Most accepted definitions of reactive arthritis (ReA) consider it a type of spondyloarthritis (SpA) precipitated by a gut or urogenital infection. A wider definition considers any arthritis that occurs after a mucosal surface infection as ReA. There is limited consensus regarding a working definition, status of HLA-B27, or even classification criteria for ReA. This may also contribute to a lack of systemic studies or clinical trials for ReA, thereby reducing further treatment recommendations to expert opinions only. The emergence of post-COVID-19 ReA has brought the focus back on this enigmatic entity. Post-COVID-19 ReA can present at extremes of age, appears to affect both sexes equally and can have different presentations. Some present with small joint arthritis, others with SpA phenotype-either with peripheral or axial involvement, while a few have only tenosynovitis or dactylitis. The emergence of post-vaccination inflammatory arthritis hints at similar pathophysiology involved. There needs to be a global consensus on whether or not to include all such conditions under the umbrella of ReA. Doing so will enable studies on uniform groups on how infections precipitate arthritis and what predicts chronicity. These have implications beyond ReA and might be extrapolated to other inflammatory arthritides. Key Points • Classical reactive arthritis (ReA) has a spondyloarthritis phenotype and is preceded by symptomatic gut or urogenital infection • The demonstration of antigen and nucleic acid sequences of pathogens in synovium has blurred the difference between invasive arthritis and reactive arthritis • Post-COVID-19 ReA has a transient phenotype and can have different presentations. All reported cases are self-limiting • The large amount of literature reporting post-COVID-19 ReA calls for introspection if the existing definitions of ReA need to be updated.

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