Yanagawa T, Watanabe H, Shinozaki T, Ahmed A R, Shirakura K, Takagishi K
Department of Orthopedic Surgery, Gunma University Faculty of Medicine, Maebashi, Gunma, Japan.
Clin Radiol. 2001 Nov;56(11):877-86. doi: 10.1053/crad.2001.0795.
We describe 27 cases of bone tumours or tumour-like lesions where there was spontaneous regression. The follow-up period was 2.8-16.7 years (average, 7.0 years). Fourteen of these cases were no longer visible on plain radiographs. Histological diagnosis included exostosis, eosinophilic granuloma, fibrous dysplasia, fibrous cortical defect, non-ossifying fibroma, osteoid osteoma and bone island. Most cases began to reduce in adolescence or earlier, although sclerotic type lesions showed their regression in older patients. All lesions thought to be eosinophilic granuloma began to regress after periods of less than 3 months, while the duration of the other lesions showed wide variation (1-74 months). As resolution of the lesions took between 2 and 79 months (mean, 25.0 +/- 20.3 months) we consider that the most likely mechanism was recovery of normal skeletal growth control. In exostosis with fracture, alteration of vascular supply may contribute to growth arrest, but not to subsequent remodelling stage. In inflammatory-related lesions such as eosinophilic granuloma, cessation of inflammation may be the mechanism of growth arrest, whilst temporary inflammation may stimulate osteogenic cells engaged in remodeling. In the sclerotic type, growth arrest is a less probable mechanism. Necrosis within the tumour and/or local changes in hormonal control, plus remodelling of the sclerotic area takes longer. Knowledge of the potential for spontaneous resolution may help in management of these tumour and tumour-like lesions of bone.
我们描述了27例发生自发消退的骨肿瘤或肿瘤样病变。随访期为2.8至16.7年(平均7.0年)。其中14例在X线平片上已不可见。组织学诊断包括骨疣、嗜酸性肉芽肿、骨纤维异常增殖症、纤维皮质缺损、非骨化性纤维瘤、骨样骨瘤和骨岛。大多数病例在青春期或更早开始缩小,不过硬化型病变在老年患者中才出现消退。所有被认为是嗜酸性肉芽肿的病变在不到3个月的时间后开始消退,而其他病变的持续时间差异很大(1至74个月)。由于病变的消退时间为2至79个月(平均25.0±20.3个月),我们认为最可能的机制是正常骨骼生长控制的恢复。在伴有骨折的骨疣中,血管供应的改变可能导致生长停滞,但对随后的重塑阶段没有影响。在嗜酸性肉芽肿等炎症相关病变中,炎症的停止可能是生长停滞的机制,而短暂的炎症可能刺激参与重塑的成骨细胞。在硬化型中,生长停滞是一种不太可能的机制。肿瘤内的坏死和/或激素控制的局部变化,加上硬化区域的重塑需要更长时间。了解自发消退的可能性可能有助于这些骨肿瘤和肿瘤样病变的管理。