Levels of neuropeptide Y in synovial fluid relate to pain in patients with knee osteoarthritis

BMC Musculoskeletal Disorders

William Weijia Lu⁴  Minmin Lv³  Songlin Peng⁵  Haobo Pan³  Li Zhang¹  Lei Wang² 

[1]Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Science, 1068 Xueyuan Avenue, Shenzhen 518055, China

[2]Department of Orthopedic Surgery, People’s Hospital of Hangzhou, Nanjing Medical University, 261 Huansha Road, Hangzhou 310006, China

[3]Center for Human Tissues and Organs Degeneration, Shenzhen Institute of Advanced Technology, Chinese Academy of Science, 1068 Xueyuan Avenue, 518055 Shenzhen, China

[4]Department of Orthopaedics and Traumatology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, China

[5]Department of Orthopedic Surgery, People’s Hospital of Shenzhen, Jinan University Second College of Medicine, 1017 Dongmen North Road, Shenzhen 518020, China

关键词: Regulator;    Radioimmunoassay;    Synovia;    Arthrophlogosis;    Pathogenesis;   

Others  :  1122043
DOI  :  10.1186/1471-2474-15-319

 received in 2014-01-15, accepted in 2014-09-23,  发布年份 2014

【 摘 要 】

Background

The precise etiology of knee osteoarthritis (KOA) pain remains highly controversial and there is no known effective treatment. Due to the known and suggested effects of neuropeptide Y (NPY) on pain, we have sought to investigate the relationship between the concentration of NPY in synovial fluid of knee, pain of KOA, and structural severity of KOA.

Methods

One hundred KOA patients and twenty healthy participants (control group) were recruited. The pain and the radiographic grade of KOA were assessed separately by Hideo Watanabe’s pain score and Tomihisa Koshino’s scoring system. Synovial fluid of knee from all participants was collected with arthrocentesis. Radioimmunoassay was used to examine the concentration of NPY in synovial fluid of knee.

Results

Concentrations of NPY in synovial fluid were significantly higher in KOA patients (124.7 ± 33.4 pg/mL) compared with controls (64.8 ± 26.3 pg/mL) (p = 0.0297). According to Hideo Watanabe’s pain score, 100 KOA patients were divided into 5 subgroups: no pain (n = 12), mild pain (n = 25), moderate pain (n = 37), strong pain (n = 19) and severe pain (n = 7). Within the KOA group, significantly higher concentrations of NPY were found in each subgroup as pain intensified (no pain 81.4 ± 11.7 pg/mL, mild pain 99.1 ± 23.2 pg/mL, moderate pain 119.9 ± 31.5 pg/mL, strong pain 171.2 ± 37.3 pg/mL and severe pain 197.3 ± 41.9 pg/mL). Meanwhile, according to Tomihisa Koshino’s scoring system, 100 KOA patients were divided into 3 subgroups: early stage (n = 30), middle stage (n = 53), advanced stage (n = 17). Concentrations of NPY in middle and advanced stage groups of KOA patients were significant higher than early stage group of KOA patients (early stage 96.4 ± 27.1 pg/mL, middle stage 153.3 ± 16.9 pg/mL, advanced stage 149.5 ± 36.7 pg/mL) (p = 0.0163, p = 0.0352). Concentrations of NPY in advanced stage group of KOA patients has no significant difference compare with middle stage group of KOA patients (p = 0. 2175).

Conclusions

This study demonstrated the presence and variation of concentrations of NPY in the KOA joint fluid, suggesting a role for NPY as a putative regulator of pain transmission and perception in KOA pain.

【 授权许可】

   
2014 Wang et al.; licensee BioMed Central Ltd.

【 图 表 】

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