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Deterioration of Trabecular Architecture in Hypogonadal Men

Departments of Medicine (M.B., P.J.S.), Radiology (B.G., F.W.W., R.H.W., A.C.W., H.K.S.), and Bioengineering (B.G.), University of Pennsylvania; General Clinical Research Centers (B.Z.), Children’s Hospital of Philadelphia; and Hospital of the University of Pennsylvania (A.C.), Philadelphia, Pennsylvania 19104

Address all correspondence and requests for reprints to: Peter J. Snyder, M.D., 778 Clinical Research Building, 415 Curie Boulevard, Philadelphia, Pennsylvania 19104-6149. E-mail: pjs{at}pobox.upenn.edu.

Bone strength depends on trabecular architecture, characterized by interconnected plates and rods. In osteoporosis, the plates become fenestrated, resulting in more rods that deteriorate and become disconnected. In men, hypogonadism is a common cause of osteoporosis. To determine whether male hypogonadism affects trabecular architecture, we selected 10 men with severe, untreated hypogonadism, and for each hypogonadal man, we selected a eugonadal man matched for race and age. Trabecular architecture in the distal tibia was assessed by magnetic resonance microimaging. Two composite topological indices were determined: the ratio of surface voxels (representing plates) to curve voxels (representing rods), which is higher when architecture is more intact; and the erosion index, a ratio of parameters expected to increase upon architectural deterioration to those expected to decrease, which is higher when deterioration is greater. The surface/curve ratio was 36% lower (P = 0.004), and the erosion index was 36% higher (P = 0.003) in the hypogonadal men than in the eugonadal men. In contrast, bone mineral density of the spine and hip were not significantly different between the two groups. We conclude that male hypogonadism is associated with marked deterioration of trabecular architecture and to a greater degree than bone densitometry of the spine and hip suggests.

This work was supported by National Institutes of Health Grants MO1-RR00041 (to the General Clinical Research Center, University of Pennsylvania), M01-RR00240 (to the General Clinical Research Center, Children’s Hospital of Philadelphia), R01 AR41443 and T32 CA74781 (to F.W.W.), and T32 AR07481 (to P.J.S.); and by a grant from the Endocrine Fellows Foundation (to M.B.).

Abbreviations: CT, Computed tomography; FOV, field of view; µMRI, magnetic resonance microimaging; NEX, number of excitations; TR/TE, repetition time/echo time.

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