Fig. 6.

Proposed molecular basis for putative overlap between PsA and OA

A common factor is biomechanical stress, microdamage or both at the entheses in some types of OA and also in PsA. For pure PsA, with gain of function in immune system (e.g. CARD14 or IL36RA) genes, this may manifest as an exaggerated inflammatory response instead of a physiological level of inflammation involved in tissue repair with cells of the innate and adaptive immune system driving disease. At the other end of the spectrum, usually in older subjects, the same inciting events may manifest in a dominant tissue repair response in the same territories with pronounced remodelling. The proposal is that there may be overlap with involvement of both aberrant inflammation and remodelling pathways, giving a mixed phenotype or a scenario whereby it is impossible to state with certainty whether it is OA or PsA. IL36RA: interleukin-36 receptor antagonist; CARD: caspase recruitment domain family, member 14.