Bone histomorphometry in the pathophysiological evaluation of primary and secondary osteoporosis and various treatment modalities.
In normal individuals, peak bone mass is reached at 25-35 years of age and thereafter a decrease with age occurs in both sexes. An acceleration in the bone loss is observed in normal women at menopause. Because of either a low peak bone mass or a more pronounced bone loss with age or during menopause, some individuals reach the fracture threshold for bone mass and suffer spontaneous fractures. To understand the mechanism behind age related bone loss, one must recognize that bone in adults is continually renewed through internal reorganization by which bone is turned over by localized osteoclastic resorption followed by osteoblastic formation (remodelling). A total reconstruction of the resorptive and formative phase can be performed by histomorphometric methods applied on iliac crest bone biopsies and thereby give a detailed description of resorptive and formative events. By the remodelling process bone may be gained or lost by 3 mechanisms: 1. Reversible bone loss depending on the magnitude of the remodelling space, which is the amount of bone resorbed and not yet reformed during the remodelling sequence. 2. Irreversible thinning of the trabeculae due to a negative balance at the remodelling site. 3. Irreversible loss of whole trabecular elements caused by deep resorption lacunae perforating the trabecular plates. Although the bone mass is significantly reduced by 20-30% in postmenopausal osteoporotic patients with vertebral fractures compared with normal controls a substantial overlap exists. Our study and several other studies have shown that beside the slight reduction in trabecular bone volume significant differences in microstructure exist between osteoporotic patients and normal controls. These changes in structure are probably a consequence of trabecular plate perforations. Although osteoporotic patients in term of remodelling (bone turnover) are a very heterogeneous group, with patients having a low, normal and even increased bone turnover, no signs in the ongoing remodelling process was found in our study that could explain why these patients had developed osteopenia and changes in the trabecular structure. The bone balance was in the patients slightly negative but no different from the balance found in normal controls. The cause of osteoporosis may therefore be factors occurring earlier in life, maybe long before the manifestation of the disease. Bone mass at any age is the result of two variables--the amount of bone achieved during growth and the subsequent rate of bone loss. Peak bone mass at maturity may be of great importance in determining the risk of developing symptomatic osteoporosis.(ABSTRACT TRUNCATED AT 400 WORDS)
Steiniche
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Department of Pathology, Aarhus Amtssygehus, Aarhus University Hospital.
D000328:Adult; D000368:Aged; D000375:Aging / Q000473:pathology; D001581:Benzothiadiazines; D001842:Bone and Bones / Q000473:pathology* / Q000503:physiopathology; D002118:Calcium / Q000652:urine; D004232:Diuretics; D004967:Estrogens / Q000627:therapeutic use; D012968:Etidronic Acid / Q000627:therapeutic use; D005260:Female; D006801:Humans; D006961:Hyperparathyroidism / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D015663:Osteoporosis, Postmenopausal / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D049993:Sodium Chloride Symporter Inhibitors / Q000627:therapeutic use
D001581:Benzothiadiazines; D004232:Diuretics; D004967:Estrogens; D049993:Sodium Chloride Symporter Inhibitors; D012968:Etidronic Acid; D002118:Calcium