High melatonin levels are related to spinal ossification in patients with ankylosing spondylitis. Issue 2 (3rd March 2020)

• Record Type: Journal Article
• Authors: Li, Yanshan; Cui, Xiaomeng; Li, Zunzhong; Jia, Qian; Jiang, Li; Zhang, Zhenchun; Lu, Qing; Wang, Jibo; Jiang, Lindi
• Is Part Of: Modern rheumatology. Volume 30:Issue 2(2020)
• Page Start: 373
• Page End: 378
• Publication Date: 2020-03-03
• Subjects: Ankylosing spondylitis -- cytokine -- melatonin -- mSASSS -- ossification; Rheumatology -- Periodicals; 616.723005
• DOI: 10.1080/14397595.2019.1601854
• Languages: English
• ISSNs: 1439-7595

Abstract

Abstract: Objectives: To investigate associations of serum melatonin with spinal ossification and cytokines in ankylosing spondylitis (AS). Methods: Serum was obtained from 52 AS patients and 25 healthy controls. Melatonin was measured by ELISA kit; bone morphogenetic protein (BMP)-2, dickkopf-related protein (Dkk)-1, IL-1β, IL-6, IL-17 and TNF-α concentrations were assayed using Luminex multiplex bead system. Osteocalcin and β isomer of C-terminal telopeptide of type I collagen (β-CTX) were measured using electrochemiluminescence immunoassay. Spinal damages were assessed using the modified Stoke Ankylosing Spondylitis Spinal Score (mSASSS) on radiographs. Results: Serum melatonin was significantly increased in AS patients. Serum melatonin correlated positively with mSASSS after multivariate adjustment for age and disease duration ( r = 0.70, p < .01). Patients with spinal bone bridge have higher levels of melatonin than those without spinal bone bridge [16.69 (4.65, 41.10) pg/ml vs. 7.43 (3.29, 15.30) pg/ml, p = .03]. The multiple linear regression analysis found that melatonin was a risk factor for spinal bone formation ( β = 0.35, p < .05). Additionally, melatonin correlated positively with osteocalcin ( r = 0.34, p = .04) and IL-1β ( r = 0.39, p = .04) in AS. Conclusion: Melatonin is increased in AS patients, especially in patients with spinal bone bridge. It suggests that melatonin may play an important role in the pathological osteogenesis of AS.