Seeman E
Austin Hospital, University of Melbourne, Australia.
Am J Med. 1995 Feb 27;98(2A):76S-88S. doi: 10.1016/s0002-9343(05)80082-8.
Hip fractures in men account for one third of all hip fractures and have a higher mortality than in women. The age-specific incidence of hip fractures is increasing so that the public health burden will increase out of proportion to the burden imposed by the increase in the numbers of elderly men in the community. Vertebral fractures are a public health problem of lesser magnitude in terms of morbidity, mortality, and cost, but they are debilitating and are seen commonly in clinical practice. (Forearm fractures should probably not be regarded as a public health problem.) The pattern of earlier gain/later loss of bone during ageing in healthy men is well documented. Peak bone mass is higher in men than women because men have bigger bones. Peak bone density is the same. The absolute 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. It is less because endocortical resorption is less, and periosteal formation is greater, in men. Bone loss may accelerate in elderly men and women (rather than decelerate), perhaps because endocortical resorption and increasing cortical porosity increase the effective surface available for resorption in cortical bone. Thus, bone fragility is less in men because (a) the cross-sectional surface of the vertebral body 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 bone density in men with fractures may be due to reduced peak bone density and bone loss. As found in women with spine fractures, men with fractures have smaller bone size. Bone loss occurs by reduced bone formation and increased bone resorption. Loss of connectivity appears to predominate in men with vertebral fractures; trabecular thinning appears to predominate in men with hip fractures. 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 be concomitants of ageing or may contribute to reduced bone-formation and bone loss. Men with vertebral fractures may be more deficient in growth hormone and insulin-like growth factor 1. Thy often have illness, hypogonadism, or illnesses associated with hypogonadism that should be sought with a high index of suspicion.(ABSTRACT TRUNCATED AT 400 WORDS)
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。髋部骨折的年龄特异性发病率正在上升,因此公共卫生负担的增加将与社区中老年男性数量增加所带来的负担不成比例。就发病率、死亡率和成本而言,椎体骨折是一个规模较小的公共卫生问题,但它们会使人虚弱,在临床实践中很常见。(前臂骨折可能不应被视为一个公共卫生问题。)健康男性在衰老过程中早期骨量增加/后期骨量丢失的模式已有充分记录。男性的峰值骨量高于女性,因为男性的骨骼更大。峰值骨密度相同。男性和女性在衰老过程中脊柱和髂嵴处小梁骨丢失的绝对量相似。男性的皮质骨丢失较少。这是因为男性的骨内膜吸收较少,而骨膜形成较多。老年男性和女性的骨丢失可能会加速(而非减速),这可能是因为骨内膜吸收和皮质骨孔隙率增加会增加皮质骨可用于吸收的有效表面积。因此,男性的骨脆性较小,原因如下:(a)椎体的横截面积较大;(b)小梁骨丢失占较高峰值骨量的百分比较小;(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密度降低和骨丢失。正如在脊柱骨折女性中所发现的那样,骨折男性的骨骼尺寸较小。骨丢失是由于骨形成减少和骨吸收增加所致。在椎体骨折男性中,连接性丧失似乎占主导;在髋部骨折男性中,小梁变薄似乎占主导。骨折男性是否由于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是衰老的伴随现象,也可能导致骨形成减少和骨丢失。椎体骨折男性可能生长激素和胰岛素样生长因子1缺乏更严重。他们常常患有疾病、性腺功能减退或与性腺功能减退相关的疾病,对此应高度怀疑并进行排查。(摘要截取自400字)