Does intradiscal steroid injection accelerate the histological degeneration of the human disc?
10.1016/j.afos.2024.06.001
- Author:
Jin Hwan KIM
1
;
Sunhee CHANG
;
Byung Ho KIM
;
Gyu Heon LEE
;
Sung Tan CHO
Author Information
1. Department of Orthopaedic Surgery, Inje University Ilsan Paik Hospital, 170 Juhwa-ro, Ilsanseo-gu, Goyang-si, Gyeonggi-do, South Korea
- Publication Type:Original article
- From:Osteoporosis and Sarcopenia
2024;10(3):108-113
- CountryRepublic of Korea
- Language:English
-
Abstract:
Objectives:Intradiscal steroid injection (ISI) use has been proven as a low-risk and rapid treatment for disc degeneration disease (DDD). However, the histological effects of steroids on human discs remain poorly understood. The purpose of this study is to investigate whether ISI induces histologic degeneration of the disc.
Methods:In this study, a histological analysis was carried out on the nucleus pulposus obtained from 150 patients who underwent posterior lumbar interbody fusion. Among these individuals, 59 received ISI before the surgery, while 91 did not. After staining with hematoxylin and eosin, the histological classification was performed based on chondrocyte proliferation (C1, C2, and C3) and granular matrix change (M1 and M2). Logistic regression analysis was used to identify the main factors influencing chondrocyte proliferation and granular matrix change.Additionally, histological differences between the ISI group and the non-ISI group were analyzed.
Results:Chondrocyte proliferation and granular matrix changes were not significantly different between the ISI and non-ISI groups. The logistic regression analysis indicated that age is the most significant risk factor for both chondrocyte proliferation (P = 0.02) and granular matrix changes (P < 0.01).
Conclusions:The most crucial factor in disc degeneration is age. ISI does not accelerate the histological degeneration of chondrocyte proliferation and granular matrix. Therefore, the ISI could be considered as a histologically safe alternative in patients with DDD.
