Pediatr Nephrol (2011) 26:1937–1946 DOI 10.1007/s00467-010-1733-5 REVIEW The impact of inflammation on bone mass in children Wai W. Cheung & Jian-Ying Zhan & Kyung Hoon Paik & Robert H. Mak Received: 13 November 2009 / Revised: 30 November 2010 / Accepted: 1 December 2010 / Published online: 1 January 2011 # The Author(s) 2010. This article is published with open access at Springerlink.com Abstract Bone is a dynamic tissue. Skeletal bone integrity is maintained through bone modeling and remodeling. The mechanisms underlying this bone mass regulation are complex and interrelated. An imbalance in the regulation of bone remodeling through bone resorption and bone formation results in bone loss. Chronic inflammation influences bone mass regulation. Inflammation-related bone disorders share many common mechanisms of bone loss. These mechanisms are ultimately mediated through the uncoupling of bone remodel- ing. Cachexia, physical inactivity, pro-inflammatory cyto- kines, as well as iatrogenic factors related to effects of immunosuppression are some of the common mechanisms. Recently, cytokine signaling through the central nervous system has been investigated for its potential role in bone mass dysregulation in inflammatory conditions. Growing research on the molecular mechanisms involved in inflammation-induced bone loss may lead to more selective therapeutic targeting of these pathological signaling pathways. W. W. Cheung : R. H. Mak (*) Division of Pediatric Nephrology, Department of Pediatrics, University of California San Diego, 9500 Gilman Drive, Mail Code 0634, La Jolla, CA 92093-0634, USA e-mail: romak@ucsd.edu J.-Y. Zhan Children’s Hospital, Zhejiang University, Hangzhou, China K. H. Paik Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, South Korea Keywords Inflammation . Bone mass regulation . Osteodystrophy . Chronic kidney disease . End-stage renal disease Introduction Chronic inflammation influences bone mass regulation [1, 2]. The mechanisms underlying this bone mass regulation are complex and interrelated. Inflammation disorders, such as rheumatoid arthritis and inflammatory bowel disease, share many common mechanisms but also have unique features of bone mass dysregulation [1–4]. These mecha- nisms are ultimately mediated through the regulation of bone modeling and remodeling cycle [5, 6]. Bone modeling and bone remodeling Bone is a dynamic tissue designed to provide structural support and an important reservoir for mineral and hematopoietic cells [3]. Bone modeling adapts structure to loading by changing bone size and shape and so maintains bone strength [7]. Bone modeling is the sum of the activities of the endosteum and periosteum of bone to produce bone forms [8]. Bone modeling predominates during growth [9]. Bone formation and resorption are not coupled in time or space in skeletal modeling. This process results in an increase in bone diameter and modification of bone shape. Bone modeling results in new bone formed at a location different from the site of bone resorption [10]. Adolescence has been associated with accelerated bone maturation and bone modeling is responsible for approxi- mately 40% of peak skeletal mass [11]. Bone modeling is important for changes in cortical geometry during growth.