POS1329 A COHORT STUDY ON THE RISK OF DEVELOPING OBSTRUCTIVE SLEEP APNEA, TEMPOROMANDIBULAR JOINT DISORDERS AND CRANIOFACIAL DEFORMITIES IN PATIENTS WITH JUVENILE IDIOPATHIC ARTHRITIS

Background: Juvenile Idiopathic Arthritis (JIA), an autoimmune disease, has been proposed to be comorbid with obstructive sleep apnea (OSA). Objectives: We aimed at identifying the relationship between JIA and OSA. Methods: We performed a cohort study including JIA and OSA patients from 1999 to 2013. A total of 2791 patients diagnosed with OSA after JIA onset were recruited, which 11,164 eligible individuals without JIA history were selected as matched-controls. A Cox proportional hazard model was developed to estimate the risk of OSA in JIA patients. A cumulative probability model was adopted to assess the time-dependent effect of JIA on OSA development, implying the casual link of the association. To identify whether JIA patients have higher risks for developing temporomandibular joint (TMJ) disorders, craniofacial anomalies and deformities than non-JIA individuals, subgroup analyses was conducted. Finally, Ingenuity Systems Pathway Analysis (IPA) was conducted to identify underlying mechanisms of the above disease correlation among peripheral blood mononuclear cells (PBMCs) from rheumatic factor (RF)-positive and RF-negative JIA patients, and subcutaneous fat tissues from OSA patients, using p-value visualization for RNA-seq analyses. Results: The Cox proportional hazard model showed that JIA patients were more likely to have OSA than non-JIA individuals (adjusted hazard ratio =1.949, 95% CI =1.264–3.005). The incidence of developing OSA was particularly high among patients who developed JIA aged 18-30 years old (aHR= 2.034, 95% CI=1.305-3.169) and males (aHR=1.82, 95% CI=1.121-2.954). The risk of developing OSA increased within 0-36 months (aHR = 2.216, 95% CI = 1.001 – 4.907) and over 60 months (aHR = 2.558, 95% CI = 1.346 – 4.860) of follow-up duration after JIA onset. Subgroup analyses showed that JIA patients were more likely to have TMJ disorders (relative risk = 2.047, 95% CI = 1.446-2.898) and to receive treatment for craniofacial deformities (RR = 1.722, 95% CI = 1.38-2.148) than non-JIA controls. IPA analyses suggested that the underlying mechanisms involved activation of antigen presentation pathway followed by antigen presentation to CD4+ and CD8+ T lymphocytes, as well as B cell development. Conclusion: Our findings identified high risks of developing OSA, TMJ disorders, and craniofacial deformities following JIA onset, which the underlying mechanisms may involve both cellular and humoral immunity. Disclosure of Interests: None declared