Croucher P I, Vedi S, Motley R J, Garrahan N J, Stanton M R, Compston J E
Department of Medicine, University of Cambridge Clinical School, Addenbrooke's Hospital, UK.
Osteoporos Int. 1993 Sep;3(5):236-41. doi: 10.1007/BF01623826.
The pathophysiology of bone loss associated with inflammatory bowel disease has not been clearly defined. In this study we have performed a detailed histomorphometric analysis of iliac crest bone obtained from 19 patients with inflammatory bowel disease in whom a diagnosis of osteoporosis had been made. Eleven subjects were receiving prednisolone at the time of their biopsy. Comparison with control values demonstrated a highly significant reduction in trabecular bone area in the patient group (p < 0.001). Wall width, adjusted appositional rate and bone formation rate were all significantly reduced in the patient group (p < 0.001) and the formation period was significantly increased (p < 0.001). Resorption cavities were slightly smaller in the patient group, differences in maximum cavity depth and cavity length achieving statistical significance (p < 0.005 and p < 0.05 respectively). The mineral appositional rate was significantly reduced in the patients with inflammatory bowel disease (p < 0.001) and the mineralization lag time significantly increased (p < 0.001); however, osteoid area, perimeter and seam width were not significantly different from controls. These results demonstrate that osteoporosis associated with inflammatory bowel disease is characterized by reduced bone formation at the cellular and tissue level; the proportionately greater change in wall width than in resorption cavity depth is consistent with a negative remodelling balance. Although none of the patients had osteomalacia as defined by the criteria of increased osteoid seam width and mineralization lag time, the higher mineralization lag time in the patient group indicates a mild mineralization defect.
炎症性肠病相关骨质流失的病理生理学尚未明确界定。在本研究中,我们对19例已诊断为骨质疏松症的炎症性肠病患者的髂嵴骨进行了详细的组织形态计量学分析。11名受试者在活检时正在接受泼尼松龙治疗。与对照值比较显示,患者组小梁骨面积显著减少(p < 0.001)。患者组的壁宽、调整后的贴壁率和骨形成率均显著降低(p < 0.001),而形成期显著延长(p < 0.001)。患者组的吸收腔略小,最大腔深度和腔长度的差异具有统计学意义(分别为p < 0.005和p < 0.05)。炎症性肠病患者的矿物质贴壁率显著降低(p < 0.001),矿化延迟时间显著延长(p < 0.001);然而,类骨质面积、周长和骨缝宽度与对照组无显著差异。这些结果表明,炎症性肠病相关的骨质疏松症在细胞和组织水平上的特征是骨形成减少;壁宽相对于吸收腔深度的变化更大,这与负性重塑平衡一致。虽然根据类骨质骨缝宽度增加和矿化延迟时间的标准,没有患者患有骨软化症,但患者组较高的矿化延迟时间表明存在轻度矿化缺陷。