Introduction: The aetiology of polymyalgia rheumatica (PMR) is unknown. Recently, reports on cases of PMR following the coronavirus disease 2019 (COVID-19) have revived the role of infection as an aetiological or triggering factor. It is estimated that patients with PMR have manifestations of giant cell arteritis (GCA) in < 20% of cases. To date, little is known on the potential role of infectious agents in facilitating this association. Given this background, we performed a review of published literature. Our first aim was to review and discuss the relationship between PMR and infective agents. Secondly, we compared data of PMR-only patients with PMR and overlapping GCA to seek any commonalities or differences regarding the type of infectious agent in these two subgroups. Material and methods: We performed a non-systematic literature search on Embase and Medline (COVID interface) with the following search terms: "polymyalgia rheumatica" AND "infections" OR "infectious agents", both MESH headings and free-text (in each language they were written). Each paper's reference list was scanned for additional publications meeting this study's aim. When papers reported data partially presented in previous articles, we referred to the most recent published data. Abstracts submitted at conferences or from non-peer-reviewed sources were not included. Polymyalgia rheumatica following vaccinations was an additional exclusion criterion. Results: Several infectious agents have been held responsible for PMR. However, no definite causal link has been identified so far. According to our review, the search for a specific infectious agent, however intriguing, appears to be stagnating. Genetic background and epigenetic regulation probably play a key role. However, topical studies are lacking. Polymyalgia rheumatica as an adverse event following immunization should be kept methodologically distinct from PMR following an acute infection, as the adjuvants in the vaccine can make a significant difference. Conclusions: Finally, some infectious agents are able to replicate in human arteries or have an endothelium tropism. Whilst these can theoretically trigger GCA, their role in isolated PMR seems minimal.
