We thank Gentzel for his careful reading of our article.1 His letter to the editor2 is enriching, as it facilitates the international debate regarding pain treatment and pain mechanisms in osteoarthritis (OA). Below we respond to each of the issues raised.
As correctly indicated by Gentzel, the aim of our article was to emphasize the role of the hyperexcitability of the central nervous system (or central sensitization [CS]) on pain in patients with OA rather than updating the readers with our current understanding of OA etiology and joint pathophysiology. Considering both peripheral and central aspects for a comprehensive approach to OA pain does not imply “ignorance” of the chronic inflammatory condition, as suggested by Genztel. As the scientific community is well informed about the pathological changes in joint structures in patients with OA, the central pain mechanisms require more attention. Our article reviewed and evaluated the existing scientific evidence addressing CS in OA pain in order to establish whether there were enough arguments to support the role of CS in chronic pain related to OA. To cite our own article, “[i]n addition to the pathological changes in articular structures, changes in central pain processing or central sensitization appear to be involved in osteoarthritis pain.”1(p842)
We do not doubt the role that tissue modification and destruction, typically observed in patients with OA, can have in explaining …
