Bone hypertrophy and trabecular generation in Paget's disease and in fluoride-treated osteoporosis.
The replacement of lost trabeculae characteristic of postmenopausal osteoporosis is problematic, since a biological pathway has not been established for trabecular regeneration de novo in the healthy, intact, mature skeleton. Possible pathways for trabecular replacement may occur under pathological conditions, in particular those associated with bone hypertrophy. The topography of trabecular hypertrophy was compared in two groups of subjects with disease- or treatment-induced osteosclerosis following a period of atrophy. In Paget's disease and fluoride-treated osteoporosis a thickening of rarefied trabeculae in both was associated in Paget's disease only with an increase in the trabecular number and the transformation of a discontinuous arrangement into a more continuous network. The sequence seems to be a progression of intratrabecular resorption normally attendant upon a period of trabecular thickening. The failure of fluoride-treated bone in this respect, due to the unusual stability of the fluorotic skeleton, may provide insight to more effective anabolic regimens.
Aaron
J E
JE
WHO Collaborating Centre for Metabolic Bone Diseases, Department of Human Metabolism and Clinical Biochemistry, University of Sheffield, UK.
de Vernejoul
M C
MC
Kanis
J A
JA
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001706:Biopsy; D001857:Bone Matrix / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D005260:Female; D006801:Humans; D015576:Hyperostosis / Q000209:etiology*; D008875:Middle Aged; D010001:Osteitis Deformans / Q000473:pathology / Q000503:physiopathology*; D010024:Osteoporosis / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology*; D012969:Sodium Fluoride / Q000627:therapeutic use*
D012969:Sodium Fluoride