Seeman E
Department of Endocrinology, Austin and Repatriation Medical Centre, University of Melbourne, Heidelberg, Australia.
Baillieres Clin Rheumatol. 1997 Aug;11(3):613-29. doi: 10.1016/s0950-3579(97)80023-4.
Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The public health burden will increase as the increase in the numbers of elderly men in the community increases. In addition, the age-specific incidence of hip fractures may be increasing in some, but not all, countries. Vertebral fractures may be a public health problem as recent studies suggest that the prevalence in the community is 20-30%, similar to that reported in women. Forearm fractures should probably not be regarded as a public health problem. Peak bone mass is higher in men than women because men have bigger bones. Peak bone mineral density is the same. The amount of trabecular bone lost at the spine and iliac crest during ageing is similar in men and women. Cortical bone loss is less in men because endocortical resorption is less and periosteal formation is greater. Bone loss accelerates in elderly men because endocortical resorption and increasing cortical porosity increase the surface available for resorption. Bone fragility is less in men than women because: (a) the cross-sectional surface of the bone is larger; (b) trabecular bone loss is less as a percentage of the higher peak bone mass; (c) trabecular bone loss occurs by thinning rather than perforation; and (d) periosteal appositional growth compensates for endocortical resorption by maintaining the bending strength of bone. Reduced BMD in men with fractures may be due to reduced peak bone size and mass, and bone loss. Bone loss occurs by reduced bone formation. Whether men with fractures have increased bone fragility due to reduced periosteal appositional growth during ageing is unknown. The age-related decline in testosterone, adrenal androgens, growth hormone, and insulin-like growth factor 1 may contribute to reduced bone formation and bone loss. Men with vertebral fractures often have hypogonadism or illnesses with few clinical features that should be considered with a high index of suspicion (alcoholism, myeloma, malabsorption, primary hyperparathyroidism, haemochromatosis, Cushing's disease). Secondary hyperparathyroidism may contribute to bone loss by activating bone turnover and so increasing the number of bone remodelling units with impaired bone formation in each. There is no proven treatment for osteoporosis in men because there have been no trials using anti-fracture efficacy as an end point. Testosterone replacement should be considered in men with proven hypogonadism and vitamin D deficiency should be corrected if present. Calcium supplements and bisphosphonates are reasonable options given the lack of information.
男性髋部骨折占所有髋部骨折的三分之一，且死亡率高于女性。随着社区老年男性数量的增加，公共卫生负担也将加重。此外，在一些（但并非所有）国家，特定年龄段的髋部骨折发病率可能正在上升。椎体骨折可能是一个公共卫生问题，因为最近的研究表明，社区中的患病率为20% - 30%，与女性报告的患病率相似。前臂骨折可能不应被视为一个公共卫生问题。男性的峰值骨量高于女性，因为男性的骨骼更大。峰值骨矿物质密度相同。男性和女性在衰老过程中脊柱和髂嵴处小梁骨丢失的量相似。男性的皮质骨丢失较少，因为骨内膜吸收较少且骨膜形成较多。老年男性的骨丢失加速，因为骨内膜吸收和皮质孔隙率增加会增加可用于吸收的表面积。男性的骨脆性低于女性，原因如下：(a) 骨骼的横截面积更大；(b) 小梁骨丢失占较高峰值骨量的百分比更小；(c) 小梁骨丢失是通过变薄而非穿孔发生的；(d) 骨膜的附加生长通过维持骨骼的弯曲强度来补偿骨内膜吸收。骨折男性的骨密度降低可能是由于峰值骨大小和骨量减少以及骨丢失所致。骨丢失是由于骨形成减少。骨折男性是否因衰老过程中骨膜附加生长减少而导致骨脆性增加尚不清楚。睾酮、肾上腺雄激素、生长激素和胰岛素样生长因子1与年龄相关的下降可能导致骨形成减少和骨丢失。椎体骨折的男性通常患有性腺功能减退或一些临床特征不明显的疾病，对此应高度怀疑（酗酒、骨髓瘤、吸收不良、原发性甲状旁腺功能亢进、血色素沉着症、库欣病）。继发性甲状旁腺功能亢进可能通过激活骨转换导致骨丢失，从而增加每个骨重塑单位中骨形成受损的数量。由于尚未有以抗骨折疗效为终点的试验，因此男性骨质疏松尚无经证实的治疗方法。对于已证实患有性腺功能减退的男性应考虑睾酮替代治疗，如有维生素D缺乏应予以纠正。鉴于缺乏相关信息，补充钙和使用双膦酸盐是合理的选择。
