Schnitzler C M, Mesquita J M, Gear K A, Robson H J, Moodley G P, Smyth A E
Department of Orthopaedic Surgery, University of the Witwatersrand, Johannesburg, South Africa.
J Bone Miner Res. 1990 Feb;5(2):141-52. doi: 10.1002/jbmr.5650050207.
We attempted to establish whether systemic changes in trabecular bone explain the development of stress fractures in the lower limbs during fluoride therapy for osteoporosis. To this end we compared transiliac bone biopsies obtained before treatment with those taken around the time of stress fractures after 14.3 +/- 10.9 (SD) months of therapy in six patients (group A). Biopsies from a comparable group of six patients without stress fractures at the time of the second biopsy (after 11.9 +/- 2.7 months of treatment) served for comparison (group B). The biopsies were processed undecalcified and examined by routine histomorphometry. The second biopsies did not show any significant improvement in mean bone volume or trabecular architecture. Although the second biopsies in group A had increased erosion surfaces (p less than 0.05) and greater osteoid volume (p less than 0.05), group B biopsies showed no difference in erosion surfaces but an increase in all osteoid parameters: osteoid volume (p less than 0.05), osteoid surface (p less than 0.05), and osteoid seam thickness (p less than 0.01). We reached the following conclusions: (1) the combination of increased erosion and replacement of removed bone by as yet unmineralized osteoid in the stress fracture group must have weakened bone and allowed the development of stress fractures. (2) Stress fracture patients may have mounted a less vigorous osteoblast response to fluoride than non-stress fracture patients. Under these conditions microfractures are likely to heal poorly and propagate to develop into full stress fractures. (3) Renal failure is a contraindication to fluoride therapy.
我们试图确定骨质疏松症氟化物治疗期间小梁骨的系统性变化是否能解释下肢应力性骨折的发生。为此,我们比较了6例患者(A组)在治疗14.3±10.9(标准差)个月后应力性骨折发生时所取的髂骨活检标本与治疗前获取的标本。另一组6例在第二次活检时(治疗11.9±2.7个月后)未发生应力性骨折的患者的活检标本用作对照(B组)。活检标本进行不脱钙处理,并采用常规组织形态计量学方法检查。第二次活检时,平均骨量或小梁结构均未显示出任何显著改善。虽然A组第二次活检时骨吸收表面增加(p<0.05)且类骨质体积增大(p<0.05),但B组活检标本的骨吸收表面无差异,而所有类骨质参数均增加:类骨质体积(p<0.05)、类骨质表面(p<0.05)和类骨质缝厚度(p<0.01)。我们得出以下结论:(1)应力性骨折组骨吸收增加以及未矿化类骨质替代被吸收骨的情况必然削弱了骨骼,并导致应力性骨折的发生。(2)与非应力性骨折患者相比,应力性骨折患者对氟化物的成骨细胞反应可能较弱。在这种情况下,微骨折可能愈合不良并发展为完全性应力性骨折。(3)肾衰竭是氟化物治疗的禁忌证。