POST-VIRAL ACCELERATION OF STRUCTURAL DAMAGE IN AXIAL SPONDYLOARTHRITIS: A BIOMARKER-BASED EVALUATION OF CARTILAGE TURNOVER FOLLOWING SARS-COV-2 INFECTION

Abstract

The emergence of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in late 2019 initiated an unprecedented global health crisis. Coronavirus disease 2019 rapidly evolved into a pandemic, affecting hundreds of millions of individuals and resulting in millions of deaths worldwide. While the acute respiratory manifestations of the infection initially dominated clinical attention, it soon became evident that COVID-19 represents a systemic inflammatory condition capable of affecting multiple organ systems. Beyond pulmonary complications, SARS-CoV-2 infection has been associated with cardiovascular injury, thromboembolic phenomena, neurological dysfunction, autoimmune activation, and prolonged post-viral syndromes. Of particular concern has been its impact on patients with pre-existing chronic inflammatory diseases.

Axial spondyloarthritis, including its radiographic form commonly referred to as ankylosing spondylitis, is a chronic immune-mediated inflammatory disorder characterized by inflammation of the sacroiliac joints and spine. The disease involves complex interactions between genetic susceptibility, innate immune activation, and cytokine-mediated inflammation, leading to progressive structural remodeling of the axial skeleton. Enthesitis, osteitis, cartilage degradation, and subsequent pathological new bone formation contribute to spinal rigidity and functional impairment. Because axial spondyloarthritis is fundamentally driven by dysregulated immune pathways, the superimposition of a systemic viral infection such as COVID-19 raises important questions regarding potential disease exacerbation, structural progression, and biomarker alterations..