i141 Diagnostic challenges in SpA: differentiating PsA from OA using imaging factors

Abstract

Rheumatologists have long considered psoriatic arthritis (PsA) and osteoarthritis (OA) as two completely distinct arthropathies. Simplistically put, OA has been conceptualised in relation to joint degeneration, whereas PsA has been primarily viewed in terms of joint inflammation. Due of its heterogeneous clinical profile and the possibility of involvement of the axial skeleton, Moll and Wright originally grouped PsA under the spectrum of the spondylarthropathies (SpA). While many of the manifestations of PsA are shared with the other SpAs, DIP joint disease is very typical of PsA. This can cause a clinical dilemma, as DIP joint arthropathy is also characteristic of OA. It was proposed more than a decade ago that enthesitis may be the primary lesion in PsA and SpA. Likewise, several experimental studies have shown that spontaneous knee OA can start in the ligament and enthesis and not the articular cartilage, thus providing proof of principle of similar micro-anatomical topography for disease onset. Studies in the generalised form of human hand OA have also shown that the ligaments and enthesis are the sites of the earliest discernible pathology. Collectively this has resulted in a mechanistic anatomical classification of OA that recognises that the generalised form of disease that was previously designated as idiopathic appears to have an enthesis-associated micro-anatomical basis. MRI of peripheral joints has long demonstrated a capsular pattern of inflammation in PsA as well as evidence for diffuse enthesitis related to pathology in a proportion of patients. Also, it may be impossible to clearly differentiate OA from PsA DIP disease, with both seeming to have prominent abnormalities in the entheses and ligaments. Studies have noted that enthesitis-related bone oedema seen in PsA is also common in OA. With respect to spinal disease, an association was evident, with bone oedema at the enthesis attachment observed occasionally in healthy subjects, OA and SpA. Imaging, in particular MRI, has highlighted how some forms of generalised OA and PsA may afflict the same anatomical territory, namely the enthesis, with genes and environment modifying the clinical phenotype. While degeneration or inflammation may be clearly discernible at the two extremes, there may be a group of patients where differentiation is impossible. Appreciating OA-PsA overlap disease may help with optimal management and apparent biologic therapy failure in PsA.