ECTS2016 Poster Presentations Osteoporosis: pathophysiology and epidemiology (55 abstracts)
Effect of recent spinal cord injury on the OPG/RANKL system and its relationship with bone loss and antiosteoporotic response to denosumab therapy: preliminary results
Laia Gifre 1 , Joan Vidal 2 , Silvia Ruiz-Gaspà 3 , Enric Portell 2 , Ana Monegal 1 , Africa Muxi 4 , Nuria Guañabens 1, & Pilar Peris 1,
1Rheumatology Department, Metabolic Bone Diseases Unit, Hospital Clinic, Barcelona, Spain; 2Spinal Cord Unit, Neurorehabilitation Institute Guttmann, Badalona, Spain; 3CIBERehd. Hospital Clínic, Barcelona, Spain; 4Nuclear Medicine Department, Hospital Clínic, Barcelona, Spain.
The aims of this study were to analyze the role of the regulators of bone remodeling, OPG and RANKL, in the bone loss associated with recent spinal cord injury (SCI) as well as the effect of antiosteoporotic therapy with denosumab in these bone regulators in a prospective study.
Patients and methods: Twenty-three male patients (aged 18–67 years (mean 36±16 years)) with recent (<6 months) complete SCI were prospectively included (43.5% paraplegic, 53.5% tetraplegic). Serum levels of OPG and RANKL (Biomedica, Vienna, Austria), bone turnover markers (PINP, bone ALP, sCTX) and BMD were assessed at baseline (99±30 days after SCI), prior to initiating antiosteoporotic treatment (14±4 months post-SCI) and during antiosteoporotic therapy with denosumab (6 months after initiating treatment). The results were compared with a healthy control group.
Results: At baseline, SCI patients showed a significant increase in RANKL serum levels compared to controls (3.4±1.7 vs 2.3±1.6 pg/ml, P=0.022) which correlated with days-since-SCI (r=0.589, P=0.005) and became undetectable after denosumab treatment in 67% of the patients (P=0.001). OPG serum levels were similar to controls at baseline (87.7±38.7 vs 71.7±25.4, P=0.1) and did not change with denosumab treatment. No differences were observed in RANKL and OPG levels on comparing tetraplegic vs paraplegic patients. Neither were RANKL or OPG levels related to the increase in bone loss and bone turnover markers after SCI. Patients with undetectable RANKL serum levels after denosumab treatment did not present further sublesional bone loss but increased total hip BMD (+2.5±1.3%, P=0.005), and bone markers markedly decreased (PINP: −53%, P=0.007; sCTX: −68%, P=0.005).
Conclusion: This study shows that short-term after SCI there is an increase in RANKL serum levels which become undetectable after denosumab treatment. The preventive effect of denosumab on sublesional bone loss further suggests a contributory role of RANKL in this clinical process.
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Bone Abstracts
ISSN 2052-1219 (online)
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