Mutijima Eugène, De Maertelaer Viviane, Deprez Manu, Malaise Michel, Hauzeur Jean-Philippe
Department of Pathology, CHU Sart Tilman, Sart Tilman, 4000, Liège, Belgium,
Clin Rheumatol. 2014 Dec;33(12):1791-5. doi: 10.1007/s10067-014-2607-1. Epub 2014 Apr 15.
The pathogenesis of nontraumatic osteonecrosis (ON) remains unclear. Some studies have suggested that nontraumatic ON is attributed to increased osteocytic apoptosis. To test this hypothesis, a controlled study must compare the apoptosis of osteocytes and osteoblasts in cases of ON and osteoarthritis (OA). To assess either the localized or diffuse patterns of this increased osteocytic and osteoblastic apoptosis, we evaluated both the proximal and distal regions of necrotic areas. Femoral heads resected for total hip prosthesis were included for this study. Of these, 10 were ON cases-three were induced by corticosteroids, three by alcohol abuse, one resulted from trauma, one resulted from hyperlipemia, and two were idiopathic-10 were osteoarthritis cases, and 1 from a patient suffering from a subcapital fracture. The TUNEL reaction was used to detect the apoptosis in osteoblasts and osteocytes. A semi-quantitative evaluation was conducted, at both distal and proximal areas relative to the lesions, specifically in the area surrounding the necrotic region in the osteonecrosis cases, in the eburnated bone in the osteoarthritis cases, and in the subchondral bone fracture. The apoptosis of osteoblasts and osteocytes was statistically more frequent in the regions close to the necrotic areas in the ON group. No difference was found in the unpaired areas. In the ON group, no difference was found in terms of the etiological factors. During ON, the apoptosis of osteocytes and osteoblasts is increased proximally to the necrotic regions in the patients presenting with osteoarthritis and subcapital fractures. This increase was found not only in the corticosteroid-induced ON cases but also in the idiopathic and alcohol abuse- and trauma-induced ON cases.
非创伤性骨坏死(ON)的发病机制尚不清楚。一些研究表明,非创伤性ON归因于骨细胞凋亡增加。为验证这一假说,一项对照研究必须比较ON和骨关节炎(OA)病例中骨细胞和成骨细胞的凋亡情况。为评估这种骨细胞和成骨细胞凋亡增加的局部或弥漫模式,我们评估了坏死区域的近端和远端。本研究纳入了因全髋关节置换术而切除的股骨头。其中,10例为ON病例——3例由皮质类固醇引起,3例由酒精滥用引起,1例由创伤引起,1例由高脂血症引起,2例为特发性;10例为骨关节炎病例,1例来自股骨头下骨折患者。采用TUNEL反应检测成骨细胞和骨细胞中的凋亡情况。在相对于病变的远端和近端区域进行半定量评估,具体而言,在骨坏死病例的坏死区域周围、骨关节炎病例的硬化骨以及软骨下骨折处进行评估。ON组中,靠近坏死区域的区域内,成骨细胞和骨细胞的凋亡在统计学上更为频繁。在非配对区域未发现差异。在ON组中,病因方面未发现差异。在ON期间,骨关节炎和股骨头下骨折患者坏死区域近端的骨细胞和成骨细胞凋亡增加。这种增加不仅在皮质类固醇诱导的ON病例中发现,在特发性、酒精滥用和创伤诱导的ON病例中也有发现。