Inflammation and glucose homeostasis are associated with specific structural features among adults without knee osteoarthritis: a cross-sectional study from the osteoarthritis initiative.

Alina C Stout, Mary F Barbe, Charles B Eaton, Mamta Amin, Fatimah Al-Eid, Lori Lyn Price, Bing Lu, Grace H Lo, Ming Zhang, Jincheng Pang, Timothy E McAlindon, Jeffrey B Driban

Journal: BMC musculoskeletal disorders 2018;19(1):1

PMID: 29304778

Plain Language Summary

plain language summary logo

Individuals with osteoarthritis (OA) typically present with greater systemic inflammation and impaired glucose homeostasis. Currently it is unclear whether these factors are associated with early-stage OA, namely bone marrow lesions and swelling. The purpose of this cross-sectional study was to investigate the role of inflammation and glucose homeostasis in early-stage OA. Using baseline data from the Osteoarthritis Initiative, 343 participants were enrolled and tested for markers of inflammation and impaired glucose homeostasis. Bone marrow lesions and swelling were also assessed through imaging results. Results indicate that among individuals without OA, those with greater systemic inflammation were more likely to have bone marrow lesions and knee swelling. According to these results, the authors conclude that systemic inflammation and glucose homeostasis are related to structural features of osteoarthritis. Future studies should explore whether these factors are predictive of OA in order to identify therapeutic targets to prevent or delay the onset of knee OA.

Abstract

BACKGROUND

Greater age and body mass index are strong risk factors for osteoarthritis (OA). Older and overweight individuals may be more susceptible to OA because these factors alter tissue turnover in menisci, articular cartilage, and bone via altered glucose homeostasis and inflammation. Understanding the role of inflammation and glucose homeostasis on structural features of early-stage OA may help identify therapeutic targets to delay or prevent the onset of OA among subsets of adults with these features. We examined if serum concentrations of glucose homeostasis (glucose, glycated serum protein [GSP]) or inflammation (C-reactive protein [CRP]) were associated with prevalent knee bone marrow lesions (BMLs) or effusion among adults without knee OA.

METHODS

We conducted a cross-sectional study using baseline data from the Osteoarthritis Initiative. We selected participants who had no radiographic knee OA but were at high risk for knee OA. Blinded staff conducted assays for CRP, GSP, and glucose. Readers segmented BML volume and effusion using semi-automated programs. Our outcomes were prevalent BML (knee with a BML volume > 1 cm) and effusion (knee with an effusion volume > 7.5 cm). We used logistic regression models with CRP, GSP, or glucose concentrations as the predictors. We adjusted for age, sex, body mass index (BMI), and Physical Activity Scale for the Elderly (PASE) scores.

RESULTS

We included 343 participants: mean age = 59 ± 9 years, BMI = 27.9 ± 4.5 kg/m, PASE score = 171 ± 82, and 64% female. Only CRP was associated with BML prevalence (odds ratio [OR] = 1.43, 95% confidence interval [CI] = 1.09 to 1.87). For effusion, we found an interaction between BMI and CRP: only among adults with a BMI <25 kg/m was there a significant trend towards a positive association between CRP and effusion (OR = 1.40, 95% CI = 1.00 to 1.97). We detected a U-shaped relationship between GSP and effusion prevalence. Fasting glucose levels were not significantly associated with the presence of baseline effusion or BML.

CONCLUSIONS

Among individuals without knee OA, CRP may be related to the presence of BMLs and effusion among normal weight individuals. Abnormal GSP may be associated with effusion. Future studies should explore whether inflammation and glucose homeostasis are predictive of symptomatic knee OA.

Address: Division of Rheumatology, Tufts Medical Center, 800 Washington Street, Box #406, Boston, MA, 02111, USA.; Department of Anatomy and Cell Biology, Temple University School of Medicine, 3500 North Broad Street, Philadelphia, PA, 19140, USA.; Center for Primary Care and Prevention, Alpert Medical School of Brown University, 111 Brewster Street, Pawtucket, RI, 02860, USA.; The Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, 800 Washington Street, Box #63, Boston, MA, 02111, USA.; Tufts Clinical and Translational Science Institute, Tufts University, 800 Washington Street, Box #63, Boston, MA, 02111, USA.; Brigham & Women's Hospital and Harvard Medical School, 75 Francis Street PBB-B3, Boston, MA, 02115, USA.; Medical Care Line and Research Care Line, Houston Health Services Research and Development (HSR&D) Center of Excellence Michael E. DeBakey VAMC, 2002 Holcombe Blvd, Houston, TX, 77030, USA.; Section of Immunology, Allergy, and Rheumatology, Baylor College of Medicine, 1 Baylor Plaza, BCM-285, Houston, TX, 77030, USA.; Department of Electrical Engineering, Tufts University, 161 College Avenue, Medford, MA, 02155, USA.; Division of Rheumatology, Tufts Medical Center, 800 Washington Street, Box #406, Boston, MA, 02111, USA. [email protected].
Bant logo

© Copyright 2026, Nutrition Evidence

NED wishes to thank the following organisations for their support:

We use cookies to improve your experience and analyze site traffic with Google Analytics. By continuing to use our site, you agree to our use of cookies. Learn more.