Lian Øystein, Scott Alex, Engebretsen Lars, Bahr Roald, Duronio Vincent, Khan Karim
Oslo Sport Trauma Research Center, Department of Sports Medicine, Norwegian School of Sport Sciences, Ullevål Stadion, Oslo, Norway.
Am J Sports Med. 2007 Apr;35(4):605-11. doi: 10.1177/0363546506295702. Epub 2007 Jan 23.
The pathogenesis of tendon overuse injuries is poorly understood. The histopathology underlying tendinopathy at various anatomical locations is similar and may reflect a common pathologic process.
Apoptosis contributes to the pathophysiology in patellar tendinopathy.
Case control study; Level of evidence, 3.
We compared biopsy specimens from the patellar tendon in patients with patellar tendinopathy diagnosed clinically and with typical magnetic resonance image findings with biopsy specimens from a control group without any previous or current knee complaints to suggest patellar tendinopathy. The presence of apoptosis was examined with immunohistochemical methods using a polyclonal antibody recognizing active caspase-3, confirmed by labeling DNA strand breaks (F7-26 antibody) and nuclear morphology (fragmentation and condensation).
The number of apoptotic cells per unit area (4.5 mm(2)) was 0.91 +/- 0.81 (SD) in tendinopathic samples and 0.21 +/- 0.21 in controls (P = .026). Although the tendinopathic samples displayed increased cellularity (average 162.5 nuclei/mm(2) vs 98.9 nuclei/mm(2)), the apoptotic index was higher (0.42% vs 0.17%, P = .014).
Increased apoptotic cell death is a feature of patellar tendinosis. The role of apoptosis within the broader framework and time course of tendon overuse injury remains to be established.
肌腱过度使用损伤的发病机制尚不清楚。不同解剖部位肌腱病的组织病理学相似,可能反映了一个共同的病理过程。
细胞凋亡参与髌腱病的病理生理过程。
病例对照研究;证据等级,3级。
我们将临床诊断为髌腱病且磁共振成像表现典型的患者髌腱活检标本,与无既往或当前膝关节疾病提示髌腱病的对照组活检标本进行比较。使用识别活性半胱天冬酶-3的多克隆抗体,通过免疫组织化学方法检测细胞凋亡的存在,并通过标记DNA链断裂(F7-26抗体)和核形态(碎片化和凝聚)进行确认。
髌腱病样本中每单位面积(4.5平方毫米)的凋亡细胞数为0.91±0.81(标准差),对照组为0.21±0.21(P = 0.026)。尽管髌腱病样本显示细胞增多(平均162.5个细胞核/平方毫米对98.9个细胞核/平方毫米),但凋亡指数更高(0.42%对0.17%,P = 0.014)。
凋亡细胞死亡增加是髌腱病的一个特征。细胞凋亡在肌腱过度使用损伤的更广泛框架和时间进程中的作用仍有待确定。