ECTS2013 Poster Presentations Other diseases of bone and mineral metabolism (48 abstracts)
Circulating sclerostin level in patients with ossification of the posterior longitudinal ligament of the spine
Masafumi Kashii 1 , Yohei Matsuo 1 , Tsuyoshi Sugiura 1 , Takahito Fujimori 1 , Yukitaka Nagamoto 2 , Hirotsugu Honda 1 , Takashi Kaito 1 , Motoki Iwasaki 1 & Hideki Yoshikawa
1Osaka University Graduate School of Medicine, Suita, Osaka, Japan; 2Osaka National Hospital, Osaka, Japan.
Backgrounds: Ossification of the posterior longitudinal ligament (OPLL) is characterized by pathological ectopic ossification of the posterior longitudinal ligament. Development of OPLL induces compression myelopathy or radiculopathy by spinal stenosis and the loss of spinal flexibility by ankylosing spinal hyperosteosis (ASH). Although the etiology of OPLL has not been fully elucidated, systemic and local bone formation factors may play a role in the pathogenesis of OPLL. The SOST gene encoding sclerostin is an osteocyte derived negative regulator of bone formation. Sclerostin is a Wnt/β-catenin signal antagonist necessary for bone formation. There is no reports regarding the relationships between OPLL and sclerostin.
Objective: This study aim to compare serum sclerostin levels between OPLL patients and control patients, and to identify the relationship between serum sclerostin level and bone turnover markers, OPLL localization and numbers of ossified vertebra.
Methods: Seventy-eight OPLL patients were studied and compared with age and sex matched 39 control patients with spinal canal stenosis without OPLL. Serum sclerostin and Dickkopf-1 (Dkk1) levels were measured by ELISA.
Results: Serum sclerostin levels in OPLL patients is significant higher than controls (OPLL: mean 64.1, S.D 39.3 pmol/l; control: mean 44.9, S.D 17.7 pmol/l; P=0.005). On the other hand, serum Dkk1 level in OPLL patients is significant lower that controls (OPLL 2016±836 pmol/l, control 2394±959 pmol/l, P=0.03). In OPLL patients, the positive correlation between age and sclerostin levels was found in male OPLL patients (r=0.43, P=0.002). There are no relationship between serum sclerostin levels and bone turnover markers, OPLL localization and numbers of ossified vertebra.
Conclusion: Systemic secretion of sclerostin by osteocytes increased in OPLL patients with advancing age, and there will be a negative feedback system to suppress progression of OPLL and hyperosteosis by sclerostin in OPLL patients.
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Bone Abstracts
ISSN 2052-1219 (online)
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