The correlation between inflammatory markers and bone turnover markers in acute Charcot neuro-osteoarthropathy

doi:10.3969/j.issn.1009-976X.2015.03.019

Abstract

Abstract: 【Abstract】〓Objective〓To investigate the correlation between serum level of inflammatory markers and serum level of bone turnover markers in patients with acute Charcot neuro-osteoarthropathy (CNO). Methods〓Data of 15 patients with acute CNO in our hospital from January 2010 to December 2014 was retrospectively analyzed. Serum level of inflammatory markers and bone turnover markers were recorded and correlation analyses were conducted. Results〓Levels of serum TNF-α, β-crosslaps, N-MID osteocalcin (N-MID.Os), procollagen type I amino-terminal propeptide (PINP) and bone alkaline phosphatase (BALP) were increased in acute CNO patients. Serum TNF-α was positively correlated to β-crosslaps, N-MID.Os, PINP and BALP, while IL-10 was negatively correlated to N-MID.Os, PINP and BALP. In addition, IL-6, IL-8 and IL-1β were not associated with bone turnover markers. Conclusion〓The abnormal level of TNF-α and bone turnover markers in acute CNO patients revealed inflammatory joint disease with bone metabolism derangement. The correlationship of TNF-α and bone turnover markers might specifically be found in acute CNO patients, which could be valuable in early clinical diagnosis of CNO.

Key words: Charcot neuro-osteoarthropathy, Inflammatory, Bone turnover, Correlation analysis

摘要： 【摘要】目的探讨Charcot神经性骨关节病(CNO)急性期患者临床检验中炎症指标与骨转换率的相关性。方法对2010年1月至2014年12月在我院住院的15例确诊为CNO急性期的患者进行回顾性分析,记录患者入院时炎症指标及骨转换指标,分析两者之间的相关性。结果 CNO患者血清TNF-α以及多项成骨及骨吸收指标均有上升,且TNF-α与β-胶原降解产物(β-crosslaps)、N端骨钙素(N-MID.Os)、总I型胶原氨基端前肽(PINP)以及骨碱性磷酸酶(BALP)均成正相关;IL-10与N-MID.Os、PINP及BALP均成负相关;IL-6、IL-8及IL-1β与骨转换指标没有明显相关性。结论〓CNO患者血清中TNF-α与多项骨转换指标的异常提示炎症性关节病的存在及骨代谢的紊乱,成骨及破骨活性均增强。TNF-α与多项骨转换指标相关,该相关性可能特异存在于炎症性骨关节病中,可能为CNO的早期诊断提供一定的价值。

关键词: Charcot神经性骨关节病, 炎症, 骨转换, 相关性分析

CLC Number:

R684

Chen Binghao, Song Weidong. The correlation between inflammatory markers and bone turnover markers in acute Charcot neuro-osteoarthropathy[J]. Lingnan Modern Clinics in Surgery, 2015, 15(03): 311-315.

陈炳豪宋卫东. Charcot神经性骨关节病急性期炎症指标与骨转换率的相关性分析[J]. 岭南现代临床外科, 2015, 15(03): 311-315.

References

[1]Molines L, Darmon P, Raccah D.Charcot's foot: newest findings on its pathophysiology,diagnosis and treatment[J].Diabetes Metab, 2010, 36(4):251-255
[2]Jeffcoate W J, Game F, Cavanagh P R.The role of proinflammatory cytokines in the cause of neuropathic osteoarthropathy (acute Charcot foot) in diabetes[J].Lancet, 2005, 366(9502):2058-2061
[3] Charcot J.Sur quelques arthropathies qui paraissent dépendre d’une lésion du cerveau ou de la moelle épinière[J].Arch Physiol Norm Pathol, 1868, 1(1):161-178
[4]Dissanayake S U, Bowling F L, Jude E B.The diabetic Charcot foot[J].Curr Diabetes Rev, 2012, 8(3):191-194
[5]Fabrin J, Larsen K, Holstein P E.Long-term follow-up in diabetic Charcot feet with spontaneous onset[J].Diabetes Care, 2000, 23(6):796-800
[6]Thompson P, Hanson D, Langemo D K, et al.Diabetic foot: Charcot neuropathic osteoarthropathy[J].Adv Skin Wound Care, 2009, 22(2):72-73
[7]Sommer T C, Lee T H.Charcot foot: the diagnostic dilemma[J].Am Fam Physician, 2001, 64(9):1591-1598
[8]Mabilleau G, Edmonds M E.Role of neuropathy on fracture healing in Charcot neuro-osteoarthropathy[J].J Musculoskelet Neuronal Interact, 2010, 10(1):84-91
[9]Mabilleau G, Petrova N, Edmonds M E, et al.Number of circulating CD14-positive cells and the serum levels of TNF-alpha are raised in acute charcot foot[J].Diabetes Care, 2011, 34(3):e33-34
[10] Solus J F, Chung C P, Oeser A, et al.Genetics of serum concentration of IL-6 and TNFα in systemic lupus erythematosus and rheumatoid arthritis: a candidate gene analysis[J]., 2015, :-
[11]于卫永，徐建民，孙进，等.关节病的影像学表现[J].中国康复理论与实践, 2010, 16(11):1018-1020
[12]Azuma Y, Kaji K, Katogi R, et al.Tumor necrosis factor-alpha induces differentiation of and bone resorption by osteoclasts[J].J Biol Chem, 2000, 275(7):4858-4864
[13]Kobayashi K, Takahashi N, Jimi E, et al.Tumor necrosis factor alpha stimulates osteoclast differentiation by a mechanism independent of the ODFRANKL-RANK interaction[J].J Exp Med, 2000, 191(2):275-286
[14] Kitaura H, Kimura K, Ishida M, et al.Immunological Reaction in TNF-α-Mediated Osteoclast Formation and Bone Resorption In Vitro and In Vivo[J]., 2013, 2013:1-8
[15]Kim N, Kadono Y, Takami M, et al.Osteoclast differentiation independent of the TRANCE-RANK-TRAF6 axis[J].J Exp Med, 2005, 202(5):589-595
[16]Hess K, Ushmorov A, Fiedler J, et al.TNFalpha promotes osteogenic differentiation of human mesenchymal stem cells by triggering the NF-kappaB signaling pathway[J].Bone, 2009, 45(2):367-376
[17]Briolay A, Lencel P, Bessueille L, et al.Autocrine stimulation of osteoblast activity by Wnt5a in response to TNF-alpha in human mesenchymal stem cells[J].Biochem Biophys Res Commun, 2013, 430(3):1072-1077
[18]Glass G E, Chan J K, Freidin A, et al.TNF-alpha promotes fracture repair by augmenting the recruitment and differentiation of muscle-derived stromal cells[J].Proc Natl Acad Sci U.S. A, 2011, 108(4):1585-1590
[19]Lu Z, Wang G, Dunstan C R, et al.Short-term exposure to tumor necrosis factor-alpha enables human osteoblasts to direct adipose tissue-derived mesenchymal stem cells into osteogenic differentiation[J].Stem Cells Dev, 2012, 21(13):2420-2429
[20] Zhang Q, Chen B, Yan F, et al.Interleukin-10 Inhibits Bone Resorption: A Potential Therapeutic Strategy in Periodontitis and Other Bone Loss Diseases[J]., 2014, 2014:1-5
[21]Fujioka K, Kishida T, Ejima A, et al.Inhibition of osteoclastogenesis by osteoblast-like cells genetically engineered to produce interleukin-10[J].Biochemical and Biophysical Research Communications, 2015, 456(3):785-791
[22]Carrasco R, Lovell D J, Giannini E H, et al.Biochemical markers of bone turnover associated with calcium supplementation in children with juvenile rheumatoid arthritis: Results of a double-blind,placebo-controlled intervention trial[J].Arthritis & Rheumatism, 2008, 58(12):3932-3940