Of mice and men: pathophysiology of male osteoporosis

Abstract

In both old and young men osteoporosis is a severe but frequently neglected condition. This review deals with the multifactorial pathogenesis of impaired bone strength in men. Male bones are not only influenced by androgens, but, somewhat surprisingly – according to the current state of knowledge –female sex hormones may be the major players in calcified tissue remodelling. As a matter of principle, gender shapes bone geometry on a life-long basis. In men, age-dependant bone loss is outweighed by increased periosteal apposition. Contrary to women, the male gender-specific resorption pattern is mainly based on trabecular thinning. Therefore the connectivity remains rather intact, which again positively influences the biomechanical tissue properties and the resistance to fractures. Since affected patients often present with a family history of fractures or low bone density, the genetics of male osteoporosis is one of the main fields of interest in current bone research. Several gene polymorphisms involving the α1 chain of type 1 collagen (COLIA-1), aromatase, vitamin D receptor (VDR), low-density lipoprotein receptor-related protein 5 (LPR5) and the lactase phlorizin hydrolase (LCT) have recently been described. But apart from such exciting research novelties, the classical every-day violaters of both male and female bone health (vitamin D deficiency, low calcium intake and inadequate life-style) must still be taken into account.