EVALUATION COMMITTEE

The Faculty Council has appointed the following adjudication committee to evaluate the thesis and the associated lecture: 

• Professor Patrick Finan, University of Virginia, School of Medicine
• Professor Anders Holsgaard Larsen, University of Southern Denmark, Department of Clinical Research

Chairman: Associate professor Andrew James Thomas Stevenson, Department of Health Science and Technology (HST), Aalborg Universitet

Moderator: Associate professor Kristian Kjær-Staal Petersen, Department of Health Science and Technology (HST), Aalborg Universitet

ABSTRACT

Knee osteoarthritis is a leading cause of chronic pain and disability worldwide. Despite similar radiographic findings of joint degeneration, patients report varying pain intensities. This suggests that factors beyond the joint influence pain perception. Pain in knee osteoarthritis is increasingly being recognized as multifactorial. Altered pain sensitivity, psychological distress, poor sleep, and knee biomechanics have all been linked to increased pain burden. Variation within these factors likely places an individual somewhere on a spectrum from being ‘pain resilient’ to ‘pain vulnerable’. These factors have previously not been studied in combination. This thesis will address this by integrating these domains into multivariate models to explain variability in experimental and clinical knee pain. Currently, there are no curative treatments for osteoarthritis, and treatment instead focuses on pain relief.  Some patients experience limited effects of these standard joint-directed therapies. Uncovering the underlying mechanisms driving pain and ultimately using this knowledge to select the right patient, at the right time, for the right treatment, could improve patient care.

Three studies form the basis of this thesis. Study I examined patients before and after undergoing a three-week pharmacological treatment and explored the individual and combined contributions of pain sensitivity, psychological factors, and quality of life. Findings from Study I demonstrated that increased pain sensitivity and higher levels of catastrophizing were related to increased pain before and after treatment. Studies II and III induced experimental knee pain in healthy volunteers using hypertonic saline, with Study III combining this model with short-term forced awakenings to introduce a potential central driver of pain. Studies II and III investigated how pain sensitivity, psychological factors, sleep, and biomechanics measured before pain impacted the intensity of experimental knee pain. Findings of studies II and III showed that high pain sensitivity, poor sleep quality, catastrophizing, symptoms of anxiety, and low propulsion impulses identified individuals vulnerable to experimental knee pain. The findings of this thesis highlight the multifactorial background of individual vulnerability to pain and indicate that this might be important for the effect of pharmacological treatment. In the future, this knowledge might be leveraged to inform personalized pain management in knee osteoarthritis.