsistent or discordant results, which, from time to time, have been attributed to participant selection, outcome measures, sample size, vitamin D dosage and/or follow-up duration. Nevertheless, the potential mechanisms by which vitamin D might exert analgesic effects remain poorly understood.
Clinical research in the area of the correlation between chronic pain and vitamin D deficiency is limited. There are still very few randomised, controlled, and blinded studies. Regardless, clinical trials have shown that vitamin D is able to exert anatomical and physiological influence on the manifestation of pain, thus playing a positive role in the aetiopathogenesis and maintenance of chronic pain states and associated comorbidities. Manifestations of pain associated with immunological, hormonal, and neuronal changes are potentially influenced by vitamin D levels. Indeed, low vitamin D levels have been found in patients with various pain states such as headache, abdominal pain, knee pain, low back pain, persistent musculoskeletal pain, costochondritis chest pain, “failed back syndrome” and fibromyalgia.