Qiu Shijing, Rao D Sudhaker, Palnitkar Saroj, Parfitt A Michael
Bone and Mineral Research Laboratory, Henry Ford Hospital, Detroit, Michigan 48202-2689, USA.
J Bone Miner Res. 2003 Sep;18(9):1657-63. doi: 10.1359/jbmr.2003.18.9.1657.
Iliac cancellous osteocyte density declines with age, but its relationship to vertebral fracture pathogenesis is unknown. We performed iliac bone biopsy in 44 women with clinical vertebral fracture and 56 healthy women. The fracture patients had 34% fewer osteocytes but no reduction in percent occupied lacunae. Some patients destined to sustain vertebral fracture make cancellous bone with fewer osteocytes.
Patient's with vertebral fracture have less bone than appropriate healthy controls, but other factors may contribute to bone fragility. Iliac cancellous osteocyte density declines with age in healthy women; we asked whether this variable differed between fracture patients and healthy controls.
Two groups of women were assembled. Forty-four (mean age, 66.2 years) had unequivocal evidence of bone fragility manifested as painful nontraumatic vertebral fracture, and 56 (mean age, 62.2 years) were skeletally healthy. All subjects underwent iliac bone biopsy. From archival embedded biopsy cores, new sections were stained with Goldner's trichrome, in which we enumerated osteocyte-occupied lacunae (stained), empty lacunae (unstained), and total lacunae per bone area.
Cancellous osteocyte density was 34% lower in the fracture group than in the controls (p < 0.001); this difference was not a consequence of higher turnover, having less bone, or the small difference in age. The area under the receiver operating characteristic (ROC) curve for discrimination between the groups was >90% for osteocyte density and <75% for bone volume/tissue volume (BV/TV). The disease-related osteocyte deficit was accompanied by a proportionate reduction in empty lacunae and no change in percent occupied lacunae; therefore, it was not the result of premature death. Both superficial bone (<25 microm from the surface) and deep bone (>45 microm from the surface) were affected. In contrast, the age-related deficit is accompanied by an increase in empty lacunae and fall in percent osteocyte-occupied lacunae and occurs only in deep bone, but not in superficial bone.
In some patients destined to sustain spontaneous vertebral compression fracture, iliac cancellous bone is made with fewer osteocytes than normal; the mechanism of osteocyte incorporation into bone needs more detailed study. Osteocyte deficiency could contribute to bone fragility, either by impairing the detection of fatigue microdamage or by reducing canalicular fluid flow. Current practices of defining vertebral fracture based on morphometry alone regardless of symptoms, and diagnosing osteoporosis based on bone densitometry alone regardless of fracture history, should be reexamined.
髂骨松质骨骨细胞密度随年龄下降，但其与椎体骨折发病机制的关系尚不清楚。我们对44例临床椎体骨折女性和56例健康女性进行了髂骨活检。骨折患者的骨细胞减少34%，但骨陷窝占有率无降低。一些注定会发生椎体骨折的患者形成的松质骨骨细胞较少。
椎体骨折患者的骨量低于适当的健康对照，但其他因素可能导致骨脆性增加。健康女性的髂骨松质骨骨细胞密度随年龄下降；我们询问该变量在骨折患者和健康对照之间是否存在差异。
组建两组女性。44例（平均年龄66.2岁）有明确的骨脆性证据，表现为疼痛性非创伤性椎体骨折，56例（平均年龄62.2岁）骨骼健康。所有受试者均接受髂骨活检。从存档的包埋活检芯中，新切片用Goldner三色染色，我们计算每骨面积中骨细胞占据的陷窝（染色）、空陷窝（未染色）和总陷窝数。
骨折组的松质骨骨细胞密度比对照组低34%（p<0.001）；这种差异不是由于更高的骨转换率、骨量减少或年龄差异小所致。用于区分两组的受试者工作特征（ROC）曲线下面积，骨细胞密度>90%，骨体积/组织体积（BV/TV）<75%。与疾病相关的骨细胞缺乏伴随着空陷窝的相应减少，骨陷窝占有率无变化；因此，这不是过早死亡的结果。表层骨（距表面<25微米）和深层骨（距表面>45微米）均受影响。相比之下，与年龄相关的缺乏伴随着空陷窝增加和骨细胞占据陷窝百分比下降，且仅发生在深层骨，而不在表层骨。
在一些注定会发生自发性椎体压缩骨折的患者中，髂骨松质骨的骨细胞比正常情况少；骨细胞整合到骨中的机制需要更详细的研究。骨细胞缺乏可能通过损害疲劳微损伤的检测或减少骨小管液流动而导致骨脆性增加。当前仅基于形态学定义椎体骨折而不考虑症状，以及仅基于骨密度测定诊断骨质疏松而不考虑骨折病史的做法，应重新审视。
