ARTHRITIS & RHEUMATOLOGY Vol. 68, No. 2, February 2016, pp 392–397 DOI 10.1002/art.39438 V C 2016, American College of Rheumatology BRIEF REPORT Association of Inflammation With Development of Erosions in Patients With Hand Osteoarthritis: A Prospective Ultrasonography Study Marion C. Kortekaas, 1 Wing-Yee Kwok, 2 Monique Reijnierse, 2 Theo Stijnen, 2 and Margreet Kloppenburg 2 Objective. To investigate the association between features of ultrasound-detected inflammation and de- velopment of erosive disease in patients with hand oste- oarthritis (OA) over 2.3 years of followup. Methods. The study group comprised 56 consecu- tive patients with hand OA (mean age 61 years, 86% female) fulfilling the American College of Rheumatolo- gy criteria. Effusion, synovial thickening, and power Doppler signal in all interphalangeal (IP) joints were assessed with ultrasonography, using standardized methods, at baseline and followup. Radiographs were scored at both time points for osteophytes/joint space narrowing using the Osteoarthritis Research Society International method and for erosive disease (E phase [erosive] and R phase [remodeling]) using the method described by Verbruggen and Veys. Erosion develop- ment was defined as progression from N phase (nor- mal) to E phase or R phase. Joints that were in E phase or R phase at baseline were excluded. Associations were analyzed using generalized estimating equations with adjustment for age, sex, body mass index, and baseline structural abnormalities. Results. At baseline, 51 IP joints (in 18 patients) and at followup 89 IP joints (in 26 patients) had erosions; thus, erosions developed in 38 IP joints. Moderate/severe synovial thickening and a power Doppler signal at base- line were associated with erosion development (adjusted odds ratio [OR] 8.8, 95% confidence interval [95% CI] 2.4–32.3 and OR 7.1, 95% CI 1.9–26.9, respectively). Persistent inflammation was particularly associated with the development of erosions. Conclusion. Ultrasound-detected features of inflam- mation are associated with the development of erosions in patients with hand OA, suggesting that inflammation plays a role in the pathogenesis of hand OA and could be a thera- peutic target. Erosive hand osteoarthritis (OA) is a subset of hand OA that is defined radiographically by subchondral central erosions, cortical destruction, and subsequent reparative change, which may rarely include bony anky- losis (1). Currently, the pathogenesis of erosive hand OA is not understood, and it is unclear whether erosive hand OA is a separate disease entity or reflects a severe disease stage. What we do know is that erosive OA has a high clinical burden and can progress relatively fast (2). Few studies have investigated the underlying mecha- nisms or risk factors associated with development of erosions. A sibpair study in patients with hand OA showed that erosion development clusters in patients and families (3). These studies showed that joints that were painful or showed soft tissue swelling or joint space narrowing (JSN) on radiographs were at especially high risk for the development of erosions over time (3,4). These findings suggest that underlying systemic process- es, such as inflammation, play a role in erosion develop- ment. Inflammation is often seen in erosive OA (5,6). A previous study showed that features of inflammation are more frequent in erosive compared with nonerosive hand OA (6,7), not only in joints with erosions, but also in joints without erosions (7). Therefore, the objective of the present study was to investigate the association between erosion development and ultrasound-detected features of inflammation in patients with hand OA. PATIENTS AND METHODS Patient population and OA diagnosis. Consecutive patients were recruited at the rheumatology outpatient clinic of the Leiden University Medical Center from May 2008 until January 2010. Followup visits took place between January 2011 and April 2012. Patients were included after providing informed consent; the 1 Marion C. Kortekaas, MD: Leiden University Medical Center, Leiden, The Netherlands, and Flevoziekenhuis, Almere, The Netherlands; 2 Wing-Yee Kwok, MD, PhD, Monique Reijnierse, MD, PhD, Theo Stijnen, PhD, Margreet Kloppenburg, MD, PhD: Leiden University Medical Center, Leiden, The Netherlands. Address correspondence to Marion C. Kortekass, MD, Depart- ment of Rheumatology, Leiden University Medical Center, PO Box 9600, 2300 RC, Leiden, The Netherlands. E-mail: m.c.kortekaas@lumc.nl. Submitted for publication November 29, 2014; accepted in revised form September 10, 2015. 392