New insights into IL‑17/IL‑23 signaling in ankylosing spondylitis (Review)
Beatrice Andreea Chisălau, Laura-Ioana Cr�nguș, Florentin Ananu Vreju, Cristina P�rvănescu, Sineta Cristina Firulescu, Ștefan Cristian Dinescu, Dana Ciobanu, Andrei Adrian Tica, Raluca Elena Sandu, Isabela Siloşi, Mihail Virgil Boldeanu, Ioan Sabin Poenariu, Anca Ungureanu, Lidia Boldeanu, Andreea Lili Bărbulescu
Abstract
Ankylosing spondylitis (AS) is a progressive common autoimmune inflammatory disease, part of the spondylarthritis group, characterized, besides clinical spinal and peripheral joint inflammation, by enthesitis and new bone formation, that can lead to severe functional impairment. Beyond intensive and continuous research on the pathogenic process extensively performed in recent years, their impact on therapeutic management remains open to future development. Better knowledge of AS pathogenesis have shown results progressively and studies are being performed to advance our current understanding of the disease. It is well known that tumor necrosis factor (TNF) exerts a central role, along with interleukin-17 (IL-17) and interleukin-23 (IL-23), demonstrated by several clinical studies. Similar to other rheumatic inflammatory conditions, SA is associated with an early process of systemic bone loss, both trabecular and cortical, consecutive osteopenia, osteoporosis, and high fracture risk. Current personalized therapeutic options benefit from new published data, to prevent future complications and to improve quality of life.