79 102 HE 1 102 45 44.1% 45 37 LCA 32 KP-1 5 KP-1 2 3 MRI 1-2 3 MRI 4 1
The role of chronic inflammation in pathogenesis of cervical spondylosis. Supervisor: Prof. Cai Qinlin, Prof. Wang Shaobo. Graduate student: Wang Shenglin Abstract Objective: To study whether the inflammation exists in herniated cervical intervertebral discs from patients with cervical spondylosis, the role of inflammation in pathogenesis of cervical spondylosis, the cause of inflammation, and its imageological signs. Method: 79 patients were studied, and 102 discs were obtained during operation. The 102 discs were used for histologic and immunohistochemical examination, and their clinical presents and images were studied. Results: (1) 45 discs(44.1%) were shown proliferating small vessels and inflammatory cells. The inflammation were all in the margin of herniated tissues of the discs. In the 45 inflammatory discs, 37 had many LCA-positive cells, and 32 discs were infiltrated by KP-1 positive cells. In the 57 discs which had no inflammation, 5 had KP-1 positive cartilage cells. (2) The course of patients with inflammation had significant difference with patients that had no inflammation; so do the spinal cord function improvement. (3) Inflammation was significantly correlated with special history of cervical spondylosis, cervical instability and special signs on MRI. Conclusion: (1) Patients with cervical 2
spondylosis have inflammation in the tissues of herniated discs, and most of the inflammatory cells were monocytes- macrophages and lymphocytes;(2) Cervical instability may be one of the causes of inflammation in the herniated discs; (3) The inflammation had its special signs in MRI; (4) Chronic inflammation participated in pathogenesis of cervical spondylosis. 3
[1] [2] [3 8] [9] (inflammation) 4
alteration exudation (proliferation) 5- NO TNF 1. 5
[6,10] [11 13] [10,14 15] Mc carron [14] 4 21 Olmarker K [15] 1 3 7 [16] -20 0 C 24 2 Olmarker K [15] 7 Mochida K [17] Bush K [18] 6
3 [2] Mochida K [17] Yasuma T [19] Yamashita K [20] Gd-DTPA( ) MRI Mochida K [17] MRI 7
Doita M [21] PBM PBM PBM Virri J [22] Haro H [23] -1 monocyte chemotactic protein-1 MCP-1 MCP-1 macrophage inflammatory protein-1 3 Doita M [24] Haro H [23] Kang JD [25] NO IL-6 Takahashi H [26] 8
IL-1 IL-6 TNF- Rand N [27] IL-6 IL-10 IL-6 IL-10 IL-1 GM-CSF - Haro H [23] CD14+ T- Habtemaridm A [28] CD68+ Saal J [6] CD45+ CD68+ [17] 1 2 3 9
Mochida K [17] 1 35 7 CD14+ Kanemoto M [29] [7] 51.4% - A2 PLA 2 NO E2(PGE 2 ) [15,25,30] IL MMPs 1 NO PGE 2 Kang JD [4] 18 NO PGE 2 NO PGE 2 NO [31] NO [4] 10
E2(PGE 2 ) [9] 2 IL-1,IL-6 TNF- MMPs [32] [7] IL-1 IL-6 TNF- Kang JD [4] IL-6 MMPs IL-1 IL-6 TNF- IL-1 MMPs IL-1 IL-6 TNF- [7] IL-1 A2 PLA 2 PLA 2 PLA 2 [6] Kang JD [25] IL-1 NO IL-6 PGE 2 MMPs TNF - [32] MMPs [21] MMP-1 MMP-3 [4 21] 11
1994 Maigne JY [33] 21 CT 5 0 35% 6 35 75% 10 75 100% CT Mochida K [17] MRI 38 15 40% MRI Bush K [18] 13 MRI 4 31 12 MRI 13 12 MRI Matsumoto M [34] 17 MRI 10 59% 12
MRI JOA 2 [2] [4 21] MMPs Doita M [21] TNF- IL-1 MMPs MMPs MMP-3 MMPs-7 TIMP-1( ) Mochida K [17] MRI Matsumoto M [34] Aprill BC [35] MRI T2 13
High-Intensity Zone, HIZ HIZ T2 HIZ MRI MRI HIZ MRI HIZ T2 Ito M [36] MRI T2 HIZ HIZ [2] MRI T1 T2 Rothoerl RD [37] Saal JS [6] [8] 55% Kang JD [4] NO IL-6 PGE2 Takahashi H [26] 14
1 Cooper RG [38] Gronblad M [39] 2 PLA 2 2 Mochida K [17] MRI 40% Maigne JY [33] CT Heithoff KB [40] CT MRI T1 MRI T2 MRI T2 15
[1] 1. 2. 3. 4 MRI [2] 16