Trabecular architecture can remain intact for both disuse and overload enhanced resorption characteristics

It is unknown what stimulus initiates the cascade of signaling processes Ibat make osteoctasts resorb bone at particular sites on the trabecular surface. It is thought that this must be relatod to mechanical disuse, bUt also the emergence of micro-damage in the tissue matrix. has been suggested as a control factor. However, the latter assumption creates a contradiction, as tbe locations of damage are those likely to be frequently high stressed in daily activity. Thus, osteoclasts would remove from the trabecular structure that material it needs most for maintaining strength. This is the more irrational because osteoblasts need much more time to repoir the structuml integrity, Iban osteoclasts need to reduce it. We have developed a FEA-based computer-simulation model which couples the morphological and mechanical effects of local bone metabolism to changes in trabecular architecture and density at large [Nature 404 (2000), in press], suitable to address the apparent contradiction. We asked the question of how alternative strain-based local stimuli fur osteoclasis to resorb bone would affect the maintenance and adaptation of architecture and mass at large. For this purpose, 5 different resorption characteristics were studied in the model: (I) resorption occurs spatially random, (11) resorption is enhanced where there is disuse, (III) resorption is strongly enhanced where there is disuse, (IV) resorption is enhanced where there are high strains, and (V) resorption is strongly enhanced where there are high strains. We found that the rates of remodeling, and structural adaptation to alternative loading, were higher for disuse-controlled resorption than for overload-controlled resorption. However, architecture and mass remained intact for all cases except (V). In the latter, strongly overload-enhanced process, the structure deteriorated as in osteoporotic bone; trabeculae became progressively thinner, nnd some were lost. We conclude that, given the potential of osteoblasts to fonn bone in highly strained areas, based on signals from osteocytes, osteoclastic resorption can be compensated for; the architecture remains stable witllin a wide margin of resorption characteristics, even when resorption is enhanced at locations where high strains are frequent. This explains the above contradiction. We hypothesize, however, that micro-damage in osteoporosis is likely to accelerate the process of architectural deterioration by enhanced ostecclast stimulation, creating instability in the control of the metabolic regulatory process. This may explain the occurence of spontaneous vertebral fractures in the elderly.