Results There is good evidence for a role of central sensitisation in chronic OA pain in a subgroup of patients .
Biomarkers may be helpful for confirming the presence of central sensitisation , especially when there is diagnostic uncertainty .
Several non‐pharmacological and pharmacological treatments may be effective in OA patients with central sensitisation features .
Multimodal therapy may be required to achieve control of symptoms .
Summary Aims The aim of this non‐ systematic review was to provide a practical guide for clinicians on the evidence for central sensitisation in chronic osteoarthritis ( OA ) pain and how this pain mechanism can be addressed in terms of clinical diagnosis , investigation and treatment .
Clinical ly , a central sensitisation component in chronic OA pain can be suspected based on characteristic pain features and non‐pain features seen in other conditions involving central sensitisation .
Duloxetine added to oral nonsteroidal anti-inflammatory drugs for treatment of knee pain due to osteoarthritis: results of a randomized, double-blind, placebo-controlled trial
Abstract Objective : To determine the efficacy , tolerability , and safety of duloxetine when added to oral nonsteroidal anti-inflammatory drugs ( NSAIDs ) in patients with osteoarthritis ( OA ) of the knee with pain of moderate or greater severity . Research design and methods : This was a 10-week r and omized , double-blind , flexible-dose ( duloxetine 60/120 mg/day ) , placebo-controlled trial that enrolled adult out patients who had persistent moderate pain ( ≥4 on a 0–10 numerical rating scale ) due to OA of the knee , despite , per protocol , having received optimized oral NSAID therapy  ( specific drug , dose , and frequency at investigator discretion ) . Clinical trials registration : Trial registration : Clinical Trials.gov identifier : NCT01018680 . Main outcome measure : Patients entered daily pain ratings in a telephone-based diary . The primary efficacy outcome was the weekly mean of the daily average pain rating at week 8 . Safety outcomes were assessed during the entire 10-week study . Results : A total of 524 patients r and omly received duloxetine 60/120 mg/day ( N = 264 ) or placebo ( N = 260 ) . In total , 74 % of the patients completed the study . Mean age was 61 years ( SD 9.2 ) , 57 % were female , and 81 % were white .  Duloxetine-treated patients had significantly greater pain reduction at week 8 ( p < 0.001 ) than placebo-treated patients . In addition , relative to placebo at week 8 , duloxetine-treated patients had significant improvements in physical function as measured by the Western Ontario and McMaster Universities Osteoarthritis Index ( p < 0.001 ) , and Patient Global Impression of Improvement ( p < 0.001 ) . Compared to placebo , significantly more nausea , dry mouth , constipation , fatigue and decreased appetite were reported by patients taking duloxetine ( each p < 0.05 ) . Discontinuation due to adverse events occurred more commonly in the duloxetine group than the placebo group ( p = 0.03 ) . Conclusion : Duloxetine added to oral NSAID therapy provided additional significant pain reduction , improved function , and patient-rated impression of improvement . Adverse events were consistent with those seen in previous duloxetine trials . The short duration of the study may not reflect the longer term efficacy and safety of NSAID/duloxetine cotherapy
Results There is good evidence for a role of central sensitisation in chronic OA pain in a subgroup of patients .
Biomarkers may be helpful for confirming the presence of central sensitisation , especially when there is diagnostic uncertainty .
Several non‐pharmacological and pharmacological treatments may be effective in OA patients with central sensitisation features .
Multimodal therapy may be required to achieve control of symptoms .
Summary Aims The aim of this non‐ systematic review was to provide a practical guide for clinicians on the evidence for central sensitisation in chronic osteoarthritis ( OA ) pain and how this pain mechanism can be addressed in terms of clinical diagnosis , investigation and treatment .
Clinical ly , a central sensitisation component in chronic OA pain can be suspected based on characteristic pain features and non‐pain features seen in other conditions involving central sensitisation .