Improving the clinical diagnosis of Osteoarthitis by assessing pain using neurological techniques and biomarkers

Osteoarthritis is the most common joint disorder worldwide. Symptomatic osteoarthritis (OA) results in significant physical and psychosocial disability. OA is a complex disease with an etiology which encompasses biological and mechanical factors. According to the World Health Organization an estimated 10% to 15% of all adults over 60 are affected by some form of OA. The primary complaint reported by most patients with OA presenting to an orthopedic surgeon is pain. Furthermore, pain has been shown to be the most important determinant of disability in patients with OA.
OA pain presents several dilemmas to clinicians. It is difficult, to predict which patients will experience pain. There is often a discord between the physical findings and the amount of pain experienced and surgical interventions do not always provide a solution for the patients’ symptoms. Currently, there are no conclusive diagnostic or prognostic tools which would allow clinicians to predict the onset progression and disease course of osteoarthritis for individual patients. We hoped to use clinical assessment, radiographs, somatosensory evoked potentials, (SSEP) functional MRI, (fMRI) and serum biomarkers to find a comprehensive diagnostic tool for OA.
We recruited 30 patients with OA of their hip and10 healthy age matched controls for the study. Clinical assessment included a history and physical examination, collection of several questionnaires. Patients were asked to report their average pain over the previous four weeks using a visual analogue scale (VAS) for pain. Radiographs of the hip were also obtained and graded using the Kellgren and Lawrence scale. All patients presented with grade 3- 4 OA. When the results were plotted using dispersion analysis there was no relationship between the OA grades and the other variables. Collection of a VAS score for pain produced two distinct groups, which provided a way to divide the patients for the study. The first group reported their pain as being 1-4 on the VAS scale and were referred to as the OA low pain (OALP) group the second group reported their pain at a level of 6-9 using the VAS and were referred to as the OA high pain group (OAHP). Data was analysed using comparisons all arthritic (OACMBD) with OAHP, OALP, and the controls.
SSEP confirmed that there was no evidence of peripheral sensitization, therefore peripheral somatosensory processing was unaffected by hip OA. However, there was some evidence of central sensitisation seen in the ratios of the amplitudes. Resting-state fMRI defined the brain signature for chronic pain secondary to OA of the hip joint. In addition, an acute component post-exercise was demonstrated. Our results show that there is a response of the central nervous system as part of the progression of the osteoarthritic hip. Finally, we looked to see if there were any biological markers that could also discriminate between the OAHP and OALP groups at the same high grade of OA. Several biomarkers were found to be statistically significant, these included monocyte chemotactic protein-3 (MCP-3) and Interleukin 8 (IL-8) Cartilage Oligomeric Matrix Protein (COMP) and monocyte chemotactic protein-1 (MCP-1).
In conclusion it is clear from the findings of this study that there are diagnostics available which can aid in distinguishing between normal, OA-low pain and OA-high pain patient groups. This knowledge may eventually be useful in predicting prognosis, modifying patient-specific management and improving outcomes.